Miscellaneous Flashcards
Awareness Under Anesthesia
Background
Considerations
Prevention
Management
Awareness Under Anesthesia
Background
Also referred to as “accidental awareness during general anesthesia” (AAGA)
Most occur during induction & emergence, less during maintenance
Range from auditory to being full awake and in pain
Patients may suffer from PTSD-like symptoms afterwards
Considerations
Rare event (1 in 1000 anesthetics) –> incidence can be reduced by certain measures but not eradicated completely
Risk factors
Use of NMBA - biggest risk factor
TIVA
Trauma & Emergency surgery, Cardiac surgery with CPB, C-section
Difficult intubation
Obesity
Personal & Family Hx
Chronic drug use (EtOH, opioids, benzos)
Prevention
Manage patient expectations (explain GA vs MAC)
Recognize HR and BP alone are unreliable for determining anesthetic depth
Avoid muscle relaxants if possible, otherwise use twitch monitor
Consider use of BIS, raw EEG is even better
End-tidal monitoring of volatile agents
Aim for MAC>0.7
Provides safety margin b/c MAC-movement > MAC-awake & MAC-amnesia
Use target-controlled infusion (TCI) for TIVA
Use isolated forearm technique
Before NMBA given, tourniquet applied to a forearm, so that later an aware patient can alert team
Management
If AAGA has suspected to have occured:
Give benzodiazepines for amnesia, opioids or other analgesics for pain
Discuss event with patient afterwards for reassurance & potential further counselling
Beach Chair Position
Background
Physiologic Effects of Sitting Position
Potential Complications
Beach Chair Position
Background
Beach chair or sitting positioning
Used for post fossa craniotomy, post c-spine surgery, shoulder surgery
Physiologic Effects of Sitting Position
CNS
↓ cerebral perfusion
correct MAP for hydrostatic diffn b/w BP cuff & brain; place transducer @ level of external auditory meatus if art line
1 cm rise = 0.75 mmHg drop in MAP
Compounded by effects of GA & sitting position on cerebral autoregulation
Possible cerebral O2 desaturation (unrelated to hemodynamics)
CVS
Venous pooling in lower extremities –> ↓ preload, SV, MAP, CO (~20%), & CPP
Mitigated w/ IV fluids, flexing hips w/ legs elevated, compression stockings, gradual head elevation
Respiratory
↑ FRC, lung compliance
Potential Complications
Nerve injuries
Brachial plexus, ulnar nv, & sciatic nv can be stretched/compressed
Spinal cord injury - if sig neck flexion
Pressure injury over ischial tuberosity
Excessive neck flexion - vascular obstruction in neck, kinking/obstruction of ETT/SGD, tongue/oropharyngeal swelling
Venous air embolism
Pneumocephalus
Stroke, ischemic brain injury, and death
Corneal Abrasions
Background
Considerations
Prevention
Management
Corneal Abrasions
Background
Definition: Injury to the epithelial layer of the cornea (4-6 cell layers thick); the outermost layer of the globe of the eye
Cornea is avascular and very densely innervated
Most common ocular complication in surgery (0.01-0.1% incidence)
Considerations
Signs/symptoms: pain, tearing, blurry vision, photophobia
Risk factors:
General anesthesia
Hx of dry eyes
Advanced age
Proptosis or exorbitism
Hx of corneal trauma
Longer procedures >60 mins
Pre-op anemia
Prone, lateral or Trendelenburg position
Procedures near head/neck
Intra-op hypotension
Potential Sources (true cause is often unknown):
After induction:
laryngoscope, face mask, watch, ID badge
Before incision:
surgical prep, gauze/sponges, surgical drapes
During procedure:
instruments, chemical solutions, heat sources, globe pressure, eye shields
Extubation:
O2 mask, patient fingers
Diagnosis:
Ophthalmology consult for slit lamp exam to rule out more serious injury (i.e. penetrating injury)
Corneal abrasion dx confirmed with fluorescein exam of the ocular surface under blue light
Prevention
Staff education about eye care
Secure eye lids in closed position after induction
Use Tegaderm/OpSite > tape in high risk patients
Use of preservative-free ocular lubricants
