Chapter 28 Ophthalmology and Otolaryngology
Ophthalmology
1. What is normal intraocular pressure (IOP)?
2. How is IOP created and maintained?
3. Why and to what extent does IOP increase during coughing or vomiting?
4. What factors during the course of a general anesthetic increase IOP?
5. What physiological factors (CO2, temperature) during the course of a general anesthetic decrease IOP?
6. 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?
7. How much does IOP increase with the intravenous administration of succinylcholine? What is the duration of this effect?
8. What is the mechanism for the increase in IOP following administration of succinylcholine?
9. What maneuvers may attenuate the rise in IOP associated with succinylcholine use for laryngoscopy and intubation?
10. How do paralyzing doses of nondepolarizing neuromuscular blocking drugs affect intraocular pressure?
11. How do inhaled anesthetics affect IOP? What is the effect on IOP of most intravenous anesthetics?
12. How do changes in arterial blood pressure affect IOP?
13. What topical ophthalmic medicines may be absorbed sufficiently to exert systemic effects?
14. What systemic effects have been attributed to the use of topical ophthalmic β-adrenergic blocking medications?
15. What are the systemic effects of topical phospholine iodide (echothiophate)?
16. Why is phenylephrine administered as a topical ophthalmic medicine? What systemic effect has been attributed to the topical ophthalmic application of this drug?
17. 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?
18. What is the oculocardiac reflex? What is its reported incidence? When is it most likely to occur?
19. When is the oculocardiac reflex most often encountered?
20. What cardiac rhythms are likely to result from the oculocardiac reflex?
21. How does arterial hypoxemia or hypercarbia affect the oculocardiac reflex? How does the depth of general anesthesia affect the oculocardiac reflex?
22. What is the first line of treatment of the oculocardiac reflex? What measures may be taken if the reflex persists?
23. Is prophylactic use of anticholinergics fully effective in preventing the oculocardiac reflex? What problems may arise from use of an anticholinergic?
24. What are some important demographic characteristics of patients scheduled for eye surgery?
25. Should antiplatelet or anticoagulant medications be discontinued prior to surgery?
26. What is a key anesthetic consideration for the patient scheduled for ophthalmic surgery with uncontrolled cough, untreated Parkinsonian tremor, severe claustrophobia, or pathological anxiety?
27. What are the anesthetic options for patients having eye surgery?
28. What is the significance of the extraocular muscle cone for eye blocks?
29. What is the ultimate needle tip position for a retrobulbar (intraconal) block?
30. What is the rationale behind extraconal (peribulbar) anesthesia? Where is the ultimate needle tip position?
31. What are some complications of a retrobulbar block?
32. What is the differential diagnosis of altered physiological status (blood pressure, heart rate) after a needle-based ophthalmic regional eye block?
33. How does a sub-Tenon block differ from a needle-based eye block?
34. Which patients are at high risk for retinal detachment?
35. What are the anesthetic considerations for patients undergoing surgery to repair a retinal detachment?
36. 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?
37. What is glaucoma? What are its variants?
38. What are the anesthetic goals in the management of glaucoma patients?
39. What are some special anesthetic considerations in children undergoing strabismus surgery?
40. What is the most common reason for an inpatient admission for children following strabismus surgery?
41. What factors must be considered in the anesthetic management of patients with traumatic eye injuries?
42. Why is “awake” endotracheal intubation hazardous for patients with open globe injuries?
43. What anesthetic maneuvers may attenuate increases in IOP in traumatic eye injury?
44. Is regional anesthesia contraindicated in traumatic eye injuries?
45. What is the most common ocular complication following general anesthesia for non-ophthalmologic surgery? What other condition can mimic it?
46. Why are patients who are undergoing a surgical procedure via general anesthesia at risk for corneal abrasion?
47. What are clinical signs of corneal abrasion?
48. What are some measures that can be taken to reduce the risk of corneal abrasion in patients under general anesthesia? What are some of the potential problems with routine use of ophthalmic ointment?
