UBP book 2 Flashcards
Anesthetic concerns with autonomic neuropathy
-inc risk for aspiration (gastroparesis)
-inc risk for significant hypotension (impaired peripheral vasoconstriction and baroreceptor fxn)
-silent ischemia
-intraop hypothermia (impaired peripheral vasoconstriction)
-impaired ventilatory response to hypoxia and hypercapnia (inc risk of drug induced resp depression)
Start a beta blocker on day of surgery?
No -> inc risk of bradycardia, hypoTN, stroke, total mortality
When to start a beta blocker preop?
2-7 days
-if have more than 3 RF: CAD, stroke, CHF, renal insuff, DM
Effects of beach chair position on anesthetized patient
-decreased CPP, dec SV, dec cardiac output
no compensatory inc in SVR if under GA -> inc risk of cerebral ischemia
chest tube placement location
-4th or 5th intercostal space, just anterior to midaxillary line
how to do a needle decompression for tension PTX
14 gauge needle, second intercostal space, midclavicular line
**will still need a chest tube
beach chair, shoulder surgery, interscalene block w/ GA ETT, OSA, GERD, difficult airway, O2 sat falls, diminished breath sounds on L
-100% FiO2, hand ventilate
-using a fiberoptic to confirm tube placement is accurate
-if placement adequate -> consider PTX, L phrenic n paralysis)
-consequences of PTX -> do a bedside POCUS looking for lung sliding
-look for tracheal devision, goal w/ spontaneous ventilation (minimize PPV in PTX)
Risks for cerebral ischemia in beach chair
-if under GA, cannot compensate w/ inc in SVR
-beach chair position dec SV, cardiac output, and CPP
-if pt has autonomic neuropathy -> further risk of cerebral ischemia
If arterial line at circle of Willis -> what is the goal MAP?
80.
cerebral autoregulation maintains BF w/ what pressure?
MAP 60-150
Normal CPP
70-80
**if chronic HTN -> goals towards 80 due to possible R shift of curve
with aspiration event, how long to monitor?
24-48 hours for concern of aspiration pneumonitis
cricoid pressure if actively vomiting?
NO -> risk of esophageal ruputure
Pathophysiology of aspiration pneumonitis
aspiration of gastric contents w/ low pH => damage to surfactant producing cells and the pulmonary capillary endotheliulm -> atelectasis, pulm edema, bronchospasm, larygospasm
-intense inflammatory response -> ARDS
-if particulate stuck/caught in airways -> abscess formation
symptoms of corneal abrasion
-red eye, watery
-foreign body sensation
-photophobia
-exacerbated w/ blinking
steps if concerned for corneal abrasion
-evaluate pt -> H&P
-c/s optho
-consider abc ointment
prevent corneal abrasion
-taping eyes after induciton, prior to intubation
-avoid direct contact w/ eyes
-apply appropriate eye lubricant
How is pheochromocytoma diagnosed?
-history and physical -> symptoms of uncontrolled HTN, dizziness, HA, N/V, orthostasic hypoTN
-free metanephrines in plasma
-urinary catecholamines
-urinary metanephrines
-urinary vanillylmandelic acid (catecholamine metabolite)
confirmatory:
=plasma conc of chromogranin-A
-clonidine suppression test (catecholamines dec if essential HTN, don’t if pheo)
symptoms of pheochromocytoma
HTN
diaphoresis
HA
tachycardia
orthostatic hypoTN (chronic vasoconstriction, volume depletion, impaired reflex responses)
flushing
tremors
N/V
weight loss
hyperglycemia
encephalopathy
anxiety
dilated cardiomyopathy -> MI
pre-pheochromocytoma optimization
-alpha blockade 7-10 days
-BP < 165/90 for AT LEAAST 48 hours
-no significant orthostatic hypoTN
-HR 60-80: can beta blockade after adequate alpha if needed
-give fluids (likely depleted)
-eval cardiac fxn: EKG, CXR, TTE
Why alpha blockade before beta?
want to avoid blocking beta vasodilation if no alpha -> can lead to unopposed vasoconstriction at alpha
why put a foley in
-allow for bladder emptying (esp in laproscopy)
-monitor UOP in setting of potential hemodynamic instability
monitors for pheo surgery
standard ASA (5 lead EKG)
foley (UOP, bladder decomp)
a line
central line
TEE
fluids pre pheo surgery?
