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Ophthalmological and dermatological applications onlyrequire the delivery of a bare beam to the tissue in air. Todeliver laser energy percutaneously to an obstructed bloodvessel a quartz optical fibre has to be used. It is very difficultto transmit any short laser pulse (ie, one lasting less than 100s) down a fibre; the shorter the pulse the higher the peakpulse power and the fibre becomes disrupted at its proximalend. The problem is compounded with the excimer laserbecause the shorter and more useful wavelengths are

increasingly absorbed by quartz, especially in the presenceof impurities. Probably the major thrust of American laserangioplasty research is in this area; the originaldemonstration of precise craters cut by the excimer invascular tissue generated tremendous interest. Lengtheningthe wavelength used relaxes the requirements for a fibre andit is now possible to transmit up to 40 mj per pulse down a600 pn diameter fibre at 308 nm, which is enough toproduce tissue ablation in human cadaver arteries.14 Atshorter wavelengths a fibre of at least 1 mm internaldiameter is required and this is naturally less flexible andtherefore less adaptable when used in the vascular tree.Another approach is to build an excimer laser with a longerpulse (more than 180 ns) of lower peak pulse power, atechnically difficult feat which has nevertheless beenachieved. 12We do not yet have any clinical data for excimer lasers.

Major worries which must be resolved before human workstarts include the possible mutagenic effect of short

wavelength UV light on DNA. This is only likely to be aproblem in the skin, where cells rapidly divide. It has alsobeen shown that there is a pressure wave of up to 200

atmospheres propagated through tissue beyond the point ofimpact, the ablated tissue fragments moving at speeds of upto 100 m/s.5 Though cadaver specimens show no evidence oftissue disruption the effect on living tissue may be different.Early medical laser research was held back by lack ofunderstanding of the physical processes seen at the laser-tissue interface and by poor or non-existent deliverysystems. Excimer laser research is proceeding much morequickly with an informed multidisciplinary approach andmay well lead to important advances in the treatment ofcommon diseases.

TRANSTENTORIAL HERNIATION

TEXTBOOK explanations of the mechanisms wherebyrapidly expanding supratentorial masses cause brainstemdysfunction and ultimately coma have largely emanatedfrom human necropsy studies. It is generally accepted thatpressure exerted by such lesions leads to displacement ofcerebral structures through the tentorial opening, withdistortion of the brainstem. In their classic monograph,Plum and Posner codified such transtentorial herniationsyndromes into uncal and central types. In uncal herniation,a portion of the medial temporal lobe is displaced throughthe tentorial opening resulting in early compression of theipsilateral third nerve with both lateral shift of the upperbrainstem and late caudal shift of the midbrain and pons. Incentral transtentorial herniation, which is caused by diffuseparenchymal disease or by expanding masses near the

14 Mohr FW, Greulich O, Weller R, et al The use of an excimer with a coupled opticalfibre. In- Proceedings of the 4th Annual Conference on Lasers in Medicine andSurgery. London: British Medical Laser Association, 1986.

vertex, there is very little horizontal shift of midlinestructures and, as the third nerve is not compressed, signs ofdiencephalic dysfunction develop in the absence of pupillarydilatation.

With the introduction of high-resolution computerisedtomography (CT) it is now possible to assess the extent oftranstentorial herniation during life, provided that carefulattention is paid to radiological technique.3,4 Lateral

displacement of midline structures such as the cerebralaqueduct and the pineal gland may be determined to within1-2 mm. Under normal circumstances the pineal is visibleon the same horizontal section as the undisplaced calcifiedchoroid plexus of the lateral ventricle (contralateral to themass), but if there is caudal shift the gland is identified onlower cuts. In cases of frank uncal herniation, descent ofthe temporal lobe causes progressive obliterationof the parasellar and intrapeduncular cisterns with

hydrocephalus of the contralateral lateral ventricle, and inthe later stages of transtentorial herniation there is

progressive distortion of the brainstem making anatomyhard to delineate.

