Oral Boards Background info Flashcards
GCS scoring
EYES
4: spontaneous
3: voice
2: pain
1: none
VOICE
5: comprehensible
4: confused
3: inappropriate
2: incomprehensible (sounds)
1: none
MOTORS
6: spontaneous
5: localizes pain
4: withdraws to pain
3: decorticate flexion
2: decerebrate extension
1: none
Trauma difficult airway, but spontaneously ventilating, AMS, inc ICP, intubate?
Due to significant head injury pt would not tolerate hypercapnia induced increase in CBF, subsequent inc in ICP assoc with hypoventilation or apnea
-dec risk of aspiration
-avoid having to manage potentially difficult airawy in more emergent circumstances
-ensure difficult airway equipment availabilty and surgeon at bedside ready to perform trach if needed
how to intubate AMS combative difficult airway
-ensure availability of difficult airway equipment
-surgeon at bedside ready to perform trach
-pt in 30 deg RT to improve respiratory mechanics, facilitate intubation, red passive regurgitation (if hemodynamically will tolerate)
-pre oxygenate
-carefully titrate IV ketamine to maintain spontaneous ventilation but adequate depth of anesthesia
-ensure manual in line stabilization
-remove front of c collar to allow for cricoid pressure
-perform larygnscopy for ETT placement
Inc ICP, head trauma and intubation avoid:
-factors that will inc ICP: hypoxia, hypercapnia, sympathetic stimulation
-hypoTN: decrease CPP (MAP-ICP)
-c spine injury
-aspiration of gastric contents
Head trauma, high ICP, difficult airway, ketamine?
-benefits outweigh risk, to maintain spontaneous respirations throughout induction and intubation
-acknowledge that ketamine inc sympathetic tone, inc CRBG and regional CMRO2, which is undesirable in this patient, outweighs the possibly inc in ICP assoc w/ hypoxia, hypercarbia, and loss of airway
succinylcholine in trauma with high ICP and difficult airway
no
-want to maintain spontaneous resp to avoid hypoxia and hypercarbia, inc ICP
-avoid transient inc in ICP with succ and fasciculations
-instead, i would give aspiration ppx, apply cricoid pressure, and secure airway as quickly as possible without succ
how to clear C-spine
- absence of cervical pain or tenderness
- absence of paresthesias or neuro deficits
- normal mental status
- no distracting pain
- age > 4
if can’t meet criteria for c spine clearance, what imaging?
cross-table lateral c spine film showing C1 to T1, open mouth odontoid view, and thoracolumbar, anterior/posterior and lateral plain films
periorbital ecchymosis and hemotympanum, difficulty w/ DL, nasal intubation suggested, response?
No, periorbital ecchymosis and hemotympanum suggest basilar skull fracture -> run the risk of putting the ETT in the brain w/ nasal intubation
-instead, call for help, release cricoid pressure, use a video laryngoscopy, if still unsuccessful ventilate as necessary and attempt with fiberoptic bronchoscope, boughie, lighted stylet or surgical access
trauma w/ AMS and bleeding into leg, VS:
HR 134, RR 24, BP 178/108 O2 96% on NRB temp 33C
-can get hyperdynamic circulatory response w/ head surgery -> surge of epinephrine
-pain, hypoxia, hypercarbia, anemia, or hypovolemia can contribute
-optimize by controlling pain, replacing fluid losses w/ blood products or crystalloid as necessary and ensure adequate ventilation
-mild hypothermia beneficial dec CMRO2
head trauma, fluids currently D5LR, what woudl you do w/ fluids?
-D/c D5LR, hyperglycemia can worsen ischemic brain injury, switch to normal saline
-access fluid status w/ UOP, mucous membranes, cap refill, blood loss (taking into accound that there could be blood in abd compartmet or possible femur fx)
-goal is to maintain CPP by restoring circulating blood volume and avoiding hypotension, while reducing risk of cerebral edema by maintaining serum osmolality and avoid reduction in colloid oncotic pressure
head injury BP inc to 205/118, what to do?
difficult to tell if part of the reflex of inc ICP, or due to hypoxia, hypercarbia, pain, anemia, hypovolemia
-but needs to be addressed due to concern for MI and/or cerebral infarction
-1. take steps to dec ICP, consult neurosurgeon for possible ICP monitoring
2. ensure adequate analgesia, intravasc volume replacemet, and ventilation
-if need to give a medication i would use something short acting: esmolol, nicardipine, clevidipine
ideal CPP for traumatic head injury
optimal unknown
normal is 70-85
some studies show > 70 inc ARDS, w/ cerebral ischemia below 50-60, so ideal 60-70
cerebral autoregulation
absence of chronic HTN, maintains CBR w/ MAP 60-150
Causes of tachycardia
- Primary: SVT, VT
- Secondary: hypoxia, hypercarbia, hypovolemia, pain, dec O2 delivery (anemia, dec cardiac output)
bradycardia causes
- primary: sick sinus syndrome, complete HB
- secondary: medication induced (beta blockers, dig, anticholinesterases, dexmedetomidine, narcotics), vagal stimulation (oculocardiac reflex, baroreceptor reflex [carotid surgery], larygnscopy, traction on viscera)
hypotension causes
-dec preload
-inc intrathoracic pressure (tamponade, PPV, PEEP, TPX, aorto-caval compression)
-heart itself: cardiomyopathy, infarcted muscle, HR too low or too high, arrhythmia
-afterload low: anaphylaxis, spinal show
-blood: not enough, not enough viscosity
Open femur fx, surgeon wants to go to OR, but head trauma, req ICP monitoring?
-If result in a significant delay, would not necessarily require
-However, would allow me to improve CPP, by knowing MAP required to combat inc ICP
-would also allow for CSF drainage to optimize CPP
-discuss w/ ortho and neurosurgeon feasibility in case delay to establish
MOA mannitol
Reduces ICP by osmotically shifting fluid from brain compartment to intravascular compartment
-Dec production of CSF
-induces reflex cerebral vasoconstriction 2/2 decreased blood viscosity
***if BBB not intact, could worsen cerebral edema, could result in expansion of intracranial hematoma
Reduce ICP in head trauma victim
- Elevate HOB 15-30 deg as hemodynamically tolerated
- Ensure no venous obstruction (esp w c Collar in place)
- Mannitol: osmotic diuresis
- Furosemide (acknowledge can cause hypoTN in Hypovolemic, possible worsening of cerebral ischemia)
- Barbiturates by Dec CMRO2 and red ICP -> likely hypoTN w/ doses required for cerebral protection
**do not hyperventilate in TRAUMA b/c red in CBR in head trauma in the first 24 hours -> but if nothing else works, yes.
Hyperventilate w/ head trauma
If other methods to reduce ICP unsuccessful, and ICP enough to be concerned fro brainstem herniation, yes to CO2 25-30 b/c cerebral vasoconstriction would Dec ICP
-however risk of cerebral ischemia, esp in the first 24 hours
-hyperventilation effects temporary, HCO3 levels in CSF adjust to compensate in 24-48 hours
Hypothermia effects
Coagulopathy
Poor wound healing
Arrhythmias
Impaired renal function
-theoretical neuro protection, but not enough evidence to show improved neurological outcomes
N2O w/ TBI
-NO
-want them breathing 100% O2, inc CBF, could expand air pocket furthering inc ICP
DDx w/ femur fx, TBI, hypoTN, PIP 40s, O2 Dec to 80s
-ETT migration
-PTX
-cardiac tamponade
-fat emboli
-allergic reaction
-aspiration pneumonia is
Next steps if femur fx, TBI, hypoTN, inc in peak insp pressure, O2 falls
-hand ventilate, auscultation, make sure FiO2 100%, verify ETT positioning, order CXR
-if still unclear, ABG, TTE, consider pulm a catheter
Femur fx, TBI, PAC: PA pressure 55/47, PWCP 16, Mixed venous 60%, CI 1.7, subconjunctival petechiae
Fat embolism Syndrome
-however to confirm you need 1 major, and 4 minor criteria
-MAJOR: petechial rash, hypoxia PaO2 <60 w/ fiO2 <.4, CNS depression unexp by hypoxia, pulm edema
-MINOR: tachypnea > 110, pyre is, jaundice, unexpl anemia, unexpl thrombocytopenia, inc ESR, retinal fat emboli, fat microglobulinemia, fat globules in sputum, urinary fat globules
**acknowledge that these criteria can be confounded by conditions w/ trauma
Normal cardiac index
2.6 - 4.2
Normal PCWP
2-15
Normal PA pressure
15-30/4-12
Mixed venous O2 saturation
65-75%
What to do if dx fat emboli syndrome?
-administer 100% O2
-treat hypoTN
-correct Hypovolemic
-replace blood and plts as needeD
-continue mechanical ventilation
-monitor pt for further deterioration
-inform surgeon of condition
PaO2 68 with FiO2 50%, CXR shows b/l infiltrates ddx?
-ARDS (2/2 fat embolism syndrome, head trauma, or aspiration)
-Aspiration pneumonia
-Pulmonary edema (cardiogenic, neurogenic)
-if req blood products: TRALI or TACO
Pathophysiology of ARDS
Pulm manifestation of systemic inflammatory response syndrome
-injury to capillary-alveolar membrane -> b/l diffuse infiltrates, severe dyspnea, and hypoxemia
Req for diagnosis of ARDS
- PaO2: FiO2 ratio < 300 (300-200: mild, 200-100:mod, <100:severe)
- Diffuse b/l infiltrates on CXR
- Acute onset (w/i 7 days of event [sepsis, trauma, aspiration])
- Respiratory failure not explained by cardiac failure or fluid overload
Treatment of ARDS
-Treat causative events (DIC, sepsis, hypoTN)
-supportive mechanical ventilation
-sufficient PEEP to recruit collapsed alveoli and improve gas exchange, while avoiding high pressures and large volumes
-goal: TV 6 cc/kg or less and static airway pressures < 30
-permissive hypercapnia may be needed to avoid higher TV and airway pressures
-FiO2 < 50
nitric oxide, prone, temporarily improve, none show long term outcome differences
Steroids in ARDS?
