ORTHOPEDIC, OPHTHALMIC, AND ENT ANESTHESIA
From the Cleveland Clinic’s Comprehensive Anesthesiology Review, presented April 30 to May 5, 2005
| ORTHOPEDIC ANESTHESIA —John E. Tetzlaff, MD, Professor of Anesthesiology, Cleveland Clinic Lerner College
of Medicine of Case Western Reserve University, and Program Director, Center for Anesthesiology Education, Division
of Anesthesiology and Critical Care Medicine, Cleveland Clinic Foundation, Cleveland
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| Pneumatic tourniquet: selected by surgical colleagues to provide optimum surgical field; exsanguination of limb and
prevention of arterial inflow provides bloodless surgical field; also reduces blood loss, allows identification of structures,
and permits careful dissection while sparing delicate structures; theoretically, used to limit spread of systemic
infection in limb; used by anesthesia provider for intravenous (IV) regional anesthesia; must be applied correctly to
avoid injuring skin, underlying subcutaneous tissue, and muscles; should be used with properly calibrated manometer;
anesthesia provider has tradition of keeping track of time tourniquet has been in place and notifying surgeon
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 | Limitations: difficult to use near sterile field; difficult to use in morbidly obese patient because of configuration of
limbs and potential for eccentric inflation and injury to tissues; calcific arterial disease also interferes; may result in
situation referred to as “venous tourniquet”; arterial flow continues, venous flow obstructed; use caution with asymmetric
application, especially in limbs with dramatic change in circumference from one side of tourniquet to other
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| Consequences of normal use: direct pressure-induced changes (eg, anaerobic metabolism; mediators of cell injury occur
below tourniquet as result of ischemia)
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| Consequences of abnormal use: if duration >≈2 hr, incidence increases (more with upper extremity); initially, cellular
swelling in skeletal muscle; after time, cell wall damage occurs; in cases of extreme acidosis, elevated creatine kinase
(CK) and lactate; tissue biopsy shows reversible cell damage at 120 min, overt cellular death 15% to 40% at 180 min;
≤20% of patients have some compartment syndrome below tourniquet
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| Patient response
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| Sedated under regional anesthesia: discomfort with inflation; anesthesia in ≈5 min; progressive neuropathic pain in
30 to 45 min; usually involves somatic block, so initial response to inflation minimal; neuroendocrine response attenuated
by sympathectomy associated with regional block; hemodynamic response also attenuated by sympathectomy;
tourniquet pain visceral, not somatic; occurrence time-related; more common in lower extremity; may be
neurometabolic; related to anesthetic techniques
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| Sedated under general anesthesia: nociceptive pain possible; definite stimulus from inflation; ischemia occurs for 10 to
30 min; neuroendocrine (stress) response; release of vasopressors; hemodynamic response includes hypertension and
tachycardia; incidence begins to increase at 60 min; phenomenon short lived (may result in hypotension)
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| Theories of tourniquet pain: not solely ischemia of nerve trunk; may be differential blockade, frequency-dependent
block, elements of ischemia or anaerobic metabolism recruiting receptors in dose-response manner, or related to
tissue injury mediator
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| Tourniquet deflation: consequences time-related; strictly related to products that occur in anaerobic area (eg, CO2 ,
lactate, acid ions, embolic products); hemodynamic consequences include universal vasodilation (from lactate and
anaerobic metabolites); patient becomes hypercarbic from accumulation of CO2 and metabolism of extra lactate;
results in brief intense metabolic acidosis; vasodilation related to variety of products; endpoint hypotension and tachycardia;
hypotension universal with lower extremity tourniquet deflation after 90 min, but may be sustained in
hemodynamically compromised; release of fat may occur. with propensity for fat embolism syndrome; fulminant
pulmonary embolism may occur occasionally; acute arterial occlusion requiring interventional treatment from vascular
surgeon or radiologist; always risk for compartment syndrome; acute coronary vasospasm also reported with
deflation of pneumatic tourniquet
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| Fat embolism: more common in young healthy person; occurs with high-velocity fracture (eg, motorcycle or skiing accident);
associated with pelvic fracture and 1% to 2% of long-bone fractures (eg, femur, tibia)
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| Pathophysiology: related to deposition of fat in variety of tissues and body’s response; anticellular enzymes in skin,
central nervous system (CNS), and lung cause digestion of structures, with specific consequences; excess fat on pulmonary
artery side can cause right heart failure
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| Diagnosis: cutaneous signs include petechiae on trunk and face; CNS signs indirect and include agitation and signs consistent
