OPHTHALMOLOGY AND OTOLARYNGOLOGY Flashcards
What is normal intraocular pressure (IOP)?
○ Intraocular pressure ranges between 10 to 22 mm Hg.
○ In the intact normal eye there
is a typical diurnal variation of 2 to 5 mm Hg.
○ Small changes can occur with
each cardiac contraction and with closure of the eyes, mydriasis, and changes inposture
How is IOP created and maintained?
○ Intraocular pressure is primarily a balance between the production of aqueous humor and its drainage.
○ Aqueous humor is actively secreted from the posterior
chamber’s ciliary body and flows through the pupil into the anterior chamber where it becomes mixed with aqueous fluids, which are passively produced by blood vessels on the iris’s forward surface.
Why and to what extent does IOP increase during coughing or vomiting?
○ Any obstruction of venous return from the eye to the right side of the heart can raise IOP.
○ Coughing or straining can increase intraocular pressure by 40 mm Hg
or more.
What factors during the course of a general anesthetic increase IOP?
○ Any maneuver that increases venous congestion will increase IOP. ○ These include: Trendelenburg positioning, tight cervical collar, straining, retching, vomiting,
and coughing.
○ Direct laryngoscopy and intubation also increase intraocular pressure
What physiological factors (CO2, temperature) during the course of a general anesthetic decrease IOP?
During general anesthesia hyperventilation and hypothermia decrease IOP
How does ketamine affect intraocular pressure? What other attributes of ketamine
make it a less than ideal choice for anesthesia in patients undergoing
ophthalmologic procedures?
○ Ketamine can induce a rotatory nystagmus, cycloplegia, and blepharospasm (tight
squeezing of the eyelids).
○ Additionally, it is proemetic and increases secretions.
○ Anticholinergic agents may be administered with ketamine to diminish secretions.
○ There is controversy surrounding the effect of ketamine on IOP.
How much does IOP increase with the intravenous administration of
succinylcholine? What is the duration of this effect?
○ Succinylcholine can produce an increase in intraocular pressure of about 9 mm Hg 1 to 4 minutes after intravenous administration.
○ This effect can last up to 7
minutes
What is the mechanism for the increase in IOP following administration of
succinylcholine?
○ Increases in IOP secondary to the administration of succinylcholine are due to a number of mechanisms including tonic contraction of the extraocular muscles, relaxation of the orbital smooth muscle, choroidal vascular dilation, and cycloplegia, which impedes aqueous outflow.
What maneuvers may attenuate the rise in IOP associated with succinylcholine use
for laryngoscopy and intubation?
Pretreatment with a small dose of nondepolarizing neuromuscular blocker, lidocaine, b-blocker, or acetazolamide may attenuate increases in IOP associated with use of succinylcholine prior to direct laryngoscopy and endotracheal
intubation
How do paralyzing doses of nondepolarizing neuromuscular blocking drugs affect
intraocular pressure?
Nondepolarizing neuromuscular blocking drugs will decrease IOP by relaxing theextraocular muscles
How do inhaled anesthetics affect IOP? What is the effect on IOP of most intravenous anesthetics?
○ Both inhaled and most intravenous anesthetics produce dose-related reductions in
intraocular pressure.
○ This is probably due to multiple mechanisms including central nervous system depression, decreased production of aqueous humor, enhanced outflow of aqueous humor, and relaxation of the extraocular muscles.
○ The effect of ketamine on IOP is controversial.
How do changes in arterial blood pressure affect IOP?
○ Arterial hypertension has minimal influence on IOP.
○ Venous drainage is the key factor affecting IOP
What topical ophthalmic medicines may be absorbed sufficiently to exert systemic effects?
○ Topical ophthalmic agents can be absorbed systemically via the conjunctiva or drain down the nasolacrimal duct and be absorbed through the nasal mucosa.
○ These agents include acetylcholine, anticholinesterases, cyclopentolate,
epinephrine, phenylephrine, and timolol
What systemic effects have been attributed to the use of topical ophthalmic b-adrenergic blocking medications?
Topical ophthalmic b-adrenergic blocking medications may produce atropine
resistant bradycardia and bronchospasm, and exacerbate congestive heart failure.
