2. CEREBROSPINAL FLUID
ā¢ CSF IS FOUND IN THE CEREBRAL VENTRICLES AND CISTERNS AND IN THE
SUBARACHNOID SPACE SURROUNDING THE BRAIN AND SPINAL CORD.
ā¢ MOST OF THE CSF IS FORMED BY THE CHOROID PLEXUSES OF THE CEREBRAL
(MAINLY LATERAL) VENTRICLES.
ā¢ IN ADULTS, NORMAL TOTAL CSF PRODUCTION IS ABOUT 21 ML/HR (500 ML/D),
YET TOTAL CSF VOLUME IS ONLY ABOUT 150 ML.
3. ā¢ CSF FLOWS FROM THE LATERAL VENTRICLES THROUGH THE INTRAVENTRICULAR
FORAMINA (OF MONRO) INTO THE THIRD VENTRICLE, THROUGH THE CEREBRAL
AQUEDUCT (OF SYLVIUS) INTO THE FOURTH VENTRICLE, AND THROUGH THE
MEDIAN APERTURE OF THE FOURTH VENTRICLE (FORAMEN OF MAGENDIE) AND
THE LATERAL APERTURES OF THE FOURTH VENTRICLE (FORAMINA OF LUSCHKA)
INTO THE CEREBELLOMEDULLARY CISTERN (CISTERNA MAGNA).
4. ā¢ FROM THE CEREBELLOMEDULLARY CISTERN, CSF ENTERS THE SUBARACHNOID
SPACE, CIRCULATING AROUND THE BRAIN AND SPINAL CORD BEFORE BEING
ABSORBED IN ARACHNOID GRANULATIONS OVER THE CEREBRAL HEMISPHERES.
ā¢ ABSORPTION OF CSF INVOLVES THE TRANSLOCATION OF FLUID FROM THE
ARACHNOID GRANULATIONS INTO THE CEREBRAL VENOUS SINUSES.
5.
6. ā¢ ACCORDING TO THE MONROE-KELLIE DOCTRINE THE CRANIAL VAULT IS A FIXED
SPACE OF ABOUT 1400 TO 1700 ML IN AVERAGE-SIZED ADULTS.
ā¢ IT CONTAINS THREE COMPARTMENTS: BLOOD (10 PERCENT ~150 ML),
CEREBROSPINAL FLUID (CSF) (10 PERCENT ~150 ML), AND BRAIN TISSUE (80
PERCENT ~1400 ML).
7. ā¢ IN ORDER TO MAINTAIN A CONSTANT ICP, ANY INCREASE IN THE VOLUME OF
AN INTRACRANIAL ELEMENT MUST BE EQUALLY COMPENSATED BY A DECREASE
IN THE VOLUME OF ANOTHER COMPONENT, OTHERWISE ICP WILL INCREASE.
8. ā¢ THE NORMAL SUPINE INTRACRANIAL PRESSURE IS 10ā15 MMHG, MEASURED AT A POSITION
EQUAL TO THE LEVEL OF THE FORAMEN OF MONRO.
ā¢ THE INTRACRANIAL PRESSURE IS DIRECTLY RELATED TO THE VOLUME OF THE INTRACRANIAL
CONTENTS WITHIN THE SKULL.
9. ā¢ INITIALLY, A SMALL VOLUME EXPANSION CAUSES ONLY A SLIGHT ELEVATION IN
ICP. CSF IS DISPLACED THROUGH THE FORAMEN MAGNUM INTO THE
PARASPINAL SPACE, BLOOD IS DISPLACED FROM THE INTRACRANIAL TO THE
EXTRACRANIAL VENOUS SYSTEM, AND THE BRAIN PARENCHYMA IS
COMPRESSED.
10. ā¢ HOWEVER, THE COMPLIANCE CURVE IS NONLINEAR; WHEN THESE MECHANISMS
ARE EXHAUSTED INTRACRANIAL COMPLIANCE (āVOLUME/āPRESSURE) FALLS
SHARPLY, AND EVEN SMALL INCREASES IN INTRACRANIAL VOLUME CAN LEAD TO
DRAMATIC ELEVATIONS IN ICP.
ā¢ THE PRESSURE-VOLUME RELATIONSHIP BETWEEN ICP, VOLUME OF CSF, BLOOD,
AND BRAIN TISSUE, AND CEREBRAL PERFUSION PRESSURE (CPP) IS KNOWN AS
THE MONROKELLIE DOCTRINE OR THE MONRO-KELLIE HYPOTHESIS.