Giving steroids early has been assoc w/ increased mortality
Post TBI, POD 5, Na is 129, urinary Na high. Dx?
Cerebral salt wasting or SIADH
-can best be differentiated by volume status of the patient
-CSW Hypovolemic, SIADH euvolemia
Diff b/w SIADH and CSW?
SIADH: euvolemia, inc ADH levels, urine Na rarely >100
CSW: hypovolemic, normal ADH levels, UNa > 100
Why important to distinguish b/w CSW and SIADH
Treatment is different!
-SIADH: water restriction, diuresis, DEMECLOCYCLINE (inh ADH effect on renal tubules), Na replacement
-CSW: water restriction, direusis could worsen the Hypovolemic
Proper Machine Check
- Turn on the machine and monitors -> verify presence of emergency ventilation equipment
- Calibrate or set the capnometer, pulse oximeter, O2 analyzer, and pressure monitors and alarms
- Check the high pressure system: opening the E-cylinders to ensure adequate gas pressure (O2 must be half full, 1000 pasig)
- Verify the central pipeline hoses properly connected -> confirm pipeline gauges read 50 psig
- Check the low pressure system by ensuring filled vaporizers, check for leaks (machine dpt), testing flow meters
- Check scavenging system, calibrate the O2 monitor, ensure proper ventilator function
- Check integrity of unidirectional valves, inspect circuit, verify adequate CO2 absorbent
- Ensure availability of airway equipment and suctioning
How to check for leaks in the low pressure system?
Low-pressure leak test used to verify integrity from flow control valves to the common outlet
-verify the proper method of testing for the workstation I’m using
Low-pressure leak test in a machine without a check valve near the common outlet
Ex: Drager
-traditional positive pressure leak reset
Low-pressure leak test for machines w/ a check valve near the common outlet
Ex: Datex-Ohmeda
-perform negative-pressure leak test by turning off the anesthesia machine, attach a suction bulb to common gas outlet, squeeze bulb until collapsed, and observing stayed collapsed for 10 seconds
-repeat w/ each vaporizer opened one at a time
Protects against delivery of hypoxic mixture?
Safety devices
-fail safe alarms: sound if the pressure in the O2 pipeline falls below 30 psig
-O2 failure cut off valves, Dec of d/c the flow of other gasses when O2 pressure Dec below the a certain threshold
***do not definitively prevent -> best is vigilance and proper monitoring of the O2 analyzer
Desflurane vaporizer
Electrically heated to create a vapor pressure of 2 atms -> pure des vapor is mixed w/ fresh gas prior to exiting vaporizer
Sevoflurane vaporizer
Variable-bypass vaporizer -> variable amount of gas is directed into vaporizing chamber -> mixes w/ volatile agent -> returns to mix w/ the rest of the carrier gas directed to bypass chamber
Pathogenesis of SCD
Hemoglobinopathy mutation of chromosome 11 (substitution of valine for glutamic acid) in beta changes of Hg -> HgS
-deformation of RBC membrane into sickled shape -> hemolysis (shorted RBC lifespan), microvascular occlusion, ischemic injury to organs, infarcts, hemolytic crisis
Comorbidities w/ SCD
Chronic hypoxia, anemia, hemochromatosis (iron overload)
-cardiomegaly
-CHF, pulm HTN
-neuro deficits
-renal insuff/failure
-painful crisis
-acute chest syndrome
-retinopathy
-aseptic necrosis of femoral head
-asplenic (multiple infarcts) -> in fxn from encapsulated organisms
Exchange transfusion prior to surgery
If moderate or high risk surgery, transfuse to a Hct > 30% w/ goals of increasing O2 carrying capacity and prevent suckling
Prevent sickling in SCD
-avoid hypoxemia, hypotension, hypothermia, acidosis, Hypovolemic
-use suppl O2, adequate hydration, Hct 30-40%, avoid hypothermia w/ fluid warmers and forced warming units, provide adequate postoperative pain control
Treatment of sickle cell crisis
-ensure adequate pain control
-provide adequate IV hydration
-supplemental O2
-adequate Hct levels
-to infection
-consider exchange transfusion to reduce HgbS to less than 40%
Morbidly obese pt, BMI >50, do to at an outpatient facility
-Assuming medically optimized and no hx of OSA possibly, because outpt reduces costs on pt and inc convenience
-need to perform a thorough history and physical exam to determine extent/severity of coexisting disease, incl OSA, type of surgery performed, capabilities of outpt facility, adequacy of post-d/c care (family, friends), post op opioid requirements
Identify pts w/ undiagnosed OSA
Large # of patients w/ undiagnosed OSA
-STOPBANG
-Snoring, daytime Tiredness, Observed apnea, Pressure (HTN), BMI >35, Age > 50, Neck circ >40, gender male
**< 3: low risk, >3 high risk, 5-8: mod to severe OSA
BMI 70s, asthma, DM, mod to severe OSA, possible periop complications?
-difficult airway management
-aspiration
-bronchospasm
-labile BP
-hyperglycemia
-difficulty evaluating cardiac/pulm status due sedentary lifestyle
-difficult patient position, rapid desaturation (Dec FRC), obesity hypoventilation syndrome
-OSA, postop apnea, stroke, CAD, altered drug effete, DVT/PE
Preop labs for low risk surgery DM, BMI 50s
Pregnancy, blood glucose, results of sleep study, hx of difficult airway
Premeds for DM, BMI 50s, HTN, asthma, GERD
-obesity, possible diabetic neuropathy, gastric reflex -> inc risk of aspiration -> H2 rec agonist, metochlopramide, nonparticulate antacid
-discuss w/ surgeon abx, DVT ppx
-beta 2 agonist to optimize breathing
BMI 50s, asthma, DM, crying, give Midas?
Yes, small dose, since excessive anxiety, crying -> complicate airway conditions,
-also possible undiagnosed OSA -> assess risk for OSA and consider risk of respiratory depression 1st
BMI 50s, asthma, HTN, IDDM, how to evaluated her given concerns of cardiac disease?
-thorough H&P -> r/o any active cardiac issues unstable angina, decompensated HF, severe arrhythmias
-access her risk for a major adverse cardiac event using revised cardiac risk index
-determine functional capacity -> given hx of diabetes possible she cannot experience angina warning signs -> if > 4 METs proceed, if < 4 -> discussion w/ patient and surgeon if prep stress test PCI/CBG considerations would alter surgical plan
Revised Cardiac risk index
2 or more assoc w/ inc risk of major adverse cardiac event
-IDDM
-hx of ischemic heart disease
-hx of compensated or prior HF
-hx of cerebral vascular dx
-renal insuff
-Supra-inguinal vascular, intraperitoneal, or intrathoracic surgery
Umbilical hernia repair, BMI 50s, asthma, HTN, GERD, IDDM. Monitors?
Standard ASA monitors, paying special attention to BP cuff fitting -> ensure bladder of cuff encircled at least 75% of upper arm -> too small, falsely elevated BP
-if unable to get adequate BP cuff -> consider a line
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM neuraxial?
Yes -> avoid airway instrumentation and GA in obese pt w/ inc risk of aspiration
-reduce periop requirements for opioids
-would avoid opioids in the spinal straight local anesthesia
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, induce?
Assuming reassuring airway:
-aspiration ppx w/ H2 blocker, metochlopramide, nonparticulate antacid
-beta 2 agonist to optimize asthma
-place in RT (improves resp mechanics, red risk of passive reg)
-preoxygenate
-apply cricoid pressure
-IV lidocaine blunt resp to laryngoscope
-RSI
-rapidly secure airway w/ cuffed ETT
-RSI inc risk of bronchospasm due to inadequate depth of anesthesia -> be prepared to treat this complication
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, mallampati III on airway, induction plan?
-While Mallampati is only part of airway exam, inc concern w/ super morbid obesity
-inc risk for aspiration, with difficult intubation
-aspiration ppx, and discuss awake fiber optic intubation
-minimal sedation (avoid risk of resp depression), adequately anesthetize airway to prevent bronchospasm
***if pt refuses, difficult airway equipment in room, asp ppx, Albuterol, RT, cricoid pressure, no muscle realaxant, adequate depth of anesthesia to avoid bronchospasm
Obese pt, pts closing capacity when moved to supine?
Closing capacity is unaffected -> relationship w/ FRC worsening -> early airway closure and shunting -> rapid desaturation
Morbid obesity, adjust protocol dose?
-induction dose of propofol is based on ideal body weight, maintenance on total body weight
-lipophilic drugs in obese pts have a higher volume of distribution -> start w/ ideal body weight, and titration to effect
Midazolam dosing in obese pts
Loading and maintenance based on TBW
succinylcholine dosing in obese pts
Based on TBW
Vec/roc dosing in obese pts
IBW
atracurium/cisatracurium dosing in obese pts
TBW
Fentanyl dosing obese pts
Loading dose: TBW
Maintenance: IBW
Remifentanil dosing obese pts
Ideal body weight
Ideal body weight in men
IBW = 50 kg + 2.3kg/in over 5 ft
ideal body weight in women
IBW = 45.5 kg + 2.3 kg/in over 5 feet
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, opioids on induction?
I would use a small dose of narcotics at induction to reach depth of anesthesia to avoid bronchospasm during laryngoscope
-recognize w/ mod-sever OSA inc risk for postop opioid induced resp depression -> only small dose of short acting narcotic
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, give muscle relaxant?
