Neurocritical Care Management of the Neurosurgical Patient E-Book

Monisha Kumar, Joshua Levine, James Schuster, W. Andrew Kofke, Andrew W. Kofke, Monisha Kumar, Joshua Levine, James Schuster, Andrew W. Kofke

• Publisher: Elsevier
• Year: 2017
• eBook ISBN:
  9780323322225
• Topic: Medicine
• Subtopic: Neurology

Kumar and colleagues' Neurocritical Care Management of the Neurosurgical Patient provides the reader with thorough coverage of neuroanatomical structures, operative surgical approaches, anesthetic considerations, as well as the full range of known complications relating to elective and non-elective neurosurgical procedures. Drawing upon the expertise of an interdisciplinary team of physicians from neurosurgery, neurology, anesthesiology, critical care, and nursing backgrounds, the text covers all aspects intensivists need to be aware of in order to provide optimal patient care.- Expert Consult eBook version included with purchase. This enhanced eBook experience allows you to search all of the text, figures, images, and references from the book on a variety of devices.- Over 100 world-renowned authors from multispecialty backgrounds (neurosurgeons, neuro-interventionalists, and neurointensivists) and top institutions contribute their unique perspectives to this challenging field.- Six sections cover topics such as intraoperative monitoring, craniotomy procedures, neuroanesthesiology principles, spine and endovascular neurosurgery, and additional specialty procedures.- Includes 300 tables and boxes, 70 line artworks, and 350 photographic images.- Clinical pearls pulled out of the main text offer easy reference.

Section 1

Neuroanesthesia and Perioperative Care

1

Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia

Zirka H. Anastasian; John G. Gaudet

Introduction

Even after completion of a neurosurgical intervention, intraoperative factors, including anesthetic agents, pharmacotherapy, and surgery, may have lasting effects that persist through recovery. The goal of this chapter is to discuss the effects of intraoperative factors, such as anesthetic effect and surgical manipulation, on postoperative recovery, including respiratory function, nausea and vomiting, glucose control, temperature variations, pain management, and delirium and cognitive dysfunction.

Key Concepts

• Anesthetics, sedatives, and opioids impair respiratory arousal by reducing chemoresponsiveness to hypoxemia and hypercarbia.

• The effect of anesthetics on respiratory muscles depends on the agent, the dose, the patient’s state of consciousness, and the specific muscle group.

• Risk factors for postoperative respiratory depression in patients with obstructive sleep apnea include the severity of sleep apnea, the dose of systemic opioids, the use of sedatives, the site and invasiveness of surgical procedure, and the potential for apnea during rapid eye movement (REM) rebound.

• When neuromuscular blockade is employed, it is necessary to monitor the degree of neuromuscular blockade and consider adequacy and potential side effects of reversal of neuromuscular blockade.

Respiratory Muscle Effects

The muscles involved in respiration are skeletal muscles and can be classified by their anatomical function into two groups: (1) upper airway dilators and (2) respiratory pump muscles. Upper airway dilator muscles counterbalance the negative inspiratory pressure generated by the respiratory pump muscle to permit airflow during inspiration.¹

Surgery itself can have direct effects on respiratory pump muscles by functional disruption (injury of muscle), postoperative pain leading to restrictions on ventilation, and phrenic nerve injury resulting in diaphragm dysfunction. Other factors that affect diaphragmatic dysfunction postoperatively include inflammation² and reflex vagal inhibition.³ Indirect effects of abdominal surgery may increase intraabdominal pressure. Increased intraabdominal pressure decreases chest wall compliance and increases the work of breathing, further taxing the muscles of the respiratory pump.¹

