• Consider bronchoscopy
• Consider bag ventilation
• Treat underlying problem
BRONCHOSPASM
Causes
• Preexisting reactive airway disease (asthma)
• Manipulation of upper airway (oral endoscopy)
• ETT with inadequate anesthesia
• ETT causing carinal or bronchial stimulation (endobronchial intubation)
• Excessive histamine release (morphine, atracurium) or β-blockade
• Anaphylaxis
• Pulmonary edema
Investigations
• Examine ETT for patency (secretions, kinks) & proper position
• Examine for wheezing, air movement
• Capnograph → shows expiratory upsloping
• High peak airway pressures, hypoxia & hypercarbia
• Rule out: Pneumothorax, pulmonary embolus, & pulmonary edema
Management
• ↑ FiO2
• ↑ Anesthetic depth (inhalational agents are bronchodilators)
• ↑ Expiratory time, ↓ RR as this helps decrease gas trapping
• Give nebulized albuterol via ETT (not effective in severe bronchospasm/lost airway)
• Epinephrine IV/SC (esp for anaphylaxis) → titrate to effect
• Aminophylline (2nd line treatment—6 mg/kg bolus, then 0.5 mg/kg/hr)
• Hydrocortisone (long term)
HYPOTENSION
MAP <60 mm Hg or 20–25% reduction from baseline
Differential Diagnosis
• Decreased preload
• ↓ Blood volume (hemorrhage, inadequate fluid replacement, third spacing)
• ↓ Venous return (change in pt position, i.e., Trendelenburg)
• Pericardial tamponade, pneumothorax, surgical compression of venous structures, pneumoperitoneum from laparoscopy, excessive PEEP
• Decreased afterload
• Sepsis, vasodilating drugs (anesthetics), anaphylactic reaction neurologic injury
• Decreased contractility
• MI, arrhythmias, CHF, anesthetic effect, electrolyte imbalances
Investigations
• Examine BP cuff for fit
• Examine preoperative BP trends
• Calculate fluid balance (including blood loss)
• Ensure that the IV site is intact & not infiltrated
• Examine arterial line waveform for respiratory variation
Treatment Options
• Administer fluid bolus
• ↓ Anesthetic agents
• Administer vasopressors (phenylephrine 40–100 mcg/ephedrine 5–10 mg)
• Administer other vasoactives/inotropes (norepinephrine, dobutamine, milrinone, dopamine)
• Consider invasive monitoring (CVP, arterial line, PA catheter, echocardiogram)
HYPERTENSION
BP >140/90 mm Hg or MAP >20–25% baseline value
Differential Diagnosis
• Primary HTN
• HTN with no known cause (70–95% of hypertension)
• Secondary HTN
• Pain/surgical stimuli (inadequate anesthesia, tourniquet pain), ETT stimulation, bladder distention
• Hypercarbia, hypoxia, hypervolemia, hyperthermia
• Intracranial pathology (↑ ICP, herniation, hemorrhage)
• Endocrine problems (pheochromocytoma, Cushing syndrome, hyperthyroidism, hyperparathyroidism)
• Alcohol withdrawal
• Malignant hyperthermia
• Inadvertent vasoactive drug administration
• Antihypertensive medication withdrawal
• Consider timing of HTN with case events:
→ HTN prior to induction
Withdrawal from antihypertensive medications, essential hypertension, pain
→ HTN postinduction
Laryngoscopy effect, improper ETT placement, hypercarbia from esophageal intubation, misplacement of gastrostomy tube into trachea, pain, hypoxia
→ HTN during the case
Inadequate pain control, hypercarbia, pneumoperitoneum, fluid overload, drugs (vasopressors), bladder distention, tourniquet pain
Investigations/Treatment Options
• Examine BP cuff size & placement, arterial line waveform
• Review anesthetic/surgical events of the case
• Check for hypoxia/hypercarbia
• Check vaporizer agent level
• Administer antihypertensives (β-blockers/vasodilators)
