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Ophthalmologists sometimes inject a small bubble of gas into the vitreal cavity during surgical reattachment of the retina. The goal is to have a sustained bubble of stable size holding the retina in place. The gases commonly used, sulfur hexafluoride (SF6 ) and carbon octofluorine (C3 F8 ), are inert, very insoluble in water, and poorly diffusible. Nitrous oxide (N2 O) is 117 times more diffusible than SF6 and rapidly enters the gas bubble. If administration of N2 O continues after the injection of gas into the vitreal cavity, the injected gas bubble rapidly increases to three times its original size,[58] which causes IOP to increase from 14 to 30 mm Hg. Within 18 minutes of discontinuation of N2 O, however, both the bubble size and IOP will decrease (from 29 to 12 mm Hg).[59] These rapid and wide variations in bubble size during general anesthesia may adversely affect the outcome of surgery.
Washout of N2 O from the lung is 90% complete within 10 minutes, so administration of N2 O should be discontinued at least 20 minutes before an intravitreal injection of gas. Bubble size and IOP should then remain stable. Some anesthetists avoid N2 O altogether when intravitreal gas injection is planned. Wolf and colleagues[59] noted that SF6 gas bubbles remain present for at least 10 days. Other intravitreal gases may remain for as long as 21 to 28 days. N2 O should be avoided in any patient returning for a general anesthetic within 3 to 4 weeks of undergoing intravitreal gas injection. The second exposure to N2 O might cause re-expansion of the bubble and elevated IOP with resultant occlusion of the retinal artery and loss of vision. This event is more likely if hypotension occurs during general anesthesia. When subjected to ambient pressures simulating those of commercial air travel, monkeys with an initial intraocular air bubble of only 0.25 cc experienced an average increase in IOP of 42 mm Hg; IOP decreased to lower than normal after return to preflight pressures. In addition, the retinal artery became temporarily occluded. Therefore, patients with intravitreal gas bubbles may risk ocular damage during air travel.
Management of emergency anesthesia for a patient with a full stomach and an open eye injury requires balancing the need to prevent aspiration of gastric contents against prevention of sudden significant increases in IOP that may cause further eye damage and loss of vision.[2] [47] [48] [60] If possible, early administration of an H2 receptor antagonist such as metoclopramide (0.15 mg/kg IV) will decrease gastric volume and provide some protection.
Before rapid-sequence induction of anesthesia, several precautions may be taken to blunt the cardiovascular and IOP response to laryngoscopy and tracheal intubation. Intravenous administration of lidocaine (1.5 mg/kg) and remifentanil (0.7 µg/kg) 3 to 5 minutes before induction may help attenuate the increase in IOP after tracheal intubation. A β-adrenergic receptor blocking drug such as labetalol (0.05 to 0.10 mg/kg IV) may also be useful in blocking the cardiovascular response to tracheal intubation, especially in patients with angina or hypertension.
A dose of thiopental (6 mg/kg IV) or propofol (3.0 mg/kg IV) will ensure adequate depth of anesthesia during tracheal intubation. The effectiveness of using a succinylcholine pretreatment technique in these cases is controversial. [60] Although IOP may increase with this method, no published reports have described further eye damage after rapid-sequence induction of anesthesia with d-tubocurarine, thiopental, and succinylcholine. In their large clinical experience using this technique to manage open eye injuries, Libonati and coworkers[61] did not encounter aspiration of gastric contents or extrusion of eye contents (also see Chapter 13 ).
Because nondepolarizing muscle relaxants reduce IOP, a modified rapid-sequence technique consisting of preoxygenation, thiopental or propofol induction, a large dose of nondepolarizing muscle relaxant,[60] and application of
During general anesthesia for open eye surgery, the depth of anesthesia must be sufficient to ensure lack of movement[17] or coughing. It is advisable to use nondepolarizing neuromuscular blockers (and document full neuromuscular blockade with a train-of-four response) to prevent coughing caused by accidental carinal stimulation (see Chapter 13 ).
When a full stomach is a possibility, the endotracheal tube is best removed while the patient is awake, breathing spontaneously, and receiving oxygen and the head is turned toward the side. Smooth emergence from anesthesia can be aided by administering an antiemetic drug before or during surgery and by giving lidocaine (1.5 mg/kg IV) or remifentanil (0.5 µg/kg IV) approximately 5 minutes before the patient awakens.
