complications of anesthesia patti murphy md, frcpc department of anesthesia university of ottawa
TRANSCRIPT
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Complications of Anesthesia
Patti Murphy MD, FRCPCDepartment of Anesthesia
University of Ottawa
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Thank you, Dr. Kelly Shinkaruk, for
presenting this talk!
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Complications of Anesthesia
• So many from which to choose! Could be a course in itself.
• Tried to avoid repeating too much of what you’ve had elsewhere (airway, for example)
• Case- based• Unusual cases to illustrate common problems• You’ll be asked questions – please participate!
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension– Myocardial ischemia
• Neurologic– Postop altered mental status– Awareness
• Immunologic– Anaphylaxis
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Peri-operative Risk
Patientdisease
Anesthesia
OutcomeSurgery
Co-morbidities
Mishaps
Mishaps
PACU
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension
• Neurologic– Postop cognitive dysfunction– Awareness
• Immunologic– Anaphylaxis
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Death
• Difficult to study– Rare event, need a huge number of patients– Uncertainty about cause of death– Difficulty comparing patients to each other– Difficulty defining time course (just intra-op,
within 24 hours, 48 hours...)– Seldom have an anesthetic without surgery!
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Death Totally Attributable to Each Component of Risk in the Confidential Enquiry into Perioperative Deaths
Adapted from Buck N, Devlin HB, Lunn JL: Report of a Confidential Enquiry into Perioperative Deaths, Nuffield Provincial Hospitals Trust. London, The King's Fund Publishing House, 1987.
Component Mortality Rate ContributionPatient 1 : 870
Operation 1 : 2860
Anesthetic 1 : 185,056
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Risk of death from anesthesia
• 0.82 in 100,0000Epidemiology of Anesthesia-related Mortality in the United States,
1999-2005, Anesthesiology - Volume 110, Issue 4 (April 2009)
• 5 per 100,000Gibbs N, Borton C: Safety of Anaesthesia in Australia: A Review of
Anaesthesia Related Mortality, 2000-2002. Report of the Committee convened under the auspices of the Australian and New Zealand College of Anaesthetists, Australian and New Zealand College of Anaesthetists Melbourne2006.
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Adapted from Lagasse RS: Anesthesia safety: Model or myth? A review of the published literature and analysis of current original data. Anesthesiology 97:1609,
2002
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Causes of death under anesthesia
• Epidemiology of Anesthesia-related Mortality in the United States, 1999-2005, Anesthesiology - Volume 110, Issue 4 (April 2009)
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Type of Complication %Complications of anesthesia during pregnancy, labor, and puerperium
3.6
Cardiac complications 2.7
Overdose of anesthetics 46.6
Inhaled anesthetics 10.5
Intravenous anesthetics 19.0
Other and unspecified general anesthetics
11.5
Local anesthetics 3.9
Unspecified anesthetics 1.7
Adverse effects of anesthetics in therapeutic use
42.5
Opioids and related analgesics 19.9
Benzodiazepines 1.9
Other and unspecified general anesthetics
1.8
Local anesthetics 6.2
Unspecified anesthetics 11.6
Other complications of anesthesia 7.3
Malignant hyperthermia 1.0
Failed or difficult intubation 2.3
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Bottom line
• Giving exact statistics about death is difficult• Chance of death is related to patient co-
morbidities and surgical procedure as well as anesthesia
• Death from purely anesthetic causes is rare• Anesthesia is dramatically more safe than it
used to be
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension– Myocardial ischemia
• Neurologic– Postop cognitive dysfunction– Awareness
• Immunologic– Anaphylaxis
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Respiratory Complications
• Failed airway, hypoxia and aspiration are well covered in other lectures
• I do have an interesting case to discuss that will test your knowledge...
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Respiratory Complications
• A 16 year old male presents with severe Ludwig`s angina (severe sublingual infection) and impending airway obstruction.
• In the OR, tracheostomy is started under local anesthesia with no sedation.
• Before the airway is secured, the airway completely obstructs.
• Oral intubation, airway, LMA are impossible. Bag mask ventilation with nasal airways is attempted.
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Respiratory Complications
• The surgeon becomes more aggressive in his attempts to find the trachea, which is difficult because of the anatomy distortion in the area.
• After several minutes, he is successful.• The saturation increases from 40 to 80%, but
will go no higher.
What is your differential diagnosis, and what will you do?