49. Which surgical procedures are associated with increased risk of postoperative visual loss?
50. What action(s) should be taken if the patient complains of postoperative visual loss?
Otolaryngology
51. What special airway considerations pertain to ENT surgery?
52. Why are posterior pharyngeal packs used during ENT surgery and what precautions are required with their use?
53. What supplemental airway devices may be needed for a difficult airway during ENT surgery?
54. What is laryngospasm? How is the reflex mediated?
55. What is the treatment for laryngospasm?
56. Why are children at particular risk for laryngospasm?
57. Should scheduled ENT surgery be postponed if the child has an upper respiratory infection (URI)? What are the risks associated with proceeding with anesthesia in a child with an active upper respiratory infection?
58. What risks are associated with general anesthesia in a patient with massive epistaxis?
59. What are some symptoms that may alert the anesthesiologist to the presence of obstructive sleep apnea (OSA)?
60. What features may be noted in the airway examination of a patient with OSA?
61. What are the anesthetic implications of OSA?
62. What elements are necessary to generate an airway fire?
63. Are airway fires possible with monitored anesthesia care (MAC)?
64. What are the main anesthetic considerations for middle ear surgery?
65. What effects may nitrous oxide (N2O) exert during ear surgery?
66. How is surgical identification of the facial nerve performed intraoperatively in patients undergoing otologic surgery? How might this affect the anesthetic management?
67. Why do otolaryngologists use epinephrine intraoperatively? What are the anesthesia implications of its use?
68. What concentration of epinephrine is considered safe in ear microsurgery?
69. During otolaryngology surgery how can bleeding in the surgical field be minimized?
70. What is an optimal anesthetic plan for emergence from general anesthesia in the patient who has undergone middle ear surgery?
71. Why are patients who have undergone middle ear surgery at risk for postoperative nausea and vomiting?
72. What anesthetic strategies minimize postoperative nausea and vomiting after ear surgery?
73. What factors contribute to airway obstruction in children undergoing tonsillectomy and adenoidectomy?
74. What is negative pressure pulmonary edema?
75. Why is blood loss often underestimated during and after tonsillectomy and adenoidectomy?
76. What are some considerations for the anesthetic management of patients who return to surgery because of significant bleeding after tonsillectomy and adenoidectomy?