HYPERCARBIA
↑ CO2 levels (as measured by blood gas or end-tidal gas analysis) (normal values 38–42 mm Hg)
Differential Diagnosis
• ↑ CO2 production
• Malignant hyperthermia
• Sepsis
• Fever/shivering
• Thyrotoxicosis
• ↓ CO2 elimination
• Reduced minute ventilation
Altered lung mechanics (atelectasis, pneumoperitoneum with CO2, surgical retractors preventing lung expansion)
Airway obstruction (secretions, mucous plugging)
Inadequate ventilator settings (↓ volumes, ↓ fresh gas flows)
Oversedation
• Increased dead space
ETT malfunction (kinks, endobronchial intubation)
Exhausted CO2 absorber
• Drug effects (muscle relaxants/narcotics/benzodiazepines)
• Consider timing of ↑ CO2 with case events:
→ ↑ CO2 at the start of a case
• Improper ETT placement, inadequate ventilator settings, oversedation of spontaneously breathing pt
→ ↑ CO2 postinduction/during case
• MH, neuroleptic malignant syndrome (NMS), improper vent settings, thyrotoxicosis, release of tourniquet, exhausted CO2 absorber
→ ↑ CO2 during emergence
• Inadequate reversal of muscle relaxants, residual narcotic/anesthetic effects, neurologic causes, electrolyte disturbances, hypoglycemia
Investigations/Treatment Options
• Examine pulse oximeter
• Ensure appropriate ventilator settings
• Examine CO2 absorber for exhaustion
• Consider ABG
• If spontaneously breathing: Assist breathing, lighten sedation
• If mechanically ventilated: Increase minute ventilation
HYPOCARBIA
↓ CO2 levels (as measured by blood gas or end-tidal gas analysis)
Differential Diagnosis
• Hyperventilation
• ↓ Metabolic rate (hypothermia, hypothyroidism)
• Pulmonary embolism
• Air embolus
• Cardiac arrest (hypoperfusion)
• ETT dislodgement/circuit disconnect
Investigations/Treatment Options
• Check breathing circuit
• Check blood pressure, heart rate, SpO2
• Check/modify ventilator settings
• Treat underlying cause
↑ PEAK AIRWAY PRESSURES
Differential Diagnosis
• Circuit problem (stuck valve, PEEP valve on wrong, kinked hose)
• ETT problem (kinked/bitten, plugged with mucus, bad positioning)
• Drug induced (opiate chest wall rigidity, inadequate paralysis/anesthesia, MH)
• ↓ Pulmonary compliance (asthma, insufflation, pneumothorax, aspiration)
Treatment
• Check tubes, hand ventilate, 100% FiO2
• Listen to lungs, suction ETT, add bite block, consider paralysis
OLIGURIA
Urine production <0.5 mL/kg/hr (also see Chapter 22, Renal System)
Differential Diagnosis
• Prerenal: Intravascular fluid depletion
• Renal origin: Lack of renal perfusion (hypotension, cross clamping, renal artery stenosis), intrinsic renal damage (nephrotoxic drugs/vasculitis)
• Postrenal: Ureteral obstruction/disruption, obstruction of Foley catheter
Investigations/Treatment Options
• Examine vital sign monitors to establish hemodynamic stability
• Examine/irrigate Foley catheter for obstruction/improper placement
• Review possible nephrotoxic drugs & withdraw
• Examine fluid administration/blood loss/surgical manipulation
• Consider fluid challenge to treat prerenal oliguria
• Treat underlying cause
MYOCARDIAL ISCHEMIA/INFARCTION
Damage to heart muscle from imbalance between myocardial O2 supply & demand
Etiology
• Atherosclerosis (accounts for 90% of MIs)
• Coronary aneurysms
• Coronary artery spasm
• O2 demand outweighs supply (e.g., aortic stenosis)
• Blood viscosity changes (polycythemia)
• Embolic sources (endocarditic vegetations)
Investigations
• Lead II—best for arrhythmia detection (RCA association & nodal system)