Management of eye anesthesia in children involves special considerations (see also Chapter 60 ).[60] [63] [64] Children sustaining eye trauma may also have cranial injuries. If administration of narcotics is necessary to control pain, an antiemetic should also be given. Regional eye anesthesia is not suitable in patients with eye trauma, young age, and lack of cooperation. Awake endotracheal intubation may increase IOP, is difficult in this age group, and should therefore be avoided in open pediatric eye injuries.
With the aid of a topical anesthetic cream it is usually possible to gently start an intravenous line. Induction of anesthesia may then proceed as described for adults. If no intravenous line is reasonably possible, rapid, gentle induction of anesthesia by mask (with 7% to 8% sevoflurane) must be performed despite a possibly full stomach while avoiding positive pressure and direct mask pressure on the injured eye. An intravenous line is secured as soon as possible.
If the patient has eaten recently, the risk of aspiration of gastric contents can be minimized by delaying these urgent cases a few hours. However, waiting is still no guarantee that the stomach will become empty. Further precautions include the administration of metoclopramide and an H2 receptor antagonist as with adults.
The stomach should be decompressed during surgery and the patient extubated while awake, with the protective airway reflexes intact. To facilitate tolerance of the endotracheal tube and minimize bucking in an awakening patient, a narcotic may be given 10 to 20 minutes before the end of surgery and lidocaine (1.5 mg/kg) administered intravenously 5 minutes before extubation of the trachea.
ROP is an abnormal proliferation of undifferentiated primitive mesenchymal cells in the retina (see also Chapter 59 and Chapter 60 ). These cells form arteriovascular shunts, and proliferation can lead to traction and detachment of the retina with blindness.[65]
As a result of improved neonatal care, more than 65% of premature infants (750 to 1000 g) now survive the neonatal period. ROP develops in more than 50% of these survivors; therefore, the incidence of this condition is increasing. Though usually associated with hyperoxic periods during neonatal care, the cause of ROP is complex and uncertain. Full-term nonhyperoxic infants can also have this condition, as can premature infants who have never received oxygen therapy. It may also be associated with factors such as hypoxia, hypercapnia, hypocapnia, sepsis, and apnea.[66] ROP occurs despite efforts in neonatal nurseries to control and monitor oxygen delivery. The retina is not completely vascularized at birth. Even at 8 months of age, the temporal retina may remain avascular. Hypoxia causes immature vessels to constrict, and such constriction leads to peripheral retinal hypoxia. This condition stimulates the formation of vascular shunts, vasoproliferative factor, and vessel proliferation. Leaking fluid causes hemorrhage, fibrosis, and scarring. As the scars contract, the retina becomes detached. Very early surgical intervention (i.e., at 1 to 4 weeks of age) with cryotherapy has been advocated to ablate the avascular retina and eliminate the release of vasoproliferative factor.
Babies with ROP also often have a history of general immaturity, apnea, bradycardia, jaundice, patent ductus arteriosus, intraventricular dysplasia, hypoxia, and developmental delays.[67]
Anesthetic management of these "ex-premies" requires attention to the details of maintaining normothermia by the use of forced warm air systems, overhead warming lamps, raised operating room temperatures, and temperature monitoring. Precise intravenous fluid management, including monitoring of serum glucose levels, is important. The hospital facility should be capable of providing the presurgical and postsurgical ventilation, monitoring, and apnea-bradycardia management that these ex-premies require. Outpatient procedures for ex-premies with a history of apnea-bradycardia are not recommended until a postconception age of at least 48 weeks. Ideally after a general anesthetic, these patients should be monitored for apnea-bradycardic episodes at least overnight before discharge.
Capillary oxygen tension should be kept at 35 to 40 mm Hg and arterial oxygen tension maintained at around 70 mm Hg in premature infants. One problem for anesthesiologists giving general anesthesia to a premature infant is to balance the risk of hypoxic damage with the respiratory problems frequently encountered in these sick, frail preterm infants[68] (see Chapter 59 and Chapter 60 ).
