Clinical Anatomy Reference should be made to Chapter ▶ 1 for an understanding of the significant clinical anatomy pertinent to anesthesiological care. The optic nerve consists of the bundled axons of the large ganglion cells in the third neuron of the retina; unlike the other cranial nerves it is not a peripheral nerve but a continuation of the diencephalon and is surrounded by a fluid-filled sheath. The osseous channel, the dural sheath and the connective tissue bordering the chiasmatic groove—inter alia the rigid annulus of Zinn—encase the optic nerve and the ophthalmic artery. This optic sheath exhibits high elastance, whereby it is potentially at risk in the event of a mass. In this respect the optic nerve is not directly at risk from pressure; the risk is more that compression of the nutritive vessels from the pia mater will jeopardize supply (see Chapter ▶ 2). A continually raised intracranial pressure (ICP) is transmitted into the optic sheath, where it can induce papilledema in the ocular fundus (edema of the optic nerve papilla) through the increase in the pressure of the fluid. The orbit—the bony capsule of the eye—is a non-expandable casing, like the skull (the bony capsule of the brain). This and other analogies form the common anatomical-physiological basis of ophthalmic anesthesia and neuroanesthesia ( ▶ Table 17.1). Eye Brain Anatomy Capsule Orbit Skull Casing Sclera Dura mater Substance Vitreous body Brain Liquid Aqueous humor Cerebrospinal fluid Production Ciliary body Choroid plexus Fluid spaces Anterior and posterior chamber Ventricle system Arterial supply Ophthalmic artery Carotid and vertebral arteries Venous drainage Jugular vein Jugular vein Physiology Perfusion barrier Autoregulation of retinal perfusion Autoregulation of cerebral blood flow (CBF) Diffusion barrier Blood–humor-barrier Blood–brain-barrier Internal pressure Intraocular pressure (IOP) Intracranial pressure (ICP) Control parameter Intraocular fluid balance Cerebrospinal fluid balance Relevant factors Chronobiology, PaCO2, AWP Chronobiology, PaCO2, AWP Pathophysiology Bleeding Vitreous hemorrhage Intracerebral bleeding, subarachnoid bleeding Drainage disorder Buphthalmus Hydrocephalus Rise in pressure Glaucoma Intracranial pressure syndrome Abbreviations: Pa, arterial partial pressure. AWP, airway pressure. Similar aims of anesthesiological care also result from these common features ( ▶ Table 17.2). Intracranial pressure (ICP) is the pressure that the contents of the skull exert on the dura mater. This pressure—in line with the hydrostatic gradients and the compartmentalization of the intracranial space—is nonuniform. Under pathological conditions the regional difference can be ≥20 mm Hg. This is to be noted when placing a pressure sensor and interpreting the readings. The ICP is the “sum of the partial pressures” of the brain tissue (80%), cerebrospinal fluid (8–12%) and blood (ICP = pcerebrum + pfluid + pblood). Depending on position, the ICP amounts to 0 to 15 mm Hg. Readings of 15 to 20 mm Hg/25 to 40 mm Hg show a “slightly/moderately raised” ICP; readings above 40 mm Hg show a “severely raised” ICP. ICP is an organ constant, which is kept constant within narrow limits under physiologic conditions. The increase in the partial pressure of one component (brain tissue, cerebrospinal fluid) is compensated by a change in the intracranial blood volume in response (Monro–Kellie hypothesis). The ICP is one determinant of cerebral perfusion pressure (CPP = MAP – ICP) and thus also of cerebral blood flow (CBF = CPP/CVR). In line with the principle “function drives metabolism, metabolism drives flow,” the CPP, as the determinant of the driving force of perfusion, is a proxy variable for cerebral blood flow, which is clinically hardly measurable and in the pre-hospital setting not at all. A persistently elevated ICP damages the tissue of the brain not only directly (pressure damage) but also indirectly (perfusion damage). For patients with craniocerebral trauma or aneurysmal subarachnoid hemorrhage, persistently elevated ICP heralds unfavorable neurologic outcome. Pathologic ICP waves (A to E waves as per Nils Lundberg) are likewise indicators of a poor prognosis. Reduction of pathologically raised ICP requires it to be measured beforehand; this can only be done invasively. Established locations for measurement are the epidural space, CSF, and brain tissue. The measurement is made using the principle of communicating tubes (e.g., in the CSF space), electronically, or fiberoptically. Direct measurement of the pressure via a catheter in the lateral ventricle (official gold standard) enables—in addition to manometry and zero point alignment—the pressure to be reduced by draining CSF, the