ā¢ AS ICP REACHES 50 TO 60 MM HG, IT APPROACHES ARTERIAL PRESSURE IN THE
VESSELS OF THE CIRCLE OF WILLIS AND BRINGS ABOUT GLOBAL BRAIN ISCHEMIA.
11. CEREBRAL BLOOD FLOW AND PERFUSION
PRESSURE
ā¢ SYSTEMIC MEAN ARTERIAL PRESSURE (MAP) IS A MAIN FACTOR IN MAINTAINING
CEREBRAL PERFUSION. CEREBRAL PERFUSION PRESSURE (CPP), DEFINED AS THE
MEAN ARTERIAL PRESSURE (MAP) MINUS ICP (CPP = MAP- ICP) PLAYS AN
IMPORTANT ROLE IN ICP MANAGEMENT.
ā¢ NORMALLY CEREBRAL BLOOD FLOW (CBF) IS ABOUT 50 ML/100 G PER MINUTE
AND EQUALS TO CPP DIVIDED BY CEREBRAL VASCULAR RESISTANCE (CVR) (CBF
= CPP / CVR).
12. ā¢ THIS AUTOREGULATION MAINTAINS
CBF AT A CONSTANT LEVEL OVER A
WIDE RANGE OF CPPS (FROM 50 TO
150 MMHG). WHEN CBF FALLS BELOW
12 ML/100 G PER MINUTE,
IRREVERSIBLE ISCHEMIC INJURY
OCCURS .
ā¢ OPTIMALLY, CPP SHOULD BE KEPT
ABOVE 70 MMHG TO AVOID ISCHEMIA
AND BELOW 120 MMHG TO AVOID
HYPERPERFUSION
13.
14. CAUSES OF INCREASED INTRACRANIAL PRESSURE
ā¢ INTRACRANIAL MASS LESIONS.
ā¢ INCREASED CSF VOLUME.
ā¢ INCREASED BLOOD VOLUME (VASOGENIC EDEMA, BREAKDOWN OF TIGHT
ENDOTHELIAL JUNCTIONS WHICH MAKE UP THE BLOOD-BRAIN BARRIER (BBB).
17. SIGNS AND SYMPTOMS
ā¢ TWO MAJOR CONSEQUENCES OF ELEVATED ICP ARE HYPOXIC-ISCHEMIC INJURY
RESULTING FROM REDUCTION OF CPP AND CBF, AND MECHANICAL
COMPRESSION AND HERNIATION OF BRAIN TISSUE LEADING TO BRAIN DAMAGE
OR DEATH.
20. ICP MONITORING
ā¢ GUIDELINES FOR THE USE OF ICP MONITORING WERE ESTABLISHED FOR
TRAUMATIC BRAIN INJURY, AND FOR INCREASED ICP ASSOCIATED WITH
CONDITIONS OTHER THAN TRAUMA THE GUIDELINES ARE LESS CLEAR.
21.
22. INVASIVE ICP MONITORING DEVICES
ā¢ THERE ARE FOUR MAIN ANATOMICAL SITES USED IN THE CLINICAL MEASUREMENT
OF ICP: INTRAVENTRICULAR, INTRAPARENCHYMAL, SUBARACHNOID, AND EPIDURAL
[12]. EACH TECHNIQUE REQUIRES A UNIQUE MONITORING SYSTEM, AND HAS
ASSOCIATED ADVANTAGES AND DISADVANTAGES.
ā¢ INTRAVENTRICULAR CATHETERS
ā¢ INTRAPARENCHYMAL PRESSURE TRANSDUCERS
ā¢ SUBARACHNOID BOLTS
ā¢ EPIDURAL TRANSDUCERS
23.
24. ā¢ INTRAVENTRICULAR CATHETERS :
ā¢ THESE DEVICES ARE CONSIDERED THE GOLD STANDARD OF ICP MONITORING,
AND DIRECTLY CONNECT THE INTRACRANIAL SPACE TO AN EXTERNAL PRESSURE
TRANSDUCER.
ā¢ CONTINUOUS ICP MONITORING WITH INTERMITTENT CSF DRAINAGE OR
CONTINUOUS DRAINAGE WITH INTERMITTENT ICP MEASUREMENT.
ā¢ THE MAIN DISADVANTAGE IS THE HIGH RISK OF INFECTION (VENTRICULITIS OR
MENINGITIS) OCCURRING IN10-20% OF PATIENTS AND INCREASES
DRAMATICALLY AFTER 5 DAYS.
