Respiratory variation of arterial pulse pressure (ZPP) Since the arterial pulse pressure (s ystolic minus diastolic pressure) is directly proportional to LV stroke volume, the magnitu de of \210\206PP has been proposed as a predictor of \202 uid responsiveness in patients equipped with an arterial catheter. The \210\206PP is calculated as the difference betwee n the maximal (PPmax) and the minimal (PPmin) value of pulse pressure over a single respira tory cycle divided by the average of the two values, and expressed as a percentage: ZPP (%) = (PPmax \200\223 PPmin)/((PPmax + PPmin)/2) x 100. In numerous categories of mechanicall y ventilated patients (septic shock, acute respiratory distress syndrome, cardiac surgery, liver transplantation, etc.), \210\206PP was demonstrated to be an accurate marker of \202 uid responsiveness. Threshold values of \210\206PP ranging from 10 to 17% have been r eported. Moreover, the \202 uid-induced decrease in \210\206PP correlates well with the percentage changes in cardiac output induced by 500ml \202 uid infusion. Thus, the \210 \206PP can be used not only to predict \202 uid responsiveness but also to assess the act ual haemodynamic response to volume infusion. Finally, \210\206PP better predicts \202 u id responsiveness than the systolic pres- sure variation or its \210\206down component. \200 How to detect \202 uid responsiveness? Because clinical evaluation is of poor value for d etecting \202 uid responsiveness, sophisticated parameters have been proposed to help the clinician in the therapeutic decision- making process. Static markers of cardiac preload Considering the Frank \200\223Starling relationship (stro ke vol- ume vs ventricular preload; Fig. 7.13.1), the response to volume infusion is more l ikely to occur when the ventricu- lar preload is low than when it is high. Stroke Volume no preload reserve Pulse contour-derived stroke volume variation Pulse contour cardiac output monitoring devices can con- tinuously measure and display stro ke volume variation (SVV) which represents the variation of pulse contour stroke volume ove r a \202 oating period of a few seconds. In patients fully adapted to their ventilator, S VV accurately predicts \202 uid responsiveness. Threshold values of SVV range between 9.5 and 12.5%. preload reserve Ventricular preload Fig. 7.13.1 Ventricular function curve demonstrating relationship between stroke volume and ventricular preload. 127 CHAPTER 7.13 Detection of \202 uid responsiveness from the lower limbs toward the intrathoracic compart- ment and thus increases cardiac prel oad. An increase in cardiac output or stroke volume in response to PLR is sug- gestive of t he presence of cardiac preload reserve and hence predictive of \202 uid responsiveness. B ecause of the short duration of this test ( 1min), a real-time cardiac out- put or stroke v olume measurement method is mandatory. In patients with spontaneous breathing activity and/ or cardiac arrhythmias, a PLR-induced increase (>10%) in descending aorta blood \202 ow ( oesophageal Doppler) or a PLR-induced increase (>12.5%) in pulsed Doppler stroke volume (ec hocardiography) can accurately predict \202 uid responsiveness. Respiratory variation of the peak Doppler aortic blood velocity (ZVpeak) Doppler echocardiography allows aortic blood velocity to be measured at the level of aortic annulus (left ventricle out \202 ow track). A value of \210\206Vpeak >12% is predictive of \202 uid responsiveness. \200 Respiratory variation of descending aorta blood velocity (ZABV) or blood \202 ow (ZABF) Oesophageal Doppler monitoring devices allow for the measurement of descending aorta blood velocity or blood \202 ow on a beat to beat basis. A value of \210\206ABF >18% is pre- d ictive of \202 uid responsiveness. Since the aortic diameter also varies over the ventila tory cycle, \210\206ABF is a better pre- dictor of \202 uid responsiveness than \210 \206ABV. \200 Conclusion Minimally invasive ( \210\206PP, SVV) as well as non-invasive dynamic parameters ( \210\206Vpeak, \210\206ABV, \210\206ABF, \210\206DIVC, \210\206Ppleth) testing the s ensitivity of the heart to changes in intratho- racic pressure during a mechanical breath c an accurately discriminate between responders and non-responders to \202 uid infusion. In the cases where these indexes are not interpretable (inspiratory efforts, cardiac arrhythm ias, low tidal volume), the response of stroke volume (or its surrogates) to PLR is helpful to predict \202 uid responsiveness. Respiratory changes in inferior vena cava diameter ( \210\206DIVC) The IVC diameter can be measured using echocardiogra- phy from short axis or long axis subc ostal views. A value of \210\206DIVC ((maximal diameter \200\223 minimal diameter))/mean of the two values) >12% is predictive of \202 uid responsiveness. \200 Superior vena cava (SVC) collapsibility The diameter of the SVC can be measured using