Transcript Complications of Anesthesia

Complications of Anesthesia
Patti Murphy MD, FRCPC
Department of Anesthesia
University of Ottawa
Thank you,
Dr. Kelly Shinkaruk, for
presenting this talk!
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!
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
– Myocardial ischemia
• Neurologic
– Postop altered mental status
– Awareness
• Immunologic
– Anaphylaxis
Peri-operative Risk
Co-morbidities
Patient
disease
Anesthesia
Surgery
Mishaps
Mishaps
Outcome
PACU
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
• Neurologic
– Postop cognitive dysfunction
– Awareness
• Immunologic
– Anaphylaxis
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!
Death Totally Attributable to Each Component of Risk
in the Confidential Enquiry into Perioperative Deaths
Component
Patient
Mortality Rate Contribution
1 : 870
Operation
1 : 2860
Anesthetic
1 : 185,056
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.
Risk of death from anesthesia
• 0.82 in 100,0000
Epidemiology of Anesthesia-related Mortality in the United States,
1999-2005, Anesthesiology - Volume 110, Issue 4 (April 2009)
• 5 per 100,000
Gibbs 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.
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
Causes of death under anesthesia
• Epidemiology of Anesthesia-related Mortality
in the United States, 1999-2005,
Anesthesiology - Volume 110, Issue 4 (April
2009)
Type of Complication
%
Complications of anesthesia during
pregnancy, labor, and puerperium
Cardiac complications
3.6
Overdose of anesthetics
46.6
Inhaled anesthetics
10.5
Intravenous anesthetics
19.0
Other and unspecified general
anesthetics
Local anesthetics
Unspecified anesthetics
Adverse effects of anesthetics in
therapeutic use
Opioids and related analgesics
Benzodiazepines
Other and unspecified general
anesthetics
Local anesthetics
Unspecified anesthetics
Other complications of anesthesia
2.7
11.5
3.9
1.7
42.5
19.9
1.9
1.8
6.2
11.6
7.3
Malignant hyperthermia
1.0
Failed or difficult intubation
2.3
Bottom line
• Giving exact statistics about death is difficult
• Chance of death is related to patient comorbidities and surgical procedure as well as
anesthesia
• Death from purely anesthetic causes is rare
• Anesthesia is dramatically more safe than it
used to be
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
– Myocardial ischemia
• Neurologic
– Postop cognitive dysfunction
– Awareness
• Immunologic
– Anaphylaxis
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...
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.
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?
Hypoxia DDx
(in general, not just this case)
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Artifact
Inadequate PO2
Hypoventilation
VQ mismatch
Decreased SVO2
Artifact
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Motion
Perfusion
Hemoglobinopathy
Nail polish
Check probe placement
Check plethysmograph
ABG
Inadequate PO2
• Decreased FIO2
Administer 100% O2
Confirm FIO2 on monitor
• Decreased pressure
– Altitude
Doesn`t apply to this case
Hypoventilation
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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
Hypoventilation
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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 these
Check CO2, PAW, TV, RR, auscultate chest
Bronchoscopy
CXR
VQ Mismatch
• Shunt
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Atalectasis
Endobronchial intubation
Negative pressure pulmonary edema
Aspiration
• Dead space
– Pulmonary embolism
Could be shunt, unlikely dead space. Same management
as hypoventilation, + PEEP
Decreased SVO2
• Increased O2 extraction - unlikely
– Fever
– Thyroid storm
– MH
Check for T°, hemodynamics, rigidity
• Decreased O2 delivery - unlikely
– Decreased cardiac output
Check hemodynamics
DDx summary for this case
Could be –
• ETT placement, or problem
• Vent problem
• Pneumothorax
• Atalectasis
• Negative pressure pulmonary edema
• Aspiration
More info about the patient
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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
Narrowed DDx
• Atalectasis
• Neg pressure pulmonary edema
• Pneumothorax
What would you do next?
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.