-avoid atracurium/mivacurium b/c histamine release avoid in asthmatics
-atracurium/cisatracurium: dose on TBW
-vec/roc dose to ideal body weight
Inhalational agents in obesity
If less than four hours, no delay in wakening w/ more soluble agents like iso (compared to less soluble sevo)
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, during case pulse o Dec to high 80s, what to do?
-switch to 100% O2, hand ventilate, auscultation chest, ensure adequate ETT placement, check airway pressures, check circuit and machine
-assess pt position, if trendelenberg -> flatten or RT
-consider giving albuterol
-if ETT in good place, and no wheezing -> consider inc PEEP
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, wheezing, what to do?
100% O2 -> inc conc of inh agent -> give albuterol (bronchodilation and inc depth of anesthesia to avoid stimulation-induced bronchospasm)
-if no improvement -> give epi
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, how to extubate?
Deep plane of anesthesia to prevent further bronchospasm
-understand inc risk of aspiration due to obesity, DM, GERD, empty stomach w/ OGT and have suction nearby in case
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, how to transport to PACU?
obesity and OSA: optimize resp mechanics: suppl O2, applying CPAP, HOB up
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, pulse ox 83% in PACU, ddx?
-airway obstruction due to OSA
-bronchospasm
-resp depression 2/2 narcotics
-aspiration
-atelectasis w/ pulm shutting
-possible PE
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, desalting to 80s after morphine
-position head of bed up, administer 100% O2, apply CPAP
-consider narcan, while giving non-opioid analgesics (acetaminophen, ketorloac)
-monitor for extended period of time -> consider redoing narcan
Umbilical hernia repair, BMI 50s, asthma, GERD, IDDM, epidural for analgesia? Dosing?
If pain insufficient w/ non-opioid analgesics, yes I would place
-however given risk for DVT and resp depression -> use low conc of local anesthetic only, non opioid
-minimize m weakness and inc mobility
Peds pt, hx of massester muscle spams, periop questions?
Complete H&P -> circumstances related to muscle spasm -> type of anesthesia provided, severity of spasm, how treated -> any work up?
-family hx of anesthesia complications, incl master spasm or malignant hyperthermia
Hx of masseter muscle spasm, mom had no surgery, and family have no history of anesthetic complications
Assuming no testing has been done to r/o MH -> provide TIVA with non-trigger agents including fentanyl and prop infusions
-massester muscle regidity following triggering agents (succ or volatiles) -> susceptibility to MH
MH concern, succ is given, cant open pts jaw, what now?
-mask ventilate w/ 100%
-if difficult -> call for help, place nasal airway, attempt nasal intubation, prepare for surgical airway
-consider risk of MH rhabdo
-admit to hospital for 12-24 hours, monitor EtCO2, CK, temp, acid-base status, electrolyte levels (concern for rhabdo induced hyperK)
-continued evaluation of pigmenturia, myoglobinuria, generalized rigidity, signs of hyper metabolism
-order neuro c/s for preexisting myopathies
-recommend testing for MH susceptibility
Succ-induced trismus, cancel the case?
Yes, d/c all triggering agents, cancel case, monitor pt for 12-24 hours
Recommend caffeine halothane contracture test
pregnant pt, obtunded, bite bark on tongue
likely seizure -> preeclampsia until proven otherwise
ddx: cerebral hemorrhage, cerebral infarction, placental abruption (AFFE), medication, trauma, encephalitis, epilepsy, meningitis, hypoNa, hypoglycemia
Diagnostic criteria for PEC
- 2 BP readings > 4 hours apart, systolic > 140, diastolic > 90
- proteinuria 24 hour urine level > 300, Urine protein:Cr ratio of 0.3
- > 20 weeks gestation
Severe PEC
- BP > 160 or d > 110 4 hours apart
- renal insuff, Cr > 1.1 or x2
- new CNS disturbance (HA, vision changes)
- pulm edema
- liver dysfxn (AST/ALT x2)
- epigastric or RUQ pain
- thrombocytopenia < 100
pregnant pt obtunded, bit her tongue, what to do?
-quickly assess VS, O2 sat, EKG
-ensure adequate oxygenation, uterine displacement, and IV access
-eval baby’s FH tracting
-quick physical exam fosuing on neuro (MS, signs of in ICP), airway, cardiopulm fxn, signs of coagulopathy
-if felt her mental status was impaired -> secure her airway ASAP to reduce risk of aspiration
-adequate ventilation more important if concerned w/ ICH -> hypoventilation -> acidosis, hypoxia, worsening ICP
pregnant pt, concerns for difficult airway, awake fiberoptic intubation, use benzocaine?
-benefit: rapid onset and short duration of action
-risk: inc risk for Met-Hg, dec O2 carrying capacity and impaired O2 delivery to tissues -> confuse clinical picture w/ airway management
-alternative: give glyco to dec secretions, apply topical anesthetic w. spray or local-anesthetic soaked gauze, supplement w/ appropriate airway blocks
Airway blocks:
glossopharyngeal, SLN, and transtracheal blocks
Glossopharyngeal nerve block
sens: posterior 1/3 of tongue, vallecula, gag reflex
-submucosa at posterior tonsillar pillar (caudal aspect) -> 2 to 5 cc of 2% lidocaine
Superior Laryngeal nerve block
sens: laryngeal structures above VC
-inferior to greater cornu of the hyoid bone -> 2cc of 2% lidocaine
Recurrent laryngeal nerve block
sens: VC and trachea, motor supply to all m of larynx except cricothyroid
-transtracheal block -> cricothyroid membrane -> 22 or 20 guage needle continuous aspiration of syringe -> rapid injxn of 5cc 4% lidocaine -> coughing normal and helps disperse LA
pulse ox and Met-Hg
-false reading of 85% b/c Met-hg absorbs the same amount of light at the 660nm and 960nm wavelength
Met-Hg and toxicity
<30%: no tissue hypoxia
30-50%: signs and symptoms of tissue hypoxia
> 50%: lead to coma and death
tx for Met-Hg in G6PD
-Met-Hg were mild -> identify and avoid any additional oxidizing agent
-tissue hypoxia does not develop until Met-Hg until levels > 30%
-Can’t use Methylene Blue in G6PD -> IV Vitamin C
Methylene Blue Dosing
2 mg/kg of 1% solution in saline over 3-5 minutes, may be repeated after 30 minutes if needed
What is G6PD def?
-enzymatic disorder, inhibits regeneration of glutathione in red blood cells -> more susceptible to oxidative damage -> shortening RBC half-life
-X-linked d/o
-can cause: fatigue, cyanosis, jaundice, anemia, hypoTN, lumbar and abd pain, hemolysis, hematuria, renal failure
-normocytic anemia, inc serum bili, inc retic count, Heinz bodies
Meds to avoid in G6PD def
Benzocaine
Lidocaine
Prilocaine
Sodium nitroprusside
Siler Nitrate
Nitrofurnatoin
Methylene Blue
High Dose Aspirin
Methyldopa
Hydralazine
Procainamide
Quinidine
can precipitate hemolysis
Anesthetic Management Changes in G6PD def
-Disease hx (hemolysis, precipitating factors, renal failure)
-Hct and retic count preop
-avoid drugs that induce Met–Hg (benzocaine, prilocaine, sodium nitroprusside)
-avoid specific abx (nitrofurnatoin, chloramphenicol, cotrimoxazole)
-avoid/treat factors known to precipitate hemolysis: hypothermia, acidosis, hypoxia, hyperglycemia, infxn
-continue to monitor pt’s Hg, retic count, and UOP
GA and G6PD def
-no anesethetics implicating as hemolytic agents
-can mask hemolysis: important to monitor postop for signs and labs ofhemolysis
-CPB has initiated hemolysis
Factors that precipitate hemolysis in G6PD def
Hypothermia
Acidosis
Hypoxia
Blood products
Stress
Hyperglycemia
Infection
Food (fava beans)
Methylene Blue, antimaliral drugs
Abx (nitrofurantoin)
High dose ASA
Procainamide
Quinidine
awake fiberoptic impossible, found down, with swollen tongue, spontaneous breathing, do you intubate? how?
-yes intubate, while spontaneously ventilating
-ensure presence of difficult airway equipment
-position pt in 30 deg RT (dec risk of aspiration, venous drainage from intracranial compartment, improve resp mechanics)
-be prepared for emergency trach
-apply cricoid pressure
-maintain spontaneous vent: slow controlled induction w/ ketamine, recognizing that could potentially inc CBF and/or CMRO2 -> inc ICP
OB, found down, AMS, CT scan prior to her c/s?
I would recommend she obtain CT scan of her head -> benefit from neurosurgical consult and treatment prior to undergoing stresses assoc with delivery
-however would require transporting her to a location -> secure airway and ensure hemodynamic stability prior to transport (optimize uteroplacental BF)
-FHR monitoring -> be prepared to quickly return
OB, AMS, babys heart tones down, consider c/s prior to head CT/MRI?
-if heart tones down: lay mom flat, left uterine displacement, give O2, assure adequate blood pressure
-proceed with GA for emergent c/s, using a high narcotic neuroprotective technique -> goal to avoid inc ICP or compromise cerebral perfusion pressure -> notify the neonatologi giving large amount of narcotics since likely to depress compromised neonate
Pt found down, AMS, pregnant, baby heart tones down, emergency c/s needed, regional anesthetic?
No, mental status can deteriorate -> inc risk for hypoventilation and aspiration
-GA help in avoiding hypovent-induced hypercapnia, hypoxia, resp acidosis -> inc risk for inadequate CPP and/or hemolysis
-regional would cause sympathectomy-induced hypotension -> compromise CPP w/ elevated ICP
-difficult airway -> prior to inducing have difficult airway equipment available and surgeon establishing airway if needed
HIV okay in neuraxial?
