2.2 Anesthesia



10.1055/b-0038-162741

2.2 Anesthesia



2.2.1 Principles of Anesthesia



Modes of Anesthesia


General anesthesia: This mode is characterized by total loss of consciousness with blunted (or absent) protective upper airway reflexes and the use of an endotracheal tube (ETT) or supraglottic device (e.g., laryngeal mask airway).


Sedation: This mode aims to maintain protective upper airway reflexes in patients with iatrogenically altered levels of consciousness. Supplemental oxygen is often required (e.g., nasal cannula), with or without the assistance of an oral/nasopharyngeal airway. It can range from minimal (i.e., patient is responsive to verbal command) to deep (i.e., no response to procedural stimulation).


Regional anesthesia: This mode involves the use of local anesthetics in conjunction with sedation or general anesthesia to improve analgesia, expedite recovery, and reduce overall IV/inhalational anesthetic requirements. It can be used as a sole anesthetic for minor or superficial procedures.



Factors of Anesthesia


An ideal anesthetic strikes a balance between the following four essential factors, which in turn are influenced by independent patient risk factors, unique surgical requirements, and circumstances under which recovery is to occur.


Amnesia/anxiolysis: Management of preoperative anxiety and control of intraoperative awareness is a cornerstone of anesthetic care. Various oral, IV, and/or inhalational agents may be used, depending on the desired effect. Analgesia: Multimodal therapy is the preferred method of achieving intra- and postoperative pain control with a combination of opioids, COX-2 selective and nonselective nonsteroidal antiinflammatory drugs (NSAIDs), and local anesthetics, and/or adjuvants, especially in patients suffering from chronic pain (e.g., the calcium channel α2δ antagonists gabapentin and pregabalin, the N-methyl–aspartate [NMDA] receptor antagonist ketamine, or α 2agonists such as clonidine).


Muscle relaxation: Depolarizing and/or nondepolarizing muscle relaxants facilitate optimal airway conditions for laryngoscopy and surgical manipulation.


Antiemetics: Postoperative nausea and vomiting (PONV) is a strongly undesirable complication in patients following head and neck surgery. High-risk procedures include otology surgery, adenotonsillectomy, and thyroidectomy as well as head and neck cancer surgery. PONV influences patient satisfaction, length of stay, recovery, and surgical outcome. Multimodal and prophylactic therapy improves outcomes. Emesis may predispose development of wound hematoma, which can become an airway emergency in the presence of a neck wound.



Phases of Anesthesia


Preinduction: This phase begins in the preoperative area and continues to the point where a patient is positioned on the operating room (OR) table with standard monitors (electrocardiogram [ECG], noninvasive blood pressure, pulse oximetry, capnography) and has been adequately preoxygenated. Induction: General anesthesia in patients with established IV access is initiated with rapid-acting parenteral drugs to facilitate airway control. Otherwise, inhalational anesthetics are administered via a face mask; once an adequate depth of anesthesia is achieved, IV access is established and is followed by the placement of an ETT or supraglottic device (unless a very brief procedure is planned). For sedation cases, IV agents are titrated to effect while maintaining spontaneous ventilation. For difficult airway situations, awake fiberoptic nasotracheal intubation or awake tracheotomy may be indicated to secure the airway, prior to induction of general anesthesia.


Maintenance: Global amnesia is maintained during surgery with inhalational agents and/or parenteral drug infusions. Surgical analgesia is maintained either with a well-established regional block, generous local anesthetic infiltration, intermittent opioid boluses, and/or IV narcotic infusion. Duration of required muscle paralysis depends on several factors and may be just long enough to facilitate ETT placement. In some instances (e.g., cases involving extensive neuromonitoring), anesthesia may be maintained through the predominant or exclusive use of parenteral infusions (total intravenous anesthesia, TIVA). TIVA is sometimes useful to reduce vasodilation and bleeding (e.g., in endoscopic sinus surgery).


Emergence: Extubation is performed upon the patient′s meeting the criteria of spontaneous ventilation, reversal of neuromuscular blockade, suctioning of airway.


Table 2.8 provides an overview of the key aspects of each phase of anesthesia.




