tran- soesophageal echocardiography. A value of SVC collapsibil- ity (difference between maximal and minimal diameter divided by maximal diameter) >36% allowed excellent pre- diction of \202 uid responsiveness. \200 Further reading Feissel M, Michard F, Mangin I, et al. Respiratory changes in aortic blood velocity as an indicator of \202 uid responsiveness in ventilated patients with septic sh ock. Chest 2001; 119: 867 \200\22373. Respiratory changes in pulse oxymetry plethysmo- graphic waveform amplitude ( \210\206Pplet h) Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vena cava dia meter as a guide to \202 uid therapy. Intensive Care Med 2004; 30: 1834 \200\2237. A value of \210\206Ppleth >14 \200\22315% is predictive of \202 uid respon- siveness in mechanically ventilated patients. Feissel M, Teboul JL, Merlani P, et al. Plethysmographic dynamic indices predict \202 uid responsiveness in septic ventilated patients. Intensive Care Med 2007; 33: 993 \200\2239. Limitations of using heart \200\223lung interaction indexes \200 Michard F, Teboul JL. Predicting \202 uid responsiveness in ICU patients: a critical analysis of the evidence. Chest 2002; 121: 2000 \200\2238. Volume responsiveness is a physiological phenomenon related to a normal preload reserve. Th us, detecting volume responsiveness must not systematically lead to the decision of infusin g \202 uid, in particular in the absence of clinical or biological signs of tissue hypope rfusion. The respiratory variation of surrogates of stroke volume cannot be used to assess \202 uid responsiveness in patients receiving a tidal volume <7ml/kg, in patients with sp onta- neous breathing activity and in patients with arrhythmias (except for respiratory var iation of vena cava diameter). Monnet X, Rienzo M, Osman D, et al. Esophageal Doppler monitor- ing predicts \202 uid res ponsiveness in critically ill ventilated patients. Intensive Care Med 2005; 11: 1195 \200 \223201. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts \202 uid responsiveness in the critically ill. Crit Care Med 2006; 34: 1402 \200\2237. Natalini G, Rosano A, Taranto M, et al. Arterial versus plethysmo- graphic dynamic indices to test responsiveness for testing \202 uid administration in hypotensive patients: a cli nical trial. Anesth Analg 2006; 103: 478 \200\22384. Preisman S, Kogan S, Berkenstadt H, et al. Predicting \202 uid res- ponsiveness in patien ts undergoing cardiac surgery: functional haemodynamic parameters including the respiratory variation test and static preload indicators. B J Anaesth 2005; 95: 746-55. Vieillard-Baro n A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004; 30: 1734 \200\2239. Passive leg raising In the cases where the dynamic indices using heart \200\223lung interac tion cannot be used (see above), the passive leg raising (PLR) maneuver can be used as a te st to detect \202 uid responsiveness. Indeed, lifting the legs by 45 from the horizonta l position induces a gravitational transfer of blood This page intentionally left blank 129 Chapter 8 Neurological monitoring Chapter contents Intracranial pressure monitoring 130 Intracranial perfusion 132 EEG and CFAM monitoring 134 Other forms of neurological monitoring 138 130 A EYNON Intracranial pressure monitoring Introduction In adults, the normal resting intracranial pressure (ICP) is 0 \200\22310mm Hg . ICP may rise to 50mm Hg or so during strain- ing or sneezing, with no impairment in funct ion. It is not, therefore, ICP alone that is important but rather the inter- pretation of t he measurement in pathological conditions. Many of the clinicopathological changes associat ed with brain injury are the result of pressure differences between the intracranial compar tments, with consequent shift of brain structures, rather than the absolute level of ICP. T he deterioration in conscious level accompanying eleva- tion in ICP is probably caused by d ownward displacement of the diencephalon and midbrain structures. Herniation of the tempora l lobe between the brainstem and the tento- rial edge into the posterior fossa (tentorial o r uncal hernia- tion) causes pupillary dilatation, ptosis, limitation of upgaze and extenso r posturing. Tonsillar herniation occurs when the tonsils of the cerebellum herniate throug h the foramen magnum into the spinal canal. This causes compression of the midbrain with ch anges in blood pressure, pulse rate and respiratory pattern. Cushing \200\231s response, th e combina- tion of hypertension and bradycardia, is seen in roughly 1/3 of cases of tonsill ar herniation. Fig. 8.1.1 Common techniques for measuring ICP. Indications for ICP monitoring The Brain Trauma Foundation recommends ICP monitor- ing in a ll patients with a closed head injury and a Glasgow Coma Score (GCS) of \211 8 and either (1) an abnormal CT scan or (2) a normal scan and the presence of two of the following three risk factors: age >40 