with hypoxia; pulmonary signs include alveolar-arterial (A-a) O2 gradient (>100 mm); cardiovascular signs
nondescript; shake test most sensitive laboratory test; truncal flushing and petechiae and retinal cotton-wool exudates
related to blood vessels being destroyed by antifat enzymes; altered level of consciousness in trauma setting should be
indicator, especially in relatively healthy person; focal neurologic signs rare but ominous; seizure activity usually related
to cerebral edema and/or increased intracranial pressure (ICP); pulmonary signs include tachycardia and dyspnea
(nonspecific to fat embolism syndrome); worse when wheezing associated with hemoptysis (active destruction of pulmonary
system); can evolve to noncardiogenic pulmonary edema when pulmonary artery filled with fat, causing obstruction
of right heart
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| Procedures: include open reduction and internal fixation of long bones (endomedullary nails), medullary reaming (total
hip repair without tourniquet), pelvic fracture procedure, joint replacement (pressurized methylmethacrylate), and
knee fusion
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| Treatment: identify; stop features of condition causing fat movement; if possible, inflate tourniquet; support cardiovascular
system with volume, inotropes, and vasopressors; support O2 any way necessary (steroids controversial); support
CNS by reducing acute ICP and cerebral edema; support blood pressure
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| Methylmethacrylate: bone cement; becomes as dense and structurally solid as bone itself; if monomer enters circulation,
it becomes potent hemodynamically active agent; profound vasodilator; effective at degranulating mast cells,
with release of massive amounts of histamine; now, less monomer as cement hardens; bone plugs used to restrict
flow of cement; some surgeons use venting devices to allow pressure release
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| Circumstances: revision hip procedure requires large amount of cement; bone often abused from chronic failure of device,
infection, or both; previously infected bone increases mobilization; exposure to circulation poorly tolerated in dehydrated
patient, especially intravascular volume dehydration in patient with limited cardiac reserve; gross embolization occurs
during endoprosthesis insertion if cement in liquid state
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| Signs: tachycardia, hypotension, abrupt decrease in level of consciousness; in extreme situation, wheezing, right heart
failure, cyanosis, myocardial ischemia from histamine release, and cardiac arrest
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| Treatment: supportive; volume (preferably given before methylmethacrylate); support cardiac output with inotropes;
support preload with vasopressors
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| OCULOCARDIAC REFLEX (OCR)—Maria Rica Inton-Santos, MD, Staff Anesthesiologist, Department of General
Anesthesiology, Cleveland Clinic Foundation, Cleveland
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| Definition: change in heart rate with certain stimuli during ophthalmic surgery; ranges from pain, pressure on eyeball,
manipulation of extraocular muscles (during strabismus surgery), retrobulbar blockade, or pressure on tissue remaining
in orbital apex upon enucleation
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| Incidence: 33% to 90%; higher incidence in pediatric population undergoing strabismus surgery
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| Pathophysiology: pathway consists of fibers from short and long ciliary nerves that run to ciliary ganglion; proceeds to
gasserian ganglion along ophthalmic division of trigeminal nerve; terminate in main sensory nucleus of trigeminal
nerve in floor of fourth ventricle, then stimulates vagus nerve, producing bradycardia associated with OCR; graded
phenomenon (strength and acuity of force of stimulus affects likelihood of occurrence); higher incidence with hypercapnia;
widely accepted that medial rectus muscle has lowest threshold for OCR; however, recent study shows no significant
difference between medial rectus and other muscles of eye
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| Diagnosis: most common manifestations include bradycardia, ventricular arrhythmia, and even periods of asystole; vagal
response may produce hypotension; heart rate returns to baseline in 10 to 15 sec; recurrence of OCR subject to fatigue
(subsequent stimuli do not produce OCR)
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| Treatment: first, ask surgeon to stop manipulation; wait for return to baseline before fatiguing reflex; surgeon can reduce
OCR by exerting gentle tension when restarting surgery; if arrhythmia persists, treat with IV atropine 0.007 mg/
kg; glycopyrrolate probably equally effective (compared to atropine); may have slower onset but produces less tachycardia;
surgeon may also place topical lidocaine on field to stop OCR; if arrhythmias persist, anesthesia provider should
ensure adequate depth of anesthesia, with controlled ventilation maintaining normocapnia
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| COCAINE OR ANOTHER CHOICE FOR NASAL SURGERY —Dr. Tetzlaff