ā¢ BLOCKAGE, INCREASED RISK OF HEMORRHAGE, NECESSITY TO READJUST THE
TRANSDUCER POSITION WITH THE LEVEL OF THE PATIENTāS HEAD.
25. INTRAPARENCHYMAL PRESSURE TRANSDUCERS
ā¢ FIBEROPTIC OR ELECTRONIC PRESSURE TRANSDUCER AT THEIR TIP, AND ARE
INSERTED INTO THE BRAIN PARENCHYMA VIA A SMALL BURR HOLE DRILLED IN
THE SKULL.
ā¢ EASIER TO PLACE AND HAVE LOWER RISK OF INFECTION AND HEMORRHAGE
COMPARED TO INTRAVENTRICULAR CATHETERS
26. EPIDURAL TRANSDUCERS
ā¢ INSERTED DEEP INTO THE INNER TABLE OF THE SKULL AND REST AGAINST THE
DURA.
ā¢ HAVE A LOWER INFECTION RATE, BUT ARE PRONE TO MALFUNCTION,
DISPLACEMENT, AND BASELINE DRIFT AFTER MORE THAN A FEW DAYS OF USE.
ā¢ INACCURACY RESULTS FROM HAVING THE RELATIVELY INELASTIC DURA
BETWEEN THE SENSOR TIP AND THE SUBARACHNOID SPACE
ā¢ PATIENTS WITH COAGULOPATHY SUCH AS THOSE WITH HEPATIC
ENCEPHALOPATHY
27. ICP WAVEFORMS
ā¢ NORMAL ICP WAVEFORMS ARE SIMILAR TO THE ARTERIAL WAVEFORM, WITH A
FIRST PEAK (PERCUSSION WAVE) CORRELATING WITH SYSTOLE, A SECOND PEAK
(DICROTIC WAVE) CORRELATING WITH AORTIC VALVE CLOSURE, AND A THIRD
PEAK (TIDAL WAVE) CORRELATING WITH ANTEGRADE ARTERIAL FLOW DURING
DIASTOLE.
ā¢ AS INTRACRANIAL COMPLIANCE FALLS, THE MORPHOLOGY OF THE ICP
WAVEFORM ALSO CHANGES, IN THAT THE AMPLITUDE OF THE DICROTIC WAVE,
THE SECOND PEAK, INITIALLY EQUALS AND THEN EXCEEDS THE AMPLITUDE OF
THE PERCUSSION WAVE.
28.
29.
30.
31. ā¢ THE SPONTANEOUS CHANGES IN VENTRICULAR FLUID PRESSURE (VFP) CURVE
WERE OF TWO MAIN TYPES, PLATEAU WAVES AND RHYTHMIC OSCILLATIONS.
ā¢ LUNDBERG STATED THAT THE FORMER COULD CAUSE BOTH TRANSIENT AND
PERSISTENT DAMAGE TO THE BRAIN AND THEREFORE DIAGNOSIS, UTILISING A
VENTRICULAR CATHETER, AND PREVENTION OF SUCH PRESSURE VARIATIONS
WERE OF CLINICAL IMPORTANCE.
32. ā¢ A WAVES OR āPLATEAU WAVESā HAVE AMPLITUDES OF 50ā 100 MMHG, LASTING
5ā20 MIN. THESE WAVES ARE ALWAYS ASSOCIATED WITH INTRACRANIAL
PATHOLOGY (FIG. 1). DURING SUCH WAVES, IT IS COMMON TO OBSERVE
EVIDENCE OF EARLY HERNIATION, INCLUDING BRADYCARDIA AND
HYPERTENSION
33.
34. ā¢ B WAVES ARE OSCILLATING AND UP TO 50 MMHG IN AMPLITUDE WITH A
FREQUENCY 0.5ā2/MIN AND ARE THOUGHT TO BE DUE TO VASOMOTOR CENTRE
INSTABILITY WHEN CPP IS UNSTABLE OR AT THE LOWER LIMITS OF PRESSURE
AUTOREGULATION
35.
36. ā¢ C WAVES ARE OSCILLATING AND UP TO 20 MMHG IN AMPLITUDE AND HAVE A
FREQUENCY OF 4ā8/MIN. THESE WAVES HAVE BEEN DOCUMENTED IN HEALTHY
INDIVIDUALS AND ARE THOUGHT TO OCCUR BECAUSE OF INTERACTION
BETWEEN CARDIAC AND RESPIRATORY CYCLES.