-HIV is not a contraindication to regional anesthesia -> no evidence that HIV progression is increased by CNS blockade
AMS, PEC, emergent c/s, place an a line?
-yes do want an arterial line to monitor and tx BP to avoid inc in ICP, and maintain adequate CPP
-understand delay in intubation and c/s for arterial placement inc risk of aspiration and poor outcome -> proceed with case and place a line as soon as feasible
OB AMS, baby delivered, BP 189/105, HR dec to 48, L pupil dilated, not reactive to light, thoughts?
Consistent w/ Cushing response -> inc in ICP -> inc in BP, reflex slowing of HR, and irregular respirations
-dilated, non reactive pupil suggests CN III compression 2/2 uncal herniation
-take measures to reduce ICP -> d/c volatile agents, make sure no venous obstruction, elevate HOB to 30 deg, and give mannitol
-last resort hyperventilation
Hyperventilation in TBI
hyperventilation not recommended due to risk of inducing cerebral ischemia (reduction in CBF during the first 24 hours) -> warranted a as a treatment of last resort in this situation if uncal herniation eminent
How does mannitol dec ICP
-osmotically shifting fluid from intracranial compartment to intravascular compartment
-dec production of CSF
-inducing reflex cerebral vasoconstriction
-potential complications: worsening cerebral edema if BBB not intact, or expansion of intracranial hematoma where intracranial bleeding (osm diuresis -> shrinkage of surrounding brain)
OB crash c/s, TBI, GA with ETT, pt taking longer to wake up than expected, what to do?
-check vital signs
-ensure adequate BP, O2, ventilation
-possible manifestation of worsening cerebral pathology -> c/s neurosurgeon plan for immediate transport to get a CT scan -> take steps to dec ICP and maintain CPP
-other possible causes: Mg tox, or high dose narcotics
OB crash c/s, TBI, GA with ETT, concern for inc ICP, going to CT, widened QRS on EKG, what to do?
-check her vital signs
-compare current EKG to previous one to rule in/out previous condition
-continue efforts to control ICP, recognizing inc ICP -> widened QRS complex
-plan for CT head to r/o ICH
-another cause could be Mg toxicity -> order Mg level and check Deep tendon reflexes
-if Mg toxicity -> d/c infusion, prepare to treat sz, give diuretic to inc renal excretion of Mg, give calcium gluconate
Serum Mg level, SE?
1.4-2.5
Normal
Serum Mg level, SE?
4-7
Therapeutic Range
Serum Mg level, SE?
7-10
loss of patellar reflexes, hypoTN, CNS depression
Serum Mg level, SE?
13-15
Respiratory Paralysis
Serum Mg level, SE?
16-25
EKG changes (prolonged PR interval, widened QRS, prolonged QT interval)
Serum Mg level, SE?
20-25
cardiac arrest
POD2 OB PEC, jaundice and develops dark urine
signs/symp with hemolytic anemia
-evaluate pt for signs of hemolytic anemia: pallor, SOB, fatigue, substernal pain
-CBC, retic count, peripheral blood smear (Heinz bodies), LFTs (inc bili), urinalsysi (hemosiderin, urobilinogen, brown)
-eliminate any preciptating factors: hypothermia, acidosis, hypoxia, hyperglycemia, infxn
-give fluids and mannitol to maintain UOP
-consider transfusion if needed
Hemolysis POD 2-5 with no blood products given, thoughts?
G6PD deficiency
Nurse sticks herself with needle after drawing on HIV positive pt, what to tell her?
-immediately wash the wound with soap and water, and report to employee health to get blood draw for testing
-reassure her telling her the transmission rate even with HIV positive source 0.3%
-likely to get post exposure ppx and should avoid risk transmitting dx like blood donation or sexual activity until labs are negative for HIV
PEA what to do?
-Call for help
-Start CPR
-verify rhythm is not v fib or v tach
-secure airway with ETT
-ensure PIV access
-give 1mg epi, repeating every 3-5 minutes as needed
-treat any reversible causes: Hypovolemic, hypoxia, acidosis, hyper/hypoK, hypothermia, drug tox, tamponade, PTX, MI, PE
-continue to check for shockable rhythm
**consider TTE
When to use post ROSC hypothermia?
-unable to meaningfully respond to verbal commands after treating precipitating causes, optimizing vent and oxygenation and optimizing cardio pulm fxn (fluids, introns, vasopressors MAP > 65)
-believed to provide protection for the brain and organs in comatose pts post cardiac arrest
ROSC determined by:
-presence of pulse and BP
-abrupt inc in EtCO2 > 40
-spontaneous arterial pressure waves on a line
When to use hypothermia post cardiac arrest?
-comatose post ROSC after being resuscitated for out of hospital v fib cardiac arrest
-in hospital arrest w/ any initial rhythm
-out of hospital arrest w/ initial rhythm PEA
How to induce therapeutic hypothermia
-cooling blankets
-ice packs
-rapid infusion of 30 cc/kg ice cold LR or normal saline
-goal temp: 32-34 C
-monitor temperature (esophageal, bladder, or pulm a catheter (if already in place))
-maintain 12-24 hours
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometimes, what causes her SOB?
-compression of the airways 2/2 mediastinal mass
-mass compression of heart or great vessels
-mass-induced V/Q mismatch
-mass obstructive PNA
-SVC syndrome (obstruction of venous drainage)
-possible myasthenia gravis (assoc w/ thymoma MC anterior mediastinal mass)
-poorly controlled asthma
-severe GERD, aspiration, aspiration PNA
-cardiac assoc w/ Down Syndrome (endocardial cushion defects)
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometime, next steps?
History and Physical
-CT scan, CXR, PFTs, and TTE -> identify any airway and/or cardiac compression, signs of COPD
-signs/sym of SVC: JVD, head and upper limb edema, dysphagia, nasal stuffiness, papilledema, CP, lightheadedness, orthopnea
-Sym of myasthenia gravis: dyspnea, diplopia, ptosis, dysphagia, slurred speech, m weakness
-H&P on severity, course, to of HERD and asthma
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometimes, could SOB due to myasthenia gravis?
-Yes, resp m compromise assoc w/ MG can contribute to SOB
-thymoma is one of the MC anterior mediastinal masses, and significant number of pts w/ thymoma develop MG
-if after further examination concerned for MG: c/s neurologist for definitive dx and tx
Pathophys of myasthenia gravis
-autoimmune disease
-antibodies to postsynaptic ACh receptors -> Dec in number of receptors in NMJ -> m weakness, esp in eyes, face, throat. Neck, limbs
-weakness worsens with activity and improves w/ rest
-symp: diplopia, ptosis, dysphagia, diff chewing, slurred speech, dyspnea
-can affect heart: mild HTN, 1st deg AV block, a fib, myocarditis, cardiomyopathy, diastolic dysfunction
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometimes. She says that she gets lightheaded while laying down, concerned?
-very concerning -> setting of anterior mediastinal mass, hx of presyncope w/ supine position -> assoc w/ inc periop risk of cardiovascular collapse
-likely caused by mass compression of heart, SVC, or pulm artery > inc risk for complete cardiovascular collapse in periop period
-other causes contributory: cardiac manifestations (mild HTN, 1st deg AV block, a fib, diastolic dysfunction
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometime. Says she gets lightheaded when lying on her back, what do you do?
-examine pt, and review CXR, CT scan, TTE, PFTs
-looking for any mass involvement in heart or great vessels and identify RF for periop cardiopulm complications:
-tracheal compression > 50%
-tracheal compression > 30% with bronchial compression
-strider
-orthopnea
-cyanosis
-jugular distinction
-SVC syndrome
-pericardial effusion
-pleural effusion
-combined obstructive and restrictive pattern on PFTs
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometimes, CT scan shows 50% tracheal compression, concerning?
Yes, this degree of tracheal compression is assoc w/ inc risk of complete airway collapse
-this w/ SOB, presyncope in supine position, and possible subglottic tracheal stenosis assoc w/ down syndrome -> substantial risk of periop airway compromise
-chronic compression or tumor invasion of tracheobronchial tree can affect structural integrity of trachea -> more susceptible to collapse w/ direct mass compression, forced expiration, inc negative intraluminal pressures
-review CT scan -> airway compression below carina may inc her risk making passage of ETT beyond area of compression impossible
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometime, Per CT compression of trachea 50%, next steps?
-ask pt symp of airway compression: dyspnea, tachypnea, wheezing (recognizing confounded by asthma/COPD) and if worsened w/ laying flat
-discussion w/ surgeon about performing surgery under local anesthesia
-attempting to reduce size of tumor w/ chemo, radiation or steroids before proceeding
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometime, TTE?
-SOB could be cardiac in nature, esp if compression involved -> TTE sitting up and supine to see effects of mass and positioning on cardiac function
-can identify any cardiac defects or dysfunction assoc w/ Down syndrome or myasthenia gravis
Anterior mediastinal mass, Down syndrome, mod to severe asthma, severe GERD, smoker, SOB sometime, flow volume loops?