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
– Myocardial ischemia
• Neurologic
– Postop cognitive dysfunction
– Awareness
• Immunologic
– Anaphylaxis
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
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...
Hypertension
• Definition
– BP > 160/100
– > 20% increase from baseline
Hypertension Complications
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Myocardial ischemia
Intracerebral bleed/ stroke
Increased intracerebral pressure
Left heart failure/ Pulmonary edema
Increased surgical bleeding
Hypertension artifact
• NIBP cuff too small
• Art line transducer
– Too low
– Not zeroed
– Malfunction
– Under-damped (ringing)
Hypertension
• Pre-existing
– Essential
– Pregnancy- induced (Pre-eclampsia)
– Renal failure
– Pheochromocytoma
– Hyperthyroidism
– Autonomic dysreflexia (spinal cord injury +
stimulus in lower body)
Hypertension
• Catecholamine release
– Intubation
– Pain/ light anesthesia/ full bladder
– Anxiety
– Hypoxia/ Hypercarbia
• Medication error
• Increased ICP
• Cocaine intoxication
Hypertension - prevention
• Continue preop antihypertensive meds
• Postpone elective surgery if diastolic BP>
110mmHg
• Anticipate levels of surgical stimulation
Hypertension - prevention
• Induction
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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)
Hypertension - treatment
• Verify the measurement
– Repeat NIBP
– Check artline transducer position, waveform,
tubing
• Check medications, infusions, calculations
• “There’s no anesthetic like no anesthetic”
Hypertension - treatment
• Deepen the anesthetic
– Volatile
– Opioids
– Propofol
– Epidural local anesthesia
Hypertension - treatment
• Treat the BP
– B blocker
– Hydralazine
– Nitrpglycerine
– Nitroprusside
– Alpha blockade (phentolamine)
– Calcium channel blockade
– ACEI
Case #2
• Getting back to our pregnant woman... DDx?
Case #2
• She received esmolol and her BP went UP!
• Does this tell you anything about the etiology?
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.
Case #2
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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
Case #2
• Pre- intubation BP 100/70
• BP still went up to 180/ 110 on intubation!
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?
Case #3
• Hypotension
• Definition
– > 20 fall in the BP below baseline
– Systolic < 90 mm Hg
– MAP < 60 mm Hg
Hypotension Complications
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Cerebral anoxia
Myocardial ischemia/ infarction
Renal failure
CHF/ Fluid overload
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
Hypotension DDx
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Hypovolemia (Preload)
Cardiogenic (HR, Contractility)
Obstructive (Preload )
Distributive (Afterload, SVR)
Hypotension DDx
• Hypovolemia (decreased preload)
– Dehydration
• GI (nausea, vomiting, diarrhea, bowel prep, NG, 3rd
space in bowel obstruction)
• GU (DI, DM, diuretics)
– Bleeding
Hypotension DDx
• Cardiogenic (rate, contractility)
– Muscle
• Cardiomyopathy
• Ischemia
• Myocardial depression (drugs, acidosis)
– Rhythm
• Tachycardia
• Bradycardia
– Valves
• Stenosis
• Regurgitation
Hypotension DDx
• Obstructive
– Intra-abdominal mass (gravid uterus)
– Tension pneumothorax
– Mediastinal mass
– Tamponade
– Pulmonary embolism
– Pulmonary hypertension
Hypotension DDx
• Distributive (decreased SVR)
– Neurogenic shock (includes regional blocks)
– Sepsis
– Addisonian crisis (steroid withdrawal)
– Hypothyroidism
– Post resection of pheochromocytoma
– Anaphylaxis
– Drugs
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
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)
Case #3
• The bradycardia quickly turned into asystole
• What do you do next?
Case #3
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Inform OR personnel/ Call for help
Release the pneumoperitoneum
Stop volatile
100% O2
Start CPR
Fluid bolus
Atropine 1 mg
Epinephrine 1 mg
Intubate
Case #3
• Presumed diagnosis is vagal response
• What next?
Case #3
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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
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?