Although there have been numerous necropsy accounts oftranstentorial herniation, there have been isolated

postmortem reports of patients who were comatose shortlybefore death from a supratentorial mass and in whom therewas no pathological evidence of herniation. Indeed, Fisher6and Ropper have proposed that in most instances

expanding supratentorial masses cause stupor and coma inthe absence of transtentorial herniation, which they suggestmay develop as a terminal event or even postmortem.Ropper’ carefully evaluated the conscious level and CTscans of twenty-four patients with unilateral cerebral

masses, after excluding patients in whom alertness wasdepressed by factors other than secondary tissue shifts (eg,vasospasm after subarachnoid haemorrhage or haemorrhageinto the thalamus or midbrain). He found a clear correlationbetween the extent of horizontal displacement of the upperbrainstem, as represented by a shift of the pineal from themidline, and the degree of impairment of consciousness.Displacement of the pineal by 0-3 mm was associated withalertness; 3-4 mm with drowsiness; 6-8-5 mm with stupor;and 8-13 mm with coma. Signs of minor uncal herniationwere present in several patients, but were not related to thedegree of impairment of conscious level and, as in Fisher’sseries of twenty patients, there was no evidence of centraltranstentorial herniation as indicated by caudal

displacement of the pineal. In the occasional patient Ropperargues that stupor may be caused by massive horizontalshifts of the cerebral hemispheres anteriorally (transfalcineherniation) as reflected by displacement of the septumpellucidum, but in his original series there were patients inwhom such distortion was apparently well tolerated.Ropper and Fisher’s findings may prove to have

important implications for the management of acute

1. McNealy DE, Plum F. Brain stem dysfunction with supratentorial mass lesions. ArchNeurol 1962; 7: 10-32.

2. Plum F, Posner JB. The diagnosis of stupor and coma 3rd ed Philadelphia FA Davis,1980.

3. Osbom AG. Diagnosis of descending transtentorial herniation by cranial computedtomography. Radiology 1977, 123: 93-96

4. Hahn F, Gurney J. CT signs of central descending transtentorial herniation. Am JNeuroradiol 1985; 6: 844-48.

5. Munro D, Sisson WR. Hernia through the incisura of the tentonum cerebelli inconnection with craniocerebral trauma N Engl J Med 1952, 247: 699-709

6. Fisher CM. Acute brain hemiation-a revised concept Semin Neurol 1984; 4: 417-21.7. Ropper AH. Lateral displacement of the brain and level of consciousness in patients

with an acute hemispheral mass. N Engl J Med 1986; 314: 953-58

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cerebral haemorrhage, for which the indications for surgicalintervention are presently unclear. It might be expected thatsurgery would only be of value when stupor or coma isassociated with significant horizontal shift of the pineal ormassive displacement of the septum pellucidum. In theabsence of such signs, mass effect alone is unlikely to beresponsible for the impairment of consciousness and surgerywould not be expected to help. This prediction requiresconfirmation in a prospective trial.

INHALATIONAL INDUCTION OFANAESTHESIA—NEW INSPIRATION?

CONVENTIONAL inhalational induction of anaesthesia isseldom undertaken in adults because of patients’ fears of theanaesthetic mask, slow onset of hypnosis, and a moderatelyhigh incidence of excitatory phenomena. Intravenousanaesthetic agents provide a means of rapid, pleasantinduction. However, these drugs may induce unacceptabledegrees of hypotension, have a "hangover" effect, and tendto cause apnoea, rendering more difficult the administrationof inhalational agents for subsequent maintenance ofanaesthesia. Furthermore, they may occasionally cause

severe adverse reactions. A new technique of inhalationalinduction has now been describedI and proposed as analternative to intravenous induction in healthy adult patientsundergoing day-case surgery.With inhalational anaesthetic agents, unconsciousness

ensues when an effective drug concentration is achieved inbrain tissue. Because of the high lipid solubility of theseagents, there is a close relation between drug concentrationsin arterial blood and in brain, and, unless there is severe lungdisease, concentrations in alveoli and pulmonary end-capillary blood are virtually equal. Rate of onset ofanaesthesia is therefore dependent primarily upon the rate atwhich alveolar drug concentration increases. Duringinduction, uptake of drug by blood produces a largereduction in alveolar concentration; it is necessary to

administer an inspired concentration much higher than thealveolar concentration required to produce anaesthesia ifinduction is to be achieved rapidly. Alveolar concentrationincreases slowly with conventional inhalational techniquesfor two principal reasons: drug concentrations are diluted bythe air present in the lungs at functional residual capacitywhen the anaesthetic mask is applied and, with most agents,the inspired concentration must be increased slowly toprevent unacceptable subjective sequelae.A new technique for inhalational induction by means of a

single vital capacity breath was described in 1982;2 thisshortened induction time by producing a more rapidincrease in alveolar anaesthetic concentration. The subjectexhaled to residual volume, took a single vital capacitybreath of an anaesthetic gas mixture from a breathingsystem, and held his breath. A mixture of 4% halothane inoxygen reduced mean induction time to 112 s with thistechnique compared with 164 s for conventional inhalationalinduction.3 More recent work has demonstrated thataddition of nitrous oxide to the inspired gas mixture (4%halothane in 67% nitrous oxide/33% oxygen) reduces

1. Wilton NCT, Thomas VL Single breath induction of anaesthesia, using a vitalcapacity breath of halothane, nitrous oxide and oxygen. Anaesthesia 1986; 41:472-76.