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Hypoxia DDx (in general, not just this case)
• Artifact• Inadequate PO2• Hypoventilation• VQ mismatch• Decreased SVO2
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Artifact
• Motion• Perfusion• Hemoglobinopathy• Nail polish
Check probe placementCheck plethysmographABG
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Inadequate PO2
• Decreased FIO2Administer 100% O2Confirm FIO2 on monitor
• Decreased pressure– AltitudeDoesn`t apply to this case
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Hypoventilation
• Central CNS e.g. respiratory depression
• Spinal cord e.g. # C5
• Phrenic/ intercostal nerves e.g. Guillan Barré
• Neuromuscular junction e.g. Myesthenia gravis, NMB agents
• Muscle weakness e.g. muscular dystrophy
• Chest wall e.g. flail chest, rigidity, restriction
None of these apply to this case
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Hypoventilation
• Pleura e.g. pneumothorax
• Lung e.g. decreased compliance, bronchospasm
• ETT e.g. endobronchial, kink, obstruction, placement
• Ventilator e.g. settings or malfunction
Could be any of theseCheck CO2, PAW, TV, RR, auscultate chestBronchoscopyCXR
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VQ Mismatch
• Shunt– Atalectasis– Endobronchial intubation– Negative pressure pulmonary edema– Aspiration
• Dead space– Pulmonary embolism
Could be shunt, unlikely dead space. Same management as hypoventilation, + PEEP
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Decreased SVO2
• Increased O2 extraction - unlikely– Fever– Thyroid storm– MH
Check for T°, hemodynamics, rigidity• Decreased O2 delivery - unlikely– Decreased cardiac output
Check hemodynamics
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DDx summary for this case
Could be – • ETT placement, or problem• Vent problem• Pneumothorax• Atalectasis• Negative pressure pulmonary edema• Aspiration
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More info about the patient
• 100% FIO2, PEEP• Vent settings are appropriate, normal PAW• CO2 present, normal waveform• Bronchoscopy confirms ETT placement, no
secretions• ABG confirms SPO2• Chest auscultation: AE bilaterally, bronchial
breath sounds
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Narrowed DDx
• Atalectasis• Neg pressure pulmonary edema• Pneumothorax
What would you do next?
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The diagnosis
• CXR showed bilateral pneumothorax• PAW was normal. May not increase until
pneumothorax is large or tension develops.• Air entry was equal bilaterally, because the
pneumothorax was equal bilaterally. The change in quality of sound was subtle.
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension– Myocardial ischemia
• Neurologic– Postop cognitive dysfunction– Awareness
• Immunologic– Anaphylaxis
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Case #2
• A patient is 36 weeks pregnant. She is booked to have her C section in the main OR because she has a large ovarian mass which will be resected after the baby is delivered.
• Completely healthy• Plan is for GA, as patient does not want
regional, and possible prolonged surgical time• BP is 180/120
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Case #2
• What are the potential causes of this BP?• Will you do this case?• What is your plan?
• We’ll come back to this patient in a moment...
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Hypertension
• Definition– BP > 160/100– > 20% increase from baseline
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Hypertension Complications
• Myocardial ischemia• Intracerebral bleed/ stroke• Increased intracerebral pressure• Left heart failure/ Pulmonary edema• Increased surgical bleeding
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Hypertension artifact
• NIBP cuff too small• Art line transducer– Too low– Not zeroed– Malfunction– Under-damped (ringing)
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Hypertension
• Pre-existing– Essential– Pregnancy- induced (Pre-eclampsia)– Renal failure– Pheochromocytoma– Hyperthyroidism– Autonomic dysreflexia (spinal cord injury +
stimulus in lower body)
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Hypertension
• Catecholamine release– Intubation– Pain/ light anesthesia/ full bladder– Anxiety– Hypoxia/ Hypercarbia
• Medication error• Increased ICP• Cocaine intoxication
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Hypertension - prevention
• Continue preop antihypertensive meds• Postpone elective surgery if diastolic BP>
110mmHg• Anticipate levels of surgical stimulation
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Hypertension - prevention
• Induction– Larger dose of opioids e.g. 5 mcg/kg Fentanyl– Lidocaine 1- 1.5 mg/kg a useful adjunct– Avoid large dose ketamine– Consider deepening with Sevo before intubation – Short-acting vasodilators (NTG 50 mcg) or beta
blockers (esmolol 10-30 mg)– Ensure adequate interval between drug
administration and stimulus (e.g. Fentanyl peaks in 3-5 minutes)
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Hypertension - treatment
• Verify the measurement– Repeat NIBP– Check artline transducer position, waveform,
tubing
• Check medications, infusions, calculations • “There’s no anesthetic like no anesthetic”
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Hypertension - treatment
• Deepen the anesthetic– Volatile– Opioids– Propofol– Epidural local anesthesia
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Hypertension - treatment
• Treat the BP– B blocker– Hydralazine– Nitrpglycerine– Nitroprusside– Alpha blockade (phentolamine)– Calcium channel blockade– ACEI
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Case #2
• Getting back to our pregnant woman... DDx?