• Lead V5—best for ischemia detection (LAD & anterior/lateral areas of heart)
• Both lead II & V5 will detect >90% of ischemic events
• ST-segment depression ≥0.1 mV
(usually subendocardial pattern → due to partially obstructed coronary)
• ST-segment elevation ≥0.2 mV
(usually transmural pattern → due to thrombosed coronary)
• T-wave inversions & Q-waves
• Dysrhythmias
• Hypotension
• TEE (most sensitive method for determining early ischemia)
• CK, CK-MB, troponins, cardiac consult (for possible coronary intervention)
Treatment Options
Goal: Maintain acceptable balance of myocardial O2 supply & demand (Note: If ↑ afterload, preload, contractility, & heart rate → ↑ myocardial O2 demand)
• Maintain BP within 20% of preoperative levels
• Confirm correct placement of ECG leads, consider 5- or 12-lead ECG
• Notify surgeon of ischemia & coordinate completion of surgical procedure
• Place patient on 100% FiO2 & ensure adequate ventilation
• Consider reducing anesthetic agents
• Consider β-blocker administration if tachycardic
• Evaluate BP stability & consider invasive monitoring (arterial line/CVP/PA)
• If hypotensive with ischemic ECG changes ↑ BP with pressors to ↑ myocardial perfusion pressure
• Consider fluid therapy & inotropic agents to support myocardial contractility
• Consider anticoagulation (aspirin, heparin)
• Obtain intraoperative cardiology consult to coordinate care
MALIGNANT HYPERTHERMIA (SEE APPENDIX C)
• Definition: Inherited syndrome of skeletal hypermetabolism after exposure to a triggering agent
• Mechanism: ↓ reuptake of ionized Ca2+ by sarcoplasmic reticulum
→ Intracellular Ca2+ accumulation/potentiation of muscle contraction
→ ↑ Aerobic/anaerobic metabolism
• Triggering drugs: Succinylcholine, potent volatile agents (sevoflurane, desflurane, isoflurane)
• Nontriggering drugs: N2O, narcotics, local anesthetics, nondepolarizing muscle relaxants (cisatracurium, vecuronium, rocuronium), IV induction agents (propofol, ketamine, etomidate, barbiturates)
• Prevention: For MH-susceptible patients, use a “clean” machine (remove vaporizers, change CO2 absorber, flush with high flow O2 for 20 min)
Differential Diagnosis
• Neuroleptic malignant syndrome (NMS)
• Thyrotoxicosis
• MAOI reactions
• Pheochromocytoma
• Inaccurate end-tidal CO2 monitoring
Clinical Presentation/Investigation
• Can occur anytime during an anesthetic & postoperatively (up to 24 hrs)
• Early signs: ↑ end-tidal CO2 levels despite adjustment of ventilation, tachycardia
• Late signs: ↑ temp, rhabdomyolysis & myoglobinuria, metabolic & respiratory acidosis, rigidity, dysrhythmias, HTN, cardiac arrest, masseter spasm, hypoxemia, hyperkalemia
• Lab testing: ABG (check for acidemia, elevated CK, myoglobinuria, elevated K+) ↑ difference in mixed venous CO2 & arterial CO2
Treatment
• Call for help & notify surgeon
• Discontinue triggering agents
• Hyperventilate with 100% FiO2
• Administer dantrolene (2.5 mg/kg IV)
→ Repeat dantrolene until MH controlled (up to 10 mg/kg IV)
→ May need to administer for up to 72 hrs after episode
• Monitor ABG, vital signs, serum CK
• Treat acidemia with sodium bicarbonate
• Cool patient with IV fluids, cold water lavage in stomach & bladder to temp <38°C
• Treat arrhythmias & promote renal function with fluids/mannitol/furosemide
• Contact Malignant Hyperthermia Hotline as needed: 800–644-9737
BRADYCARDIA
Heart rate <60 bpm
Differential Diagnosis
• Altered impulse formation (↑ vagal tone or ↓ SA node automaticity)