2. Ruffle JM, Latta WB, Snider MT. Single breath halothane oxygen induction in man.Anesthesiology 1982; 57: A461.

3. Ruffle JM, Snider MT. Onset of hypnosis with halothane induction using singlebreath, triple breath and conventional techniques. Anesthesiology 1984; 61: A498.

induction time even further, to a mean of 83 s.l Thereduction results partly from the additive pharmacologicaleffect obtained with combinations of anaesthetic agents, butis probably contributed to also by the rapid uptake of largevolumes of nitrous oxide from the alveoli, resulting in anincrease in the alveolar concentration of halothane (secondgas effect).4 The latter phenomenon also tends to increase, orat least maintain, alveolar oxygen concentrations duringthe breath-holding manoeuvre.s Although excitatoryphenomena still occur with this technique, their incidence islow. The degree of arterial hypotension appears to be similarto that seen after slow intravenous induction withbarbiturates.6 91% of patients found the technique to beacceptable.The single-breath technique has advantages over

intravenous induction of anaesthesia. Venepuncture is

unnecessary while the patient is awake; the risk of

anaphylaxis with intravenous agents, although small, isavoided; there is a generally smooth transition frominduction to maintenance phases; and the hangover effectassociated with intravenous anaesthetic agents particularlybarbiturates, should be avoided, although this has not beenstudied. There are disadvantages, however. Intravenousaccess before loss of consciousness is felt by most

anaesthetists to be mandatory; the technique is unsuitablefor patients with airway obstruction or those unable tocooperate fully; and induction time remains shorter withintravenous agents (15-30 s for thiopentone8). Moreover,there is increasing concern about the incidence of liverdamage following administration of halothane, highlightedin a recent Lancet editorial.9 Both of the agents which mightreplace halothane in single-breath induction-isofluraneand enflurane-have a more pungent aroma and their MAC(minimum alveolar concentration of an inhalationalanaesthetic agent required to produce a lack of movement inresponse to surgical stimulation) is considerably higher.Although the rate of increase of alveolar concentrationrelative to inspired concentration is more rapid forisoflurane and enflurane than for halothane because of theirlower blood/gas solubility coefficients, induction wouldalmost certainly be slower and much less acceptable to thepatient.The principal indication for inhalational induction inadults is anticipated difficulty in control of the airway.Although computer simulationsl° suggest that rapid returnof consciousness should occur in the event of total airwayobstruction, the single-breath technique cannot berecommended in such situations at present. For patients inwhom intravenous access is impractical, the single-breathtechnique represents a considerable advance over

conventional methods of inhalational induction. However, itdoes not appear to offer significant advantages over

intravenous induction of anaesthesia for most patients.

4. Epstem RM, Rackow H, Salanitre E, Wolf GL. Influence of the concentration effecton the uptake of anesthetic gas mixtures: the second gas effect Anesthesiology 1964;25: 364-71.

5. Stoelting RK, Eger EI. An additional explanation for the second gas effect: Aconcentrating effect. Anesthesiology 1969; 30: 273-77.

6. Elder JD, Nagano SM, Eastwood DW, Harnagel D. Circulatory changes associatedwith thiopental anesthesia m man. Anesthesiology 1955; 16: 394-400

7. James RH. Day case anaesthesia. In: Smith G, Aitkenhead AR, eds. Textbook ofAnaesthesia. Edinburgh: Churchill Livingstone, 1985: 346-51.

8. Vickers MD, Wood-Smith FG, Stewart HC. Drugs m Anaesthetic Practice, 5th ed.London: Butterworths, 1978: 59.

9. Editorial. Halothane-associated liver damage Lancet 1986; i: 1251-52.10. Ruffle JM, Robbins ME, Snider MT. Computer strategies for optimizing rapid

inhalation induction. Anesthesiology 1983; 59: A513.