Intraoperative Management


It is well recognized that the intraoperative management of the patient is a significant determinant of the postoperative course and overall clinical outcome. In light of the frequent associated comorbidity, advanced age, lack of physiologic reserve, complexity of many therapeutic procedures, and other factors, vascular surgical patients can be particularly challenging to manage intraoperatively. The aim of this chapter is to review the important intraoperative considerations the surgical team will face during the conduct of a vascular surgery operation.

Anesthesia

Appropriate anesthesia is tailored to the procedure to allow safe and comfortable interventions that the patient would otherwise not tolerate. A breakdown of the levels of anesthesia as described by the American Society of Anesthesiologists (ASA) is presented in Table 35.1 .

TABLE 35.1
Continuum of Depth of Sedation: Levels of Sedation/Analgesia
From American Society of Anesthesiologists Committee on Quality Management and Departmental Administration. Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation/Analgesia. Approved by the ASA House of Delegates on October 13, 1999 and last amended on October 23, 2019. Anesthesiology . 2002;96:1004.
Minimal Sedation (Anxiolysis) Moderate Sedation/Analgesia (Conscious Sedation) Deep Sedation/Analgesia General Anesthesia
Responsiveness Normal response to verbal stimulation Purposeful response to verbal or tactile stimulation Purposeful response after repeated or painful stimulation Unarousable, even with painful stimulation
Airway Unaffected No intervention required Intervention may be required Intervention often required
Spontaneous ventilation Unaffected Adequate May be inadequate Frequently inadequate
Cardiovascular function Unaffected Usually maintained Usually maintained May be impaired

Anesthesia Techniques and Complications

Local/Regional Anesthesia

Local anesthetics produce their effects by interfering with nerve conduction through blockade of neuronal sodium channels. , Most local anesthetics contain an aromatic ring, have a basic pH, and are lipid soluble. They are made soluble in an acidic aqueous vehicle for administration. In tissue, neutral pH is required to achieve neuronal blockade. There are several agents currently available in contemporary practice ( Table 35.2 ). Today, most vascular surgeons use lidocaine, taking advantage of its rapid onset of action; or bupivacaine, because of its long duration of effect.

TABLE 35.2
Clinical Features of Individual Local Anesthetic Drugs
Class Drug Main Use Potency a Onset Duration Toxicity Maximal Single Dose Comments
Esters Cocaine Topical 1 slow 30–60 min Very high 150 mg Addictive, vasoconstriction, “fight or flight response”
Benzocaine Topical NA slow 30–60 min Low 200 mg Topical only
Procaine Infiltration, nerve block 2 fast 30–60 min Low 1000 mg Allergic potential
Chloroprocaine Infiltration, nerve block 1 fast 30–60 min Low 1000 mg No longer available
Tetracaine Topical ¼ slow 30–60 min High 20 mg No longer available
Amides Lidocaine Topical, infiltration, nerve block, epidural 1 fast 1–2 h Medium 300–500 mg Versatile agent
Mepivacaine Infiltration, nerve block, epidural 1 fast 1–3 h Medium 400–500 mg No longer available
Prilocaine Infiltration, nerve block, epidural, intravenous regional 1 fast 1–3 h Low 600 mg Methemoglobinemia at >600 mg
Ropivacaine Infiltration, nerve block, epidural ¼ slow 2–12 h Medium 20 mg Enantiomer of bupivacaine
Bupivacaine Infiltration, nerve block, epidural ¼ fast 2–12 h Medium 225 mg Ventricular arrhythmias, cardiovascular collapse at high doses
Etidocaine Infiltration, nerve block, epidural ½ fast 2–12 h Medium 300–400 mg No longer available

a Relative to lidocaine.

Ester-containing local anesthetics are cleared by plasma cholinesterase, but amide-based local agents, including lidocaine and bupivacaine, require liver metabolism. Toxic central nervous system effects follow a dose-related progression from vertigo and tinnitus, to anxiety and fear, and subsequently to tremors, seizures, and coma. Benzodiazepines, which increase the seizure threshold related to local anesthetics use, may mask some of the other neurologic signs of local anesthetic toxicity, so particular care is needed in the setting of concomitant sedation. Direct cardiovascular toxicity is seen at levels exceeding the threshold for seizure and is manifested as arrhythmia and myocardial depression.

