白袍恐懼症

IICP

1.      The Monro-Kellie hypothesis

cranial compartment= brain tissue+ CSF+ blood= 定值(1400 to 1700 mL)

2.      Introduction

Normal ICP<15 mmHg, if ICP> 20 mmHg: IICP

3.      Factor regulating cerebral blood flow

(1). Autoregulation

Cerebral perfusion pressure= MAP - ICP 

-為了保持cerebral blood flow(CBF)，腦中mean artery blood pressure維持在50-140mmHg。由MAP調節CPP。

(2). PaCO2

-血液中PaCO2正常約為35-40mmHg：下降時，身體消耗速度減慢，產生vasoconstriction，使CBF下降；反之上升時，要加速新陳代謝，產生vasodilatation，使CBF上升。

-降低PaCO2來降低血流量是臨床上最常用而且最快速的處理方法。

(3). PaO2

-氧氣分壓高時血管收縮；分壓低時血管擴張，與PaCO2作用相反。但PaCO2影響較大，所以臨床上主要以控制PaCO2來控制IICP，而非PaO2。

(4). Blood viscosity (Hct)

-Hct下降，blood viscosity下降，則血液流通性越好，CBF會上升。

-但如果RBC太稀，CBF會很快，但攜氧量卻下降，因此Hct最好保持在30-35，有足夠攜氧量又不會太濃稠。

(5). Body temperature

-每上升1℃，腦部新陳代謝加快，可使CBF上升約5~7%。但是，上升太多(40度以上)，反而會造成腦部傷害，如IICP。

(6). Neurogenic control

-交感神經興奮，造成vasoconstriction，CBF下降；副交感神經興奮，造成vasodilatation，CBF上升。但控制交感神經影響CBF是最沒效的方式，臨床少用。

PS.以Autoregulation和PaCO2最重要

4.      Etiology

(1)   Brain edema: acute hypoxic ischemic encephalopathy, large cerebral infarction, severe traumatic brain injury

(2)   Hydrocephalus:

(3)   Space-occupying lesion: tumor, hematoma

5.      IICP sign

Headache, vomiting, papilledema, conscious disturbance

6.      Cushing triad

bradycardia, respiratory depression, and hypertension

為克服增加的腦壓而把血打進腦中，故血壓上升；為增加心輸出，故心跳減慢。

7.      CT image

(1). Loss of sulci

(2). Compressed ventricles, loss of fourth ventricle

(3). Loss of cisterns

(4). Midline shift

8.      Indication of ICP monitor

(1). comatose head injury patients with Glasgow Coma Score (GCS) 3 to 8, and with abnormal cranial findings on CT scan.

(2). Comatose patients with normal CT scans have a much lower incidence of elevated ICP unless they have the following features at admission:

- Age >40 years

- Unilateral or bilateral motor posturing

- Systolic blood pressure (SBP) <90 mmHg

9.      Herniation

(1). Subfalcial

(2). Transtentorial

(3). foramen magnum

10.  Treatment

<GENERAL MANAGEMENT>

(1). Resuscitation: Head elevation, Hyperventilation to a PCO2 of 26 to 30 mmHg, Intravenous mannitol(1 to 1.5 g/kg)

(2). Monitoring and the decision to treat: The goal of ICP monitoring and treatment should be to keep ICP <20 mmHg and CPP between 60 and 70 mmHg

(3). Sedation: Propofol is useful

(4). Antiepileptic therapy: Seizures can both complicate and contribute to elevated ICP. If seizures are suspected; prophylactic treatment may be warranted in some cases.

<SPECIFIC THERAPIES>

(1). Mannitol: Osmotic diuretics reduce brain volume by drawing free water out of the tissue and into the circulation, thus dehydrating brain parenchyma. The effects are usually present within minutes, peak at about one hour, and last 4 to 24 hours.

(2). Other diuretics: Furosemide(0.5 to 1.0 mg/kg, IV), may be given with mannitol to potentiate its effect. (this effect can also exacerbate dehydration and hypokalemia.)

(3). Hyperventilation: Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of intracranial blood. The effect of hyperventilation on ICP is short-lived (1 to 24 hours); a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF.

(4). Barbiturates: reduce brain metabolism and cerebral blood flow

(5). Removal of CSF: When hydrocephalus is identified, a ventriculostomy (EVD) should be inserted.

(6). Decompressive craniectomy