-yes if volume depleted to avoid hypoTN w/ induction or pneumoperitoneum
-no if not volume depleted _< avoid CHF exacerbation, and avoid edema w/ steep trendelenberg position
-can use CVP/TEE to guide fluid replacement
can you do a spinal for laparoscopic surgery
-avoid -> could not toelrate inc abd pressures from pneumoperitoneum, lead to respiratory compromise
-req NG/OGT placement for stomach decompression -> not tolerlate
-muscle relaxation red risk of serious injury, and prevents coughing/bucking
position for pheo
-lateral 60 deg flank position
metochlopramide in pheo?
can stimulate secretions of cetecholamine from pheo
-avoid if needing to give aspiration ppx
when not to give metochlopramide for asp ppx
-SBO
-pheo (inc catecholamine secretion)
RSI in pregnant smoker, pheo surgery?
Yes -> high risk of aspiration
-acknowledge: goal to minimize catecholamine surge (despite inc in catecholamines w/ fasciulations w/ succ and intubating in not deep enough)
-acknolwedge inc risk of bronchospasm if not deep enough
-GOAL: ensure adequate alpha blockade and intravascular voleume replacement, difficult airway equipment available, RT, topical lidocaine and fent (dec symp resp), RSI prop and ROC
Meds to avoid in pheo
-ephedrine: inc release of catehcolamines
-ketamine
-succ (stimulate tumor cells to release)
-morphine, atracurium: histamine releasing drugs
-meotchlopramide
-droperidol
laparoscopic case, ABG PaCO2 54, ddx?
-normal inc in CO2 w/ pneumoperitoneum (first 15-30 minutes) -> V/Q mismatch from pt position,
-inadequate ventilation
-CO2 emphysema
-capnothorax
-CO2 embolism
-PTX (alveolar rupture)
-aspiration
-MH
inc EtCO2, PaCO2, subq crepitating of head, neck, face
subcutaneous emphysema
Capnothorax presentation
Inc EtCO2
Dec O2 sat
Inc airway pressure
Dec breath sounds
hyperresonance
CO2 embolism presentation
Dec EtCO2
Dec O2 sat
no change in airway pressures
R heart strain EKG
hypoTN
aspiratiory of foamy blood from CVC
inc pulm artery pressure
PTX presentation
EtCO2 dec
O2 sat dec
airway pressures inc
hyperresonance
dec breath sounds
laproscopic surgery UOP low, what to do
Transient oliguria common w/ laparoscopic surgery: hypercarbia, inc intra-abd pressures (dec CO, catecholamines, ADH)
-give volume cautiously: consider fluid losses and invasive monitoring data (pulse pressure variation, CVP)
what to do if subq emphysema?
-consider possibility of PTX or capnothorax: look at EtCO2, PaCO2, auscultate b/l
-if 2/2 insufflation: d/c insufflation, hyperventilate, and w/ improvement of hypercapnia, reinflate w/ lower insufflation pressure
-consider prolonged intubation dept on comorbidities (COPD w/ inc CO2 -> inc postop work of breathing)
pheo surgery, massive inc to 200/100, what to do?
-verify BP
-ask surgeon to stop manipulation
-check vitals, look at oxygenation, ventilation, EKG
-Check TEE and CVP
-ensure adequate depth of anesthesia: inc volatiles, consider pain meds
-if no improvement give short acting anti-HTN: nicardipine, clevidipine, nitroglycerin, nitroprusside, phenotalmine
signs/symp of cyanide toxicity 2/2 nitroprusside
metabolic acidosis
hypoxemia
confusion
palpitations
Mg sulfate in pheo
inhibits catecholamine release from adrenal medulla and peripheral n terminals
direct vasodilator
reduces the sensitivity of the alpha receptors to catecholamines
pheo surgery BP dec to 74/46 after vein ligation to tumor, ddx?
-tumor has been adequately isolated, so dec in plasma catecholamines
OTHER
-residual alpha blockade
-hypovolemia
-cardiomyopathy (catecholamine induced)
-CO2 embolism
-PTX
-CHF
-MI
-massive blood loss
-vagal activation
post pheo surgery -> pt has conjunctival edema and subq emphysema, extubate?