What are the systemic effects of topical phospholine iodide (echothiophate)?
○ Phospholine iodide (echothiophate) is a miosis-inducing anticholinesterase that profoundly interferes with metabolism of succinylcholine.
○ Patients with low levels of plasma cholinesterase are at risk for prolonged paralysis.
Why is phenylephrine administered as a topical ophthalmic medicine? What systemic effect has been attributed to the topical ophthalmic application of this
drug?
○ Phenylephrine is an a-adrenergic that causes mydriasis (pupil dilation).
○ Systemic absorption of phenylephrine can induce transient malignant hypertension.
Why are carbonic anhydrase inhibitors, such as acetazolamide, administered as topical ophthalmic medicines? What systemic effects have been attributed to the
topical ophthalmic application of this drug?
○ Acetazolamide inhibits the production of aqueous humor.
○ Its systemic effects include diuresis and hypokalemic metabolic acidosis
What is the oculocardiac reflex? What is its reported incidence? When is it most likely to occur?
○ The oculocardiac reflex is a vagal-mediated response that manifests with an abrupt, profound decrease in heart rate.
○ It occurs in response to extraocular muscle traction or external pressure on the globe.
○ The reported incidence varies widely from 15% to 80%.
When is the oculocardiac reflex most often encountered?
○ The oculocardiac reflex is most often encountered during strabismus surgery.
○ However, it can arise during any type of ophthalmic surgery as well as some otolaryngology procedures.
○ A regional anesthetic eye block can ablate it.
○ Paradoxically, it may be triggered during the administration of this block.
What cardiac rhythms are likely to result from the oculocardiac reflex?
○ The oculocardiac reflex can manifest as a variety of dysrhythmias including junctional or sinus bradycardia, atrioventricular block, ventricular bigeminy, multifocal premature ventricular contractions, ventricular tachycardia, and asystole.
How does arterial hypoxemia or hypercarbia affect the oculocardiac reflex? How does the depth of general anesthesia affect the oculocardiac reflex?
○ Hypercarbia, hypoxemia, and light planes of general anesthesia all augment the incidence and severity of the oculocardiac reflex.
What is the first line of treatment of the oculocardiac reflex? What measures may be taken if the reflex persists?
○ Prompt removal of the surgical stimulus often results in rapid recovery.
○ At the first sign of any dysrhythmia, surgery must stop and all pressure on the eye or traction on extraocular muscles must be discontinued.
○ Other measures that can be taken include the administration of a parasympatholytic such as atropine or glycopyrrolate.
○ Consider increasing the depth of general anesthesia (provided that
the patient is hemodynamically stable).
○ Alternatively, infiltration of local
anesthetic attenuates recurrence of the reflex
- Is prophylactic use of anticholinergics fully effective in preventing the
oculocardiac reflex? What problems may arise from use of an anticholinergic?
○ The prophylactic use of an anticholinergic is not 100% effective in preventing the oculocardiac reflex.
○ Side effects that may result from the use of an anticholinergic include persistent tachycardia.
○ This may have serious
consequences in geriatric patients and those with a history of heart disease
What are some important demographic characteristics of patients scheduled for eye surgery?
○ Eye surgery patients are often at the extremes of age, and range in age frompremature newborns to nonagenarians.
○ Age-specific considerations such as altered pharmacokinetics and pharmacodynamics apply.
○ The elderly, syndromic pediatric patients, and premature infants commonly have comorbidities that carry important anesthesia implications.
Should antiplatelet or anticoagulant medications be discontinued prior to
surgery?
○ The cessation of antiplatelet or anticoagulant drugs prior to ophthalmic surgery is controversial.
○ One must weigh the risks of intraocular bleeding versus the risks
of perioperative stroke, myocardial ischemia, or deep venous thrombosis.
What is a key anesthetic consideration for the patient scheduled for ophthalmic
surgery with uncontrolled cough, untreated Parkinsonian tremor, severe
claustrophobia, or pathological anxiety?
○ An important component of the preoperative assessment is to gauge the likelihood of patient movement during surgery.
○ An inability to remain supine and
relatively still during eye surgery under monitored anesthesia care may result in eye injury with devastating long-term visual consequences.