Moderate Sedation

The term moderate sedation (often referred to as “conscious sedation”) describes a drug-induced depression of consciousness that facilitates intervention but does not depress the ability of patients to protect their airway. By definition, moderate sedation does not impair independent respiration and normal cardiovascular function and may be administered by non-anesthesiologists who have appropriate training and credentialing.

In preparation for moderate sedation, patients should be fasting. A careful history of allergies, adverse reactions, current medications, and conditions recognized to compromise cardiopulmonary function under sedation (e.g., sleep apnea) should be elicited. The facility should have devices and medications for rescue in the event of oversedation. Intraprocedural and postprocedural monitoring should include continuous electrocardiographic and pulse oximetry, in addition to frequent assessment of blood, respiratory rate, and level of consciousness. There are several agents utilized in modern practice ( Table 35.3 ). Reversal agents, naloxone for opiates as well as flumazenil for benzodiazepines, must be immediately available. These receptor antagonists may have durations of action shorter than the agents they are used to block, and therefore continued careful observation of patients after any use of rescue agents is mandated since repeat dosing may be required.

TABLE 35.3
Properties of Drugs Commonly Used for Moderate Sedation
Modified from Lubarsky DA, Candiotti K, Harris E. Understanding modes of moderate sedation during gastrointestinal procedures: a current review of the literature. J Clin Anesth . 2007;19:397.
Drug Pharmacologic Class Pharmacologic Effects Onset of Action Duration of Action Adverse Effects
Midazolam Benzodiazepine Sedation
Amnesia
Anxiolysis
1–5 min, peak in 3–5 min 1–3 h Hypotension, hypoventilation, decreased tidal volume, increased respiratory rate, apnea, increased upper airway resistance
Diazepam Benzodiazepine Sedation
Amnesia
Anxiolysis
1–5 min 20–60 min Hypotension, hypoventilation, respiratory depression
Meperidine Opioid Sedation
Analgesia
5 min, peak in 10 min 2–4 h Hypoventilation, hypotension, lower seizure threshold, respiratory depression, decreased tidal volume, nausea, vomiting
Propofol Ultrashort-acting sedative, hypnotic Sedation
Hypnotic
30–60 s 3–10 min Dose-dependent hypotension, hypoventilation, respiratory depression, pain at injection site
Droperidol Neuroleptic Neuroleptic
Anxiolytic
30 min 1–4 h Hypotension, tachycardia, hypoventilation, prolonged QT interval
Fentanyl Opioid Sedation
Analgesia
<1 min, peak in 5–8 min 30–60 min Hypoventilation, respiratory depression, decrease in tidal volume

Regional Anesthesia

Regional anesthetic techniques include peripheral nerve blocks, cervical and brachial plexus blocks, spinal anesthesia, and epidural anesthesia. Peripheral nerve blocks can be utilized for extremity and digital procedures with effects lasting well after the operation is complete.

Spinal and Epidural Anesthesia

Spinal anesthesia refers to the injection of medications through the dura directly into the cerebrospinal fluid from lumbar levels. Spinal anesthesia is contraindicated when hemodynamic instability is expected since this technique often produces a sympathetic blockade with some loss of arterial and venous tone. Hypotension associated with spinal anesthesia is treated with fluid resuscitation, Trendelenburg positioning, or inotropic or pressor agents if the patient has underlying heart failure.

Complications of spinal anesthesia include postdural puncture headache, nausea and emesis resulting from unopposed parasympathetic efferents, and respiratory depression particularly in patients with high punctures and chronic obstructive pulmonary disease. Other complications include direct neurologic injury, cauda equina syndrome, arachnoiditis, spinal hematoma, meningitis, and idiopathic cardiovascular collapse. Complications are rare, with the exception of postdural puncture headache which may occur in 25% of patients undergoing spinal anesthesia. The headache may be associated with cranial nerve symptoms such as diplopia, tinnitus, and nausea and is classically relieved by assuming a supine posture. Patients are treated with bed rest, caffeine, hydration, and analgesics. , This complication may be treated by the administration of an epidural blood patch which is thought to work by sealing the meningeal puncture site.