Table 2.8 Key areas in each phase of anesthesia

Preinduction


Induction


Maintenance


Emergence


Airway assessment


Intravenous access


Anxiolysis


Aspiration precautions


Positioning for safety and patient comfort


Baseline vital signs


Preoxygenation


Adequate depth of anesthesia (to prevent awareness or laryngospasm)


Aspiration precaution (cricoid pressure, rapid sequence induction)


Positioning for optimal view of the airway upon direct laryngoscopy


Securing the airway (confirmed by auscultation, inspection, and capnography)


Maintenance of end organ perfusion


Adequate fluid administration


Normothermia


Appropriate anesthetic depth


Procedural analgesia


Facilitation of optimal surgical field (e.g., controlled hypotension)


Extubation upon meeting criteria (spontaneous ventilation, reversal of neuromuscular blockade, suctioning of airway)



Stages of Anesthesia


Stage 1: The period between initial delivery of induction agents and loss of consciousness. Patients experience analgesia without amnesia and can often carry on a conversation during this time.


Stage 2: More commonly known as the “excitement stage,” this stage follows loss of consciousness and is characterized by delirious, uninhibited, and often spastic activity. Cardiovascular and respiratory patterns are erratic.


There is also an increased risk for aspiration. The goal of any anesthetic induction is thus to minimize time spent in this stage.


Stage 3: In this stage, also known as “surgical plane,” procedural stimulation causes minimal, if any, cardiovascular and/or respiratory changes.


Stage 4: This stage occurs when a massive anesthetic overdose causes severe depression of brainstem activity, leading to respiratory and/or cardiovascular collapse. This stage should never be reached, as it may be lethal even with appropriate cardiovascular and/or respiratory support.



2.2.2 Regional Anesthesia Techniques



Benefits of Regional Anesthesia


When combined with a general anesthetic, regional nerve blocks reduce narcotic requirements and their subsequent side effects, such as nausea, vomiting, somnolence, and respiratory depression. Time to discharge is reduced.



Contraindications to Regional Anesthesia


Contraindications to regional anesthesia include lack of patient consent and interference with surgical field/technique. Relative contraindications include coagulopathy, infection at the skin site, and presence of neurologic disease.



Complications Common to All Nerve Blocks


Complications common to all nerve blocks include local anesthetic complications (intravascular injection, overdose, and allergic reaction), nerve damage (needle trauma, intraneural injection), infection, and hematoma.



Blocks of the Scalp and Face



Supraorbital and Supratrochlear Nerve

Indications: Closure of lacerations, forehead and ear procedures


The forehead and anterior scalp can be rendered insensate by blocking the supraorbital and supratrochlear nerves, branches of the ophthalmic division of the trigeminal nerve (CN V1), where they exit from their respective foramina along the brow line.


A skin wheal is placed over the glabella. A 25-gauge needle, bent to aid in superficial placement, is inserted through the anesthetizing wheal and advanced laterally along the brow. A total of 8 mL of local anesthetic is applied from the glabella to the lateral edge of each brow.



Greater and Lesser Occipital Nerves

Indications: Closure of lacerations


By blocking the greater and lesser occipital nerves, the posterior scalp can be anesthetized. By placing a track of local anesthetic from the mastoid process to the inion (i.e., external occipital protuberance) along the highest nuchal line from each side, both the greater and lesser occipital nerves will receive a dose of local anesthetic, and the posterior scalp will become anesthetized.


A large skin wheal is placed over the mastoid process on each side using a 27-gauge needle. Then, through this wheal, a wheal is placed from the mastoid process to the inion using a 25-gauge Quincke needle that is bent to facilitate a superficial injection.



Infraorbital Nerve

Indications: Closure of lacerations, facial surgery


The maxillary division of the trigeminal nerve (CN V2) innervates the midface, from the inferior portion of the orbit to the mandible. This area includes the area overlying the zygoma, the maxilla, and most of the nose, as well as the philtrum and the hard and soft palate.


The infraorbital foramen is palpable 2 to 3 mm below the rim of the orbit, just medial to the equator of the orbit. A small-gauge needle is used to inject local anesthesia just outside the foramen. Avoid injection into the foramen, as the nerve is located in a confined space.


A small amount (2–4 mL) of local anesthetic is sufficient, and it should be injected based on which area is to be anesthetized. Specifically, emphasize above the foramen for lower lid work, medial to the foramen for lateral nasal work, and inferomedial to the foramen for work on the philtrum.



Blocks of the Neck



Superficial Cervical Plexus

The cervical plexus is composed of four nerve roots, C1–C4, and terminates in four branches: the lesser occipital, great auricular, transverse cervical, and supraclavicular nerves. The terminal branches emerge superficially at the posterior border of the sternocleidomastoid (SCM) muscle along the midportion of the muscle.


This is a purely cutaneous nerve block; there is no motor block with the superficial cervical plexus block. Neuromonitoring and stimulation of the recurrent laryngeal nerve are not compromised when using this block.