Management
Corneas heal on their own without scar formation within 72 hrs
Goal is to minimize pain & prevent infection
Pain typically improves within 24-48 hrs
If not improving, need to rule out infection / missed dx
Pain management:
Oral NSAIDs PRN
Preservative-free 0.5% methylcellulose lubricant drops PRN
Topical anesthetics (e.g. 1% tetracaine HCl)
Persistent pain >24-48 hrs should warrant ophthalmology
Infection prevention:
topical antibiotics x 2-3 days (e.g. Erythromycin 0.5% ointment)
Avoid:
eye patches
topical NSAIDs
topical steroids
Geriatric Patient
Considerations
Geriatric Patient
Considerations
↑ post-op morbidity and mortality
Screen for dementia → try prevent post-op delirium & POCD with:
↓ anesthetic doses
employ BIS/EEG monitoring to titrate minimum anesthetic
MSK Δ’s with aging predispose to ↑ risk of nerve, joint & skin injury
Pre-operative frailty assessment tool can risk stratify patients much better than just using “age”
Multiple co-morbid conditions + potential for polypharmacy
Pharmacologic considerations:
↓ dose requirements for IV anesthesics
↑ sensitivity to opioids
↑ duration of neuromuscular blockers except cis-atracurium
Avoid ketamine to avoid risk of post-op delirium
Undesirable side-effects from diphenhydramine, anti-cholinergics, benzos, metoclopramide, NSAIDs, meperidine
Consider neuraxial anesthesia > GA to:
↓ risk of post-op delirium & POCD
↓ post-op pulmonary complications
Decreased physiologic reserve and Δ’s in all organ systems
CVS
↓ tachycardic response to hypotension → CO is preload dependent
↓ baroreceptor sensitivity → limited response to hypovolemia & ↓ contractility
Rigid arteries → wider pulse pressure + labile blood pressures
Increasing prevalence of:
LV hypertrophy
CAD
Aortic valve disease
Arrhythmias esp. afib
Resp
↑ WOB with age
Emphysematous-like changes → VQ mismatching
↓ FRC, ↑CC → ↑shunting
PFTs: ↓FEV1, ↓DLCO, ↑A-a gradient
Weaker pharyngeal muscles and ↓ effective cough → ↑aspiration risk
CNS
↓ MAC requirements
↓ requirements of all IV anesthetics
↑ duration of action of most medications
Avoid: diphenhydramine, anti-cholinergics, benzos, metoclopramide, NSAIDs, meperidine
↑ prevalence of dementia
↑ risk of post-op delirium and POCD
Renal
eGFR ↓ with age
↑ prevalence of: HTN, DM, vascular dz → ↓ renal dysfunction
Endo
Malnutrition is common & ↑ morbidity & mortality
Impaired thermoregulation → ↑risk of hypothermia
↑ prevalence of T2DM
Laparoscopic Surgery
- Physiologic Effects of Laparoscopy:
CVS
Respiratory
Regional ciculatory changes - Potential complications
Laparoscopic Surgery
Physiologic Effects of Laparoscopy
Goal = intraabdominal pressure (IAP) ≤15 mmHg to minimize physiologic effects
CVS:
Variable & dynamic
generally well tolerated if healthy
significant cardiac dysfxn can occur in elderly & comorbid pts (eg. COPD, CHF, pulm HTN, valve dz)
↑MAP, SVR, & CVP
↓CO & SV
∆s are due to:
Pneumoperitoneum/↑ IAP
Release of catecholamines & RAS activation: release of vasopressin
Vagal stimulation: bradyarrhythmias
Dynamic mechanical effects
Depend on vol status, insufflation pressure & position
Arterial compression: ↑SVR & PVR
CVS effects usually resolve rapidly as pneumoperitoneum is maintained
Position ∆s
Head-up/Reverse Trendelenburg (ex cholecystectomy): venous pooling w/ ↓ venous return
Head-down/Trendelenburg (ex pelvic surgery): ↑venous return & cardiac filling pressures
Hypercarbia
Direct effects: ↓ cardiac contractility, sensitization to arrhythmias, systemic vasodilation
Indirect effects: symp stimulation (tachycardia, vasoconstriction, ↑SVR/PVR)
Respiratory
Mechanical
Cephalad displacement of diaphragm & mediastinal structures: ↓FRC & pulm compliance; atelectasis, ↑peak airway P, V/Q mismatch
Endobronchial migration of ETT
Hypercarbia
MV must ↑ to compensate
Can lead to ↑intrathoracic P w/ ↑SVR & PVR
Regional circulatory changes
Splanchnic blood flow: no clinically sig effect