37.
38. NORMAL ICP WAVEFORM
THE NORMAL ICP WAVEFORM CONTAINS
THREE PHASES:
ā¢ P1 (PERCUSSION WAVE) FROM ARTERIAL
PULSATIONS
ā¢ P2 (REBOUND WAVE) REFLECTS
INTRACRANIAL COMPLIANCE
ā¢ P3 (DICHROTIC WAVE) REPRESENTS VENOUS
PULSATIONS
39. NONINVASIVE ICP MONITORING
ā¢ SEVERAL METHODS HAVE BEEN EMPLOYED TO ESTIMATE INTRACRANIAL
PRESSURE, INCLUDING COMPUTED TOMOGRAPHY, MAGNETIC RESONANCE
IMAGING, TRANSCRANIAL DOPPLER SONOGRAPHY, NEAR INFRARED
SPECTROSCOPY, AND VISUAL-EVOKED POTENTIALS.
40. ā¢ TRANSCRANIAL DOPPLER (TCD) ULTRASONOGRAPHY
ā¢ TRANSCRANIAL DOPPLER (TCD) ULTRASONOGRAPHY, WHICH MEASURES THE
VELOCITY OF BLOOD FLOW IN THE BASAL CEREBRAL ARTERIES, SHOWS
CHARACTERISTIC CHANGES WITH INCREASING ICP.
ā¢ TCD CAN BE USED TO ESTIMATE ICP BASED ON CHARACTERISTIC CHANGES IN
WAVEFORMS THAT OCCUR IN RESPONSE TO INCREASED RESISTANCE TO CEREBRAL
BLOOD FLOW .
ā¢ IT ALLOWS THE ESTIMATION OF CPP THROUGH PULSATILITY INDEX (PI) [PI = PEAK
SYSTOLIC VELOCITY - END DIASTOLIC VELOCITY / MEAN FLOW VELOCITY]. IT HAS
EMERGED AS A SURROGATE MARKER FOR ICP, ESPECIALLY IN CASES, SUCH AS THOSE
OF SEVERE COAGULOPATHY WITH HEPATIC FAILURE.
41. ā¢ TCD PI IS A HELPFUL TOOL TO GUIDE THE USE OF HYPEROSMOLAR THERAPY IN
VARIOUS CONDITIONS WITH INTRACRANIAL HYPERTENSION .
ā¢ AS CPP FALLS, DIASTOLIC VELOCITY DECREASES AND PULSATILITY INCREASES,
REFLECTING INCREASED DISTAL VASCULAR RESISTANCE TO FLOW.
ā¢ IN INTRACEREBRAL HEMORRHAGE WITH SPACE OCCUPYING LESION,
LATERALIZED ASYMMETRIES IN TCD PULSATILITY INDEX CORRELATE WITH
COMPARTMENTALIZED ICP GRADIENTS .
42. ā¢ TCD SENSITIVITY FOR VASOSPASM VARIES BETWEEN 50 AND 100% AND IS
VESSEL-DEPENDENT DUE TO LOCATION AND SIZE, BUT HAS A SPECIFICITY OF
>90% AS COMPARED TO THE GOLD STANDARD OF DIGITAL SUBTRACTION
ANGIOGRAPHY.
43. OPTIC NERVE SHEATH DIAMETER
ā¢ A NUMBER OF STUDIES HAVE FOUND THAT DIAMETERS OF 5 TO 6 MM HAVE
THE ABILITY TO DISCRIMINATE BETWEEN NORMAL AND ELEVATED ICP IN
PATIENTS WITH INTRACRANIAL HEMORRHAGE AND TRAUMATIC BRAIN INJURY .
ā¢ LIMITATION TO ITS USE ARE PATIENTS WITH CHRONIC OCULAR DISEASE AND
MALIGNANT HYPERTENSION.
44.
45. MANAGEMENT
1. MAINTAIN ICP AT LESS THAN 20 TO 25 MM HG.
2. MAINTAIN CPP AT GREATER THAN 60 MM HG BY MAINTAINING ADEQUATE MAP.
3. AVOID FACTORS THAT AGGRAVATE OR PRECIPITATE ELEVATED ICP.
46.