Even though no convincing evidence has indicated that ROP has ever occurred solely because of oxygen given during anesthesia,[66] in addition to the usual anesthesia requirements and precautions for these young, immature patients,[66] [69] prolonged exposure to high intraoperative concentrations of oxygen is best avoided during the period of retinal immaturity (i.e., until 8 months of age). Arterial oxygen tensions of 60 to 90 mm Hg may be achieved by giving mixtures of air and oxygen or N2 O and oxygen and by documenting arterial oxygen saturation at 90% to 95% by finger-pulse oximetry.[70]
Halothane, isoflurane, and enflurane can affect visual evoked potentials (VEPs).[71] [72] Halothane and isoflurane decrease the amplitude and increase the latency of VEPs. A 0.9% or higher concentration of isoflurane can prolong the latency of VEPs.[72] Although some studies claim that this relationship is dose dependent, at least two studies have failed to demonstrate significant differences with various concentrations of anesthetics. Neuroleptanalgesia seems to increase the latency of P2 slightly without changing the amplitude of evoked potentials. The effect of isoflurane on VEPs may be minimized by using low-concentration muscle relaxants, if necessary, and supplemental opioids.
Ketamine, a phencyclidine derivative, is a unique anesthetic because it increases the electrical activity of the brain. This increased activity could alter the amplitude of VEPs and distort the conclusions of testing. Ketamine has been used for anesthesia in rabbits without affecting the electroretinographic response. [73]
Unlike the VEP, which is a complex cortical response, the electroretinographic response is a simple reflex occurring within eye. Therefore, it is unlikely that such a response would be affected significantly by general anesthetics.
Treatment of poor alignment of the visual axis with amblyopia (strabismus) in children 1 to 6 years of age usually consists of surgery on the extraocular muscles. Surgical intervention must occur by 4 months of age if proper stereoscopic visual development is to proceed.[74] Strabismus repair in an older child is performed for cosmetic purposes.
Three problems associated with strabismus are of particular interest for the anesthetist: the possible increased risk of malignant hyperthermia, the high incidence of postoperative nausea and vomiting (PONV), and the likelihood of an OCR.
Strabismus is considered by some to be associated with an underlying myopathy, and such patients are assumed to have an increased risk for malignant hyperthermia. [75] The incidence of isolated masseter spasm after administration of halothane and succinylcholine was higher in children with strabismus (2.8% versus 0.72%) than in those without strabismus.[76] In patients with strabismus who were intubated after the administration of pancuronium, isolated masseter spasm did not develop.[77] Furthermore, in one study, approximately 50% of patients in whom malignant hyperthermia developed also demonstrated isolated masseter spasm after induction of anesthesia.[78] Because the overall incidence of malignant hyperthermia in children is only 1 in 15,000, the frequent incidence of masseter spasm after succinylcholine administration in patients with strabismus suggests that malignant hyperthermia may be more likely to develop in such patients. The relationship between isolated masseter spasm and malignant hyperthermia has been discussed and reviewed by Rosenberg and Shutack. [79]
The risk of malignant hyperthermia may be lessened by avoiding succinylcholine and halothane. Moreover, because succinylcholine increases extraocular muscle tone, it interferes with the forced duction test (which evaluates muscle tone) for approximately 15 minutes. By contrast, vecuronium, rocuronium, cisatracurium, and mivacurium render the extraocular muscles flaccid, thereby minimizing the afferent stimuli for nausea, vomiting, and OCR. To ensure that an episode of malignant hyperthermia is detected promptly, body temperature, ECG, and especially the end-tidal concentration of carbon dioxide should be monitored carefully during general anesthesia in patients with strabismus (also see Chapter 29 ).