77. What organism is frequently responsible for acute epiglottitis?
78. What are the clinical features of acute epiglottitis?
79. What anesthetic precautions are necessary in acute epiglottitis management?
80. What are the clinical features of foreign body aspiration into the airway?
81. What anesthesia precautions are necessary in addressing the patient with an airway foreign body?
82. What postoperative measures are necessary after the removal of a foreign body from the airway?
83. Why has cocaine been used for nasal surgery?
84. What are the disadvantages of using cocaine? Are there alternatives?
85. What considerations are important for general anesthesia emergence in nasal and sinus surgery?
86. What preoperative investigations may be useful in a patient undergoing endoscopic surgery?
87. What techniques may be used to maintain ventilation and oxygenation during airway endoscopy?
88. What risk is associated with the use of a manual high-pressure jet ventilator (Sanders’ injector apparatus)?
89. What is a laser? What advantages does it offer for surgical procedures?
90. Name some hazards that are associated with laser surgery.
91. What is the purpose of a smoke evacuator used during laser surgery?
92. What measures can be taken during laser surgery to minimize the risk of an endotracheal tube fire?
93. Why should the ETT cuff be filled with saline or an indicator dye during laser surgery?
94. What medical issues are frequently encountered in patients undergoing radical neck dissection?
95. How does a history of radiation to the larynx, pharynx, or oral cavity affect anesthetic management?
96. What arrhythmias may be precipitated during radical neck dissection, and why?
97. What known injuries may be encountered postoperatively after radical neck dissection?
98. What catastrophic postoperative event may occur after neck surgery?
99. How may hypocalcemia present after thyroid surgery?
100. The patient is unable to grimace after a parotidectomy. Why? What monitor(s) may help prevent this complication?
Answers*
Ophthalmology
1. 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 in posture. (487)
2. 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. (487)
3. 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. (487)
4. 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. (487)
5. During general anesthesia hyperventilation and hypothermia decrease IOP. (487)
6. 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. (487)
7. 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. (487)
8. 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. (487)
9. Pretreatment with a small dose of nondepolarizing neuromuscular blocker, lidocaine, β-blocker, or acetazolamide may attenuate increases in IOP associated with use of succinylcholine prior to direct laryngoscopy and endotracheal intubation. (487)
10. Nondepolarizing neuromuscular blocking drugs will decrease IOP by relaxing the extraocular muscles. (487)
11. 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. (487)
12. Arterial hypertension has minimal influence on IOP. Venous drainage is the key factor affecting IOP. (487)
13. 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. (487, Table 31-1)
14. Topical ophthalmic β-adrenergic blocking medications may produce atropine resistant bradycardia and bronchospasm, and exacerbate congestive heart failure. (487, Table 31-1)
15. 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. (487, Table 31-1)
16. Phenylephrine is an α-adrenergic that causes mydriasis (pupil dilation). Systemic absorption of phenylephrine can induce transient malignant hypertension. (487, Table 31-1)
17. Acetazolamide inhibits the production of aqueous humor. Its systemic effects include diuresis and hypokalemic metabolic acidosis. (487, Table 31-1)
18. 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%. (487)
19. 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. (487)
20. 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. (487-488)
21. Hypercarbia, hypoxemia, and light planes of general anesthesia all augment the incidence and severity of the oculocardiac reflex. (488)
22. 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. (488)
23. 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. (488)
24. Eye surgery patients are often at the extremes of age, and range in age from premature 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. (488)
25. 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. (488)
26. 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. (488)
27. The anesthetic options for ophthalmic procedures include general anesthesia, retrobulbar (intraconal) block, peribulbar (extraconal) anesthesia, sub-Tenon block, and topical analgesia. (488)
28. 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. (489, Fig. 31-1)
29. 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). (489, Fig. 31-1)
30. The boundary separating the intraconal from extraconal space is porous. Local anesthetics 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. (489, Fig. 31-1)
31. 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. (489, Table 31-3)
32. 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. (489, Table 31-4)
33. 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. (490, Fig. 31-2)
34. Diabetics and patients with severe myopia are at particular risk for retinal detachment. (490)
35. 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. (490)
36. 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. (490)
37. 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. (491)
38. 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. (491)
39. 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. (491)
40. The most common reason for pediatric inpatient admission following strabismus surgery is postoperative nausea and vomiting (PONV). (491)
41. The anesthetic plan for patients with traumatic eye injuries must balance the specific risks of increasing IOP and exacerbating the ocular insult versus anesthetizing a non fasted patient at risk for aspiration upon the induction of general anesthesia. Increasing IOP via a tightly applied facemask, laryngoscopy and intubation, or from coughing or bucking may result in extrusion of vitreous, and jeopardize ultimate visual outcome. A rapid sequence induction is indicated for the non fasted patient. (491)
42. Awake endotracheal intubation may be appropriate in patients with difficult airways. However, in the setting of a disruptive globe increases in IOP can lead to adverse visual outcomes. The risks associated with rises in IOP produced by an awake intubation must be weighed against the inherent dangers of the difficult airway. (491)
43. It is important to avoid maneuvers that increase IOP in patients with a traumatic eye injury. The patient should be positioned in a slight anti-Trendelenburg tilt. If no airway problems are anticipated, consider the rapid sequence induction of anesthesia with a large dose of nondepolarizing neuromuscular blocking agent. The systemic hypertension and rise in IOP that follows the administration of succinylcholine can be attenuated by the preinduction administration of intravenous medications such as lidocaine and opioids. Also, pretreatment with a small dose of a nondepolarizing neuromuscular blocking agents is useful. (491)
44. Regional anesthesia may be an option for select injuries, and in patients at higher risk from general anesthesia. (491)
45. The most common ocular complication following general anesthesia for non-ophthalmologic surgery is corneal abrasion. It is important to remember a painful eye may also be a manifestation of acute glaucoma.