determination of the intracranial elastance (ΔP/ΔV), and microbiological and metabolic diagnostics. Placing the catheter is traumatizing (drill hole 4.4 mm, brain passage 4.5 cm), and the risks of bleeding (1.4%) and contamination (≤3%) are not trivial. Measurement using a fiberoptic or electronic sensor in the brain tissue is less traumatic (drill hole 2.8 mm, brain passage 1.4 cm) and burdened with fewer complications. Parenchymal pressure measurement has been established as the de facto standard in many places. ICP measurement should be considered if intracranial hypertension is suspected. ICP monitoring cannot be replaced by CT checks. Organs close to the orbit exhibit hemodynamically relevant peculiarities. Thus the frontal brain lobe lying over the roof of the orbit has the highest oxygen requirement of the body, the choroid in the orbit the highest perfusion. Perfusion of the brain, as well as that of the retina, is subject to autoregulation; that of the choriocapillaris, owing to the absence of precapillary sphincters, is not. 1 The last-mentioned difference is clinically significant. A rise in mean arterial pressure (MAP; driving force of organ perfusion) brings about a drop in intracranial pressure (ICP), in contrast, a rise in intraocular pressure (IOP) ( ▶ Fig. 17.1). The cause is the autoregulatory response of the blood vessels of the brain, which respond to the rise in MAP with vasoconstriction: the consecutive drop in the cerebral blood volume (CBV) lowers the ICP. The choroidal blood volume, in contrast, rises pressure-passively, and with it so does the IOP. Awareness of these connections enables targeted control of the hemodynamics by anesthesiological measures with the aim of optimizing not only patient safety but also the surgical conditions (see also “Controlled Reduction of Blood Pressure” in Chapter ▶ 17.5.6). Fig. 17.1 Autoregulation. Effect of raising the cerebral and ocular perfusion pressure through angiotensin-induced arterial hypertension (arterial pressure, AP; arrow) on intracranial pressure (ICP) and intraocular pressure (IOP). The ICP falls as a result of autoregulation-triggered vasoconstriction; the IOP rises—due to the absence of autoregulatory competence of the choroid—in parallel with the blood pressure (pig model). 26 The intracranial pressure (ICP) is the pressure that the contents of the skull exert on the craniodural envelope ( ▶ Table 17.2). ICP is position-dependent and is physiologically lower than 10 mm Hg. The pressure is built up by the blood volume expelled into the cerebral vascular bed during systole. A clearly raised ICP can affect perfusion of the brain. For the purpose of a rough assessment of cerebral perfusion, the cerebral perfusion pressure (CPP) is used, the calculated difference between mean arterial pressure and ICP (CPP =MAP – ICP). The perfusion of the brain is subject to autoregulation (myogenic autoregulation, Bayliss effect); that is, it takes place for the most part independently of the systemic blood pressure and is controlled to meet metabolic requirements (CMRO2: cerebral metabolic rate for oxygen). In metabolically highly active areas of the brain, CO2 accumulates as the end product of aerobic metabolism, which dilates blood vessels and thus fosters regional substrate supply via vasodilatation. In less-active areas, relative hypocarbia results in vasoconstriction. This marked CO2-responsiveness of the cerebral blood vessels enables the fine control required for the perfusion of the brain. Due to the same mechanism, hypoventilation-induced hypercapnia causes global cerebral vasodilatation with corresponding rise in the CBV and consequent rise of the ICP ( ▶ Fig. 17.2). Conversely, a raised ICP can be reduced promptly through hyperventilation. This “controlled hypocapnia” may be used only for a limited time, however, as the vasoconstriction induced is associated with the risk of cerebral ischemia. Fig. 17.2 CO2 responsiveness. The capnographic rebreathing-induced hypercapnia causes a parallel course of the intracranial pressure (ICP) via cerebral vasodilatation (pig model). 