years, unilateral or bilateral motor posturing or a systolic blood p ressure <90mm Hg. These patients have a roughly 60% chance of having raised ICP. Both an el evated ICP and an inadequate cerebral perfusion pressure (CPP; see Chapter 8.2) have been s hown to correlate with poorer outcome following traumatic brain injury. The optimal levels for the mainte- nance of ICP and CPP are still debated, but most recom- mend keeping ICP <2 0 \200\22325mm Hg and CPP >60mm Hg. Monitoring of ICP may be useful in other conditions. Mo rtality is improved if ICP is measured in patients who are comatose following intracerebral hemorrhage, and an elevated ICP is a poor prognostic factor in patients with aneurysmal su barachnoid hemorrhage. ICP monitoring in anoxic injury following cardiac arrest or near dro wning may be useful in guiding prognosis. ICP measurement may also be of use in hepatic enc ephalopathy, bacterial meningitis, encephalitis and in conditions such as hydro- cephalus o r benign intracranial hypertension. ICP monitor- ing in acute stroke is of little bene \201 t over clinical monitoring alone. pressure prior to insertion. Intraparenchymal monitors are usually inserted into the non-do minant frontal lobe, or the dominant frontal lobe if the non-dominant lobe is the primary s ite of injury. Intraventricular catheters These allow measurement of ICP as well as drainage of cerebrospi nal fluid (CSF) to help relieve raised ICP. Placement can be done at craniotomy or through a burr hole. Simple ventriculostomies are tunneled subcutane- ously to reduce the risk of i nfection and are connected to an external pressure transducer placed at the level of the fo ramen of Munro or, for clinical purposes, the external auditory meatus. Bolt-drains are lar ger in diameter and have a pressure transducer within their lumen. They are placed through a hole drilled in the skull vault and secured using a bolt screwed into the skull. Ultrasou nd or stereo- tactic guidance is used to direct the catheter if the ventri- cles are small, whereas normal or large ventricles can usually be found \200\230free-hand \200\231. ICP i s measured by a strain gauge and the trace is generally of better quality and undamped comp ared with a ventriculostomy with an external transducer. Complications of ICP monitoring The transducer drift of modern intraparenchymal moni- tors is small, infection rates are low and there is no need to change them routinely if prolonge d monitoring is required. The risk of signi \201 cant intracranial bleeding requiring drai n- age is <1%. Tunneling of simple ventriculostomies helps to reduce bacterial colonization and ventriculitis. The use of antibiotic-coated or silver-impregnated catheters may also h elp to reduce infection rates. With bolt-drains, the ICP should not be measured if the drai n is open. This leads to a pressure gradient from one end of the drain to the other that is not always uniform. If drainage holes are partially blocked, a pressure gradient develops between the outside and the inside. Catheters with a transducer within them may then undere stimate ICP. Methods of measuring ICP The two most commonly used techniques for measuring ICP are intrap arenchymal monitors and intraventricular catheters (Fig. 8.1.1). Intraparenchymal monitors These are placed via a small incision in the scalp. A hollow bolt is then screwed into the skull such that it penetrates both tables. A 20G spinal needle is passed down the lumen of the bolt to puncture the dura. The transducer is then placed thro ugh the lumen of the bolt, 5mm into the brain parenchyma. The monitor should be zeroed to a tmospheric 131 CHAPTER 8.1 Intracranial pressure monitoring ICP in normal and pathological conditions The normal ICP trace looks similar to an arterial trace (Fig. 8.1.2A). The three peaks are: P1 \200\224the percussion wave caused by the art erial pressure being transmitted from the choroid plexus to the ventricle; P2 \200\224the t idal wave thought to be due brain compliance; and P3 \200\224the dicrotic wave due to aorti c valve closure. Plateau waves are always pathological and indicate greatly reduced cerebral compliance. B w aves occur at cycles of 0.5 \200\2232/min and can be seen in normal individuals (Fig. 8.1.3 ). ICP rises to levels 20 \200\22330mm Hg above baseline and then falls sharply. Absence of B waves following head injury is a poor sign and may indicate poor autoregulation. C waves are of little clinical importance. They occur with a frequency of 4 \200\2238/min and are synchronous with Traub \200\223Hering \200\223Meyer variations in blood pressure. Fig. 8.1.3 Lundberg pressure waves. Although ICP monitoring can be safely performed in non-neurosurgical centers, outcome from severe brain injury is better if patients are managed on specialized units rather than in a district general hospital. NICE guidance states that all patients with a severe head injur