The patient is positioned in the seated position. A line connecting the insertion of the SCM at the midpoint of the clavicle to the mastoid process along the posterior muscle border designates the path in which subcutaneous local anesthetic should be injected. Initially, 3 to 5 mL of local anesthetic is injected at the midpoint of the SCM using a 27-gauge needle. Using a 25-gauge Quincke point spinal needle, subcutaneous injections are then performed from this initial injection site in caudad and cephalad directions along the posterior edge of the SCM. Infiltration along these paths should require 6 to 8 mL of anesthetic in each direction. Aspiration prior to injection is important to avoid intravascular injection.



Deep Cervical Plexus

The deep cervical plexus (DCP) is the collection of the C2–C4 nerve roots as they exit the “gutter” formed by the transverse processes of the respective vertebrae. By injecting proximal to the division of the cervical roots into dorsal and ventral rami, a more complete blockade of the ipsilateral neck is achieved—including both sensory and motor elements (including the phrenic nerve, paralyzing the ipsilateral diaphragm). This is not commonly used for otolaryngology procedures.


The patient is seated upright in a high Fowler position with a small towel behind the shoulders. The above-mentioned line is drawn between the mastoid process and the anterior tubercle of C6, which is palpable in the vast majority of patients. A line parallel to this is drawn 1.5 cm behind the first, and the posterior tubercle is palpated on C2, C3, and C4. Deep palpation can be uncomfortable, and a light touch is indicated. After a small skin wheal is placed with a 27-gauge needle, a short (2.5-cm) blunt needle is advanced to the posterior process of each of the three vertebrae and then “walked” laterally and anterior to the posterior tubercle. An advance of 1 mm beyond the bony tubercle will suffice. It is not uncommon for the patient to describe a light paresthesia in the dermatome of the root being blocked. After careful aspiration, 4 to 5 mL of local anesthetic (with epinephrine) is injected at each of the three levels (C2, C3, C4). The proximity to the spinal column and major vascular structures increases the risk of intrathecal or intravascular injection.



Specific Nerve Blocks for the Upper Airway


Maxillary Division of the Trigeminal Nerve (Pterygopalatine Ganglion)



  • The transnasal topical approach to the pterygopalatine (sphenopalatine) ganglion involves application of local anesthetic to the mucous membranes surrounding the ganglion.



  • Position the patient supine with neck extension. A local anesthetic (typically 80 mg of 4% cocaine) is applied to each nostril. Cotton-tipped applicators soaked in 4% cocaine are gently swirled and advanced into the nares. Each applicator is advanced a little further than the one prior, and once placed, the applicator is left there as successive applicators are introduced. Each nostril should receive four to seven applicators as the opening allows. The applicators should remain in the nares for at least 20 minutes, allowing the local anesthetic to diffuse through the mucosa overlying the ganglion.



  • The pterygopalatine ganglion can also be approached through the greater palatine foramen, located at the posterior portion of the hard palate. In this approach, the patient is positioned in the supine position with the neck extended. The foramina can be palpated medial to the gumline of the third molar. A small-gauge needle is advanced < 2.5 cm through the foramen in a superior and slightly posterior direction. To avoid an intravascular injection, aspirate prior to injection.



Glossopharyngeal Nerve



  • The glossopharyngeal nerve (CN IX) exits the skull at the jugular foramen and passes between the internal jugular vein and the internal carotid artery. It descends just dorsal to the styloid process before curving forward and anterior to innervate the palatine tonsil, the mucous membranes of the fauces, and the base of the tongue. This nerve has motor, sensory, and autonomic components and supplies lower motor neurons to the stylopharyngeus and parasympathetic innervation of the parotid and mucous glands.



Superior Laryngeal Branch of the Vagus Nerve



  • The superior laryngeal nerve can be blocked as it passes into the thyrohyoid membrane inferior to the greater cornu of the hyoid bone and superior to the greater cornu of the thyroid cartilage. This block will provide anesthesia to the glottis above the vocal folds.



  • With the patient seated in an upright (high Fowler) position with a towel roll transversely laid behind the shoulders, the thyroid cartilage is palpated. It can be helpful to lightly displace the thyroid cartilage toward the side of the block. Using a small-gauge needle, 2 to 3 mL of local anesthetic is injected near the cartilaginous greater cornu. Aspiration prior to injection will confirm that the needle has not entered the supraglottic air column. This procedure is then repeated on the other side.