No -> could be a sign of laryngeal edema possibly 2/2 position or fluid overload
-subq emphysema = hypercapnia = inc WOB after extubation
-goals: optimize fluid status, and ventilation with easly extubation
glucose control post pheo removal
common for hypoglycemia
-w/ inc catecholamines: dec insulin,
inc glycogenolysis, and gluconeogenesis
-now dec catecholamines: inc insulin, red gluconeogenesis and glycogenolysis
-after tumor removal, should use dextrose containing solution
-monitor for 24 hours postop
how to minimize PONV in pregnant laproscopic surgery
-TIVA prop
-no volatiles or nitrous oxide
-adequate hydration
-scopolamine
-zofran (serotonin antagonist)
-aprepitant (neurokinin-1 receptor antagonist)
-acupressure
-local at port sites to minimize postop opioid needs
**NO NSAIDS IN PREGNANCY -> closure of ductus arteriosus
pheo removal POD, HTN w/ elevate catecholamines, concerned?
yes, possible residual pheo
-acknowledge that can have HTN and elevated catecholamines a few days postop due to inc stored catecholamines in peripheral nerves
-less concerned if HTN is sustained (NOT paroxysmal), and if it was lower than pre tumor removal
**HTN could be essential HTN or renal ischemia
signficant bleeding after delivy w/ echongenic mass in uterine cavity dx?
uterine inversion
Treatment of uterine inversion
-d/c all uterotonics (oxytocin)
-NG to relax uterus (can also use volatiles)
-give fluids and vasopressors tu support
POST reduction: u/s to confirm, idetnify and perofrations, lacerations or retained placenta
-now give uterotonics to minimize additional blood loss
ACA aneurysm, severe headaches, HR 92, BP 140/90, RR 16, temp 36C, inc ICP?
Possibility w/ known aneurysm and severe headache
-H&P: HA, papilledema, N/V, AMS
-Cushings triad: HTN, bradycardia, change in resp pattern (or widened pulse pressure)
-unsure: order CT: looking for bleeding, small ventricoles, or midline shift
Airway evaluation
-ability to open mouth
-cervical spine mobiltiy
-receding chin
-large tongue
-prominant incisors
-short neck
-thyromental distance (good > 6.5 cm), sternomental (good >12.5)
-mallampati
**obtain prev anesthesia records if available
difficult airway thyromental distance
<6.5 cm
monitors for ACA aneurysm clipping open
5 lead EKG
foley
a line (preinduction)
central line (vasopressors, fluid status, facilitate rescuctiation, air embolism)
SSEPs or EEG (identify cerebral ischemia)
Periods of significant stimulation in ACA clipping
laryngoscopy
endotracheal intubation
head pinning
bone flap creation
Scalp block nerves
Supraorbital
Supratrochlear
zygomaticotemporal
auriculotemporal
greater/lesser occipital
what to do if accidentally cannulate carotid artery
-cancel the case and c/s vascular surgeon
-keep in place -> concern for bleeding and hematoma formation in neck -> decrease cerebral venous return -> decrease in cerebral perfusion
-possibly compromise airway
complications w/ inadvertent cannulation of the carotid artery
-hematoma formation
-airway obstruction
-stroke
-hemothorax
-pseudoaneurysm
-AV fistula
-death
why use a lumbar drain
maintain spinal perfusion pressure to avoid SCI in thoracic aortic aneurysm repair
risks assoc w/ accidental carotid cannulation prior to ACA aneurysm repair
hematoma formation
airway obstruction
dec cerebral venous return
inc ICP
dec cerebral perfusion
Hunt and Hess classification neuro grade
non-traumatic SAH
0: no repture
I: asymptomatic w/ ruptured aneurysm: mild HA, slight nuchal ridigity
II: mod to severe HA, nuchal rigitidy, neuro deficit limited to CN
III; drowsy, confused, mild focal deficit
IV: exhibiting stupor, hemiparesis
V: deep coma, cerebrate
ACA aneurysm repair, would you lower BP prior to clipping?
-assuming deliberate hypoTN not absolutely necessary, no -> global dec in cerebral perfusion pressure -> inc ischemia -> vasospasm
-controlled hypoTN showed worsened outcomes and inc incidence of vasospasm
-cardiac concerns for hypoTN
Conditions that worsen cerebral ischemia
hyperthermia
hypoxia
hyperglycemia
anemia
hyperventilation (SAH or TBI)
what to do after a temprary clip placed on ACA for aneurysm reapir?
increase MAP -> support collateral circulation
cerebral protection while temporary ACA clip in place
-give prop/etomidate: goal to dec CRMO2
-maintain higher than normal MAPs
-minimize occlusion time
-brain relaxation: mannitol, furosemide, hypocapnia
-mild hypothermia acceptable
hypothermia with ACA aneurysm clipping
-no b/c has not proven to be of benefit, can cause delayed emergence, slow metabolism of anesthestics and muscle relaxants, inc rate of infxn, inc O2 consumption w/ shiviering, MI, coag defects
ACA aneurysm clipping, ST changes, what to do?