y should be managed in specialized centers even if the patient does not require immediate n eurosurgery. Protocols to manage severe head injuries have resulted in reduced mortality an d improved functional outcome. Rapid access to specialist neurosurgical and non-surgical th erapies such as induced hypertension, hypothermia, decompressive craniectomy and barbiturat e coma are not generally available outside the specialist centers. Fig. 8.1.2 Intracranial pressure waveforms. If intracranial volume increases, the ICP wave shows an ini- tial increase in amplitude alt hough the mean ICP remains little changed. As brain compliance reduces, the P2 compo- nent of the pressure wave exceeds P1, with the wave becoming broader (Fig. 8.1.2B). Lundberg des cribed \202 uctuations in ventricular pressure in humans in 1960. Lundberg A waves or pla teau waves are slow vasogenic waves seen in patients with critical perfusion (Fig. 8.1.3). They may reach 50 \200\223100mm Hg high and last 5 \200\22320min. Plateau waves can cause c ritical cerebral ischaemia within minutes and are thought to result from spontaneous reduct ions in arterial blood pressure resulting in cerebral vasodilatation. This increases ICP, l eading to further reduc- tions in cerebral perfusion until maximal cerebral vasodilata- tio n occurs and the wave plateaus. Termination of these waves may occur if arterial blood pres sure is increased. Further reading Huang SJ, Hong WC, Han YY, et al. Clinical outcome of severe head injury us ing three different ICP and CPP protocol-driven therapies. J Clin Neurosci 2006; 13: 818 \200\22322. National Institute of Health and Clinical Excellence. Head injury: triage, assessment, inve stigation and early management of head injury in infants, children and adults (partial upda te). 2007. http://www.nice.org.uk The Brain Trauma Foundation. The American Association of Neurological Surgeons. Management and prognosis of severe traumatic head injury. J Neurotrauma 2000; 17: 449 \200\22327. 132 A EYNON Intracranial perfusion Introduction The brain receives 15% of the cardiac output (50ml/ 100g/min) and consumes 20 % of total body oxygen supply. The gray matter of the brain, which consists primarily of th e neuronal cell bodies and synapses, has a higher blood flow compared with the white matter , which consists largely of \201 bre tracts. Critical cerebral blood \202 ow (CBF) is a round 20ml/100g/min, with the EEG becoming isolelectric at 15ml/100g/min. Brain perfusion d epends on the difference between MAP and cerebral venous pressure (cerebral perfusion press ure or CPP). As the latter is dif \201 cult to measure, ICP is used as a surrogate. Systemic factors Carbon dioxide CBF increases by 3 \200\2234% for each mm Hg increase in pC O2. The responses to changes in pCO2 occur rapidly, within 30s, and are thought to relate t o changes in extracellular or interstitial H+ concentrations. Tight control of pCO2 is esse ntial if CPP is critical; increases in CO2 cause vasodila- tation and increased ICP, wherea s decreases in pCO2 below 4kPa have been shown to result in vasoconstriction suf \201 cien t to precipitate cerebral ischaemia. Oxygen CBF is not affected by changes in paO2 within the normal range but levels <50mm Hg ( 6.65kPa) result in cerebral vasodilatation and increases in CBF. Below 30mm Hg (4kPa), CBF is roughly doubled. Again, this will result in an increase in ICP. CPP = MAP \200\223 ICP Regulation of cerebral perfusion Autoregulation (myogenic regulation) Autoregulation ensure s that CBF remains constant between MAPs from 60 to 160mm Hg (Fig. 8.2.1). The trigger for autoregulation is CPP, with re \202 ex vasoconstriction occurring in response to increases in CPP, and vasodilatation occurring in response to decreases in CPP. Above and below the values where autoregulation is effec- tive, the relationship between CBF and MAP is linear such that \202 ow is pressure dependent. Autoregulation may be impaired by hypoxia, ischa emia, hypercapnia, trauma and certain anesthetic agents. How it is impaired is likely to va ry between conditions, between patients and even in the same patient at different times in the pathological process. Temperature Brain cCMRO2 is increased by 8% for each degree Celsius increase in temperature . Outcome from brain injury has been inversely correlated with elevation in body tempera- t ure. Cooling allows the brain to tolerate periods of low blood \202 ow. Although applicat ion of cooling to an unselected group of patients with head injury has been shown to be ine ffective, its use is widespread for the control of elevated ICP. Similarly, cooling has bee n shown to improve neuro- logical outcome following resuscitation from out-of-hospital card iac arrest (from pulseless VT or VF). Anesthetic agents Thiopentone is a potent cerebrovasoconstrictor and reduces both CBF and I CP. It has been used as a cerebral protection agent for patients