46. Mechanical damage to the eye can occur during the induction of anesthesia. It can be caused by dangling eye tags, anesthesia masks, drapes, or other objects that come in contact with the open eye. Abrasions can also occur secondary to the loss of the blink reflex with subsequent drying from exposure to the atmosphere and diminished tear production. (491)
47. The clinical signs of corneal abrasion include conjunctivitis, tearing, and foreign body sensation. (491)
48. Preventative measures include gently taping the eyelid shut during mask ventilation, intubation, and thereafter. Ointments may cause an allergic reaction or blur post-emergence vision. Protective goggles may be beneficial. (491)
49. The risk of postoperative visual loss is higher in prolonged spine surgery in the prone position, and cardiac surgery. (492)
50. Early consultation with an ophthalmologist is essential when a patient complains of postoperative visual loss. Funduscopic and visual field examinations may aid in diagnosis. (492)
Otolaryngology
51. Since ENT surgery takes place around the head, the airway becomes relatively inaccessible to the anesthesia provider. Furthermore, there is a real possibility of encountering a difficult airway because of anatomic factors, surgical issues, or underlying pathology. Attention should be directed to establishing and securing the airway, preferably with an endotracheal tube. Also, the airway may become compromised in the perioperative period by undetected bleeding, edema, or surgical manipulation. (492)
52. Posterior pharyngeal packs minimize the risk of aspiration by sealing the larynx from blood that reaches the pharynx. It is vital to alert operating room personnel of their placement, and to confirm their removal prior to extubation. (492)
53. Supplemental airway devices include the video-laryngoscope or fiber-optic bronchoscope. A tracheostomy kit may be necessary for the gravely compromised airway. Ancillary equipment should be readied prior to the commencement of anesthesia. (492)
54. Laryngospasm is an abrupt, intense, and often prolonged closure of the larynx that leads to compromises in ventilation and oxygenation. The reflex is mediated through vagal stimulation of the superior laryngeal nerve. It may be precipitated by instrumentation of the endolarynx, blood or secretions on the vocal cords, and surgical manipulation at inadequate depths of anesthesia. (492)
55. Prompt recognition and intervention is key to the treatment of laryngospasm. Treatment modalities include administration of 100% oxygen via positive-pressure facemask ventilation, placement of oral or nasal airways, and deepening of anesthesia with intravenous or inhalational agents. In refractory cases, a small dose of succinylcholine may be required. (492)
56. In neonates, infants, and small children even brief laryngospasm is perilous. In this group peripheral oxygen saturation drops rapidly because of a small functional residual capacity and relatively high cardiac output. (492)
57. The child with an URI is at increased risk of airway issues, notably breath holding, oxygen desaturation, and postoperative croup. However, not all children with an URI need their ENT surgery postponed. An assessment of the benefits of surgery vs. the risk of airway compromise should be made. For example, the performance of a myringotomy with placement of ventilation tubes requires minimal airway manipulation. (492)
58. Massive epistaxis is often associated with ongoing hemorrhage and concealed swallowing of blood. These patients are at high risk for regurgitation and aspiration. Clinically, they are anxious, hypovolemic, and hypertensive. The preoperative placement of a large-bore peripheral intravenous cannula and adequate rehydration are vital. Hypertension and continued hemorrhage should be anticipated. (492)
59. OSA is characterized by upper airway obstruction and disordered breathing patterns during sleep. Symptoms include snoring, early morning headache, sleep disturbances, daytime somnolence, and personality changes. In children there may be behavioral and growth disturbances as well as poor school performance. (492-493)
60. Many patients with OSA are obese. The combination of limited mouth opening and a large tongue may make visualization of the pharynx difficult. In adult men the neck circumference is large, often exceeding 17 inches. (492-493)
61. One must anticipate difficult airway management in the OSA patient. Mask ventilation, laryngoscopy, and intubation are often challenging. Intraoperative hypertension is common. OSA patients are exquisitely sensitive to the effects of hypnotics and narcotics, and may require prolonged recovery room monitoring. (492-493)
62. There are three key elements needed to produce an airway fire:
63. During monitored anesthesia care the danger of an airway fire exists because the heat and fuel elements are still present. It is important to remove the source of oxidation, and discontinue delivery of supplemental oxygen. (493)
64. There are five primary anesthetic concerns for middle ear surgery:
65. Nitrous oxide is more soluble than nitrogen in blood and diffuses into air-filled cavities. The increases in middle ear pressure may disrupt tympanoplasty grafts. Also, the acute discontinuation of N2O may produce serous otitis. Nitrous oxide should be administered in moderate concentrations (<50%), if at all. (493)
66. The surgeon frequently uses a facial nerve monitor to prevent trauma or accidental incision of the facial nerve and its branches. The use of neuromuscular blocking drugs should be curtailed in order to prevent attenuation of the monitor’s twitch response. Succinylcholine or a single small dose of an intermediate-acting non depolarizing neuromuscular blocking agent is preferred. (493)
67. Epinephrine is injected during ear microsurgery to decrease bleeding and improve visualization within the surgical field. Systemic uptake may precipitate hypertension, tachycardia, and dysrhythmias. (493)
68. Epinephrine concentrations should be limited to 1:200,000 in ear microsurgery. (493)
69. Maneuvers to limit bleeding in the surgical field include use of topical or injected epinephrine, moderate reverse Trendelenburg (head-up) positioning, and volatile anesthetics to decrease arterial blood pressure (within an acceptable range). The use of potent vasoactive drugs and controlled hypotension is controversial. (493)
70. The risk of graft disruption or acute hemorrhage is minimized by the smooth emergence from general anesthesia. Episodic coughing and bucking will produce hypertension that may result in poor surgical outcome. In the uncomplicated airway, extubation of the trachea at a deep plane of anesthesia with spontaneous respiration may be beneficial. (493)
71. Postoperative nausea and vomiting is common after middle ear surgery because of manipulation of the vestibular apparatus. Factors that contribute to PONV include anesthesia technique (use of nitrous oxide and narcotics), inadequate hydration, and postoperative movement. (493)
72. The number of agents used to prevent PONV after ear surgery is guided by a relative risk analysis. Prophylactic agents include corticosteroids, 5HT3-receptor antagonists, neurokinin-1 receptor antagonists, scopolamine patches, and low-dose propofol. Gastric decompression is useful if blood has been swallowed. Scopolamine crosses the blood-brain barrier and may cause confusion, particularly in the elderly. (493)
73. Children undergoing tonsillectomy and adenoidectomy have upper airway obstruction that often only manifests during sleep. The routine use of premedication is controversial. Furthermore, airway obstruction is accelerated by large masses of tonsillar or adenoidal tissue, and loss of pharyngeal tone associated with the induction of anesthesia. Also, manipulation of the airway during light planes of anesthesia may result in acute airway obstruction. (493-494)
74. Negative pressure pulmonary edema clinically manifests when the patient inhales forcefully against a closed glottis. This effort generates marked negative intrathoracic pressures that are transmitted to the pulmonary interstitial tissue, and promotes fluid transition from the pulmonary circulation into the alveoli. (494)
75. Blood loss during tonsillectomy and adenoidectomy is either overt (into the suction bottle) or covert (swallowed). Blood loss is underestimated because the covert loss is not seen. (493-494)
76. Anesthesia considerations for the post-tonsillectomy bleed include the possibility of undetected and prolonged hemorrhage, concomitant hypovolemia, and regurgitation of blood swallowed into the stomach. Measures required include rehydration, rapid sequence induction of general anesthesia, protection of the airway with a cuffed endotracheal tube (minimize risk of aspiration), and drainage of gastric contents. (494)
77. Acute epiglottitis is an infectious disease caused by Haemophilus influenzae type B. It most often affects children between the ages of 2 and 7. (494)
78. There is a history of sudden onset of fever and dysphagia. Symptoms progress rapidly and the child may transition from an acute pharyngitis to complete airway obstruction and respiratory failure within a few hours. The clinical picture is of an agitated, drooling child leaning forward and holding the head in an extended position. The child becomes exhausted from the work of breathing against an almost fully occluded airway. (494)
79. Acute epiglottitis is an airway emergency. Direct visualization of the glottis should not be attempted because stimulation and struggling may produce acute airway obstruction. Emergency airway equipment should be readied. A surgeon adept at rigid bronchoscopy and tracheostomy should be present at the bedside. An inhaled induction of anesthesia maintaining spontaneous respiration is preferred. Atropine may dry secretions and prevent bradycardia. (494)
80. Tracheal aspiration of a foreign body is an airway emergency. Clinical features include sudden dyspnea, dry cough, hoarseness, and wheezing. (494)