↓ by mechanical & neuroendocrine effects - ↓hepatic blood flow & bowel perfusion
↑ by hypercapnia (direct splanchnic vasodilatation)
Renal blood flow: ↓renal perfusion & u/o
renal parenchymal compression, ↓ renal vein flow, ↑vasopressin
Cerebral blood flow: ↑CBF & ICP
↑IAP, hypercarbia, Trendelenburg
May be significant if intracranial mass, sig cerebrovascular dz - important to maintain strict normocapnia
Intraocular pressure: ↑
Potential Complications
Hemodynamic & pulmonary complications related to physiological changes of pneumoperitoneum
Initial insufflation = higher risk time
Occult hemorrhage - may not be visible due to small surgical field
Vascular or solid organ injury
Gas embolism
Subclinical embolism very common; sig emboli rare
Mechanisms:
Direct venous injection of CO2 w/ Veress needle
CO2 entrainment via severed/disrupted vein
Subcutaneous emphysema
↑ CO2 absorption ➝ hypercarbia
Potential airway compromise if crepitus/swelling in head, neck, or upper chest
Risk factors: surgery >200 mins, ≥6 ports, age >65, Nissen fundoplication
Capnothorax: suspect of unexplained ↑ airway P, hypoxemia, & hypercapnia
Capnomediastinum & capnopericardium
Complications related to positioning
Marijuana Use
Background
Withdrawal
Considerations
Marijuana Use
Background
Common names: marijuana, hashish, ganja, bud, hemp, weed, cannabis
Psychoactive compounds:
THC (delta-9-tetrahydrocannabinol)
CBD (Cannibidiol)
Cannot predict degree of intoxication from lab studies
Tissue half-life up to 30 days
Act on:
CB1 receptors: present throughout the central and peripheral nervous system
CB2 receptors: peripheral lymphoid and hematopoetic cells
Acute effects:
CNS: Euphoria vs anxiety, sedation, relaxation, altered spatial/temporal perception
CVS: tachycardia, vasodilation
Resp: bronchodilation, hyperreactivity, airway edema
GI: anti-nausea, increased appetite, abdominal pain
Chronic effects:
Atheromatous disease, chronic bronchitis/emphysema, tolerance, hyperemesis
Withdrawal
Signs & symptoms: irritability, anger, insomnia, altered dreams, anorexia, headache, tremors, fevers/chills
Onset: <1d
Duration: several weeks
Treatment: symptom mgmt, synthetic THC
Considerations
Ascertain careful history of use (frequency, route & amount)
Tox screen is not of value
Assess for the use of other drugs
R/o acute intoxication
may have more violent emergence
hypertension, fever, tachycardia may be confused with other more serious syndromes (i.e MH, serotonin syndrome)
Increased risk of MI in CAD patients 1hr after use
delay elective surgery for 1hr after acute use
Increased risk of airway hyperreactivity
Potential for:
elevated intra-op BIS (or unreliable BIS)
larger induction dose requirements
larger volatile requirements
more post-op pain, consider regional anesthesia
Methemoglobinemia
Background
Management
Methemoglobinemia
Background
MetHb = oxidized form of Hb (heme iron configuration changed from ferrous (Fe2+) to ferric (Fe3+) state)
doesn’t bind O2 –> can’t deliver O2 to tissues
causes left shift of Hb O2 dissociation curve –> further ↓ in O2 delivery
Can be congenital or acquired
Congenital - ↓ enzymatic reduction of MetHb back to Hb
may appear cyanotic but generally asymptomatic
Acquired - from drugs that can oxidize Hb to MetHb
↑ risk in infants & heterozygous CYB5R3 (cytochrome b5 reductase) mutations, G6PD deficiency
can be fatal
Drugs that can cause MetHb:
local anesthetics: prilocaine, lidocaine, benzocaine
NTG, sodium nitroprusside
Inhaled nitric oxide
Phenytoin
Sulfonamides
Metoclopramide
Diagnosis
symptoms of hypoxia that don’t improve w/ O2
blood may have “chocolate brown” colour
[MetHb] on blood gas (co-oximetry)
Nl [MetHb] <1%
> 10%: cyanosis
<20%: asymptomatic or headache, fatigue, lethargy
> 20%: resp depression, altered LOC, seizures
> 40%: life threatening
PaO2 usually normal or high
SpO2 may read 85% w/ no improvement w/ O2
Management
D/C precipitating agents
Rule out other causes of cyanosis