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| History: first local anesthetic; evidence of cocaine use to relieve pain and facilitate various interventions in 1800s in
South America; European travelers discovered topical and euphoric properties of coca leaves and brought leaves back
to Europe; German scientists discovered active ingredient and extracted cocaine crystals from coca leaves; Koller reported
first clinical use for topical anesthesia of eye; after drug introduced into medical community, it rapidly became
known to have profound effect on all mucous membranes, producing topical anesthesia and intense vasoconstriction;
development of hypodermic syringe allowed further use (eg, infiltration; subarachnoid block); others began using cocaine
for topical anesthesia of airway and gastrointestinal (GI) tract
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| Chemical properties: tissue irritation; causes rhabdomyolysis if injected into skeletal muscle; rapid, dense topical anesthesia
of mucous membranes associated with intense vasoconstriction; rapid plasma uptake from mucous membranes
(even more accelerated with infected or injured mucous membranes); reformulated from alcohol preparation to alkaloid
preparation to prevent recreational abuse
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| Metabolism: slow elimination from body; ≤10% eliminated intact in urine; 2-step metabolism includes ester hydrolysis
and conjugation; clinical metabolites, although less potent, can also contribute to toxic side effects; in patient with
decreased or atypical plasma cholinesterase, duration of action prolonged
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| Toxicity: related to vasoconstriction; potential for CNS accumulation, causing limbic and seizure activity; “most unfortunate
side effect” involves interaction with catecholamine metabolism; vasoconstriction topical and systemic, including
predisposition to arterial vasospasm, hypotension, and coronary vasospasm; local anesthetic toxicity includes direct
tissue toxicity, rapid absorbance from mucous membranes, and sustained excitation with plasma levels because of slow
elimination; seizure activity and cardiovascular collapse reported with excessive illicit use; altered catecholamine metabolism
(potent ability to block reuptake of peripheral catecholamines); subsequent increase in catecholamine levels
causes additional work for myocardium, including hypertension, tachycardia, and synergy with other systemic vasoconstrictive
events; leads to myocardial ischemia, arrhythmia, and interaction with other drugs known to do same (eg,
halothane, theophylline, tricyclic antidepressants)
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| Clinical use: used as 4% alkaloid solution in ear, nose, and throat (ENT) surgery; slower than alcohol-based solution for
topical anesthesia of eye; ≤5 min for full-depth mucous membrane anesthesia and vasoconstriction; duration 90 to 120
min; limited to 160 mg total dose (or 3 mg/kg for smaller body size); apply incrementally; effective for topical anesthesia
of tympanic membrane, oropharyngeal area, reduction of nasal fracture, nasal endoscopy, intense vasoconstriction for
transnasal approach to pituitary, and surgery around nose; also used in facial applications as mixture in tetracaine, adrenaline,
and cocaine (TAC) solutions; “diversion is a problem”; some hospitals have elaborate documentation systems that
make use in operating room cumbersome; may irritate cornea if used repeatedly; reported to be toxic when applied directly
to cartilage; may be associated with hypertension, tachycardia, arrhythmia, myocardial ischemia, and myocardial infarction,
even if not at risk
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| Alternatives: eutectic mixture of local anesthetics (EMLA; lidocaine with prilocaine) has profile comparable to topical
cocaine; better designed for dermis than mucous membrane; TAC preceded EMLA in pediatrics, but severe injuries associated
with overdosing TAC (eg, seizure, cardiac arrest) may limit pediatric use; lidocaine combined with vasoconstrictors
leading alternative (eg, epinephrine, phenylephrine, oxy-metazoline); gel-based lidocaine sustains
vasoconstrictor in direct contact with mucous membrane for longer period; 1% tetracaine gel mixed with vasoconstrictor
excellent alternative (sustained duration); airway blocks also useful; transtracheal injection provides profound anesthesia;
benzocaine also used successfully
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Educational Objectives
| The goal of this program is to educate the listener about orthopedic, ophthalmic, and otolaryngologic anesthesia. After
hearing and assimilating this program, the clinician will be better able to:
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| 1. Identify anesthetic issues associated with the use of a pneumatic tourniquet and with methylmethacrylate.
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| 2. Discuss the diagnosis and anesthetic implications of fat embolism and deep venous thrombosis.
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| 3. Diagnose and effectively treat the oculocardiac reflex and prevent complications.
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| 4. Describe the clinical use of cocaine and understand the perioperative risks.
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| 5. List the alternatives to the use of cocaine for topical anesthesia.