Epidural anesthesia refers to the placement of a catheter into the epidural space around the distal thoracic or lumbar spine, frequently with the delivery of larger quantities of anesthetic required for absorption between the spinal ligament and dura (epidural space). A major advantage of epidural anesthesia is the ability to continually deliver post-procedural analgesia via an indwelling catheter. Effective epidural postoperative analgesia may obviate the need for systemically administered opioids and the accompanying risk for respiratory depression, excessive sedation, and gastrointestinal side effects. Epidural anesthetic infusions can be maintained for 3 to 4 days as needed and should not interfere with routine postoperative mobilization.

The safe use of neuraxial anesthesia in the setting of anticoagulant therapy is summarized in Table 35.4 .

TABLE 35.4
Anticoagulation Management and Neuraxial Anesthetic Intervention
Modified from Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines. 3rd ed. Reg Anesth Pain Med . 2010;35:64–101.
Drug Waiting Time Before Neuraxial Manipulation Waiting Time After Neuraxial Manipulation to Restart
Unfractionated heparin, subcutaneous prophylaxis 4 h >60 min
Intraoperative therapeutic heparinization 2–4 h after the last heparin dose, check partial thromboplastin time >60 min (Note intravenous anticoagulation should not be continued with neuraxial catheter in place)
Low-molecular-weight heparin 12 h for prophylactic doses
24 h for therapeutic doses
Prophylaxis should be delayed 24 h after neuraxial manipulation and should be limited to once a day dosing
Delay prophylaxis until adequate hemostasis is achieved if blood is present during neuraxial manipulation
Prophylaxis can be started 2 h after neuraxial catheter removal
Warfarin When INR <1.4 When INR <1.4
Dabigatran 5 days 6 h
Apixaban 3 days 6 h
Rivaroxaban 3 days 6 h
Prasugrel 7–10 days 6 h
Ticagrelor 5–7 days 6 h
Aspirin, NSAIDs COX-2 inhibitors Can be continued Can be continued
Clopidogrel 7 days (if needed before, can perform P2Y12 assay to assess residual antiplatelet activity) Should be held until after removal

General Anesthesia

The term general anesthesia refers to a loss of consciousness with the patient being unarousable to painful stimuli. By definition, patients under general anesthesia cannot protect their airway and, in most cases, require assisted ventilation. Patients receiving general anesthesia often have depressed cardiovascular function and require attention and support by specially trained anesthetists.

All of the agents used in general anesthesia can induce peripheral vasodilation and inhibit sympathetic autonomic regulation, leaving the patient with the reduced ability to autoregulate circulation and tissue perfusion. This, plus the lack of surgical stimulation, can lead to hypotension which is frequently noted between the time of anesthesia induction and skin incision. The loss of vasoconstriction in the periphery leads to redistribution of blood flow to the skin, loss of thermoregulation, and a decrease in core temperature.

Malignant Hyperthermia

Malignant hyperthermia occurs when genetically susceptible individuals are exposed to triggering agents which are usually drugs used during the conduct of a general anesthetic including the use of succinylcholine or a halogenated anesthetic agent. Symptoms include muscle rigidity, tachycardia, hyperthermia, and cardiac arrythmias. Life-threatening aspects of this include the hypermetabolic condition, hyperthermia, and hyperkalemia.