Myocardial Ischemia
Etiology
• Coronary artery occlusion
• Myocardial O2 supply/ demand imbalance
– Increased demand
• Tachycardia
• Increased afterload
• Myocardial stretch (excessive preload)
– Decreased supply
• Tachycardia
• Hypotension
• Anemia
Myocardial Ischemia
Prevention
• Preop identification of patients at risk
– Angina, previous CAD
– Diabetes
– Hypertension
– Obese
– Smoker
– Hyperlipidemia
Myocardial Ischemia
Prevention
• Tight control of blood pressure +/- 20% of
baseline
• Avoid tachycardia
• Tight control of volume status
• Maintain adequate Hb
Myocardial Ischemia
Manifestations
• Awake patient
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Chest pain
SOB
Mental status changes
Nausea/ vomiting
• Anesthetized patient
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Hemodynamic instability
Flipped T, peaked T
ST depression, elevation
Q waves
Rhythm disturbance
Increased PA pressures
Myocardial Ischemia
Complications
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Hypotension, cardiogenic shock
Myocardial infarction
Cerebral anoxia
Pulmonary edema/ CHF
Death
Myocardial Ischemia
Management
• Assess multiple leads
• Ensure adequate oxygenation/ ventilation.
• Treat tachycardia (most important)
– Adequate depth of anesthesia
– B blockade
• Treat hypertension
– NTG
– Calcium channel blockers
Myocardial Ischemia
Management
• 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)
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
Management
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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.
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
– Myocardial ischemia
• Neurologic
– Postop cognitive dysfunction
– Awareness
• Immunologic
– Anaphylaxis
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?
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)
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
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
Case #5
• Patient needs acknowledgement and
explanation of what occurred.
• Reassurance about the next time she has an
anesthetic...
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
Case #6
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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?
Postoperative change in mental status
DDx
• Drugs
– Volatile
– Benzodiazepines
– Induction agents (PPF, STP, ketamine)
– Opioids
– NMB
– Non-anesthesia drugs (Tricyclic antidepressants,
Phenothiazines...)
– Drug withdrawal
Postoperative change in mental status
DDx
• Metabolic
– Hypoxia/Hypercarbia
– Electrolyes (glucose, Na+, Ca+)
– Endocrine (thyroid, adrenal)
– Uremia
– Hepatic encephalopathy
– Porphyria
– Hypothermia
Postoperative change in mental status
DDx
• CNS injury (ischemia, hemorrhage)
• Post-ictal
• Psychogenic
Postoperative change in mental status
Management
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Check ABCs
Neuro exam – pupils, GCS
Review medications given (errors)
Check electrolytes, glucose, ABG
ECG
CT head
Neuro consult
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???
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!!
Outline
• Death
• Respiratory
– Hypoxia
• Cardiovascular
– Hypertension
– Hypotension
– Myocardial ischemia
• Neurologic
– Postop cognitive dysfunction
– Awareness
• Immunologic
– Anaphylaxis
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
Case #7
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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?
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
Case #7 (Here’s a bit of an aside)
• TOF now has visible fade
• Why??
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
Residual NMB
• Commonly found in PACU
• Risk for
– Hypoventilation
– Decreased cough
– Aspiration
– Patient discomfort
Residual NMB
Prevention
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Minimize use of muscle relaxants
If used, minimize doses
Always check PNS if NMB used
Do not attempt to reverse a dense block
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?
Case #7
• Stayed intubated in PACU overnight
• Received
– Epinephrine 10 mcg IV prn until bronchospasm
resolved
– Histamine blockers (diphenhydramine and
ranitidine)
– Hydrocortisone
Case #7
• Allergy testing – cefazolin
• Take home messages
– Anaphylaxis can be delayed following
administration (30 minutes in this case)
– Variable in its presentation
Summary
• Complications reviewed
– Death
– Hypoxia
– Hypertension
– Hypotension
– Myocardial ischemia
– Postop cognitive dysfunction
– Awareness
– Anaphylaxis
Summary
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•
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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
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)