The Surgical Patient

Sarvie Esmaeilzadeh

Rachel E. Carlson

Louisa J. Palmer

INTRODUCTION

The surgical patient poses unique airway challenges in the critical care environment for intensivists with backgrounds in various medical and surgical fields. Intensivists must thoroughly understand these challenges, including the relevant patient population, the “typical” perioperative course, and the common surgical/anesthetic procedures and their potential complications. In this chapter, we will discuss the general approach to the postsurgical airway and considerations related to specific surgical procedures.

APPROACH TO THE POSTOPERATIVE PATIENT’S AIRWAY

Was the airway considered high-risk preoperatively?
Did the surgery increase the risk to the airway?
Did the anesthetic increase the risk to the airway?
Does the patient have sufficient physiologic reserve?

GENERAL POSTOPERATIVE CONCERNS

Airway Edema

Postoperative airway edema is a common finding in the surgical patient but varies significantly in severity and clinical significance. Direct compression (positioning, airway devices, endotracheal tube ties, etc.) may result in tissue injury, swelling, or obstruction to venous outflow. Prolonged surgery may be associated with significant volumes of intravenous crystalloid and colloid administration, especially in the setting of massive hemorrhage or the insensible losses of an open abdomen, thoracic cavity, or other exposed tissue surfaces. The systemic inflammatory response and interstitial edema often exacerbate these shifts. Additionally, prone positioning, particularly for prolonged periods, risks airway edema due to decreased venous and lymphatic drainage from paratracheal and oropharyngeal tissues. Occasionally, clinically significant airway edema may be delayed; thus, patients at the highest risk should be monitored postoperatively for symptoms.

Strategies aimed at preventing or reducing airway edema should be prioritized in all patients, but especially in high-risk patients. These strategies are numerous and are outlined in Table 37.1. Once edema is established, the treatment is supportive (see Table 37.2). Resolution may take hours to days.

TABLE 37.1 Strategies for Prevention of Postoperative Airway Edema

Prevent mechanical trauma

Careful positioning (avoid compression of the face, mouth, neck)

Avoid constricting ties/tape around the mouth, face

Minimize endotracheal tube cuff pressures

Ensure appropriate endotracheal tube size

Ensure tongue midline and decompressed

Cautious surgical technique and traction

Minimize fluid shifts

Prevent insensible losses (in-line humidification, low fresh gas flow, pack open chest/abdomen/exposed tissue when possible)

Minimize crystalloid administration, as clinically indicated

Promote venous/lymphatic drainage

Reverse Trendelenburg positioning when feasible, including prone

Avoid excessive flexion or extension of the neck

Avoid constricting ties/tape around the mouth, face, neck

Avoid large/bulky bite block placement

Miscellaneous

Consideration for “staged” procedures to avoid prolonged surgical times and physiologic stress

Adequate perfusion pressures

TABLE 37.2 Treatment of Postoperative Airway Edema

Head-up or reverse Trendelenburg positioning

Maintain euvolemia and diurese as indicated

Nebulized racemic epinephrine

Dexamethasone, high dose

Heliox inhalation to promote laminar flow

Noninvasive positive pressure ventilation (NIPPV)

Intubation and mechanical ventilation as indicated

Consider presence or absence of cuff leak when determining time of extubation

Airway Injury

Injury during airway manipulation may involve the upper airway structures, including dentition or oronasopharyngeal tissue, or the tissues of the hypopharynx, glottis, or trachea. Those at highest risk are patients with significant coagulopathy or masses, as well as patients with difficult airways. Paratracheal, submandibular, and glottic tissues (including nerves) are at risk of injury during surgical exposure or traction. Patients may present with pain, edema, bleeding, airway obstruction, dysphagia, or dysphonia, and otolaryngology or oral maxillofacial evaluation may be indicated.

Recurrent Laryngeal Nerve Palsy

Injury to the recurrent laryngeal nerve, either directly or secondary to tissue traction, deserves special mention in the surgical patient. Given its long course in the neck and into the mediastinum, this nerve is susceptible to injury during any surgery (because of patient positioning) but is particularly at risk during surgery of the head and neck, or any surgery within the thoracic cavity or
mediastinum. This nerve is the single neural supply to the abductors of the vocal cords. Unilateral injury may result in hoarseness, altered phonation, inability to Valsalva, and increased risk of aspiration. Bilateral nerve injury is most feared, as unopposed vocal cord adduction with medialization can result in acute airway obstruction postextubation (Table 37.3).