Look at surgical field about potential rupture (ST depression occurs in presence of SAH)
-ensure adequate ventilation w/ 100% O2
-monitor EKG, a line, pulse ox CVP
-order trops, assess hemodyanmic status
***ST depression often occur in presence of SAH and have not inc morbidity or mortality
ACA aneurysm repair, aneurysm rputured, what to do?
-not excessive: correct any conditions that inc ischemia: hypoxia, hypercarbia, hyperthermia, hyperglycemia, mild hypoTN to allow for repair
-excessive: compress carotid arteries, suggest temporary clipping, prepare for aggressive resucitation w/ fluids and blood products -> avoid hypoTN and cerebroprotective agents
-consider CPB
surgen put on a clip on the ACA to control bleeding -> SSEP changes
-correct any hypoxia, hyper/hypocarbia, anemia, hypotension, hypovolemia to optimize O2 delivery
-make sure depth of anesthesia has been stable
-consider inc MAP to improve collateral circulation
-consider prop/barbs to provide some ischemic protection
SIMV stands for
synchronized intermittent mandatory ventilation
POD #2 post ACA aneurysm repair, AMS, ddx?
-vasospasm (#1 M&M)
-delayed cerebral ischemia
-cerebral edema
-hematoma formation (highest 1st 12 hours)
-sz
-electrolyte abnormality
POD #2 post ACA aneurysm repair, AMS, what do you do?
evaluate patient, secure airway, ensure adequate ventilation and oxygenation
-check lytes
-EKG, trops, CK
-pain control
-BP
-urgent neuro c/s
-nimodipine for cerebral vasospasm
-transcranial doppler or angiography
Post ACA aneurysm clipping => vasopasm -> tx?
secure airway
normovolemia
inc MAP 20-30 above baseline using phenyleprhine, NE
-surgeon: transluminal angioplasty, or intra-arterial CCB
What is Triple H therapy post aneurysm repair?
Hypertension
hemodilution
hypervolemia
Neurogenic pulmonary edema
can occur after any injury to CNS -> minutes to hours
-massive sympathetic surge by injury CNS -> generalized vasoconstriction -> redistribution of blood volume to pulmonary circulation
tx of neurogenic pulm edema
treat CNS injury
reduce ICP
mechanically ventilate w/ TV 5-6 cc/kg
PEEP -> not too high, don’t want to impede cranial venous drainage
-diuretics
-optimal O2 delivery: Hg > 10. adequate cardiac ouput
ACA aneurysm repair, POD3 Na 125, differential?
-Cerebral Salt Wasting (UNa > 100, hypovolemia)
-SIADH (UNa < 100, normovolemia, elevated ADH levels)
tx for cerebral salt wasting syndrome
fluid and sodium replacement
tx for SIADH
water restriction and diuresis
Cystic fibrosis and pneumothorax
bullae formation w/ CF -> inc risk of PTX
Other system impact of cystic fibrosis
-coagulopathy (hepatic involvement and malabsorption of Vit K)
-diabetes (pancreatic involvement)
-electrolyte abnormalities (malabsorption)
PFTs for cystic fibrosis
dec max mid-exp flow rate
-inc RV to TLC’dec FEV1/FVC
Cystic Fibrosis pathophysiology
Mutation on a protein that transports chloride and bicarbonate -> impacts sodium transport across plasma membranes -> affects airways, intestines, liver, reproductive organs, sweat glands
-causes thick secretions -> Dec mucociliary cleareance, airway obstruction, bronchiectasis
Treatment for CF
-breathing/coughing maneuvers -> chest PT
-percussive vests
-inhaled airway clearance agents: Doran’s Alfa, hypertonic saline
-oral azithromycin, inh tobramycin, and inh aztreonam w/ P. Aeration’s a in fxn
-pancreatic enzyme replacement therapy, fat-soluble vitamin supplementation, insulin
-if biliary obstruction: ursodeoxycholic acid
Optimize cystic fibrosis patient for emergent surgery
-pulm: chest PT, bronchodilators, humidified nebulizers, perioop box
-GI: asp ppx
-adequate fluid resuscitation
-correct any coagulopathy or electrolyte abnormality as time allowed
Asthma and nasal polyps with NSAIDs
NSAIDs or aspiration can induce bronchospasm
Why R mainstem intubation w/ insufflation
Cephalad displacement of the diaphragm and carina with inflation of the pneumoperitoneum
EtCO2 changes w/ capnothorax, PTX, and CO2 embolism
Capnothorax: increase
TPTX: decrease
CO2 embolism: decrease
Laproscopic appendectomy, O2 sat Dec to 82%, diminished breath sounds over L lung field, what do you do?