81. A preoperative plan and mutual intraoperative cooperation between the anesthesia provider and surgeon are vital in order to avoid inadvertent distal displacement of the foreign body. Removal of the foreign body can be accomplished by either direct laryngoscopy or rigid bronchoscopy. The surgeon should be prepared for an emergency cricothyrotomy or tracheostomy in the event of acute airway occlusion. Total intravenous anesthesia with maintenance of spontaneous ventilation can eliminate operating room pollution. (494)
82. After the removal of a foreign body, postoperatively the patient should receive humidified oxygen and remain under close observation for development of airway edema. (494-495)
83. Cocaine is an effective topical anesthetic agent. Since it is also a potent vasoconstrictor, it reduces bleeding in the surgical field and shrinks the nasal mucosa. (495)
84. The disadvantages of cocaine include altered sensorium (euphoria and dysphoria) and untoward cardiac arrhythmias. For these reasons, cocaine has been surpassed by the “pseudo-cocaine” solution containing a local anesthetic and vasoconstrictor. (495)
85. The removal of posterior pharyngeal packs should be confirmed. Protective airway reflexes should be present prior to extubation because of possible airway edema and ongoing bleeding. (495)
86. Bronchoscopy, laryngoscopy, and microlaryngoscopy involve direct manipulation of the airway. In these procedures, the airway should be assessed carefully paying special attention to the presence of stridor (indicator of compromise). Preoperative investigations such as blood gas analysis, flow-volume loops, radiographic studies, and magnetic resonance imaging may be useful. (495)
87. A variety of techniques can be employed to provide oxygenation and ventilation during endoscopy. The trachea may be intubated with a small diameter pediatric endotracheal tube but this may impair visualization of the posterior commissure. An alternative technique, jet ventilation, utilizes high-flow oxygen insufflation through a small-gauge catheter placed in the trachea. (495)
88. The use of the manual high-pressure jet ventilator carries risks of pneumothorax and pneumomediastinum. (495, Fig. 31-4)
89. Laser is an acronym for light amplification by stimulated emission of radiation. It produces an intense focused light beam that allows for precise and controlled coagulation, incision, and vaporization of tissues. Advantages of laser include its ability to target difficult-to-reach lesions, provide hemostasis, produce minimal edema, and promote rapid healing. (495)
90. Hazards associated with laser surgery include atmospheric contamination by fine particles of vaporized tissues, misdirected laser energy, venous gas embolism, and ocular (retina) injury. There is also risk of endotracheal tube (ETT) fire during airway surgery. (495-496)
91. During laser surgery an efficient smoke evacuator, as well as special masks, is necessary because small, vaporized particles are easily inhaled. (495)
93. The purpose of filling the ETT cuff with saline or an indicator dye during laser surgery is to help dissipate laser heat. Furthermore, leaking dye is an indicator of cuff rupture. (496)
94. Radical neck dissection is indicated for removal of a malignancy. These patients frequently have a history of tobacco and alcohol abuse. An extensive preoperative work-up is necessary because pulmonary and cardiac disease is prevalent. (496)
95. A history of prior radiation therapy to the larynx, pharynx, or oral cavity may produce marked tissue indurations, scarring, and limitation of mobility. These may cause difficulties with airway management, particularly endotracheal intubation. (496)
96. Traction or pressure on the carotid sinus may provoke acute arrhythmias. These include prolongation of the QT interval, bradydysrhythmias, and asystole. Treatment includes early detection, cessation of the surgical stimulus, and administration of an anticholinergic agent. Another option is local anesthetic infiltration of the carotid sinus. (496)
97. Injuries to the facial (VII) nerve, recurrent laryngeal nerve, and phrenic nerve may all be encountered postoperatively after radical neck dissection surgery. (496)
98. Hematoma formation in the neck may compress the airway leading to acute obstruction. If tracheotomy is not performed during the initial surgery, then the patient requires close monitoring (for laryngeal or upper airway obstruction) in the postoperative phase. (496)
99. Hypocalcemia after thyroid surgery may present in many forms. Clinical signs may include tetany (carpal spasm), peripheral and circumoral paresthesia, QT interval prolongation, and laryngospasm. (497)
100. The inability to perform a symmetrical grimace after parotid surgery is indicative of facial nerve injury or traction. Since the parotid gland is traversed by the facial nerve, it is customary to monitor the facial nerve function with a facial nerve monitor. Occasionally, the facial nerve may need to be sacrificed. It is then reconstructed with a graft from the greater auricular nerve. (497)