47. SUMMARY OF SURGICAL
MANAGEMENT OF RAISED
INTRACRANIAL PRESSURE
ā EARLY EVACUATION OF FOCAL HAEMATOMAS: EDH, SDH
ā CEREBROSPINAL FLUID DRAINAGE VIA VENTRICULOSTOMY
ā DELAYED EVACUATION OF SWELLING CONTUSIONS
ā DECOMPRESSIVE CRANIECTOMY
48.
49. MANNITOL
MANNITOL IS THE MOST COMMONLY USED HYPEROSMOLAR AGENT FOR THE TREATMENT OF
INTRACRANIAL HYPERTENSION
INTRAVENOUS BOLUS ADMINISTRATION OF MANNITOL LOWERS THE ICP IN 1 TO 5 MINUTES WITH
A PEAK EFFECT AT 20 TO 60 MINUTES
MANNITOL USUALLY IS GIVEN AS A BOLUS OF 0.25 G/KG TO 1 G/KG BODY WEIGHT
WHEN URGENT REDUCTION OF ICP IS NEEDED, AN INITIAL DOSE OF 1 G/KG BODY WEIGHT
SHOULD BE GIVEN
WHEN LONG-TERM REDUCTION OF ICP IS NEEDED, 0.25 TO 0.5 G/KG CAN BE REPEATED EVERY 2
TO 6 HOURS
THE EFFECT OF MANNITOL ON ICP LASTS 1.5 TO 6 HOURS, DEPENDING ON THE CLINICAL
CONDITION .
50. HYPERTONIC SALINE
GIVEN IN CONCENTRATIONS RANGING FROM 3% TO 23.4%,
MECHANISM:-
CREATES AN OSMOTIC FORCE TO DRAW WATER FROM THE INTERSTITIAL SPACE OF THE BRAIN PARENCHYMA INTO THE
INTRAVASCULAR COMPARTMENT IN THE PRESENCE OF AN INTACT BLOOD-BRAIN BARRIER, REDUCING INTRACRANIAL
VOLUME AND ICP.
ADVANTAGES:-
HYPERTONIC SALINE HAS A CLEAR ADVANTAGE OVER MANNITOL IN HYPOVOLEMIC AND HYPOTENSIVE PATIENTS.
MANNITOL IS RELATIVELY CONTRAINDICATED IN HYPOVOLEMIC PATIENTS BECAUSE OF THE DIURETIC EFFECTS,
WHEREAS HYPERTONIC SALINE AUGMENTS INTRAVASCULAR VOLUME AND MAY INCREASE BLOOD PRESSURE IN
ADDITION TO DECREASING ICP.
ADVERSE EFFECTS
HEMATOLOGIC SUCH AS BLEEDING SECONDARY TO DECREASED PLATELET AGGREGATION AND PROLONGED
COAGULATION TIMES,
ELECTROLYTE ABNORMALITIES -HYPOKALEMIA, AND HYPERCHLOREMIC ACIDOSIS .
HYPERNATREMIA SHOULD BE EXCLUDED BEFORE ADMINISTERING HYPERTONIC SALINE TO REDUCE THE RISK OF
CENTRAL PONTINE MYELINOLYSIS.
51.
52. ā¢ FOR PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY, CARE FOCUSED ON
MAINTAINING MONITORED INTRACRANIAL PRESSURE AT 20 MM HG OR LESS WAS
NOT SHOWN TO BE SUPERIOR TO CARE BASED ON IMAGING AND CLINICAL
EXAMINATION.
ā¢ SURVIVAL AT 14 DAYS MUCH BETTER WITH ICP MONITORING !!!
53.
54. ā¢ IN ADULTS WITH SEVERE DIFFUSE TRAUMATIC BRAIN INJURY AND REFRACTORY
INTRACRANIAL HYPERTENSION, EARLY BIFRONTOTEMPOROPARIETAL
DECOMPRESSIVE CRANIECTOMY DECREASED INTRACRANIAL PRESSURE AND THE
LENGTH OF STAY IN THE ICU BUT WAS ASSOCIATED WITH MORE UNFAVORABLE
OUTCOMES.
55.
56. ā¢ AT 6 MONTHS, DECOMPRESSIVE CRANIECTOMY IN PATIENTS WITH TBI
AND REFRACTORY INTRACRANIAL HYPERTENSION RESULTED IN LOWER
MORTALITY AND HIGHER RATES OF VEGETATIVE STATE, LOWER SEVERE
DISABILITY, AND UPPER SEVERE DISABILITY THAN MEDICAL CARE