Supportive care - IV fluids, intubation/ventilation prn, antiseizure Rx prn
Methylene blue if concerning symptoms and/or [MetHb] >20-30%
accelerates reduction of MetHb
fast-acting; resolution w/in 20-60 mins
Contraindications:
G6PD deficiency –> can precipitate hemolysis
Caution if pt on serotonergic Rx –> can precipitate serotonin syndrome
Ascorbic acid if methylene blue contraindicated
Consider blood or exchange transfusion & hyperbaric in severe/refractory dz
Non Operating Room Anesthesia
Background
Considerations:
- Location
- Personnel
- Patient
Non Operating Room Anesthesia
Background
Non-operating room anesthesia (NORA) refers to all procedures performed in non operating room environments
Considerations
Location
Crowded and unfamiliar
Limited access to patient (i.e. C-arm at patient’s head)
Monitoring may be limited and in unfamiliar positions
Help is far away
Equipment may be lacking (difficult airway cart, emergency supplies)
Personnel
Interventionist or proceduralist or nurses/assistants may be unfamiliar with conduct of anesthesia and anesthesiologists skillset
Potential for:
ad hoq requests
scheduling inconsistencies
poor communication
less patience for “anesthesia time”
Patient
Range from “healthy” to “too sick for surgery”
Potential for inadequate preoperative anesthesia work-up
Perioperative Hypothermia
Background
Causes
Considerations
Prevention
Perioperative Hypothermia
Background
Decrease in core body temperature which develops in nearly all unwarmed surgical patients
Mild: 35-33℃
Moderate: 33-27℃
Severe: <27℃
Causes
Thermoregulatory impairment during general & neuraxial anesthesia
Decreased ambient room temperature
Increased heat loss from open body cavities
Considerations
Consequences of hypothermia
Impaired coagulation
Increased risk of infection
Prolonged drug effects (prolongs NDMRs, decreases MAC)
Delayed emergence
Potential for shivering –> ↑ metabolic rate & patient discomfort
Sympathetic stimulation –> ↑ risk of myocardial ischemia
Prevention
Pre-warm patient & use passive insulation (i.e. blanket)
Active warming techniques:
Forced air
Resistive heating
Circulating water garment devices
Use warm IV fluids & irrigation fluids
Perioperative Stroke
Background
Considerations for high risk patients
Prevention
Management
Perioperative Stroke
Background
Defn: brain infarct (ischemic or hemorrhagic) which occurs during surgery or < 30d post-op
Two types:
Overt: acute infarct, classic signs/sx, last > 24h, easily diagnosed
Covert: diagnosis made via brain imaging only, too subtle to be dx clinically at the time
Incidence = 0.1-1.9% after non-cardiac, non-neurosx
↑ disability / mortality compared to non-surgical related stroke
Etiology:
More common: cardioembolic
Less common: hypotension → hypoperfusion
Timing:
Peak POD 1-2
May contribute to Post-operative Neurocognitive Decline
Considerations for High Risk Patients
Consider EEG / Cerebral oximetry monitoring
Regional or GA are both OK
Maintain normotension → Avoid prolonged periods of hypotension
Signs/symptoms of covert stroke are sublte:
mental status changes only
no other deficits
diagnosis is made via CT/imaging only
Risk factors:
Old age, Hx of prior stroke/TIA
HTN, Afib, Valve dz, CAD, CHF, PFO
CKD, DM, Smoker/COPD
Migraines
Type of surgery: vascular, thoracic, transplant, endocrine, burn, ENT, hemicolectomy
Prevention
Identify ↑ risk pts, discuss risk/benefit profile
In pts with hx of stroke:
Delay elective surgery for 9 months post-stroke
Proceed with urgent surgery
No interventions are yet known to ↓ risk of perioperative stroke
Not recommended:
Routine bridging of anti-coagulation for afib
Perioperative ASA for stroke prevention
Treating asymptomatic carotid artery disease
Starting new beta-blocker therapy
Management
Requires ↑ degree of suspicion as mental status change may be only sign of covert stroke
Consider use of scoring tool to detect covert stroke (e.g. mNIHSS)
Perform routine investigations to rule out other causes:
Blood pressure / SpO2 / ABG / Blood glucose
CBC / electrolytes / Creatinine
If stroke is suspected:
perform neurologic assessment
immediate non-contrast CT or MRI
Once confirmed with imaging:
Consult stroke team / neurology service for further management
Consider endovascular thrombectomy
Postoperative Delirium
Background
Considerations
Prevention
Management
Postoperative Delirium
Background
Def’n: acute, fluctuating alteration in awareness and disturbance of attention
Timeline: PACU to POD5
Associated with: ↓ surgical outcomes, ↑ LOS, functional decline, ↑ cost, ↑ mortality
Two forms:
Hyperactive - classic well-known type
Hypoactive - may go unnoticed
Considerations
Risk factors:
Age > 65, pre-existing cognitive impairment, severe illness, multiple comorbid conditions, hearing/visual impairment, active infection
Major surgery, longer surgery
Need for pre-operative risk assessment
Prevention
Screen for delirium before PACU discharge
Avoid deliriogenic medications post-op: anticholinergics, benzos, meperidine
Frequent reorientation and reassurance, having familiar objects in the room
Ensure glasses/hearing aids are on as soon as possible
Good pain control via multi-modal analgesia
Ensuring circadian rhythm
Eliminate restraint use
Management
Employ prevention measures as above
Evaluate and address precipitating factors:
Pain, hypoxia, pneumonia, infection, electrolyte abn, hypoglycemia, medications
Haldol 0.5mg-1mg IV/IM when all other measures have failed
Postoperative Nerve Injury (1/2)
Background
Considerations
Prevention
Management
Prevention
Postoperative Nerve Injury
Background
Third-most common cause of anesthesia-related medical litigation
Most common nerves injured:
Ulnar nerve, brachial plexus, lumbosacral nerve roots, spinal cord
Grade of injury:
Grade I - Neurapraxia (compression) - Focal segmental demyelination (i.e. myelin sheath only)
Grade II - Axonotmesis (crush) - Damaged axon with intact endoneurium
Grade III - Axonotmesis (crush) - Damaged axon and endoneurium with intact perineurium
Grade IV - Axonotmesis (crush) - Damaged axon, endoneurium, perineurium with intact epineurium
Grade V - Neurotmesis (transection) - Complete nerve transection
Considerations
Very rare event (incidence ~ 0.03%)
U/S use in regional does NOT ↓ risk of nerve injury
Important to document pre-existing neurological deficits
Mechanisms:
Direct nerve damage from trauma
Stretch and compression
Ischemia
Toxicity from injected solutions
Second-hit on nerve with pre-existing injury
Risk factors:
Neuro, cardiac, GI, ortho sx
HTN, DM, smoking
Pre-existing peripheral neuropathies
GA, epidural
↓ Fluid status, ↓BP, electrolyte abn, ↓ temp
Signs / symptoms depend on specific nerve injured (see below)
Anesthesia, paresthesia, hypo/hyperasthesia, pain, motor deficit
Prevention
Understand which nerves are at risk with each procedure/position
Avoid ↓BP, ↓temp, dehydration
Careful positioning and judicious padding
Avoidance of contact of susceptible nerves to hard surfaces
Regional techniques:
Use less toxic LAs + vasoconstrictors for regional techniques (i.e. use Ropivicaine)
Avoid injecting during pain or paresthesia (likely perineurial injection)
Lower limb nerves:
Adequate padding when patient is in lithotomy, prone or lateral positions (hip flexion > 120 deg)
Management
Clinical exam/history to localize lesion and identify pre-existing lesions
Document sensory/motor deficits as well as severity of each
Important for prognosis
Consult neurology
Request EMG + nerve conduction studies to determine:
Complete vs incomplete lesion
Localization of lesion
Severity and age of lesion
Guide prognosis + recovery course
MRI +/- high-res U/S may help further localize otherwise ambiguous lesions
Prevention
Understand which nerves are at risk with each procedure/position
Avoid ↓BP, ↓temp, dehydration
Careful positioning and judicious padding
Avoidance of contact of susceptible nerves to hard surfaces
Regional techniques:
Use less toxic LAs + vasoconstrictors for regional techniques (i.e. use ropivicaine)
Avoid injecting during pain or paresthesia (likely perineurial injection)
Lower limb nerves:
Adequate padding when patient is in lithotomy, prone or lateral positions (hip flexion > 120 deg)
Peripheral Nerve Injuries (2/2)
Specific Nerve Injuries:
(innervation/Mechanism/Signs and symptoms/ Prevention)
- Ulnar nerve injury
- Brachial Plexus injury
- Radial nerve injury
- Median nerve injury
- Axillary nerve injury
- Musculocutaenous nerve injury
- Sciatic nerve injury
- Femoral nerve injury
- Superficial peroneal nerve injury
Specific Nerve Injuries
Ulnar Nerve Injury (C7, C8-T1)
Most common –> superficial + close to medial condyle
Men > women
Possible pre-existing subclinical neuropathy exacerbated by surgery
Symptoms can present up to 28 days post-op
Mechanism:
direct pressure on ulnar groove
prolonged forearm flexion
Signs/symptoms:
tingling/numbness along pink finger
weak add/abduction o fingers
hyperextension of MTP joints
flexion at distal + proximal ITP joints of ring + little finger
Prevention:
General considerations above
Mandatory padding
Keep forearm in supine/neutral position
Maintain flexion/extension of elbow < 90 deg
Brachial Plexus Injury (C5-T1)
Common –> superficial structure which runs btw two fixed points (intervertebral foramen + axillary sheath)
Mechanism:
Compression (e.g. retraction during median sternotomy or lateral decubitus position)
Stretching (i.e. Arm abduction + external rotation + posterior shoulder displacement)
Direct trauma during regional technique
Signs/symptoms:
C5-C6 lesions: Waiter’s tip = arm hangs by side, medially rotated + pronated
C8-T1 lesions: flexion of small muscles of hand (“claw hand”), numbness in ulnar area
Prevention:
General considerations as described above
Maintain arm ABduction < 90 deg
Radial Nerve Injury (C5-T1)
Usually injured at spiral groove of the humerus
Mechanism:
Tourniquets/BP cuff compression
Arm board at incorrect height creating a step
Signs/symptoms:
Wrist drop
Numbness along:
Posterior + distal surface of arm
Posterior surface of forearm
Dorsum of hand + lateral 3 1/2 fingers
Prevention:
General considerations as described above
Median Nerve Injury (C5-T1)
Mechanism:
Direct trauma during regional technique
Surgical procedures on elbow
Compression in the carpal tunnel
Signs/symptoms:
Paresthesias: lateral 3 1/2 fingers + palmar aspect of hand
Supinated forearm
Weakness:
Abd + opposition of thumb
Wrist flexion
Prevention:
General considerations as described above
Mandatory padding
Keep forearm in supine/neutral position
Maintain flexion/extension of elbow < 90 deg
Axillary Nerve Injury (C5, 6)
Mechanism:
Shoulder dislocation
Shoulder surgery
Signs/symptoms:
Weakness: shoulder abduction
Numbness: upper lateral border of arm
Prevention:
General considerations as described above
Musculocutaneous Nerve Injury (C5-7)
Mechanism:
Shoulder dislocation
Shoulder surgery
Signs/symptoms:
Weakness: flexion of elbow
Numbness: lateral border of forearm
Prevention:
General considerations as described above
Sciatic Nerve Injury (L4-S3)
Men > women, T2DM
Mechanisms:
Lithotomy, frog leg and seated positions (hyperflexion of hip, ABduction + extension off leg
Direct damage during: regional techniques + hip replacement surgery
Signs/symptoms:
Hamstring muscle paralysis
Weak knee flexion
Foot drop
Numbness: below knee in all areas except medial aspect of leg+foot
Prevention:
General considerations as described above
Adequate padding when patient is in lithotomy, prone or lateral positions (hip flexion > 120 deg)
Femoral Nerve Injury (L2-4)
Mechanisms:
Pelvic brim injury due to retractors in abdo/pelvic surgery
Ischemia during aortic cross clamp
Lithotomy position: extreme ABduction of thigh + ext rotation of hip
Direct damage during: vascular sx involving femoral vessels + hip replacement
Signs/symptoms:
Numbness: anterior thigh, medial leg
Weakness: hip flexion, knee extension