-i would not, flow volume loops for this patient b/c poor predictors of periop resp complications, provide little info that can’t be obtained from CT, and do not alter anesthetic plan
-INSTEAD, review CT, perform H&P, observe pt in sitting and supine positions
Benefit: PFTs to know effect on position on pulm fxn, location (intrathoracic or extrathoracic), and nature (fixed or variable), and if there is a reversible component
What flow volume loop results show inc risk of airway collapse during induction of anesthesia
Increased mix-expiratory plateau noted when position is changed from upright to supine = variable intrathoracic airway obstruction
Flow volume loop for fixed obstruction
Dec exp and insp loops
Flow volume loop for extrathoracic obstruction
(VC paralysis, tracheomalacia)
-Dec insp curve, normal exp curve
-neg pressure pulls in, causes obstruction, positive pressure pushes out
Flow volume loop for intrathoracic obstruction
Dec exp loop, more normal insp loop
-b/c positive pressure causes compression in intrathoracic cvavity, but opens up w/ neg pressure in insp
36 YOF, anterior mediastinal mass, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, anesthesia?
-local anesthesia w/ little to no sedation if possible
-concerns for general anesthesia: occurrence of presyncope and dyspnea with supine position, FEV1 and FVC < 50% of esp, 50% tracheal compression -> suggest significant risk of pulm or cardiovascular collapse on induction of GA
-abnormalities of airway w/ DS: macroglossia, subglottic stenosis, micrognathia, atlantoaxial instability, compl mask ventilation, DL
-severe GERD, dysphagia, severe asthma inc bronchospasm
Airway abnormalities assoc w/ Down syndrome -
Macroglossia
Subglottic stenosis
Micrognathia
Atlanta-axial instability
36 YOF, anterior mediastinal mass, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, pt refuses just local anesthesia, what to do?
-Would make the surgeon, pt, and her family aware of my concerns and suggest chemo, radiation or steroid therapy to reduce size of the mass prior to surgery
-and then f/u scan to see resolution of concerning symptoms and successful reduction of tumor prior to rescheduling
-acknowledge this can affect risk of diagnostic inaccuracy, risk of proceeding w/o pretreatment
36 YOF, anterior mediastinal mass, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, would you give anticholinergic for aspiration ppx
-no, reduce LES tone and have not been shown to Dec acidity or gastric volume in pts at inc risk for aspiration
-instead give H2 blocker (famotidine), metochlopramide, and nonparticulate antacid (sodium citrate)
-would also avoid anticholinergic drugs since could possible lead to inc m weakness and bulbar symptomaology in someone w/ MG
How to evaluate for Atlanta-axial instability?
-review previous anesthesia records for indication of difficult airway or Atlanta-axial instability?
-anterior atlantodental interval > 4-5 mm in any lateral view
-H&P to identify signs of symp of cord compression (gait anomalies, clumsiness, fatigue w/ ambulating, numbness/tingling, hyperreflexia
-full neck flexion and extension to see if symp -> if any symptoms would delay the case and request repeat cervical imaging and a neurosurgeon eval
36 YOF, anterior mediastinal mass, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, has never undergone cervical imaging, would you require?
-while it it’s reasonable to obtain cervical imaging in a pt with Down’s syndrome who’s never been screened, I would not require it assuming that the history and physical did not identify any signs or symptoms consistent w/ cervical instability
-however would proceed w/ extreme caution and make every effort to avoid excessive flexion, rotation or neck extension -> especially concerned b/c DS freq are difficult airways
36 YOF, anterior mediastinal mass, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected. Previous XR at 4 years old showing anterior atlantodental interval of 6mm, never had symp, would you delay the case for repeat imaging?
Would not delay needed surgical procedure unless H&P show cord compression
-would take caution to minimize head and neck movement during the case, esp w/ laryngoscopy
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, c/o numbness and tingling in her arms w/ full neck extension, what would you do?
Recognizing consistent w/ cervical spine instability -> delay nonemergent case until she could have full service l spine eval by neurosurgeon
-if surgical procedure cannot be delayed -> goal to minimize neck flexion, extension and rotation
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, how to intubate and induce this patient?
-asp ppx, pre-induction albuterol
-ensure adequate IV access, and presence of fluids, inotropes, and vasopressors
-difficult airway equipment available incl fiber optic, multiple micro laryngeal ETT sizes, surgeon in room w/ rigid bronchoscope
-put pt in position she’s the most comfortable in to minimize mass compression -> leave bed in room in event prone positioning necessary
-cannulate femoral arteries under local anesthesia w/ CPB in the room and ready
-adequate airway anesthesia
-awake fiber optic
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, awake fiber optic best approach?
Assuming GA was required, awake FOB gets
-adv: minimize movement of cervical spine w/ possible atlantoaxial instability, minimize asp b/c airway secure prior to induction, allows assessment of level and degree of compression, ensure ETT distal to obstruction
-avoids deleterious effects of general anesthesia (red preload and altered resp mechanics)
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, pt refuses awake intubation, what will you do?
-attempt to explain benefits of placing ETT prior to induction and reassure her that I would do everything I could to make her comfortable
-if still refused: optimize medical conditions (asp ppx, albuterol), ensure difficult airway equipment, surgeon present in the room with rigid bronch and eternal saw
-minimize head movement
-place her in position she is most comfortable
-cannulate femoral arteries under local anesthesia w/ CPB pump on standby
-reduce airway secretions
-induce the pt w/ small dose of ketamine followed by volatile agent -> goal to maintain depth of anesthesia sufficient to prevent bronchospasm while maintaining sp respriations and avoiding pulm asp and neck movement
-reinforced ETT
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, shortly after induction but prior to placement of ETT airway movement ceases, can’t ventilate, what to do?
-place OPA and attempt to hand ventilate w/ 100 FiO2 and CPAP, auscultation the chest
-put pt in position preop tha minimizes dyspnea and presyncope
-minimize head and neck movement
-perform laryngoscope to see if larygnoasm -> if none place an ETT
-if unable to ventilate -> pass fiber optic through ETT to identify any mass-induced obstruction
-could be. Bornchospasm -> PPV, deepen anesthetic, give albuterol, and epi
-if unable to ventilate due to obstruction, wake pt up, if unable to: attempt to advance ETT or bronchoscope beyond obstruction
-consider prone position to relieve mass obstruction
-ask surgeon to perform emergency stereo to my and manually elevate mass -> and start cardiopulm bypass
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, intubated, mass identified as thymoma, attempt to extubate?
-return of sp ventilation and chest wall tone should help maintain airway latency -> providing pt meet standard extubate on criteria, remove in RT position
-given risk of aspiration, possibility of MG and risk of airway compression from mass (since just biopsy) -> prepare for emergent reintubation, delay extubate on until fully awake
-consider ACHE inh should help w/ resp m weakness if concerned for MG
-risk of bronchospasm consider IV lidocaine or albuterol prior to extubate on
-vigilant monitoring postoperative
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, you give pyridostigmine to treat MG, after ETT removal she Delors laryngospasm and can’t ventilate
-suction airway to remove debris, blood, secretions
-apply positive pressure mask ventilation
-deepen anesthetic w/ volatile agent
-give IV lidocaine to blunt glottic closure reflex
-forceful jaw thrust (careful to avoid changes in cervical spine)
-call for help, gently attempt to pass ETT through closed CV
-avoid succ or roc if at all possible -> concern of airway collapse after cessation of spontaneous ventilation
-if last resort would give succ -> acknowledging that MG tend to be resistant, duration can be prolonged
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, larygnospasm, no succ available, would you give a nondepolarizer medication to break spasm
Due to concern for airway collapse in this pt, this would be a last resort
-MG she would be very sentisitve to NDM
-would give small dose, only if laryngospasm persisted despite other interventions (half or 1/3 dose)-> she was becoming hypoxic, intubation w/o m relaxation proved impossible and succ was unavailable
-make sure ETT beyond mass compression area
36 YOF, anterior mediastinal mass for biopsy, smoker, DS, SOB asthma mod to severe, diff swallowing, severe GERD, 50% tracheal obstruction, FEV1, PEF less than 50% expected, postop dyspneic, differential?
-mass obstruction compressing tracheal structures, cardiac structures
-bronchospasm 2/2 asthma/COPD
-laryngospasm
-upper airway obstruction 2/2 macroglossia/subglottic stenosis with DS
-airway edema
-exacerbation of myasthenia gravis or cholinergic crisis
-residual anesthesia
-pulmonary edema (neg pressure, cardiogenic)
-inadequate pain control
-aspiration pneumonitis
-cardiac tamponade/PE
Tonsilon test
Edrophonium test
-positive is muscle strengthening after edrophonium adminstration
-if symptoms worsen - > cholinergic crisis
-2-10mg of edrophonium, improvement in 5 minutes, only lasts around 10 minutes
Signs/symptoms of cholinergic crisis
-diaphoriess/diarrhea
-urinary freq and urgency
-miosis: constricted pupil size
-bradycardia, excess mucous in lungs
-emesis
-lacrimation
-lethargy
-salivation/sweating (vomiting)
-weakness/muscle fasciculations
MG and NMB
-avoid long acting nondepolarizers
-use minimum dose needed for effect
-plan to let the affects wear off, avoid giving a reversal agent
Negative pressure pulm edema
-noncardiogenic form
-large inspiratory effort against obstructed upper airway
-negative intrathoracic pressure in alveoli -> inc transcapillary pressure gradient
-may occur w/i a few minutes up to 3 hours -> coughing, tachypnea, hypoxia
Treatment of neg pressure pulm edema
Maintain upper airway latency, provide suppl O2, give diuretics, and start mechanical ventilation if necessary
Would you give steroids for SC injury?
No, not recommended, lack of evidence w/ clinical improvement
-large complications incl fluid retention, hypertension, electrolyte imbalances, hyperglycemia, impaired wound healing and immunosuppression
Hx of tobacco use, how to evaluate pulm status/fxn?
H&P!
-s/s of COPD: cough, sputum production
-freq of pulm infections, freq and severity of exacerbations, exercise tolerance, # and course of hospitalizations, efficacy of past treatments
-CXR, PFTs, ABG, consider pulm consult
When to order PFTs w/ lung hx?
Hx of long smoking hx, is hypoxic on room air, and about to undergoing surgery w/ inc risk of postop pulm complications
-PFTs give type and severity of dx, baseline pulm fxn, and presence of reversible component
FEV1/FVC < 70%, type of lung dx?