with resistant elevations in ICP, and is currently being compared against decompres- sive craniectomy as a rescue tre atment (www.RESCUEicp. com). Propofol is similar to barbiturates with regard to its cerebro vascular effects but causes greater systemic haemo- dynamic depression. Ketamine causes sig ni \201 cant vasodila- tation with increases in both CBF and ICP. CMRO2 is little changed and there is a theoretical risk of seizures. Volatile agents are all cerebrovasodilators, t hus increasing CBF and ICP to varying degrees. They also decrease CMRO2. Measurement of CBF Because of the dif \201 culties in measuring CBF at the bedside, it is not routinely monitored for the majority of brain- injured patients. CPP is used as a simpl er measure with the recommendation that it be maintained above 60mm Hg. A number of other t echniques allow estimation of either regional CGF or cerebral metabolism. Transcranial Doppler sonography Transcranial Doppler sonography (TCDs) allows calcula- tion of the \202 ow velocity of red cells in the major vessels of the circle of Willis. The t echnique may be applied continu- ously or intermittently. Most commonly, the middle cerebra l artery is studied as this carries 75 \200\22380% of the carotid blood \202 ow. TCD meas ures velocity rather than \202 ow. Although absolute CBF cannot be measured, relative cha nges in CBF can be measured. Widespread use of the technique is limited by the technical ex pertise required. TCD measurements are most commonly used to detect vasospasm following sub arachnoid hemorrhage. Clinically signi \201 cant vasospasm occurs in 20% of cases. Vasospa sm is Fig. 8.2.1 Regulation of cerebral perfusion. (A) Flow \200\223metabolism coupling. (B) Auto regulation in the normal adult and in a hypertensive adult. Flow \200\223metabolism coupling Flow \200\223metabolism coupling is the direct relationshi p of the metabolic activity of the brain to CBF (Fig. 8.2.1). The precise mechanisms that c ontrol \202 ow \200\223metabolism coupling are unknown but may involve a variety of media tors such as acetylcholine, serotonin, nitric oxide and substance P. 133 CHAPTER 8.2 Intracranial perfusion generally considered present when either the \202 ow velocity exceeds 120cm/s or the Lind egaard ratio (the ratio between the velocity in the middle cerebral artery and that in the ipsilateral carotid artery) exceeds 3. The technique can also be used to determine cerebral autoregulation and CO2 reactivity following head injury. Loss of autoregulation and CO2 re activity are poor prognostic indicators. TCD can also be used to measure the pulsatility in dex which correlates with ICP. of the sample with extracerebral blood, speed of sampling, malpositioning of the catheter a nd the position of the patient \200\231s head. Up to half of desaturations <50% may repre- sent false-positive readings. SjvO2 monitoring allows detection of episodes of desatu- rati on associated with increases in ICP. A high frequency of desaturations has been correlated with a poor outcome. Monitoring of SjvO2 allows guidance of hyperventilation strategies and helps to distinguish between hyperaemia (when the SjvO2 is high) and vasospasm (when the S jvO2 is low) in patients following subarachnoid hemorrhage. Jugular venous catheters may al so be used to measure CBF using thermodilution. Jugular venous bulb oximetry Jugular venous oximetry (SjvO2) provides a way of intermit- te ntly or continuously measuring cerebral oxygenation and metabolism. As CBF and CMRO2 are cl osely coupled, CBF can be determined using the difference in arteriovenous oxygen content ( AVDO2) between the arterial system and the jugular vein. Both SjvO2 and AVDO2 are global me as- ures and cannot be used to detect regional ischaemia. Evidence from PET scanning sugges ts that 13% of the brain must become ischaemic before SjvO2 levels fall below 50%. Radiological techniques Various radiological techniques can be used to assess cer- ebral pe rfusion and physiology. Although their use is not widespread, they are helping to de \201 ne the physiological changes that occur in disease and can be used to direct therapy. AVDO2 = Hb x 1.39 (SaO2 \200\223 SjvO2) (ignoring the amount of dissolved O2) Further reading Bhatia A, Gupta AK, Neuromonitoring in the intensive care unit. 1. Intracra nial pressure and cerebral blood flow monitoring. Intensive Care Med 2007; 33: 1263 \200 \22371. Normal values of SjvO2 range from 60 to 75% and for AVDO2 from 2.2 to 3.3 mol/ml. A cathet er is inserted into the internal jugular vein in a cephalad direction using the Seldinger t echnique. The tip of the catheter should be level with the mastoid air cells on a lateral s kull X-ray. The accuracy of jugular venous sampling can be affected by contamination Bhatia A, Gupta AK. Neuromonitoring in the intensive care unit. 2. Cerebral oxygenation mon itoring and microdialysis. Intensive Care Med 2007; 33: 1322 \200\2238. Coles JP. Imaging after brain injury. Br J Anaes 2007; 99: 49 \200\22360. 