• Pharmacologic agents (β-blockers, Ca-channel blockers, cholinergics, narcotics, anticholinesterases, α2-agonists)
• Pathologic causes (hypothermia, hypothyroidism, sick sinus syndrome, hypoxemia)
• Myocardial ischemia
• Surgical/anesthesia stimuli (traction on eye, neuraxial anesthesia, laryngoscopy)
• Reflex bradycardia
Investigations/Treatment
• Confirm correct ECG lead placement
• Check vital signs for hemodynamic stability
→ If stable, consider anticholinergics/ephedrine
→ If unstable, ↑ FiO2 to 100%, abort anesthetic, administer epinephrine/atropine/CPR, consider placement of pacing device
• Treat underlying cause
TACHYCARDIA
Heart rate >100 bpm
Differential Diagnosis
Tachycardia + Hypertension
• Pain/light anesthesia/anxiety
• Hypovolemia, hypercapnia, hypoxia, acidosis
• Drugs: Vagolytic drugs (pancuronium, meperidine), ketamine, ephedrine, epinephrine, anticholinergic drugs (atropine/glycopyrrolate), desflurane, isoflurane, β-agonists, vasodilators → reflexive tachycardia (hydralazine), caffeine
• Electrolyte abnormalities: Hypomagnesemia, hypokalemia, hypoglycemia
• Myocardial ischemia
• Endocrine abnormalities: Pheochromocytoma, hyperthyroidism, carcinoid, adrenal crisis
• Bladder distension
Tachycardia + Hypotension
• Anemia
• Congestive heart failure
• Valvular heart disease
• Pneumothorax
• Immune-mediated problems (anaphylaxis, transfusion reactions)
• Myocardial ischemia
• Sepsis
• Pulmonary embolism
Treatment Options
• Ensure adequate oxygenation and ventilation
• Verify ECG leads’ placement
• Assess BP & prepare to treat depending on scenario
• Consider arterial line placement
• Assess volume status if hypotension exists and treat accordingly
• Assess depth of anesthesia
• Treat underlying cause
DELAYED EMERGENCE
Differential Diagnosis
• Residual drug effects (volatile agents, narcotics, muscle relaxants)
• Neurologic complications (seizure with postictal state, CVA, infection, tumor effect)
• Metabolic (electrolyte abnormalities, hypoglycemia, hyperglycemia, adrenal failure)
• Respiratory failure (due to hypercarbia/hypoxia)
• Cardiovascular collapse
• Hypothermia
• Sepsis
Investigations/Treatment Options
• Check for residual neuromuscular paralysis with train of four monitor and ensure that muscle relaxants have been reversed
• Ensure hypoxia & hypercarbia do not exist (check arterial blood gas)
• Check glucose/electrolytes & replace accordingly (rule out hypoglycemia and hypo/hypernatremia
• Consider narcotic reversal with Naloxone 40 mcg IV and repeat every 2 min up to 0.2 mg
• Consider benzodiazepine reversal with Flumazenil 0.2 mg IV every 1 min up to 1 mg
• Check for hypothermia and warm if body temperature is less than 34°C
• Consider neurologic imaging if neurologic examination warrants
• Supportive care
ANAPHYLAXIS
Severe type 1 hypersensitivity allergic reaction (IgE) with degranulation of mast cells/basophils
Differential Diagnosis
• Anaphylactoid—not IgE-mediated, no prior sensitization to antigen required
• Vasovagal reactions generalized urticaria/angioedema, asthma exacerbations
• Myocardial infarction, stroke
Clinical Manifestations
• Cardiovascular collapse, tachycardia, dysrhythmias
• Bronchospasm, pulmonary & laryngeal edema, hypoxemia
• Rash, skin flushing, peripheral/facial edema
Treatment Options
• Remove stimulus (if known)
• Oxygen, consider intubation
• Give volume if hypotensive
• Hydrocortisone 250 mg to 1.0 g IV or methylprednisolone 1–2 g IV