-100% FiO2, look at peak pressures
-Look at EtCO2: if unchanged, likely too deep, w/d until b/l breadth sounds, if high possible capnothorax (ask surgeon to deflate, hyperventilate and try again)
-if low concerned for PTX -> ultrasound POCUS look for lung point, or lung pulse
-exhibit TPTX w/ hypoTN: needle thoracostomy or ask surgeon to place chest tube
Benefit of thoracic epidural for open procedure
-improved pain scores
-greater mobility
-Dec postop pulm complications: Dec pulm splinting -> Dec atelectasis, shunting, improved clearance of pulm secretions
-reduce opioid requirements
Coagulopathy and cystic fibrosis
Hepatic dysfunction and malabsorption of Vit K: reduced clotting factors II, VII, IX, and X: inc risk of epidural hematoma
Emergence ship becomes delirious, thrashing around, pulling at ETT and IV
-call for help, secure girl’s arms to prevent from pulling, consider giving a sedating dose of fentanyl, ketamine, propofol, or dexmedetomidine
-acknowledge other causes: pain, hypoxia, hypercarbia, hypotension, hypoglycemia, bladder distention
-ensure adequate oxygenation and ventilation, adequate pain control, correct hypoTN or hypoglycemia, r/o bladder distention w/ bladder scan
Limit emergence delirium how?
-reduce preop anxiety
-adequate postop pain control
-stress-free environment recovery
-preop midazolam
RF for emergence delirium
-poorly controlled pain
-preop anxiety
-young age (1-5 highest)
-sevo and does
-pt underlying temperament
-type of surgery: abd and breast
-prolonged surgery time
Extra pyramidal symptoms
Dyskinesias: repetitive, involuntary, purposeless body or facial movements
Akathisia: extreme restlessness, inability to sit still, jitteriness or shakiness
Dystopia: muscle tension strong muscle contraction
Postop shaking ddx
-extrapyramidal symptoms (if metochlopramide given/anti-DA)
-shivering
-NMS
-seizure
What causes extrapyramidal symptoms?
Treat extrapyramidal symptoms
-diphenhydramine or benztropine
-d/c offending agent (antiemetic, anti-DA)
-give supplemental O2, assess respiration and oxygenation
-explain what occurred
Diabetic undergoing outpt surgery
-reduce nighttime dose of subs insulin to 2/3 normal dose before bedtime
-hold rapid-acting or short-acting agents the morning of surgery
-check blood glucose level on arrival for surgery
-check glucose hourly during perioperative period
-goal: 120-180
Importance of good glucose control
-increased wound healing
-decreased rate of infection
-decreased dehydration 2/2 osmotic diuresis
-reduce length of stay
-reduce mortality
GOAL: 120-180
What is HgA1c?
Hg exposed to glucose -> glycosylated
-% of glycosylated Hg -> tells us glucose control over last 30-90 days
Uncontrolled DM can cause
-CAD
-autonomic neuropathy
-peripheral neuropathy
-gastroparesis
-retinopathy
-renal insufficiency
-HTN
-PVD
Revised Cardiac Risk Index
-ischemic heart disease
-heart failure
-cerebral vascular disease
-DM
-Cr of 2 or higher
-intra-thoracic, intra-abd, or supra-inguinal vascular surgery
**assess risk of major cardiac events
“In a Stroke (CVA) of genius, Debbie (diabetes) Created 2 (creatinine of 2, also 2 criteria is increased risk) HeartFelt (heart failure) Schemes (ischemic heart) to find a buff man with abs (chest, abdomen).”
1: 6%, 2: 10%, 3:15%
DEX Dual antiplt therapy?