What are the anesthetic options for patients having eye surgery?
○ The anesthetic options for ophthalmic procedures include general anesthesia, retrobulbar (intraconal) block, peribulbar (extraconal) anesthesia, sub-Tenon
block, and topical analgesia
What is the significance of the extraocular muscle cone for eye blocks?
○ The extraocular muscle cone separates the intraconal from the extraconal space and determines whether the local anesthetic is delivered as a retro- or peribulbar block
What is the ultimate needle tip position for a retrobulbar (intraconal) block?
A retrobulbar block is accomplished by inserting a steeply angled needle into the muscle cone such that the tip of the needle is behind (retro) the globe (bulbar).
What is the rationale behind extraconal (peribulbar) anesthesia? Where is the ultimate needle tip position?
○ The boundary separating the intraconal from extraconal space is porous.
○ Local
nesthetics injected outside the muscle cone diffuse inward, resulting in anesthesia of the eye.
○ An extraconal block is achieved by directing a needle with minimal
angulation to a shallow depth, such that the tip remains outside the muscle cone
What are some complications of a retrobulbar block?
○ Complications of needle-based ophthalmic regional anesthesia include superficial or retrobulbar hemorrhage, elicitation of the oculocardiac reflex, intraocular
injection of local anesthetic, penetration or puncture of the globe, optic nerve trauma, intravenous injection of local anesthetic solution and resultant convulsions, central retinal artery occlusion, brainstem anesthesia, and blindness.
What is the differential diagnosis of altered physiological status (blood pressure,
heart rate) after a needle-based ophthalmic regional eye block?
○ Intravenous sedation is the most common cause of altered physiologic status (blood pressure, heart rate, rhythm, ventilation) after a needle-based eye block.
○ More sinister complications are brainstem anesthesia and local anesthetic toxicity secondary to intravascular injection
How does a sub-Tenon block differ from a needle-based eye block?
○ A sub-Tenon block is performed using a blunt cannula inserted into the space between the globe’s sclera and surrounding the Tenon capsule. ○ Local anesthetic injected into this space blocks the optic and ciliary nerves as they penetrate the capsule.
Which patients are at high risk for retinal detachment?
○ Diabetics and patients with severe myopia are at particular risk for retinal detachment.
What are the anesthetic considerations for patients undergoing surgery to repair
a retinal detachment?
○ Retinal surgery is often prolonged and associated with greater manipulation of the eye.
○ Patients may require deeper planes of general anesthesia or a dense regional block.
○ Perfluorocarbons such as sulfur hexafluoride are relatively
insoluble gases that are surgically instilled in order to tamponade the retina; these may take up to 28 days to resorb.
When must nitrous oxide be avoided as maintenance anesthetic for patients
undergoing surgery to repair a retinal detachment? What is the risk associated
with this?
○ Nitrous oxide is 100 times more diffusible than sulfur hexafluoride and, therefore, can expand the size of a gas bubble.
○ This will raise IOP and may result in retinal ischemia with permanent loss of vision.
What is glaucoma? What are its variants?
○ Glaucoma is a condition characterized by raised IOP, optic nerve injury, and gradual loss of vision.
○ It is thought that a sustained increase in IOP results in
diminished perfusion of the optic nerve.
○ Variants include closed angle (or acute) glaucoma and open angle (or chronic) glaucoma.
What are the anesthetic goals in the management of glaucoma patients?
○ The key anesthetic goals in the management of glaucoma patients include avoiding mydriasis (by ensuring miotic drops are continued), understanding the interactions between glaucoma medications and anesthetic agents, and preventing
increases in IOP associated with the induction, maintenance, and emergence from anesthesia.
What are some special anesthetic considerations in children undergoing
strabismus surgery?
○ Special considerations for children undergoing strabismus surgery include an awareness of the high incidence of intraoperative oculocardiac reflex, an increased
risk for malignant hyperthermia, and the high incidence of postoperative
nausea and vomiting.
What is the most common reason for an inpatient admission for children following strabismus surgery?
The most common reason for pediatric inpatient admission following strabismus surgery is postoperative nausea and vomiting (PONV).