Absent knee jerk reflex
Prevention:
General considerations as described above
Adequate padding when patient is in lithotomy, prone or lateral positions (hip flexion > 120 deg)
Superficial Peroneal Nerve Injury (L4-S2)
Commonly compressed against the fibular head
Mechanism:
Direct trauma during knee arthroplasty
Lithotomy / lateral position
Signs / symptoms:
Weakness: dorsiflexion + eversion of the foot
Numbness: antero-lateral leg + dorsum of digits
Prevention:
General considerations as described above
Adequate padding when patient is in lithotomy, prone or lateral positions (hip flexion > 120 deg)
Postoperative Neurocognitive Disorder
Background
Considerations
Goals
Postoperative Neurocognitive Disorder
Background
Formerly known as Post-operative Cognitive Dysfunction (POCD)
Subtle cognitive impairment that differs from overt delirium
Consists of two syndromes:
Delayed neurocognitive recovery
patient is back to baseline by 30 days
Post-op neurocognitive disorder
cognitive decline which persists up to 12 months post-op
Mild = mild cognitive impairment (MCI) equivalent
Major = dementia equivalent
Pathophysiology
Thought to be secondary to inflammatory response of surgery
Considerations
Risk factors:
Age > 65, pre-operative cognitive impairment, critically ill, excessive EtOH use, polypharmacy, frailty, hx of stroke or TIA, other comorbid dz (DM, vascular dz), lower education level
Major ortho sx, cardiac sx, otherwise long sx
Useful to perform baseline cognitive screen (i.e. MMSSE or Mini-Cog) in suspected pts
Consider use of BIS or raw EEG monitor to avoid burst suppression
Employ cerebral oximetry to avoid drop in rSO2
No difference in incidence based on anesthetic technique (GA vs regional or inhalation vs IV)
Goals
Identify high-risk patients
If high-risk:
Avoid excessive anesthetic depth (i.e. burst suppression)
Avoid prolonged periods of hypotension
Avoid ↓ cerebral oximetry
Avoid benzos & gabapentinoids
Minimize opioids
Multi-modal analgesia for opioid-sparing effect
e.g. Acetominophen +/- NSAIDs +/- steroids +/- ketamine +/- dexmedetomidine infusion
Employ routine measures to avoid post-operative delirium (e.g. early mobilization, removing drains/restraints/lines etc.)
See post-operative Delirium
Prior Bleomycin Exposure
Background
Bleomycin-Induced Lung injury
Goals
Prior Bleomycin Exposure
Background
Bleomycin (BLM) is an antitumor antibiotic used to treat mostly germ cell tumors and Hodgkin lymphomas
Mechanism of action: works by inducing breaks in DNA through a complex of bleomycin, ferrous iron and oxygen
BLM is inactivated in the body by BLM-hydrolase (BLM-h)
BLM-h activity is lowest in skin and lungs
Skin and lungs are the organs most susceptible to BLM toxicity
Pathophys. of toxicity is poorly understood but likely through a combination of:
Oxidative damage via oxygen free radicals
Relative deficiency of BLM-h
Genetic susceptibility
Subsequent inflammatory cascade
80% renally cleared
Bleomycin-Induced Lung Injury
Life-threatening interstitial pulmonary fibrosis AKA BLM-induced lung injury
Signs and Symptoms:
Dyspnea (earliest sx), cough, chest pain, crackles
Chest opacities on CXR
Asymptomatic decline in DLCO
Develops subacutely, over days to weeks, within 1-6 months of bleomycin exposure
Assess PFTs
↓ DLCO
Restrictive pattern: ↓ FVC, TLC and FRC
Co-morbid conditions:
Testicular or ovarian germ cell tumor
Ovarian sex cord-stromal tumor
Hodgkin lymphoma
Risk factors:
↑ age
Renal insufficiency
↑ cumulative drug dose (rare if dose exceeds 270 IU)
Severity of underlying malignancy
↑ FiO2 use
Concomitant radiation therapy (i.e. thoracic irradation)
Treatment with other chemo agents (i.e. cisplatin)
Cigarette Smoking
Goals
Avoid exposure to high FiO2
Evidence is largely anecdotal
High FiO2 even years after BLM exposure can increase risk for BLM-induced lung injury
If hypoxemic, titrate minimal amount of oxygen to maintain O2 sat 89-92%
Minimize IV fluids to avoid volume overload