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Case #2
• She received esmolol and her BP went UP!• Does this tell you anything about the etiology?
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Case #2
• Systemic vasoconstriction/ dilatation is controlled by the balance of alpha and beta sympathetic activity
• Beta receptors vasodilate.• Alpha receptors vasoconstrict• Beta blockers cause unopposed alpha activity, causing intense
vasoconstriction in– Cocaine intoxication– Pheochromocytoma
Do not use them in these patients!Labetolol has mild alpha-blocking effects as well as beta. Be careful!
Vasodilators are safer.
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Case #2
• She admitted to using cocaine• Waited an appropriate interval• Arterial line• Induction with (70 kg):– Fentanyl 300 mcg– Pentothal 350 mg– Lidocaine 100 mg– Titrated NTG totalling 150 mcg– Sevo pre- intubation
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Case #2
• Pre- intubation BP 100/70• BP still went up to 180/ 110 on intubation!
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Case #3
• Healthy woman for elective tubal ligation• Uneventful induction and placement of LMA• On abdominal insufflation, heart rate
decreases to 30, BP decreases to 60 systolic.
• What do you think has happened?• What do you do?
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Case #3
• Hypotension• Definition – > 20 fall in the BP below baseline– Systolic < 90 mm Hg– MAP < 60 mm Hg
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Hypotension Complications
• Cerebral anoxia• Myocardial ischemia/ infarction• Renal failure• CHF/ Fluid overload
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Hemodynamic review
• Blood pressure depends on – Cardiac output (CO)– Systemic vascular resistance (SVR)
• CO= Heart rate x Stroke Volume• SV determined by – Preload– Afterload– Contractility
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Hypotension DDx
• Hypovolemia (Preload)• Cardiogenic (HR, Contractility)• Obstructive (Preload )• Distributive (Afterload, SVR)
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Hypotension DDx
• Hypovolemia (decreased preload)– Dehydration• GI (nausea, vomiting, diarrhea, bowel prep, NG, 3rd
space in bowel obstruction)• GU (DI, DM, diuretics)
– Bleeding
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Hypotension DDx
• Cardiogenic (rate, contractility)– Muscle
• Cardiomyopathy• Ischemia• Myocardial depression (drugs, acidosis)
– Rhythm• Tachycardia• Bradycardia
– Valves• Stenosis• Regurgitation
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Hypotension DDx
• Obstructive– Intra-abdominal mass (gravid uterus)– Tension pneumothorax– Mediastinal mass– Tamponade– Pulmonary embolism– Pulmonary hypertension
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Hypotension DDx
• Distributive (decreased SVR)– Neurogenic shock (includes regional blocks)– Sepsis– Addisonian crisis (steroid withdrawal)– Hypothyroidism– Post resection of pheochromocytoma– Anaphylaxis– Drugs
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Hypotension management
• Rule out artifact (NIBP, art line, PULSE)• Check oxygenation/ ventilation (100% O2 if severe or
prolonged)• Reduce/ turn off vasodilating drugs• Fluids (RL, NS, Pentaspan, Voluven, blood)• Vasopressors– Ephedrine 5-10 mg– Phenylephrine 40 -100 mcg +/- infusion
• Ensure adequate IV access• Underlying cause
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Case #3
• Getting back to our case, DDx– Hypovolemia – not likely– Cardiogenic – severe bradycardia (vagal stimulus)– Obstructive – gas embolus (no decrease in CO2, no
millwheel murmur, surgeons insist they are not in a vessel)
– Distributive – anaphylaxis (no other signs)
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Case #3
• The bradycardia quickly turned into asystole• What do you do next?
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Case #3
• Inform OR personnel/ Call for help• Release the pneumoperitoneum• Stop volatile• 100% O2• Start CPR• Fluid bolus• Atropine 1 mg• Epinephrine 1 mg• Intubate
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Case #3
• Presumed diagnosis is vagal response• What next?
