1、Intracranial Hypertension,张家涌 2012,Intracranial pressure,Intracranial pressure is the result of a constantly changing interplay between the CSF system, the cerebral blood volume contained in venous, capillary and arterial vessels and brain tissue with its associated intra-and extracellular fluid. Ea
2、ch of these systems exerts an influence and the end-result, at equilibrium, is called ICP.,Normal ICP,Brain tissue：85% neuron 500-700ml glial cell 700-900ml extracellular fluid 100-150ml CSF 10% 100-150ml CBF 2-7% 70-100ml,Intracranial pressure,Monro-kellie hypothesis The sum of the intracranial vol
3、umes of blood, brain, CSF, and other component is constant, and that an increase in any one of these must be offset by an equal decrease in another, or else pressure will rise.,The pressure-volume curve,ICP autoregulation,1 CSF and ICP CSF total 150ml volume formation rate 0.3-0.35ml/min ICP CSF is
4、producedCSF volumeICP ICP CSF is absorbed CSF volumeICP,2 brain tissue and ICP,3 cerebral blood flow(CBF) and ICP CPP=MAP- JVP =MAPICP,Effects of variations in CBF,Causes of raised intracranial pressure,Mass lesions intracranial haematoma,cerebral contusion, tumor,abscess Vascular factors passive ar
5、terial dilatation by loss of autoregulation and raised arterial blood pressure venous congestion by sinus occlusion Non-vascular factors hydrocephalus, edema,Mass lesions,tumor,hematoma,Vascular factors,CPP ：180mmHg - 50mmHg.,Contussion,lacerationg and edema,hydrocephalus,Presentation of IC-HTN,Head
6、aches Classically described as being worse in the morning (possibly due to hypoventillation during sleep) Often exacerbated by coughing, straining, or bending forward.,Presentation of IC-HTN,Vomiting Papilledema,Presentation of IC-HTN,Cushings triad 1 hypertension 2 bradycardia 3 respiratory irregul
7、arity,IC-HTN treatment measures,Goals: keep ICP60mmHg,IC-HTN treatment measures,IC-HTN treatment measures,“Second tier” therapy for persistent IC-HTN,High dose barbitureate therapy: initiate if ICP remains 20-25 mm Hg Hyperventilate to pCO2 = 25-30 mm Hg. Hypothermia Decompressive craniectomy: remov
8、al of portion of calvaria and /or large areas of contused hemorrhagic brain (makes room immediately; removes region of disrupted BBB). Controversial (may enhance cerebral edema formation). If contused, consider temporal tip lobectomy (no more than 4-5 cm on dominant side, 6-7 cm on non-dominant) (to
9、tal temporal lobectomy is probably too aggressive) or frontal lobectomy. Has not shown great therapeutic promise Hypertensive therapy,Brain Herniation,Shifts in brain tissue through rigid openings in the skull compress other structures of the CNS producing the observed symptoms.,一、小脑幕裂孔疝 （Transtento
10、rial herniation）,最常见的一种脑疝。颞叶的钩回、海马回和临近的舌回受颞叶或大脑半球占位的压迫，向内下移位疝入小脑幕裂孔，压迫中脑、动眼神经和后交通动脉等。,临床表现,动眼神经麻痹病理性瞳孔散大，光反射消失，眼球外展，眼睑下垂。 中脑受压意识障碍，对侧肢体瘫痪，自主运动少，肌张力增高，肌力减退腱反射亢进，锥体束征阳性。 进一步加重，昏迷加深，动眼神经核进一步受到损害，出现双侧瞳孔散大，双侧肢体瘫痪，去大脑强直。,亦称小脑扁桃体疝 后颅凹占位或幕上 占位引起的严重颅 内压高，导致小脑 扁桃体下移进入枕 大孔和锥管，使延 髓受压，延髓轴向 和偏向移位，神经 受到牵张。,二、枕大孔疝
11、（Foramen megnum herniation）,临床表现,颈神经根牵张 颈后部疼痛，颈项强直，强迫头位 四脑室激惹反复吐 后颅神经核功能紊乱，吞咽困难 ,呼吸、脉搏减慢，血压升高, 强迫头位。 进一步加重，脑脊液循环障碍。扁桃体充血、水肿、坏死以及咳嗽等用力动作，可使脑疝突然加重，昏迷，呼吸停止。,多见于一侧大脑半球 额顶区占位病变。扣 带回和临近的额回经 大脑镰的游离缘移向 对侧，大脑前动脉及 其分支胼周、胼缘动 脉可被挤压而部分堵 塞，引起大脑半球内 侧面的脑软化坏死， 出现对侧肢体偏瘫， 排尿障碍等。,大脑镰下疝,脑疝的治疗,脑疝是颅内压增高的严重后果，亦称颅压高危象必须紧急处理。 明确病变性质、部位 ，急诊手术去除病因 。 病因不明，按颅压高处理原则治疗，争取短期缓解，做好术前准备。,