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Discussed on This Program
Atropine sulfate (several trade names)
Benzocaine (ethyl aminobenzoate) [many trade names]
Bupivacaine HCl (many trade names)
Cocaine [Cocaine HCl, Cocaine Viscous]
Epinephrine [Adrenalin Chloride, others]
Glycopyrrolate [Robinul, Robinul Forte]
Halothane [Fluothane]
Lidocaine HCl (many trade names)
Lidocaine with prilocaine [EMLA Anesthetic]
Oxymetazoline HCl (many trade names)
Phenylephrine HCl (many trade names)
Tetracaine HCl [Pontocaine, Pontocaine HCl, Viractin]
Theophylline (many trade names)
Suggested Reading
Allison CE et al: A comparison of the incidence of the oculocardiac and oculorespiratory reflexes during sevoflurane or
halothane anesthesia for strabismus surgery in children. Anesth Analg 90:306, 2000; Arai YC et al: Preoperative stellate
ganglion blockade prevents tourniquet-induced hypertension during general anesthesia. Acta Anaesthesiol Scand 48:613,
2004; Ernst AA et al: Comparison of tetracaine, adrenaline, and cocaine with cocaine alone for topical anesthesia. Ann
Emerg Med 19:51, 1990; Estebe JP et al: Use of a pneumatic tourniquet induces changes in central temperature. Br J
Anaesth 77:786, 1996; Fleming JA et al: Pharmacology and therapeutic applications of cocaine. Anesthesiology
73:518, 1990; Grinspoon L et al: Coca and cocaine as medicines: an historical review. J Ethnopharmacol 3:149,
1981; Heine TA et al: Fatal pulmonary fat embolism in the early postoperative period. Anesthesiology 89:1589, 1998;
Iwama H et al: Circulatory, respiratory and metabolic changes after thigh tourniquet release in combined epidural-propofol
anaesthesia with preservation of spontaneous respiration. Anaesthesia 57:588, 2002; Jenkins K et al: Fat embolism
syndrome and elective knee arthroplasty. Can J Anaesth 49:19, 2002; Karlsson J et al: Methylmethacrylate
monomer produces direct relaxation of vascular smooth muscle in vitro. Acta Anaesthesiol Scand 39:685, 1995; Kil HK:
Hypercapnea is an important adjuvant factor of oculocardiac reflex during strabismus surgery. Anesth Analg 91:1044,
2000; Kim KJ et al: Direct myocardial depressant effect of methylmethacrylate monomer: mechanical and electrophysiologic
actions in vitro. Anesthesiology 98:1186, 2003; Milot JA et al: The oculocardiac reflex in strabismus surgery.
Can J Ophthalmol 18:314, 1983; Mirakhur RK et al: I.m. or i.v. atropine or glycopyrrolate for the prevention of oculocardiac
reflex in children undergoing squint surgery. Br J Anaesth 54:1059, 1982; Mitsuhata H et al: Methylmethacrylate
bone cement does not release histamine in patients undergoing prosthetic replacement of the femoral head. Br
J Anaesth 73:779, 1994; Ohashi T et al: Quantitative analysis of the oculocardiac reflex by traction on human extraocular
muscle. Invest Ophthalmol Vis Sci 27:1160, 1986; Sasano N et al: Cerebral fat embolism diagnosed by magnetic
resonance imaging at one, eight, and 50 days after hip arthroplasty: a case report. Can J Anaesth 51:875, 2004; Sutin
KM et al: Deep venous thrombosis revealed during ultrasound-guided femoral nerve block. Br J Anaesth 94:247, 2005;
Tetzlaff JE et al: Regional anaesthetic technique and the incidence of tourniquet pain. Can J Anaesth 40:591, 1993;
Townsend HS et al: Tourniquet release: systemic and metabolic effects. Acta Anaesthesiol Scand 40:1234, 1996;
Tuncali B et al: Controlled hypotension and minimal inflation pressure: a new approach for pneumatic tourniquet application
in upper limb surgery. Anesth Analg 97:1529, 2003; Vince KG: Bilateral total knee arthroplasty under one anesthesia:
a safe protocol. Mayo Clin Proc 72:883, 1997.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported
nothing to disclose.
Drs. Tetzlaff and Inton-Santos were recorded at the Comprehensive Anesthesiology Review, presented April 30-May 5,
2005, by the Cleveland Clinic Division of Anesthesiology and Critical Care Medicine, and held in Cleveland. The Audio-
Digest Foundation thanks the speakers and the Cleveland Clinic Foundation for their cooperation in the production of this
program.
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