Obstructive
FEV1/FVC 50% with mild improvement w/ bronchodilator therapy
Severe COPD
Smoker, hypoxia on room air, case w/ postop pulm issues, benefit of case being delayed?
Pulm status benefits from smoking cessation 8 weeks prior to surgery
Preop chest physiotherapy
Bronchodilators
Glucocorticoids
And abx if evidence of in fxn all for optimization
Timeline for symptoms for alcohol withdrawal
Tremulousness: 6-8 hours
Hallucinations and so: 24-36 hours
DTs: confusion, perceptual distortions, agitation, autonomic instability: 72 hours
Concern of alcohol hx, w/u?
History: type, frequency, quantity of alcohol consumed, last time of alcohol intake
-physical exam: looking for cirrhosis, hepatic encephalopathy, wernicke-korsakoff syndrome, gait disturbance, cardiomyopathy
-CBC, BUN, Cr, lutes, glucose, coats, LFTs
-EKG, CXR
-benzos
Anesthesia concerns w/ chronic alcohol abuse
-inc MAC req
-tolerance to other anesthetic drugs
-cognitive impairment
-cerebral atrophy
-cerebella degeneration
-peripheral neuropathy
-cardiomyopathy, cirrhosis, hypoglycemia
-thrombocytopenia, electrolyte abnormalities, GI bleeding, w/d symp, risk for aspiration, nutrition def
Risk of poor periop glucose control
Poor wound healing
Inc rate of infection
Osmotic diuresis
lab work for diabetes
CBC, BMP, glucose level, UA
-potential for arthrosclerosis and silent ischemia: EKG
Cervical Laminectomy: DM2, HTN, active smoker, daily alcohol consumption. How to optimize prior to surgery?
-c/s pul for dx and optimization of pulm dx (steroids, bronchodilator’s, abx?)
-recommend smoking cessation at least 8 weeks prior to surgery (red in carboxyHg), improved ciliary fxn, red nicotine level, red airway hyperreactivity, Dec sputum production, Dec periop pulm complications
-d/c and detox of alcohol -> correct any metabolic abnormalities or nutritional def from alcohol
-evaluate for s/s of diabetic autonomic neuropathy, eval glycemic control, see endo if inadequate
Posterior cervical laminectomy, DM, HTN, active smoker, severe spinal stenosis, poor airway, orthostatic hypoTN, wheezing, special monitors?
ASA standard (5 lead KEG): monitor for cardiac ischemia
-arterial line : hemodynamic changes
-SSEPS/MEPS: intraop SC ischemia
-foley
When to avoid MEP monitoring
Cochlea implants, active so, or vascular clips in the brain
Why do MEPS in addition to SSEPS for SC surgery?
-SSEPS anterior SC function
-possibility of false neg with SSEPs, and inc sensitive of MEPS for detecting motor injury
-would do both if SC ischemia is a significant risk
Posterior cervical laminectomy, DM, HTN, active smoker, severe spinal stenosis, poor airway, orthostatic hypoTN, wheezing, how to intubate?
-asp ppx, beta blocker, place pt in RT, ensure adequate airway analgesia prior to awake FOB w/ manual in-line stabilization
Posterior cervical laminectomy, DM, HTN, active smoker, severe spinal stenosis, poor airway, orthostatic hypoTN, wheezing, maintenance of anesthesia?
TIVA w/ prop, remi, and ketamine
-allowing an adequate depth of anesthesia w/ minimal depression of SSEPs, MEPs
**MEPs more sensitive to volatiles than SSEPs -> if volatile given use less than 0.5 MAC
How do anesthetic agents affect MEPs?
-Dec amplitude and inc latency w/ opioids, sedative hypnotics, and volatile agents
-similarly seen with SC ischemia
-no muscle relaxants
What change in MEPs are significant?
50-80% Dec in amplitude, changes in latency are less reliable
Anesthesia affect SSEPs
Decreased amplitude and inc latency
-anesthesia suppression, hypothermia, hypercarbia, hypoxia, and hypoTN have similar effects
What monitored in MEPs?
Descending motor pathways in anterior spinal cord
What monitored in SSEPs
Ascending sensory neural pathways in posterior spinal cord
After induction and prone positioning, pt hypoTN, 62/48, tx with ephedrine ineffective
-100% O2, ensure adequate ventilation, look at EKG
-give fluid bolus -> ensure positioning not obstructing venous return
-likely has significant autonomic neuropathy: small bolus of direct acting vasopressors like phenylephrine
Autonomic Neuropathy
-long standing DM -> excessive glycosylation can lead to neuropathy in Autonomic neuro us system
-Gastroporesis, GERD
-exercise intolerance
-early satiety
-bloating
-no sweating
-peripheral neuropathy
-dysrythmias
-diarrhea
-N/V, epigastric pain
-orthostasis, HTN
-lack of reflex tachycardia w/ Hypovolemic
-resistant to ephedrine (indirect)
**often affects parasympathetic 1st
Dec amplitude and inc latency in SSEP and MEPs, what do you do?
-correct any hypoxemia, hypoTN (up to 20% above normal), Hypovolemic, anemia, hypo/hypercarbia
-make sure depth of anesthesia was stable
-r/o SC injury due to excessive traction
-if no improvement as removal of instruments and consider wake up test
What change in SSEP is considered significant
50% Dec in amplitude, 10% inc in latency
What part of SC most vulnerable to ischemic injury?
Anterior spinal cord -> limited blood supply from anterior spinal artery
-additional supplied by radicular arteries: Artery of Adamkiewicz
Delayed emergence with NMB fully reversed, adequate TV, and low conc of volatile, ddx?
-neurological deficits
-hyper/hypoglycemia
-alcohol w/d
-hypoxia
-hyper/hypocarbia
-residual anesthetic
-residual NMB
-metanbolic derangements
What to do in delayed emergence?
-ensure adequate ventilation and oxygenation
-review meds given during the case
-confirm complete NMB with twitch monitor
-serum glucose and lutes
-check temp
-still unknown c/s neuro, EEG, and CT head/neck
Expected pH on PaCO2 on acute respiratory
-inc in 10 PaCO2 = Dec 0.08 pH
7.40/40
7.32/50
7.24/60
7.16/70
Difference b/w expected and actual is metabolic
Inc anion gap metabolic acidosis
Diabetic or alcoholic ketoacidosis
Accumulation of lactic acid (poor tissue oxygenation) or liver dysfunction
Intravascular dilution (hypotonic fluids )
Renal failure
Rhabdomyolsysis
How to calculate anion gap
Na - (Cl and bicarb)
12 +/- 4 is normal 8-16
How to treat combined AG metabolic acidosis
-adjust ventilator to maintain PaCO2 in low 30s to compensate for academia
-identify cause of metabolic acidosis: lactate, UOP, Cr, BUN, blood glucose and urine ketones, blood alcohol level
-treat metabolic derangement
-only if bicarb if pH < 7.1, bicarb < 10 or life threatening hyperK
Concerns of treatment w/ sodium bicarb
-generates additional CO2 (reacts w/ hydrogen ions) -> worsen acidosis
-L shift of O2 dissociation curve -> inc Hg affinity for O2 -> Dec O2 offloading
-hyperosmolar state 2/2 excessive Na
-hypoK (K moves from Extracellular to intracellular)
Patient wakes up after prone case and can’t see, what to do?
-assess pt
-correct any metabolic disturbances
-elevate HOB (facilitate venous drainage)
-ensure adequate BP, Hg, O2, and cardiac function
-urgent potholes c/s
-talk to pt and family: all precautions had been taken to minimize risk, everything being don to treat
What is posterior ischemic optic neuropathy?
-postop vision loss believed to occur when Dec O2 delivery to RETROLAMINAR PART OF THE OPTIC NERVE
-MCC of postop vision loss, 24-48 hours postop
-painless vision loss, Afferent pupillary defect, visual field defect, optic disc normal
Which pts high risk for developing posterior ischemic optic neuropathy?
Spine surgery:
-prolonged case > 6.5 hours
-substantial blood loss (45% of EBV)
RF:
Anemia, substantial blood loss, hypoTN, Hypovolemic, hypoxia, hemodilution, external ocular pressure, inc ocular venous pressure, release of endogenous vasoconstrictors, prone head-down positioning, prolonged surgery, massive fluid resuscitation
How to reduce risk of periop vision loss for a high risk patient undergoing spine surgery in prone position
-ensure head is neutral forward position, level or higher than heart
-monitor BP continuously, and maintain BP a baseline
-consider CVP and monitor and maintain intravascular volume w/ crystalloids and colloids
-monitor Hg and Hct levels (goal Hg > 9 and Hct 28%)
-consider staging spinal surgeries that are anticipated to be long and complex
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Concerns?
-cardiac status: hx of MI and HF, exertional angina and orthopnea
-poorly controlled HTN -> periop hemodynamic instability and inc postop compl
-periop complications w/ DM: hyper/hypoglycemia, hemodynamic instability (DM autonomic neuropathy), silent ischemia, neurological injury (inc risk of ischemic neural injury), and aspiration
-TIAs: inadequate collaterals through circle of Willis
-periop MI or stroke
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. How to eval preop?
-neuro exam: deficits?
-acute cardiac condition: unstable angina, unstable CHF -> both require surgical delay
-Hg, UA, EKG, CXR, ABG (baseline PaCO2)
-TTE if not done in 12 months or symp worsened
-eval signs for autonomic neuropathy (BP and HR)
-optimize blood sugar, BP, and cardiac function
-reassurance and minimal sedation to avoid any inc in HR, BP, and myocardial O2 consumption
-continue cardiac meds
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. How to eval her cardiac status?