26 The ICP increases in case of expansion of the intracranial compartment—for example, in hypercapnia-induced vasodilatation (see above). This rise is usually nonthreatening, though it is undesirable in supraorbital operations. All mechanisms that increase ICP with intact dura mater act as vis-a-tergo once the dura is opened, rendering ICP atmospheric. The surgeon identifies this force by the fact that brain tissue emerges over the edge of the craniotomy. This worsens surgical conditions, which is why medication and measures that would increase ICP with the dura intact should be avoided. The intraocular pressure (IOP)—the pressure that the contents of the eyeball exert on the corneoscleral envelope—is a result of inner pressure and outer counterpressure. IOP is an organ constant that varies only within a narrow range. The pressure is composed of the components of the aqueous humor and perfusion balance as dynamic factors and the volume of the vitreous body and osmotic pressure gradients as predominantly static factors. The mechanical and chemical effects of controlled ventilation are further controlling or disrupting forces. Acute changes in the internal pressure of the eyes in the seconds to minutes time range result from changes in tension of the extraocular striated musculature or are produced hemodynamically. As well as effects of the preoperative medication and hydration on the IOP, the positioning of the patient is significant. In addition to its significance for the diagnosis of glaucoma, measurement of the IOP serves as a global test that can be performed on the intact eyeball to record factors that–with the eye opened up–that is, at atmospheric IOP would act as vis-a-tergo expelling the contents of the eyeball. In most intraorbital operations, an IOP stable at a low level provides favorable operating conditions. With opening of the eyeball, especially extensive opening, one should refrain from using pharmaceuticals and measures that would increase the vis-a-tergo. The majority of anesthetics do not have a relevant effect on the IOP, or they reduce it dose dependently. As the cause of the latter phenomenon, a direct effect on an IOP control center, presumably located in the diencephalon, is assumed. 3 In contrast to anesthetics, the effects of depolarizing muscle relaxants are clinically significant (see Chapter ▶ 17.4.5). A number of well-controllable drugs with few side effects is available for the induction and maintenance of anesthesia and for neuromuscular blockade ( ▶ Table 17.3). The suitability of anesthetics for the goals of ophthalmic anesthesia and neuroanesthesia can be gauged from the requirements listed in ▶ Table 17.4. In addition to the desire for hemodynamic stability one should take account of the specifics of orbit surgery in relation to the pharmacodynamics with reference to the internal cranial and orbital pressures—ICP und IOP. A medication is easily controllable if it can be used with antagonists to be short-acting, or have rapid onset and offset, and be free of residual or side effects. Premedication Midazolam, clonidine, dexmedetomidine Hypnotics Propofol, etomidate Analgesics Sufentanil, remifentanil, (S)-ketamine Inhalational anesthetics Sevoflurane, desflurane Muscle relaxants Mivacurium, cisatracurium, rocuronium Antagonists Sugammadex, flumazenil, naloxone Intraoperative and postoperative analgesia Immobilization Orbital and/or intracranial hypotension Arterial normotension When needed, controlled arterial hypotension Emergence without emesis and shivering Early postoperative sensory assessability Sedatives and tranquillizers are administered as premedication or to deepen general anesthesia. Benzodiazepines are the most widely used. These interact with the benzodiazepine receptors in the CNS and intensify endogenous GABA-mediated inhibition mechanisms. Midazolam and diazepam inter alia are used for parenteral administration. Long-acting lorazepam is predominantly used in the United States. Midazolam is the one most suited to the aims of anesthesia in orbit surgery. In a low to moderate dose midazolam bolsters the opiate effect on the descending inhibitory pain pathway. Midazolam can be administered as a bolus or continuously. The dosage is calculated on an individual basis according to effect, mostly in a range from 2.5 to 10 mg/h. Despite a relatively short elimination half-life of 1 to 2 hours, high lipophilia causes evident cumulation and a lengthening of the effect, particularly when administered for a longer time. For prompt termination of undesirable or intensive effects of benzodiazepines, there is specific antidote available in flumazenil. Hypnotics and hypnoanalgesics are available for the induction of general anesthesia by injection. Ketamine and (S)-ketamine belong to the second group. These are used when circulatory stabilization or augmentation is desired or when hypnotics are contraindicated (see also Chapter ▶ 17.4.4). The significance of barbiturates (thiobarbiturates or hydroxybarbiturates) is in decline, due, among other causes, to their tendency to suppress the immune system. Myocardial depression is characteristic of the pharmacodynamics of barbiturates, while cumulation is significant with regard to the pharmacokinetics, so that administration by means of infusion is not indicated for lengthy interventions. Barbiturates are contraindicated in patients with porphyria; a niche still remaining for methohexital, where available, is the rectal induction of anesthesia in children. 