Upper airway muscles are generally more sensitive to anesthetics and sedatives than respiratory pump muscles. Animal trials have shown that although volatile anesthetics, barbiturates, and benzodiazepine anesthetics all decrease neural input to both upper airway (hypoglossal nerve) and respiratory pump muscles (phrenic nerve), the decrease of upper airway neural input is much more than respiratory pump muscles.⁴ In human clinical studies, even subhypnotic concentrations of propofol, isoflurane, and sevoflurane increase the incidence of pharyngeal dysfunction. This places patients at increased risk for aspiration of pharyngeal contents during recovery of anesthesia. The effect on the pharyngeal contraction pattern may be most pronounced in patients treated with propofol because propofol use results in markedly reduced pharyngeal contraction.⁵ In contrast, ketamine reduces neural input to both the upper airway and respiratory muscles equally. Reduction in neural input to the upper airway muscles is much less with ketamine relative to the other classes of anesthetics.⁴ Ketamine has no inhibitory effect on genioglossus activity. Unlike other anesthetics, ketamine preserves a high level of upper airway dilator muscle activity, similar to that of conscious patients.⁶ Ketamine, however, is a sialagogue, a property that can occasionally be problematic.

Opioid analgesics cause respiratory depression via both upper airway dilator and respiratory pump muscle dysfunction. Opioids reduce genioglossus activity in animals, decrease vagal motor neuron activity in the laryngeal abductors, and increase vagal motor neuronal activity in adductors.^7–9 These changes result in increased upper airway resistance and possibly vocal cord closure, as well as pharyngeal airflow obstruction.⁹ Opioid analgesia also increases abdominal muscle activity, which produces a rapid decrease in end-expiratory lung volume and functional residual capacity, contributing to a higher degree of atelectasis.¹⁰ Chest wall rigidity also occurs with the use of opioids, even when dosed conservatively.¹¹

Clinical Pearl

Upper airway muscles are generally more affected by anesthetics and sedatives than respiratory pump muscles.

Controlled ventilation immobilizes the diaphragm and disrupts diaphragmatic function. Controlled ventilation is associated with proteolysis in the diaphragm, which over a long period leads to diaphragmatic atrophy and dysfunction.¹² As little as 18 hours of controlled ventilation results in diaphragmatic atrophy and decreases contractile function.¹³ Duration of controlled ventilation correlates with thinning, injury, and atrophy of the diaphragm.^14,15

Neuromuscular blocking agents (NMBAs) are often used during surgery to provide immobility and optimal operating conditions. Train-of-four (TOF) ratios are customary measures to assess neuromuscular blockade at muscle groups. The TOF ratio value is determined by the ratio of the last twitch height to the first twitch height after a TOF twitches. Recovery at the adductor pollicis is often used for this assessment because the hand is generally convenient and available for monitoring purposes. A TOF ratio of 0.6 or more predicts acceptable recovery of forced vital capacity,^16,17 and for many years recovery to a TOF ratio of 0.7 was considered indicative of adequate recovery of neuromuscular function.¹⁸ Recovery from NMBA generally occurs sooner at the diaphragm than peripheral muscles, such as the hand muscles. Therefore tidal volumes are usually preserved, whereas residual paralysis may still be noted by peripheral monitoring.^19,20 However, a TOF ratio of 0.6 and even 0.8 may be insufficient to ensure recovery of respiratory function. TOF ratios of < 1.0 are associated with decreased forced inspiratory volume in one second (FIV1), upper airway obstruction, and impaired pharyngeal function and impaired ability to swallow.^16,21

Even when nerve stimulators are used, subjective tactile or visual evaluation of the evoked response to indirect nerve stimulation is notoriously inaccurate. Once the TOF ratio exceeds 0.4, most clinicians cannot detect the presence of any fade in the twitches upon four stimuli.²² A very strong case can be made for the routine administration of a nondepolarizing reversal agent (cholinesterase inhibitor), unless it can be objectively demonstrated that complete recovery (TOF rati...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Foreword
• Preface
• List of Contributors
• Acknowledgements
• Dedications
• Section 1: Neuroanesthesia and Perioperative Care
• Section 2: Craniotomy
• Section 3: Spinal Surgery
• Section 4: Endovascular Neurosurgery
• Section 5: Intracranial Monitors and Special Procedures
• Section 6: Specific Intensive Care Unit Complications
• Index