H&P
-assess severity and stability of her cardiac disease
-r/o any acute cardiac conditions
-any previous cardiac interventions
-determine functional status (> 4 METs proceed)
-if METS < 4 -> c/s with surgeon and patient to see if results of further cardiac testing would alter care (CABG or PCI)
-consider pharmacological stress test
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Can’t determine functional capacity. Recommend testing for cardiac ischemia?
-if cardiac risk outweighed benefits of immediate surgery, and if a positive test would alter management -> dob stress test
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Would cardiac revascularization be indicated prior to CEA?
It would if the vascular surgeon and cardiologist believed her overall outcome would be improved
-important to realize risk of periop stroke during revascularization of heart
-decision in conjunction w/ cardiologist and vascular surgeon
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Benefits/disadvantage of GA
-Benefits: still patient and operative field, definitive control of airway and ventilation, pharmacological interaction for brain protection
-Disavd: can’t perform repeated neuro exams, possibility of greater hemodynamic instability 2/2 induction, intubation, extubate on
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Regional benefits/disadvantages
Benefits: greater hemodynamic stability, avoid MI depression w/ GA, avoid tracheal intubation and symp response, reduce risk for vasopressors, continuous neurological monitoring
Disadvantages: phrenic n paralysis (commonly associated w/ cervical plexus block), limited access to unsecured airway, high level of pt cooperation (need same language). Can be insufficient if pts carotid disease extends so high incision must be extended
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Premeds?
-if pt anxious despite reassurance, small amount of narcotic prior to line placements -> periop anxiety can cause detrimental effects on heart
-give any chronic cardiovascular med pt is taking at home (make sure they get their ASA if on at home)
Regional anesthesia for carotid endarterectomy
-deep and superficial cervical plexus blocks to anesthetize C2-4 dermatomes
-superficial: posteriori border of the SCM
-deep: draw a line from mastoid process to Chassaignacs tubercle and level of cricoid cartilage -> palpate C2 transverse process 1-2 cm caudate of mastoid process with transverse process of C3 and C4 -> inject 10cc at each transverse process
Complications of deep and superficial cervical plexu blocks
-epidural and subarachnoid in Jan
-phrenic n blockade
-intravascular injection into vertebral artery
-recurrent largyneal nerve blockade
-horners syndrome (ptosis, miosis, anhydrosis)
-local anesthetic toxicity
-bleeding
Infection
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. CEA, can you use superficial cervical plexus blocks alone?
I would not
-poorly controlled HTN, CAD, CHF would not tolerate sympathetic response from inadequate analgesia
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. Monitors?
A line
5 leads EKG
computerized ST segment analysis
-central line
-possible TEE
-EEG, SSEPs
Options for neuromonitoring with CEA?
-most reliable: intraoperative exam of awake patient
-indirect if under GA: EEG, SEEPs, transcrnaial Doppler, stump pressure determinations, cerebral oximetry, measurements of regional CBF, jugular venous O2 sats
Stump pressure in CEA
Internal carotid artery
-placing a needle in the artery above the clamp to measure back pressure from collaterals through circle of Willis
-adv: inexpensive, easy to obtain, continuously available during cross-clamping
EEG in CEA
-requires stable anesthetic
-disadvantage: may not detect subcortical or small cortical infarcts, not specific for ischemia
-can be altered with changes in temp, BP, and anesthetic depth
SSEP monitoring
measures the response of the sensory cortex to electrical impulses from from peripheral n stimulation
-ascending sensory neural pathways in posterior SC
-affected by hypothermia, BP, anesthetic depth
Transcranial Doppler CEA
TCD of ipsilateral MCA: continuous measurement of mean BF velocity and detection of micro-embolic events
-helpful in evaluating shunt function, identifying shunt malfunction, determine need for shunt placement (if Dec flow during cross-clamp)
68 YOF, recurrent TIAs, presenting L CEA. PMH MI 1 year ago, poorly controlled HTN, HF, DM, tobacco, orthopnea, and angina. How to induce GA?
Goal to maintain adequate cerebral perfusion and minimize stress to heart
-avoid any hypercarbia or hypoxia
-prepare to treat any hypertension, tachycardia, bradycardia, or hypoTN that occurs during induction
-place monitors and lines
-preoxygenate patient
-start remifentanil drip
-give esmolol and lidocaine to blunt symp response to laryngoscope
-slowly titration ETT I’d ate until patient no longer responsive (Dec CMRO2 more than CBF)
-after able to mask ventilate, give a muscle relaxant
-ventilate w/ volatile agent
-perform laryngoscope after sufficient depth of anesthesia
Isoelectric EEG w/ iso during CEA correct?
-no, dose required to produce isoelectric EEG can cause significant cardiac depression and interfere with EEG monitoring for cerebral perfusion
-can use remi and low dose sevo (0.5 MAC) to allow for EEG monitoring and maintain energy of BP in the high-normal range during cross clamp
Myocardial preconditioning
-exposure to certain drugs serve to protect myocardium against subsequent myocardial ischemia and reperfusion injury
-volatiles w/ conc as low as 0.25 MAC may limit infarct size, prevent dysrhythmias, and preserve myocardial function
-done w/ iso, sevo, and does
Why is inc in PaCO2 an issue in CEA?
Can cause cerebral vasodilation in normally reactive, non-ischemic vascular beds, diverting VF away from hypoperfusion areas where vascular use is already maximally dilated (“steal phenomenon”)
-acknowledge that too low PaCO2 would cause intense vasoconstriction and L shift of the oxyHg dissociation curve -> normalize while avoiding hypocarbia
CEA, w/ dissection pts HR Dec to 48 and BP 88/40, ddx?
Reflex bradycardia 2/2 enhanced vagal tone from surgical manipulation of carotid sinus with activation of baroreceptors
-myocardial depression
-cardiac ischemia
-dysrhythmia
-preexisting autonomic neuropathy
CEA w/ dissection HR Dec to 48 bpm, BP 88/40, what do you do?
Ask surgeon to stop any further dissection, evaluate the EKG, cardiac output
-make sure adequate ventilation and oxygenation
-depending on cause I would treat w/ glyco, fluids, and/or inotropic agents
-if etiology surgical manipulation: can ask surgeon to give local anesthetic to prevent further episodes
CEA, after carotid cross clamp, ipisilateral EEG slowing is noted, significance?
May indicate cerebral ischemia
-could also be due to hypoterhmia, inc depth of anesthesia (but those are usually b/l)
-ask surgeon to remove cross clamp and consider placing a shunt
-ventilate w/ 100% FiO2, ensure adequate MAP, ensure normal apnea
CEA EEG shows slowing and surgeon wants BP at 180 (preop BP 170), agree?
If baseline 170/95 was close to her baseline -> cautiously raise her BP while monitoring EKG and CVP to improve cerebral perfusion
-inc BP could cause MI 2/2 inc myocardial O2 consumption w/ inc afterload
-10-15% above baseline
CEA, EEG slowing, Inc BP, and now new onset SET segment depression?
-optimize myocardial O2 supply and demand
-ventilate 100% FiO2
-correct any anemia, to any tachycardia -> carefully reduce afterload -> acknowledging that I might compromise cerebral perfusion
-carefully titrate NTG due to short duration of action and beneficial effects on coronary circulation
Delayed emergence ddx?
Residual anesthetic effects
Inadequate muscle relaxation
Cerebral ischemia
Hypoxia
Hypercarbia
Hypotension
Metabolic derangements
Hyperglycemia/hypo
Hypothermia
Cerebral hyperperfusion syndrome (usually several days later)
Delayed emergence after CEA, what to do?
-check vitals: EKG, CVP, EtCO2
-ensure adequate ventilation, oxygenation, and perfusion
-any neuro deficits
-reverse any residual anesthetics
-correct any hyper/hypoglycemia, hypothermia, hypoxemia, hypercarbia, HTN/hypoTN
-make surgeon aware and Doppler s for carotid blood follow
-CT scan and cerebral angio
Cerebral hyperperfusion syndrome
When previously hypoperfused areas of the brain have lost ability to autoregulate BF -> exposed to high systolic BP w/ restoration of blood flow
-HA, sz, focal neurological signs, brain edema, ICH
Post CEA BP 195/97 what to do?
Correct any hypoxemia, hypercapnia, bladder distention
-ensure adequate pain control
-could be a result of the enervation of the carotid sinus baroreceptors -> give hydral, beta blocker, NG
-goal systolic BP < 160 or w/i 20% of preop values
Post CEA HTN, while treating pt becomes dyspneic, what’s going on?
Most concerning: airway obstruction 2/2 airway edema or wound hematoma
MI
CHF
PTX
-other: bronchospasm, atelectasiis, autonomic neuropathy, carotid body denervation (impaired ventilator response to hypoxia and hypercarbia)
-undx OSA
-narocis
-inadequate reversal of NMB
Post CEA, inspiratory strider, pressure in neck underneath dressing, are you going to intubate her?
Yes, consistent with airway obstruction 2/2 expanding neck hematoma
-transport pt to OR, call surgeon, presence of difficult airway equipment, continue to tax hypertension
-have someone apply pressure to wound
Post CEA, inspiratory stridor, expanding neck hematoma, do you open the wound
-if i felt there was time, I would not open the wound prior to transport surgical and anesthesia equipment not available
-difficult airway equipment, send for surgeon, and attempt to intubate the patient
33 weeks gestational infant, copious oral secretions, gastric distention w/ PPV, polyhydramnios intern, can’t advance OGT, next steps?
Consistent w/ estophageal atresia and tracheoesophageal fistula
-nurse d/c PPV -> further gastric distention can impair ventilation
-call for surgeon to eval neonate for possible gastrostomy tube to decompress the stomach
-consider placing an ETT beyond the fistula
-neonate in head up position (minimize resurgence)
-obtain IV access
-initiate suctioning of upper esophageal pouch to prevent aspiration
-neonate NPO
-CXR to confirm dx
Tracheoesophageal fistula, gastrostomy tube placed, ETT removed, need to replace it?