TABLE 37.3 Phenotypes of Recurrent Laryngeal Nerve Palsy

Location	Presentation	Comments
Unilateral	Hoarseness/dysphonia Altered vocal pitch Dysphagia Aspiration Inability to Valsalva	Symptoms tend to be more subtle
Bilateral	All the above + Stridor Acute airway obstruction	Severity of symptoms dependent on degree of cord medialization
Complete or proximal injury	All of the above + variable stridor	Theoretically less likely to cause acute airway obstruction given involvement of the superior laryngeal branch of the vagus nerve (palsy of both the abductors AND adductors of the vocal cord) resulting in paramedian position
Incomplete or distal injury	All of the above + stridor, acute airway obstruction	Sparing of the superior laryngeal nerve may result in unopposed adduction via the cricothyroid muscle with resultant medialization of the vocal cords and acute airway obstruction

CAROTID ENDARTERECTOMY

Cervical Hematoma

Cervical hematoma formation is one of the most feared complications of carotid endarterectomy (CEA), with incidence of severe hematoma estimated at ˜3%.⁴^,⁵ Postoperative hematoma formation in the neck, from either venous or arterial sources, may result in airway compromise from direct compression. Patients with risk factors for coagulopathy, such as dual antiplatelet therapy, recent anticoagulation, intraoperative cardiopulmonary bypass for a combined cardiac procedure, or chronic renal insufficiency, are particularly prone to this complication. Avoidance of hypertension, coughing, and straining in the immediate postoperative period may decrease the likelihood of hematoma formation, and though controversial, protamine to reverse heparin anticoagulation at the completion of surgery may decrease postoperative bleeding risk.⁵

Clinically significant neck hematoma formation should prompt immediate return to the operating room for re-exploration. Early identification can allow for timely re-engagement of the surgical team, and potential patient transfer to the operating room for definitive airway management.
In the event of impending airway loss, as demonstrated by rapidly progressive dyspnea, increased work of breathing or stridor, immediate decompression of the hematoma by removal of superficial clips/sutures at the bedside should be strongly considered. Should bedside decompression be performed, significant bleeding must be anticipated. Airway management can be pursued without initial decompression, understanding that significant expansion of the hematoma may drastically alter airway anatomy and even impede oxygenation/ventilation through the endotracheal tube. If airway management is to be performed at the bedside, it is prudent to keep the patient spontaneously breathing during the procedure if at all feasible. Preparations should be made for potential awake flexible endoscopic intubation, with backup plans for RSI and surgical emergency airway (cricothyrotomy) should initial airway management techniques fail.⁴^,⁵

Cranial Nerve Injury

Cranial nerve injury may occur due to direct surgical insult, surgical traction, or secondary to hematoma formation. This may include injury to the hypoglossal, vagal, recurrent laryngeal, facial, or glossopharyngeal nerves. The vagus nerve is at risk of injury during dissection of neck vessels as it passes in the carotid sheath, injury before the takeoff of the recurrent laryngeal nerve is most common (though still rare) and results in hoarseness postoperatively. Injury to the hypoglossal nerve, caused by retraction for the surgical procedure, may lead to difficulty swallowing and risk of aspiration postoperatively.⁴^,⁵

Cervical Plexus Blocks

The superficial and deep cervical plexus blocks have been used both separately and in combination as regional anesthetic techniques to facilitate surgical anesthesia. In addition, some surgeons may opt for infiltration of local anesthetic in the surgical field during the CEA. Blockade of the deep cervical plexus, or diffusion of local anesthetic to the high cervical nerve roots, will result in temporary ipsilateral phrenic nerve palsy and possible inadequacy of ventilation postoperatively in patients with poor underlying pulmonary reserve.⁵

The degree and duration of respiratory insufficiency postoperatively in the critical care setting will depend on the type, concentration, and volume of local anesthetic used. Some patients may be well supported with noninvasive positive pressure ventilation.

ESOPHAGECTOMY

Patients undergoing esophagectomy are at high risk of postoperative respiratory complications, and often require postoperative airway management by the intensivist. In general, such patients have a high prevalence of medical comorbidities and low physiologic reserve. Considerations include
aspiration risk, pain leading to splinting and respiratory impairment, meticulous volume status assessment, and avoiding damage to the fresh anastomosis.⁶^,⁷^,⁸

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