134 A EYNON EEG and CFAM monitoring Electroencephalogram The electroencephalogram (EEG) represents the summa- tion of the elect rical activity of the brain as recorded from the scalp. Most of the recorded activity arise s from the pyramidal neurons of the cerebral cortex. The electrodes are placed according to an internationally recognized system (the 10 \200\22320 electrode system). The pattern of electrodes is called a montage. Seizures and pseudoseizures Staus epilepticus (SE) is a medical emergency. Mortality is 10 %, with deaths directly attributable to SE, rather than the underlying condition that provo ked the seizures, being 2%. 20 \200\22330% of SE is refractory to \201 rst-line measures and it is these that more commonly require general anesthesia to control the seizures and transfer to ICU for manage- ment of the airway and ventilation. The EEG is an impor- tant t ool in the management of both SE and pseudostatus. With seizures, the EEG shows rhythmic sp ike and wave activity that may be focal or generalized. Once general anesthesia is induced for refractory SE, EEG monitoring is desirable as the patient may enter a drug- induced com a with little evidence of convulsions but con- tinue to have repeated seizures (non-convuls ive status epilepticus, NCSE). A number of EEG patterns have been described in NCSE. The EE G allows titration of anesthetic drugs and the use of alternative agents if seizure control is not obtained. NCSE should be considered in patients with unexplained coma or alteration in their mental state, with or without motor signs such as facial myoclonus or nystagmus. Myoclonic SE is well recognized following anoxic injury, especially in patients resuscitate d from cardiac arrest. The EEG usually shows the myoclonic jerking to be associated with ge neralized, repetitive spikes, sharp waves or triphasic waves occurring at roughly 1s interv als. The prognosis of patients with myoclonic epilepsy associated with anoxic injury is ext remely poor. Pseudostatus due to psychogenic problems is surprisingly common, with up to 25 % of patients referred to ICU for the management of refractory seizures having pseudostatus rather than SE. Patients may have received a previous diag- nosis of epilepsy and the cond ition is often refractory to \201 rst-line therapy (indeed they often show little respons e to very high doses of benzodiazepines), resulting in the need for general anesthesia and ventilation. The EEG allows rapid diagnosis and withdrawal of inappropriate therapy; patien ts with pseudostatus may have a well-developed alpha rhythm, which can be assessed by passi ve opening and closing of the eyes. It is essential that the request for EEG details concer ns regarding the diagnosis, as <15% of the normal population may have non-speci \201 c abn ormalities and there is a danger that the EEG is overinterpreted. Such patients must be han dled sensitively and referred for appropriate support. CFM/CFAM Cerebral function monitors (CFMs) and cerebral function analyzing monitors (CFAMs) are automated EEG processors. The CFM produces a single trace of total power varying with both amplitude and frequency of raw EEG data. The CFAM produces displays of both amplitude and frequency. Both are commonly used as simpler measures of brain electrical activity comp ared with the EEG. EEG terminology The EEG is interpreted according to four main criteria: 1 Frequency The com ponent waves of the EEG are classi \201 ed according to their respective frequencies (Table 8.3.1). 2 Amplitude Most EEG activity is between 20 and 200 V. 3 Location Multi-channel EEG allows determination of whether activity is localized or generalized. Most CFM/CFAM devices are t wo channels only. 4 Paradoxical activity This refers to bursts of abnormal activity. Table 8.3.1 Clinical interpretation of EEG waves Wave Frequency (Hz) Clinical situation beta 13 \200\22330 Found mainly in the frontotemporal regions. Beta is the dominant frequency when awake and t he main frequency in drug-induced coma. Seen in the occipital cortex when awake but with ey es closed. Wanes when eyes opened. Hypoxia or brainstem lesions can produce generalized alp ha waves that are unchanged with stimulation. Equally dominant with alpha in children but r educes as ageing occurs. 