3 When circulatory depression is a concern, etomidate is used. Etomidate is substantially circulation-neutral, short-acting, and free of cumulation potential. One disadvantage and indication-limiting feature is the suppression of cortisol synthesis. 4 An undesirable effect is myoclonus, which occurs if etomidate is administered to induce anesthesia without previous administration of opioids or benzodiazepines. The induction hypnotic most often used is propofol. The cerebral pharmacodynamics of propofol are characterized by a decrease in CMRO2, cerebral blood flow (CBF), and ICP. Cerebral autoregulation and CO2-responsiveness remain intact. As propofol in individual cases, especially when administered quickly, lowers the blood pressure, it is often given by means of a syringe pump. This method is also selected when propofol is administered as the hypnotic component of total intravenous anesthesia (TIVA). The negligible cumulation of propofol, even when administered for a long period, is particularly advantageous when the patient is to wake up early after a lengthy operation on the orbit for neurologic assessment. Inhalational anesthetics are a chemically heterogeneous group of drugs, from the “simple” noble gas xenon to complex halogen-substituted hydrocarbon compounds. The only thing in common is the inhalational supply. Nitrous oxide (N2O, “laughing gas”) and diethyl ether were used in the beginning of modern anesthesiology. The importance of nitrous oxide is dwindling, not least due to the N2O-induced inhibition of methionine synthetase. This enzyme catalyzes the conversion of homocysteine to methionine and tetrahydrofolate. Inhibition results in the accumulation of homocysteine and a lack of vitamin B12. In addition to the hypovitaminosis and homocysteine-induced vascular disease, possible clinical consequences are ultimately the impairment of myelin and DNA synthesis. The future for xenon cannot be predicted at present. Its advantages (among other things, xenon as a noble gas is biochemically inert and environmentally sustainable) are indisputable. Analgesic potency and ease of control are givens; neuroprotective properties are likely. In high-performance sports, xenon has the potential for misuse as an indirect doping medium because it increases endogenous erythropoietin synthesis without being detectable. Arguments against its widespread use in clinical anesthesiology are above all its very limited availability, with the resulting high cost, and also the lack of medical devices requisite for its administration. The volatile inhalational anesthetics sevoflurane and desflurane are almost exclusively used now. Both are relatively easy to control and have few side effects. An absolute contraindication for both is the disposition to malignant hyperthermia (MHS). This is an autosomal dominant hereditary defect of the calcium-release channel in the sarcoplasmic reticulum of the skeletal musculature (“ryanodine receptor”). If genetically disposed patients receive a volatile inhalational anesthetic, a lasting opening of this calcium release channel can ensue. This then will result in calcium overloading of the sarcoplasm, with the consequence of a lasting activation of the contractile actin–myosin apparatus. The skeletal musculature will go into contracture, and perfusion ceases owing to vascular compression. Anaerobic metabolism brings about acidosis and hypoxia. Since several steps of the pathophysiologic cascade occur exothermally, in combination with perfusion-based limited thermal dissipation there results central hyperthermia. Blood gas analysis, which shows marked mixed respiratory–metabolic acidosis in addition to muscle rigor, hypercapnia, and hyperthermia, provides diagnostic guidance. In the further course, rhabdomyolysis occurs and the patient dies of circulatory failure. This course of events can be interrupted by the timely administration of dantrolene, which “seals” the calcium release channel. Further contraindications to volatile agents are marked myocardial, coronary, or liver failure and—for desflurane—a history of “halothane hepatitis.” When these contraindications are taken into account, both anesthetics are well tolerated, stabilize the hemodynamic profile of the anesthesia and, dose dependently, reduce cerebral oxygen consumption. 