If malignant hyperthermia is suspected, the surgical procedure should be stopped as soon as possible. Intravenous dantrolene at 2.5 mg/kg can be given through a large-bore IV. Doses can be repeated until decreases in end-tidal CO 2 , heart rate, and muscle rigidity are noted. Dantrolene dosing may need to be increased to 10 mg/kg if muscular contractions persist. The patient should be hyperventilated on 100% oxygen at greater than 10 L/min to lower end-tidal CO 2 and flush out volatile anesthetics. Activated charcoal filters can be placed in the ventilator circuit and replaced frequently to remove inhaled anesthetic. The patient should be cooled if temperature is greater than 38°C. Metabolic acidosis should be corrected with bicarbonate. Calcium chloride 10 mg/kg or calcium gluconate 30 mg/kg, sodium bicarbonate 1 to 2 mEq/kg IV, 50% glucose 50 mL, and regular insulin 10 units IV can be used to treat hyperkalemia. Refractory hyperkalemia should be treated with albuterol, kayexalate, or dialysis. Calcium channel blockers should be avoided for the treatment of arrhythmias. ,

Chronic Renal Failure

The number of patients with hemodialysis (HD)-dependent chronic renal failure (CRF) is increasing in parallel to the increasing prevalence of hypertension, diabetes, obesity, and an aging population. Their adjusted all-cause mortality rate is at least 10-fold higher than that of the non-CRF population, with 5-year mortality rates ranging between 39% and 60%, primarily due to cardiovascular disease. Their existing medical problems, such as the increased risk of coronary artery disease and congestive heart failure, complicate their surgical care. Their renal disease, with its resulting volume disturbances, anemia, and electrolyte disturbances, further increase their surgical risk. Not surprisingly, patients with end-stage renal disease (ESRD) undergoing elective vascular surgery have a significantly elevated risk of postoperative complications and death after major vascular surgical operations – particularly in patients over the age of 65. Their perioperative mortality following arterial reconstruction is at least three to four times that of patients without renal failure. ,

The timing of dialysis prior to an operation is a key consideration, given its accompanying volume and electrolyte shifts. The available information suggests that HD on the day before surgery is preferable to correct electrolyte imbalance, uremia, anemia, and excess body fluid.

Special attention must be directed toward intraoperative fluid management since patients may be volume overloaded related to their renal dysfunction, or hypovolemic following a dialysis treatment. Intravenous fluid administration must be considered carefully. A balanced salt solution may be advantageous due to the patient’s renal failure-related acidosis, but these solutions contain potassium. Normal saline may lead to hyperchloremia.

The underlying anemia associated with chronic renal failure is generally well tolerated but leads to a risk of compromised oxygen delivery if even relatively small amounts of blood are then lost. Transfusion and its potential risk of volume and potassium overload must be undertaken cautiously.

Intraoperative Monitoring

Continuous monitoring of the patient response to the surgical intervention is critical. This allows both the surgeon and the anesthesiologist to recognize deviations from the expected course and adapt to the changing condition of the patient.

Electrocardiography

Monitoring of the electrical activity of the heart should be applied throughout the perioperative period in almost all types of interventions. A five-electrode system with four limb leads and a single unipolar precordial lead (generally V 5 ) is standard for most vascular procedures. Leads II and V 5 are monitored continuously in most vascular cases. Some evidence suggests that V 3 or V 4 may have greater sensitivity for detection of myocardial ischemia in this setting. ,

Pulse Oximetry

Pulse oximetry is a noninvasive technique of monitoring oxygen saturation with a probe placed peripherally, often on a finger, earlobe, or toe. Evidence to support its efficacy or impact on outcomes in patients undergoing general anesthesia is scant. , Nevertheless, its use remains the standard of care.

Capnography

Continuous monitoring of the end-tidal CO 2 using infrared absorption spectroscopy is the standard of care for the assessment of ventilation during general anesthesia. This information is displayed most commonly as a continuous plot of the partial pressure of CO 2 versus time.

Arterial Pressure

In clinical practice today, intraarterial pressure is measured with an electromechanical pressure transducer system. The fluid-filled systems have the added benefit of allowing repeated sampling of arterial blood for laboratory and blood gas analysis. The arterial cannula is commonly inserted into the radial artery. Stenosis, thrombosis, and occlusion of the radial artery are possible complications of cannulation, and ischemia of the hand can result. The ulnar artery is the dominant supply of arterial perfusion to the hand in approximately 90% of people. Assessment of the adequacy of collateralization through the ulnar artery should be assessed and documented before use of the radial artery for monitoring pressure.

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