• For rapidly decompensating situations give Epinephrine 20–100 mcg IV bolus followed by infusion if necessary (can give 0.5–1.0 mg IV for cardiovascular collapse)
• Diphenhydramine 50 mg IV/ranitidine 50 mg IV
• Norepinephrine 4–8 mcg/min
• Sodium bicarbonate 0.5–1 mEq/kg for persistent acidosis
• Consider intubation (if pt not intubated)
• Evaluate airway for edema prior to extubation
Prevention
• Premedicate with diphenhydramine (H1-blocker), ranitidine (H2-blocker), prednisone
LATEX ALLERGY
Incidence/Risk Factors
• Pts with spina bifida & congenital genitourinary abnormalities
• Health-care workers (housekeepers, lab workers, dentists, nurses, physicians)
• Rubber industry workers
• Atopic patients (asthma, rhinitis, eczema)
• Pts who have have undergone multiple procedures
Mechanism
• IgE-mediated immune response
Preoperative Evaluation
• No routine diagnostic testing indicated (RAST & skin tests used occasionally)
Equipment/Drug Considerations
• Routine preop administration of H1– & H2-blockers not usually recommended
Anesthetic Considerations
• Avoid products that may contain latex (gloves, tourniquets, blood pressure cuffs, face masks, ETT tubes, PA catheters, IV tubing with latex injection ports, rubber stoppers in medication vials)
• Notify entire OR team (nurses, surgeon) & place large sign on OR door
Treatment
• Latex reaction may present as anaphylaxis (>20 min after exposure)
• Symptoms include hypotension, bronchospasm, rash
• Treatment similar to anaphylaxis treatment (see above) (remove offending agent, give 100% O2, fluid resuscitation, epinephrine, corticosteroids, diphenhydramine, aminophylline)
GASTRIC ACID ASPIRATION OR VOMITING UPON INDUCTION OF ANESTHESIA
• Can cause chemical pneumonitis
Clinical Manifestations
• Early signs: Coughing, shortness of breath, wheezing, hypoxia, & cyanosis
• Late signs: Fever, metabolic acidosis, RML & RLL infiltrate on CXR
Management
• If possible, place patient in head-down position
• Turn the patients head to the side if actively vomiting while unconscious and aggressively suction
• Administer 100% O2
• Consider placement of a suction catheter into the trachea to remove large particulate matter
• Perform rigid bronchoscopy (but no lavage)
• Obtain chest x-ray
• Antibiotics (staph, pseudomonas coverage) & steroids generally not recommended
COMPLICATIONS OF LARYNGOSCOPY AND INTUBATION
Causes
• Inexperienced use of laryngoscope
• Difficulty placing ETT
• Poor existing dentition
General complications
• Physiologic stimulation, hypercarbia, hypoxia, dental damage (#1 cause of malpractice claims)
• Airway trauma, vocal cord paralysis, arytenoid dislocation, ulceration/edema of glottic mucosa
• Tube malfunction and/or malposition
Specific complications
• Postintubation croup in children secondary to tracheal/laryngeal edema
• Recurrent laryngeal nerve damage from ETT cuff compression → vocal cord paralysis
• Laryngospasm from stimulation of superior laryngeal nerve
• Involuntary/uncontrolled muscular contraction of laryngeal cords
• Caused by pharyngeal secretions or direct stimulation of ETT during extubation
• Treatment: (1) gentle positive pressure ventilation, (2) succinylcholine (0.25–1 mg/kg to relax laryngeal muscles)
• Negative-pressure pulmonary edema
• Can occur during strong inspiratory effort caused by large negative intrathoracic pressure gradient against closed vocal cords
• Prevention: Place bite block prior to emergence
• Treatment: Maintain airway, provide O2, consider PEEP/reintubation