The incidence of nausea and vomiting in children after outpatient strabismus surgery varies from 48% to 85%.[80] Van den Berg reported that after strabismus surgery, 10% of patients had early PONV and as many as 57% had a delayed incidence of PONV caused by the ocular-emetic reflex. [81] Persistent PONV delays discharge and may even require overnight admission. Many regimens have been used in an attempt to control nausea and vomiting in these patients without also prolonging recovery time. Droperidol (75 µg/kg IV) successfully reduces the incidence of nausea and vomiting to 16% to 22% without increasing the discharge time (4.6 hours). Droperidol, however, may cause undesirable postoperative side effects such as restlessness, dyskinesia, and dysphoric reactions.[82] Lower doses of droperidol, usually effective as an antiemetic in adults, do not seem to be effective in children with strabismus.[83] Intravenous administration of lidocaine (1.5 mg/kg) before tracheal intubation also reduces the incidence of PONV to 16% to 20%.[84]
Weir and colleagues[80] have shown a significant decrease in the incidence and frequency (41%) of vomiting in the first 24 hours after strabismus surgery with the use of a propofol infusion and N2 O technique. This incidence was further reduced (24%) when opioids were avoided. Discharge times average 2 hours, but postoperative restlessness was more common than in patients who received an inhaled anesthetic.
Splinter and Rhine[85] reduced the incidence of vomiting after strabismus surgery in children to 9% by using a combined low-dose ondansetron (50 µg/kg) and dexamethasone (150 µg/kg) regimen.
The emetic symptoms associated with strabismus surgery may be caused by eye muscle manipulation or pain that induces an OCR vagal response. Prophylactic treatment with atropine or glycopyrrolate, however, does not decrease the incidence of nausea and vomiting.[83] The OCR, commonly elicited in response to traction on the extraocular muscles, is frequently associated with strabismus surgery. Previous studies have noted an
In addition to the usual practice regarding pediatric management, use of the following measures to decrease the incidence of nausea and vomiting after strabismus surgery should be considered:
The special problems of pediatric ophthalmic anesthesia make it almost a specialty in itself.[89] Congenital syndromes in which eye abnormalities are only one manifestation of a multisystem disorder present problems of overall general anesthesia management.
Patients with homocystinuria, a rare inborn error of amino acid metabolism, may present with subluxation of the lens or glaucoma. These patients are susceptible to thromboembolic complications during general anesthesia. Hyperinsulinemia and hypoglycemic convulsions are also common. Safe anesthesia management requires pretreatment with acetylsalicylic acid and dipyridamole, adequate hydration with glucose or low-molecular-weight dextran, and maintenance of good arterial blood pressure and peripheral vasodilation. In addition, to prevent venous stasis, the patient should wear elastic stockings or pneumoboots during surgery and walk as soon as possible.
Marfan's syndrome is a connective tissue disorder that causes subluxated lenses and detached retinas. Anesthesia management should consider the possibility of heart valve defects, thoracic aneurysms, and kyphoscoliosis.
Children with Down syndrome often have strabismus and cataracts. Of concern to the anesthesiologist are hypotonia, heart defects, hypothyroidism, macroglossia, seizures, and atlantoaxial instability, all of which may be associated with this syndrome.
Patients with Sturge-Weber syndrome may have secondary glaucoma. Sturge-Weber syndrome consists of cavernous cutaneous angioma of the face, cerebral cortex, and lower airway. Seizures and airway bleeding may occur.
Patients with homozygous sickle cell disease or thalassemia may present with retinitis proliferans, vitreous hemorrhage, or retinal detachment. Anesthesia management involves the treatment of anemia and avoidance of conditions that trigger sickle cell crisis, such as dehydration, acidosis, hypoxia, infection, venous stasis, and hypothermia.
Patients with craniofacial abnormalities, as in Crouzon's disease, Alport's syndrome, or Kniest's syndrome, may have myopia, detached retinas, exophthalmos, or glaucoma. The trachea can be difficult to intubate in these patients. Chapter 27 and Chapter 60 also discuss congenital syndromes involving a pathologic process of the eye.
Stead[90] has reviewed the mortality and morbidity from coexisting disease in patients undergoing ophthalmic surgery. Wu and Schachat[91] reported that 0.7% of ophthalmic patients required transfer to the medical service, usually for cardiac-related conditions.
Stead reviewed morbidity from the systemic effects of ophthalmic drugs and the complications of anesthetic techniques, monitored anesthesia care, and regional eye blocks, including optic nerve trauma, ocular penetration, retrobulbar hemorrhage, corneal injury, OCR, and the myotoxicity of local anesthetics on extraocular muscles. Stead also discussed general anesthesia, the impact of nausea and vomiting on the results of ophthalmic surgery, and the effect of general anesthesia, intubation, and N2 O on IOP.[90]
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