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Case #3
• Cancel the surgery• Emergence• PACU• ECG (non-specific changes)• TnTs• Advise the patient• Admit for observation• Next time, pre-treat with atropine, slower
insufflation of CO2
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Case # 4
• Elective AAA surgery• X clamp comes off, and the ST segments
become depressed.• BP is 80/60• Heart rate is 105• What is going on, and what do you do?
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Myocardial IschemiaEtiology
• Coronary artery occlusion• Myocardial O2 supply/ demand imbalance– Increased demand• Tachycardia• Increased afterload• Myocardial stretch (excessive preload)
– Decreased supply• Tachycardia• Hypotension• Anemia
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Myocardial IschemiaPrevention
• Preop identification of patients at risk– Angina, previous CAD– Diabetes– Hypertension– Obese– Smoker– Hyperlipidemia
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Myocardial IschemiaPrevention
• Tight control of blood pressure +/- 20% of baseline
• Avoid tachycardia• Tight control of volume status• Maintain adequate Hb
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Myocardial IschemiaManifestations
• Awake patient– Chest pain– SOB– Mental status changes– Nausea/ vomiting
• Anesthetized patient– Hemodynamic instability– Flipped T, peaked T– ST depression, elevation– Q waves– Rhythm disturbance– Increased PA pressures
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Myocardial IschemiaComplications
• Hypotension, cardiogenic shock• Myocardial infarction• Cerebral anoxia• Pulmonary edema/ CHF• Death
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Myocardial IschemiaManagement
• Assess multiple leads• Ensure adequate oxygenation/ ventilation.• Treat tachycardia (most important)– Adequate depth of anesthesia– B blockade
• Treat hypertension– NTG– Calcium channel blockers
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Myocardial IschemiaManagement
• Treat Hypotension– Must have adequate pressure at aortic root to
perfuse coronary arteries– Avoid NTG, CCB until pressure stabilized– Optimize fluids and Hb– Invasive monitoring– Inotropes (caution, may increase O2 demand)– Vasoconstrictors (caution, may decrease cardiac
output)
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Case # 4
• Ischemia related to– Wave of acidotic blood returning from ischemic
lower body depresses the myocardium– Bleeding at anastamotic site– Hypotension from hypovolemia and decreased
cardiac output
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Management
• O2• Increase ventilation to normalize pH• Fluids/ blood• Phelylephrine to increase coronary perfusion• Careful with B blockers! Fix the BP first. Still
have active blooding.
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension– Myocardial ischemia
• Neurologic– Postop cognitive dysfunction– Awareness
• Immunologic– Anaphylaxis
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Case #5
• A patient with Harrington rods is booked for an elective c section.
• She had previously had failed attempts at spinal, and just wanted a GA.
• After induction, the resident couldn’t intubate. Staff let him struggle for a minute, then took over and intubated. The case proceeded uneventfully.
• The patient remembers the incision.Why did this happen?What do you tell the patient?
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Awareness
• Predisposing factors– Cardiac anesthesia (narcotic based to avoid
myocardial depression)– OB anesthesia (minimal doses to avoid depressing
neonate)– Muscle relaxation– Hypotension– Beta blockers (masks hemodynamic response)– Increased drug metabolism (chronic opioids etc)
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Prevention of awareness
• Adequate levels of hypnotic drugs (volatiles, PPF infusion)
• Midazolam may be helpful• Minimal use of muscle relaxants• BIS monitor for patients at risk• Support BP with vasopressors rather than let
volatile get too low
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Case #5
• Peak of pentothal had passed due to extra time for intubation
• Volatile level was not yet established• Only ½ MAC used for c section to avoid excessive
uterine relaxation• No opioids or midazolam given until fetus is out• Patient already hypertensive from prolonged
laryngoscopy• Rapid progression from intubation to incision
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Case #5
• Patient needs acknowledgement and explanation of what occurred.
• Reassurance about the next time she has an anesthetic...
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Case #6
• Anxious 40 year old woman for breast biopsy under needle localization
• Induction with – Midaz 1 mg– Fentanyl 1 mcg/ kg– PPF 2 mg/kg– LMA placed, breathing spontaneously soon
resumed– Sevo in O2/ air, ET 1.2-1/4 through case
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Case #6
• Surgery done• 100% O2• Left in PACU with LMA in situ, normal vitals• 1 hour later, the nurse calls you because your
patient is not yet awake (LMA was removed by RNs)
• What are the possible causes?• What will you do?