-if following decompression, neonate showed no signs of respiratory distress (tachypnea, tachycardia, IC retractions, rales, cyanosis) -> spontaneous ventilation okay
-i would not replace ETT to avoid PPV and worsen gastric distention
-monitor neonate carefully —> if needed decompress gastrostomy tube and PPV
Types of tracheoesophageal fistula, most common?
Type A-E
Type C most common: esophageal atresia w/ blind upper pouch and a lower segment tracheal fistula
Neonate prematurity concerns
-respiratory distress syndrome
-persistent pulm HTN of newborn
-Apneic spells
-bronchopulm dysplasia
-NEC
-retinopathy of prematurity
-intraventricular hemorrhage
-red renal fxn
-impaired glucose regulation
-immature hepatic fxn
-inc susceptibility to hypothermia
Congenital abnormalities assoc w/ esophageal atresia and TEF?
VACTERL
Vertebral defects
Anal atresia
Cardiac anomalies
TEF
Radial and renal dysplasia
Limb anomalies
TEF, how to eval preop?
-identify/optimize any aspiration PNA, pneumonitis, RDS, Hypovolemic
-CXR and ABG to determine extent of pulm dx
-TTE eval cardiac defects
Renal u/s
Spinal films
CBC, BMP
-optimize pulm and cardiac fxn, avoid asp, ensure adequate hydration, establish a plan for intubation, vent, and extubate on
TEF repair, what monitors for the case?
Arterial line (femoral or umbilical)
Precordial stethoscope in L axilla
Foley
Place the gastrostomy tube under a water seal (ensure placement of ETT)
-temp monitoring
TEF repair, how to induce and intubate
-ensure proper monitors and IV access
-pt in HOB up position
-suction proximal esophageal segment, suction gastrostomy tube
-topically anesthetize the airway (minimize sympathetic stimulation)
-atropine (ablate vagal resp to laryngoscope)
-RSI
-advance ETT into R main stem bronchus and slowly w/d until breath sounds b/l
-verify PPV with ETT w/o causing excessive bubbling from submerged gastric tube (confirm w/ fiber optic)
TEF repair, if pt did not have gastrostomy tube, awake intubation?
Yes, awake intubation to minimize risk of PPV induced gastric distention and aspiration
-airway analgesia w/ topical local anesthesia and if neonate stable give minimal sedation I
-goal to blunt sympathetic response could lead too intraventricular hemorrhage in premature neonate
-consider inhalational induction to maintain spontaneous respiration
TEF, does intubation protect child from aspiration?
Not entirely, placement and inflation of cuff provides some protection, however if cuff not placed distal to fistula it will provide no protection
TEF, ex-33 weeks, what size ETT and cuffed v uncuffeD?
3.0 mm ETT to minimize risk of aspiration with goal to place ETT cuff distal to fistula
-no need for repeated laryngoscope
-acknowledge means smaller diameter -> could lead to inc airway resistance, risk of post extubate on croup
-largest allow for adequate air leak around cuff at 20-25
TEF repair, SpO2 Dec to 89%, airway pressure inc
-displacement of ETT into R mainstream
-surgical retraction of trachea, bronchus or lug
-gastric distention from PPV
-bronchospasm
-PTX
-V/Q mismatch from RDS, PNA,
-mucous plug or clot in ETT
TEF repair, SpO2 85%, inc airway pressures, what to do?
-inform surgeon
-hand ventilate w/ 100% oxygen
-auscultation breath sounds in all lung fields
-suction ETT
-peds bronch to verify placement
-check for gastric distention
-check for bubbling w/ gastric tube under wet seal
-ask surgeon to relieve traction
-check ABG
-consider POCUS or intraop CXR
TEF repair on TPN, how to manage intraop fluid replacement
-continue TPN and maintenance fluids separately
-goal of Hct > 35%, blood loss 3:1 crystalloid
-monitor UOP, HR, BP, ABGs adjust as needed
TEF repair, temp is 36.3 concerning?
Yes, while not meeting the definition of hypothermia, it is lower than normal
-neonate limited ability to maintain normothermia
-prone to hypothermia: thin skin, large surface area to body mass ratio, low sub fat, inefficient mechanism of heat production (brown fat metabolism)
-hypothermia effects: inc O2 consumption, in PVR, inc cardiac shunting, altered drug response, postop hypoventilation, apnea, coagulopathy, delayed wakening, cardiac irritability, wound healing, metabolic acidosis
Extubate pt post TEF repair?
-I would not extubate due to high risk of reintubation, causing inc risk for airway trauma, intraventricular hemorrhage (sympathetic response), disruption of anastomatic suture line
-infants often require re-intubation 2/2 atelectasis, aspiration PNA, aspiration pneumonitis, RDS, tracheomalacia, resp depression, excessive secretions
Extubation goals for TEF repair
Cardiopulm status stable
AWake
Complete reversal of NMB
Cough and gag reflex intact
Spontaneous TV of 5-7 cc/kg on CPAP
Peak inspiratory pressures below 30
O2 requirements were below 40% with a PEEP of 3-5
Regional w/ TEF repairs
Caudal anesthesia
-allows for reduction in volatiles, intraop narcotics, and NMB
Post TEF, intubated transport to NICU, hand ventilation through ETT difficult, pt hypoxic, what do you do?
-quickly transport back to NICU or back to OR, whichever is closer
-continue ventilation w/ 100% FiO2
-auscultation all over lung fields
-confirm presense of EtCO2 (possible extubation()
-confirm ETT positioning
-suction ETT
-consider CXR/bronchodilator
TEF repair ICU vent settings
SIMV
-PEEP 2
-FiO2 as low as necessary to maintain PaO2 of 60-80 mmHg
-minimize Peak inspiratory pressures to Dec stress on anastomotic suture line and Dec risk of anastomotic leak
RF for retinopathy of prematurity -
-age younger than 44 weeks post conception
-excessive FiO2
-multiple blood transfusions
-parenteral nutrition
-hypoxia
-hypercapnia/hypo
Neonate postop Hct 30%, transfuse?
Yes, I would want to avoid potential consequences of tissue hypoxia -> metabolic acidosis, necrotizing enterocolitis, impaired wound healing, MI, cerebral ischemia
-risks assoc w/ transfusions: TRALI, TACO, hemolytic transfusion reactions,
-transfuse only pRBCs O neg, irradiated (minimize transfusion gvh), leukokreduced, sickle cell negative
-goal Hct 35%
TEF 2 hours post extubation, barking cough w/ inspiratory stridor
Post-intubation croup (highest on my differential)
-also consider: epiglottis, laryngotracheobronchitis, or laryngeal foreign body
RF for post-intubation croup
Traumatic intubation
Excessively tight ETT
Prolonged intubation
Surgery yof head and neck
Intra-op changes in kid’s position
Hx of croup
Coughing w/ ETT in place
Treatment for post intubation croup
Racemic epi and IV dexamethasone
Tracheomalacia
Cartilage in the trachea has not developed properly or was damaged and collapses w/ exhalation
-expiratory stridor (intrathoracic obstruction)
TEF postop pain management
-lumbar or caudal epidural catheter w/ bulk 0.1% and feet 0.5 mcg/cc at 0.1 to 0.1 cc/kg per hour
-if neuraxial CI or technically difficult, tylenol, IV fentanyl
Postop and long term complications of TEF repair
-anastomatic leak
-recurrent laryngeal or vagal n injury
-tracheal or esophageal stricture
-GERD
-dysphagia
-tracheomalacia
-esophageal dysmotility
-recurrent or missed fistula
-recurrent aspiration pneumonitis
-Barrett’s esophagus
-freq bronchitis
-PNA
-sepsis
-mortality
What is TRALI short for
Transfusion Related Acute Lung Injury
What is TACO short for
Transfusion Associated Circulatory Overload
64 YOM 118 kg, ex lap, rupture diverticulum. HTN-induced chronic renal failure on HD. K 5.6. Temp 38.1. Concerns?
-urgency of the case -> limit the time I have to eval and optimize the pt
-chronic renal failure: inc risk for metabolic abnormalities, metabolic acidosis, cardiac conduction issues, LVH/CHF, hyperglycemia, bleeding (uremia, impaired vWF, impaired plt fxn)
-chronic HTN, anemia, Hypovolemia,
-inc risk for aspiration
-obesity: complicate airway management, surgical duration, postop pain control
-risks w/ laparoscopic surgery: capnothorax, grocer-induced trauma, hypoTN, CO2 emphysema
64 YOM 118 kg, ex lap, rupture diverticulum. HTN-induced chronic renal failure on HD. K 5.6. Temp 38.1. How to assess volume status?
Pts on HD are hypovolemic following HD, and hypervolemic prior to next session
-ask how often he was dialysed, when last HD session was, and how much fluid taken off at that time
-signs/symp of fluid overload or hypovolemia: pulm edema, HTN, peripheral edema, JVD
-versus dry mucous membranes, hhypoTN, and orthostasis
64 YOM 118 kg, ex lap, rupture diverticulum. HTN-induced chronic renal failure on HD. K 5.6. Temp 38.1. Cancel the case if K was 5.6
Assuming he’s not symptomatic or showings signs of hyperK on EKG (peaked T waves, wide QRS, prolonged PR interval), would not cancel due to urgency of procedure
-I understand hyperK inc risk for cardiac irritability and arrhythmias -> often delay elective when K > 5.5
-plan to correct any metabolic acidosis or hypoCa, avoid succ and Kk containing solutions (LR), prepare to treat hyperK w/ Calcium, glucose/insulin, albuterol, hypervent
-defibrillator in room
-proceed w/ case carefully while monitoring EKG and K