10 \200\22315% of adults have theta activity in the temperoparieta l regions. alpha 9 \200\22312 Diagnosis of speci \201 c neurological conditions \200 Creutzfeldt \200\223Jakob disease This is characterized by periodic sharp wave complexes. \200 Herpes simplex encephalitis Commonly, patients exhibit periodic, lateralized epilepti- theta 4 \200\2238 delta 0 \200\2234 Occasional delta waves are seen in the awake adult. High voltage delta waves are seen in me tabolic encephalopathies of any cause. form discharges in the temporal lobe area. Subacute sclerosing panencephalitis Patients show paroxysmal bursts of activity in the 2 \200\2233Hz region. Raised ICP Increases in ICP are commonly associated with both partial and generalized seizu res. Prophylactic anticonvulsants are commonly used in cases of severe brain injury with an ticipated seizure potential. The optimum duration of Clinical use in ICU Continuous EEG monitoring is dif \201 cult in the ICU. High frequency electrical noise is generated by an array of equipment. Ventilators, nursing procedures and physio- therapy produce mechanical noise. 135 CHAPTER 8.3 EEG and CFAM monitoring Fig. 8.3.1 EEG frequencies of patients suffering status epilepticus following out-of-hospit al cardiac arrest. Fig. 8.3.2 EEG frequencies of a patient undergoing burst suppression with thiopentone. 136 A EYNON also been used as a prognostic indicator in patients who remain comatose following injury. Burst suppression, low voltage delta activity and a generally low voltage EEG are all poor prognostic indicators. However, EEG patterns that appear more benign do not necessarily cor relate with a good outcome. anticonvulsant use and the incidence of seizure activity in unconscious patients are still unclear. Barbiturate coma is one of the rescue treatments available for intractable, raised ICP when other therapies have failed. The patient is fully loaded with IV barbiturate to p roduce an isoelectric EEG. A maintenance infusion of barbiturate is then continued and titr ated to allow only one or two bursts of activity per screen on the EEG (burst suppression) (Fig. 8.3.2). Therapy is usually continued for a number of days before gradual withdrawal. The use of barbiturate coma is currently being compared with decompressive craniec- tomy in a phase III clinical trial (www.RESCUEicp.com). Further reading Brenner RP. EEG in convulsive and non-convulsive status epilepticus. J Clin Neurophysiol 2004; 21: 319 \200\22331. Prognosis An isoelectric EEG is one of the additional tests suggested in the USA for con \201 rmation of brain death. The EEG has This page intentionally left blank 138 A EYNON Other forms of neurological monitoring Tissue metabolism Brain tissue oxygenation The Licox monitor (GMS, Kiel-Mielkendorf, German y) allows measurement of brain tissue oxygenation that can be used in conjunction with othe r monitoring modalities to measure the adequacy of cerebral perfusion. The probe is inserte d either via a single-lumen bolt, or via a triple-lumen bolt with both an ICP monitor and a microdialysis catheter. Oxygen diffuses from the tissue into an inner electrolyte chamber in the catheter which generates an electric current using a polarographic electrochemical s ensor. The probe measures tissue oxygenation from an area of 15mm3 around the tip. The ris ks of infection and signi \201 cant haemor- rhage associated with the technique are low. N ormal brain tissue oxygen values range from 25 to 30mm Hg. Levels <20mm Hg have been report ed following head injury and levels <5mm Hg are associated with increased mortality. Improv ements in mortality and functional outcome have been reported in patients treated with ther apy aimed at maintaining a brain tissue oxygen level >25mm Hg compared with patients treate d with a tradi- tional ICP/CPP-guided therapy. (primarily iron in oxyhaemoglobin and deoxyhaemoglobin, and copper in cytochrome AA3). Chan ges in the concen- tration of near-infrared light as it passes through these compounds can be measured, and this allows calculation of the oxidation status. Generally, optodes are pl aced 4 \200\2237cm apart on the scalp. Light waves of 700 \200\2231000nm can penetrate the scalp, skull and brain to a depth of a few centimeters, allowing illumi- nation of a volume of 10ml of brain. Normal values of oxygenated hemoglobin are 60 \200\22380%. NIRS has bee n used to monitor patients with brain injury or intracranial haem- orrhage, and patients un dergoing carotid endarterectomy. The major limitation to its use is the dif \201 culty in distin- guishing intracerebral and extracerebral tissues. NIRS is able to follow trends in oxygenation in individual patients. Laser Doppler \202 owmetry Doppler change of laser light can be used to measure movement of red cells within the brain microcirculation. A small Doppler probe is placed within the brain tissue itself. It can obviously only measure CBF within a small area of brain tissue. It has been used experimentally to assess therapeutic interventions, to detect ischaemia a nd to assess CO2 reactivity and autoregulation following head injury. Microdialysis Microdialysis involves placement of a \201 ne catheter into the brain paren chyma. Dialysis \202 uid is continuously perfused through the catheterm which is lined wi th a dialysis mem- brane, typically with a molecular weight cut-off of 20kDa. Low molecula r weight substances cross the membrane and their concentrations