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Postoperative change in mental statusDDx
• Drugs– Volatile– Benzodiazepines– Induction agents (PPF, STP, ketamine)– Opioids– NMB– Non-anesthesia drugs (Tricyclic antidepressants,
Phenothiazines...)– Drug withdrawal
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Postoperative change in mental statusDDx
• Metabolic– Hypoxia/Hypercarbia– Electrolyes (glucose, Na+, Ca+)– Endocrine (thyroid, adrenal)– Uremia– Hepatic encephalopathy– Porphyria– Hypothermia
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Postoperative change in mental statusDDx
• CNS injury (ischemia, hemorrhage)• Post-ictal• Psychogenic
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Postoperative change in mental statusManagement
• Check ABCs• Neuro exam – pupils, GCS• Review medications given (errors)• Check electrolytes, glucose, ABG• ECG• CT head• Neuro consult
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Back to our Case #6
• Vital signs normal, 99% SPO2 on room air, RR16, good TV, ABG normal
• PERLA• No response to deep pain stimulus (GCS3)• Cranial nerve reflexes intact• Patient’s hand dropped towards patient’s face
never landed on her face.• Neuro consult???
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Case #6
• CT head, ECG and all bloodwork normal• Patient awoke at 22:00, went home completely alert.• Came back 3 weeks later for mastectomy• 2nd anesthetist aware of previous events• Similar anesthetic given, case longer • Patient miraculously woke up in PACU shortly after
MD told RN that patient wasn’t to receive analgesia until she was awake.
• Psychogenic!!
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Outline
• Death• Respiratory
– Hypoxia• Cardiovascular
– Hypertension– Hypotension– Myocardial ischemia
• Neurologic– Postop cognitive dysfunction– Awareness
• Immunologic– Anaphylaxis
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Case #7
• 42 year old healthy woman with vaginal rupture, hemorrhagic shock
• Hx of vaginal hysterectomy 3 months ago• Post-op wound infection, now resolved• Received several litres of crystalloid as
resuscitation for hypovolemia, now stable• Routine induction, ½ hour surgery
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Case #7
• Vaginal repair finished• NMB reversed, TOF > 90%• Volatile turned off• Breathing well• Patient opens eyes to command, extubated• She tells you she can’t breathe
• What do you want to assess?
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Case #7
• Tidal volume initially good, progressively deteriorates
• No stridor• + paradoxical respirations• Looks “floppy”• Saturation initially good, progressively
deteriorates to 88%• Assisted ventilation initially good, progressively
becoming difficult
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Case #7 (Here’s a bit of an aside)
• TOF now has visible fade• Why??
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Residual NMB
• Duration of reversal agents is shorter than NMB agents
• Patient hypoventilation – Respiratory acidosis– pH change causes dissociation of NMB agent from
blood proteins– Rebound clinical effect
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Residual NMB
• Commonly found in PACU• Risk for– Hypoventilation– Decreased cough– Aspiration– Patient discomfort
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Residual NMBPrevention
• Minimize use of muscle relaxants• If used, minimize doses• Always check PNS if NMB used• Do not attempt to reverse a dense block
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Back to Case #7
• Patient was re-intubated• Airway found to be massively edematous• Within seconds later, face became markedly
edematous and chest wheezy• No urticaria• No hypotension (but had received ++ fluids for
bleeding)• What do you do now?
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Case #7
• Stayed intubated in PACU overnight• Received– Epinephrine 10 mcg IV prn until bronchospasm
resolved– Histamine blockers (diphenhydramine and
ranitidine)– Hydrocortisone
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Case #7
• Allergy testing – cefazolin• Take home messages– Anaphylaxis can be delayed following
administration (30 minutes in this case)– Variable in its presentation
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Summary
• Complications reviewed– Death– Hypoxia– Hypertension– Hypotension– Myocardial ischemia– Postop cognitive dysfunction– Awareness– Anaphylaxis
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Summary
• Many potential complications• This is the tip of the iceberg• Fortunately, they are rare• It is important to know– Who is at risk– How to prevent– What to look for– What to do
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Summary
• Important to have– A complete and systematic differential diagnosis
(for those patients who don’t behave like the books say they will)
– A plan to manage the first 5 minutes of any crisis (until you figure out what’s going on)