Topical Anesthesia of the Subglottic Airway



  • The recurrent laryngeal branch of the vagus nerve pierces the subglottic trachea to innervate all the laryngeal muscles other than the cricothyroid muscle as well as provide sensory innervation to the subglottic mucosa.



  • The patient is positioned in a high Fowler position with a towel roll laid transversely behind the shoulders. Moderate neck extension is helpful. After skin disinfection, the thyroid cartilage is identified. The next palpable cartilage inferiorly is the cricoid cartilage. The palpable gap between these two structures overlies the cricothyroid membrane. A 22-gauge needle containing local anesthetic (2 to 4 mL 3% chloroprocaine or 2 to 4 mL 4% lidocaine) is advanced perpendicular to the skin while gentle aspiration is applied to the syringe plunger. Air will be freely aspirated when the needle penetrates the cricothyroid membrane, entering the trachea. The patient should be alerted that the injection will induce coughing. The local anesthetic should be rapidly administered and the needle withdrawn. The patient will cough and should be encouraged to do so several times to enhance spread of the anesthetic.



2.2.3 Anesthesia Drugs



Opioids


Opioids work by binding to specific receptors located throughout the central nervous system (CNS) and other tissues ( Table 2.9 ). The pharmacodynamic effect of an administered opioid depends on which receptor is bound, the affinity of the binding, and whether the receptor is activated or inhibited. There are four opioid receptors: mu, delta, kappa, and sigma ( Table 2.10 ).
































Table 2.9 Opioid effects on organ systems

Organ system


Physiologic response


Cardiovascular


In general, opioids do not impair cardiovascular function.


At high doses opioids can lead to bradycardia.


Meperidine, structurally similar to atropine, can cause tachycardia.


Hypotension seen with opioid use is secondary to bradycardia and, in the case of morphine and meperidine, histamine-induced vasodilation.


Respiratory


Opioids depress ventilation, particularly respiratory rate. The hypoxic drive, the body′s ventilatory response to CO2, is decreased. The result is an increase in PaCO2 and decreased respiratory rate.


The apneic threshold, the highest PaCO2 at which a patient will remain apneic, is increased.


In patients susceptible to histamine-induced reactive airway disease, morphine and meperidine can lead to bronchospasm. Chest wall rigidity, severe enough to prevent adequate ventilation, can be seen with fentanyl and remifentanil.


Central nervous


Opioids reduce cerebral oxygen consumption, cerebral blood flow, and intracranial pressure.


Minimal changes are seen on EEG except for meperidine, which can cause an increase in EEG frequency.


Even at high doses, opioids do not reliably produce amnesia. The high doses necessary to establish unconsciousness can lead to physical dependence.


Gastrointestinal


Opioids slow peristalsis, resulting in decreased gastric emptying and constipation.


Contraction of the biliary sphincter, leading to biliary colic, is also common.


Endocrine


Opioids block the release of catecholamines, ADH, and cortisol associated with surgical stress.


Drug interactions


Barbiturates, benzodiazepines, and other CNS depressants have a synergistic effect on level of sedation and respiratory depression when combined with opioids.


Abbreviations: ADH, antidiuretic hormone; CNS, central nervous system; EEG, electroencephalogram.























Table 2.10 Opioid receptors

Receptor


Physiological characteristics


Mu




  • µ1 receptor is responsible for producing analgesia, miosis, nausea/vomiting, urinary retention, and pruritus.



  • The endogenous stimulus for µ1 receptors are enkephalins.



  • µ2 receptor activation leads to euphoria, respiratory depression, sedation, bradycardia, ileus, and physical dependence.


Delta




  • Activation leads to analgesia and contributes to physical dependence.



  • These receptors are highly selective for endogenous enkephalins.


Kappa




  • Activation leads to analgesia, sedation, dysphoria, and psychomimetic effects.



  • Pure κ agonists do not lead to respiratory depression.



  • Stimulation leads to vasopressin release and subsequent diuresis.


Sigma


Activation leads to dysphoria, hallucinations, tachypnea, and mydriasis.



Morphine

Because morphine is a hydrophilic compound, it has a slower onset with a longer clinical effect. Morphine can lead to hypotension secondary to histamine-induced vasodilation as well as decreased sympathetic tone. Morphine metabolites are excreted by the kidneys. Patients with renal failure can have prolonged duration of action given that between 5 and 10% of morphine is excreted unchanged in the urine. Morphine 6-glucuronide can lead to respiratory depression and narcosis.


Dosing: Preoperatively, postoperatively 5 to 15 mg intramuscular (IM)/IV; 0.05 to 0.2 mg/kg IV

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May 19, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on 2.2 Anesthesia

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