can be measured in the dial ysate. Unless there is total equilibration, the concentration of molecules in the dialysate will be lower than that in the extracellular \202 uid. The proportion of molecule recov- ered depends on the membrane size, membrane area, diffusion speed of the molecule and the rate of \202 ow of the dialysate. Glucose, lactate, glutamate, glycerol and the lactate/p yruvate ratio have all been used as markers of cerebral metabolism. Larger membrane sizes a llow measurement of polypep- tides and cytokines that may be implicated in the damage or re pair processes. A recent consensus statement sug- gests that catheters should be placed in the right frontal region in patients with diffuse head injury, in the area of brain at risk in patients with subarachnoid hemorrhage, and in the penumbral area and a second catheter in normal brain in patients with focal lesions. The lactate/pyruvate and lactate/glucose ra tios are sensitive markers of tissue hypoxia/ischaemia. A high lactate/pyruvate ratio corre lates with the severity of injury and outcome in head injury. Alterations in these levels m ay precede eleva- tions in ICP in acute brain injury, allowing earlier interven- tion. Simi lar changes have been seen before development of delayed ischaemic de \201 cits due to cer ebral vasospasm in subarachnoid hemorrhage. High levels of the excitatory amino acids gluta mate and aspartate have been found in areas of contusion or secondary ischaemic injury. Thermal diffusion \202 owmetry The thermal conductivity of brain tissue varies in propor- tion to CBF. Two thermistors can be placed on the brain surface, and blood \202 ow calcu lated by means of heating one plate and measuring the thermal difference between plates. Ag ain only a small amount of brain tissue can be assessed. Peripheral nerve and muscle electrophysiology Sensory evoked potentials (SEPs) These are th e electrical response of the cortex, brainstem and spinal cord to a peripheral sensory stim ulus. They can be recorded in response to stimulation of any sensory nerve, whether cranial or peripheral. The most commonly evoked SEPs are somatosensory (SSEP), visual (VEP) and br ainstem auditory (BAEPs). SSEPs are recorded commonly from the median, ulnar and posterior tibial nerves. SSEPs are a useful method of predicting outcome in post-traumatic and anoxic coma patients. Bilaterally absent SSEPs are strongly associated with poor outcome. SSEPs m ay also be used in surgery on the spinal column, carotid endarterectomy and cerebral aneury sm surgery. VEPs are measured in response to a visual stimulus (usually a flashing light or reversing checkerboard). VEPs are profoundly affected by anesthesia and are occasionally u sed to assess optic nerve function in pituitary surgery of surgery on the anterior cranial fossa. BAEPs are used in acoustic neuroma surgery where they have been shown to be useful i n preserving the function of the auditory nerve. They may also be used for monitoring durin g posterior fossa surgery. Nerve conduction studies These can be used to diagnose and classify generalized neuropathie s that may be seen on the ICU. A stimulus is applied to a nerve at two points along its cou rse, and the response recorded. In axonal neuropathies, the amplitude Cerebral blood \202 ow and metabolism NIRS Near-infrared spectroscopy (NIRS) measures reg ional cerebral oxygen saturation by measuring near-infrared light reflected from the chromo phobes in the brain 139 CHAPTER 8.4 Other forms of neurological monitoring Table 8.4.1 Nerve conduction studiy patterns in common clinical conditions Motor nerve conduction Sensory nerve conduction EMG Slowed or blocked Reduced amplitude Reduced and falls further with repetition Reduced or absent Normal Normal Later denervation Denervation widespread Increased jitter on single \201 bre testing Guillain \200\223Barr syndrome Motor neuron disease Myasthenia gravis Reduced Reduced Fibrillations Critical care polyneuropathy Further reading Bhatia A, Gupta AK. Neuromonitoring in the intensive care unit. 1. Intracra nial pressure and cerebral blood \202 ow monitoring. Intensive Care Med 2007; 33: 1263 \200\22371. of the response will fall but conduction velocity is well preserved. In contrast, in demyel inating neuropathies, although the amplitude may fall, the conduction velocity is also redu ced (Table 8.4.1). Critical illness polyneuropathy is a diffuse axonal neuropathy usually s een in patients with severe sepsis and multi-organ failure. It is usually consid- ered when the patient fails to wean from ventilation and remains profoundly weak. Patients have musc le wasting that often spares the face (although there may be evidence of facial involvement on electrophysiological testing). Bhatia A, Gupta AK. Neuromonitoring in the intensive care unit. 2. Cerebral oxygenation mon itoring and microdialysis. Intensive Care Med 2007; 33: 1322 \200\2238.