5 Sevoflurane can also be used for mask induction; desflurane is less suitable for this due to its pungent smell. Both are used as basic anesthetics, supplemented by sedatives, hypnotics, and analgesics as well as muscle relaxants where needed. The CO2-responsiveness of the cerebral vascular system is augmented rather than damped by inhalational anesthetics. As a consequence, inhalational anesthetics can also be used when it is intended to control organ perfusion by induced hypocapnia or hypercapnia. In the in vitro model, ischemia-induced release of the excitotoxin glutamate is reduced significantly by exposure to sevoflurane. 6 This may indicate some neuroprotective potential. The analgesic component of combination anesthesia is provided by opioids or ketamine. Fentanyl, sufentanil, alfentanil, and remifentanil are used. In terms of receptor affinity, sufentanil offers advantages in theory, but no results-relevant superiority could be demonstrated. With regard to influencing postischemic damage, opioids cannot be classified as neuroprotective or neurodestructive. With regard to controllability and (lack of) cumulation, remifentanil is far superior to the reference substances. For short-duration and diagnostic procedures on the orbit, this profile is thoroughly advantageous. With the other opioids there is the risk of an undesirably prolonged effect or of “remorphinization.” This can be countered effectively and promptly with naloxone, a pure competitive opiate antagonist. The risk of a severe hemodynamic reaction and, at times, the development of a pulmonary edema must be considered. The hypnoanalgesic ketamine, as racemate or as (S)-ketamine, is inherently suited to the aims of neuroanesthesia not least due to its indirect sympathomimetic properties. Earlier reservations with regard to an ICP- and CMRO2-raising effect are unfounded. (S)-Ketamine does not raise the ICP, but can, at least in children, decrease raised ICP. Relevant “neuroprotective” properties of ketamine due to NMDA-receptor-induced anti-excitotoxic effect are suspected but have not been proven. 7 Nondepolarizing muscle relaxants do not have any effect on ICP but they do minimally reduce intraocular pressure, probably through relaxation of the extraocular eye muscles. 8 If the surgical procedure requires intact neuromuscular transmission (e.g., facialis monitoring in ENT) the relatively short-acting nondepolarizing relaxant mivacurium is used and its effect is monitored relaxometrically. The reason for the predictable duration of the effect is the breakdown of mivacurium by pseudocholinesterase. If there is a surgical requirement for longer immobilization, cisatracurium or rocuronium are the drugs of choice. Cisatracurium is one enantiomer of racemic atracurium; both drugs are benzylisoquinolines, which are rapidly broken down chemically. Degradation pathways are Hofmann elimination and ester hydrolysis. Accordingly, offset of the neuromuscular block is predictable even with impaired liver and kidney function and also independent of the pseudocholinesterase concentration. A disadvantage is the accumulation of the metabolites monoacrylate and laudanosine, which maybe toxic or ictogenic in high concentration. Cisatracurium differs from the racemate in its slower onset, but also through producing less histamine release and laudanosine formation. The most rapid onset of effect among nondepolarizing relaxants is provided by rocuronium, which has a medium duration of action. Its effect is lost through redistribution; elimination is hepatobiliary. In individual cases this limits the predictability of the action; on the other hand, only with rocuronium is there the option of rapid and complete antagonization. The modified cyclodextrin sugammadex incorporates all circulating rocuronium molecules irreversibly; the complex is excreted renally. The very fast and short-acting depolarizing relaxant succinylcholine raises the IOP considerably ( ▶ Fig. 17.3), which is attributable to specific characteristics of the eye muscles. Basically, the striated muscles contain fibers with a “fibrillar structure” and others with a “field structure” 9. The fibers with “fibrillar structure” are innervated with end plates, react quickly as well as phasically, and enable eye movements. The fibers with “field structure” are multiply innervated, have grape-shaped nerve endings, and carry out the slow, tonic fusion movements. Stimulating them with succinylcholine brings about a tonic contraction without action potential, which raises the IOP via compression of the eyeball. Fig. 17.3 Effect of the administration of succinylcholine (arrow) on the intraocular pressure (IOP). As the stimulus response fades away, the IOP rises (dog model). 15
17.3 Clinical Physiology
17.3.1 Hemodynamics
17.3.2 Intracranial Pressure
17.3.3 Intraocular Pressure
17.4 Clinical Pharmacology
17.4.1 Sedatives
17.4.2 Hypnotics
17.4.3 Inhalational Anesthetics
17.4.4 Analgesics
17.4.5 Muscle Relaxants
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