6 months! to avoid stent thrombosis
-consider at 3 months if benefit of surgery outweighs risk of stent thrombosis
TURP complications w/ glycine solution
hyperammonemia -> encephalopathy, sz
visual disturbances
circulatory depression
TURP complications w/ sorbitol solution
hyperglycemia
Concerns with autonomic neuropathy
hemodynamic instability, silent MI, hypothermia
Benefits of neuraxial for TURP
awake patient to communicate CP/SOB, AMS assoc w/ TURP syndrome, pain assoc w/ bladder or prostate perforation
Sensory level goal for TURP
T10! need hyperbaric bupi for spinal
-above T9 sym/pain assoc w/ bladder perforation will not be felt
TURP mannitol solution
intravascular volume expansion
Distilled water for irrigation in TURP?-
Absolutely not -> hypervolemia, hyponatremia, intravascular hemolysis (hypotonic), shock, renal failure
20 minutes into TURP pt agitated, HTN, ddx?
-inadequate spinal anesthesia
-TURP syndrome (fluid overload, toxicity from solute)-> hyponatremia
-perforated bladder
-perforated prostatic capsule
-MI
-sympathetic response to hypoxia, hypercarbia
How does TURP syndrome occur?
hypotonic solution absorbed by venous sinuses in prostate -> circulatory overload, hypoNa, and solute toxicity
**inc risk w/ >1 hour surgical resection, bag suspended > 40cm above table (inc fluid hydrostatic pressure), disruption of prostatic capsule
TURP syndrome symptoms
cardiovascular: HTN, reflex bradycardia, pulm edema
neuro: confusion, restlessness, sz, visual changes (cerebral edema and inc ICP)
resp: pulm edema, hypoxia,
hematology: hemolysis, DIC
renal: metabolites of glycine can lead to renal failure
metabolic: acidosis -> breakdown of glycine
Treatment of TURP syndrome
-ensure adequate O2
-hemodynamic support
-invasive monitoring if unstsable
-eval blood gasses, lytes, osmolality, glucose
-12 lead EKG
-tx hypoNa: fluid restriction, diuretics, hypertonic saline, anticonvulsants as needed
TURP: pt agitated, hypertensive, bradycardic, c/o pain to abd and L shoulder, what to do?
-Communicate w/ surgeon possible bladder perforation
-also concerned for MI: 12 lead EKG
-optimize O2 and ventilation, support hemodynamically, ensure adequate analgesia, treat any hemodynamic instability
Succ given at beginning of TURP, 40 minutes later pt not breathing spontaneously, ddx?
-pseudocholinesterase def
-TURP syndrome
-toxicity from irrigation solution (glycine -> inc ammonia -> encephalopathy)
-hyperglycemia (sorbitol)
-too much narcotics
-stoke (cerebral ischemia, cerebral edema)
-hypothermia
-hypoxia/hypercarbia
Post TURP, not initiating respirations, what to do?
-ensure adequate oxygenation and ventilation
-assess residual NMB (TOF)
-auscultate the chest (asp, pulm edema, PTX)
-check EKG for signs of ischemia or arryhtmia
-ensure normothermia
-signs of narcosis (miosis)
-check lytes and ABG
Fade with TOF means?
residual nondep NMB
phase II blockade from depolarizing muscle relaxant (multiple doses, prolonged infusions, or atypical pseudocholinesterase activity)
Dibucaine number
indirect measure of pseucholinesterase activity
normal: 70s-80s
homozygous: 20s-30s
heterozygous: 50s-60s
If given succ and pt has pseudocholinesterase activity, what do you do?
continue to sedate and support mechanically ventilate
-consider extubation w/ full return of TOF and once other extubation criteria have been met
Difficulty seeing post TURP, ddx?
-2/2 glycine toxicity (transient blindness)
-anterior or posterior ischemic optic neuropathy
-acute glaucoma
-retina ischemia
-corneal abrasion
severe, diffuse periorbital pain, dry and pale eye, dilated pupil
acute glaucoma
dilated/nonreactive pupil, normal intraocular pressure, fundus exam, extra-ocular muscle movement after TURP
glycine toxicity
Anterior ischemic optic neuropathy
acute ischemic disorder of the optic nerve head supplied by the posterior ciliary artery
*assoc w/ cardiac surgery
-optic disc edema
Posterior ischemic optic neuropathy
acute optic neuropathy due to ischemia in the retrobulbar portion of the optic nerve.
*assoc w/ spine surgery
-no optic disc edema
Why is postop sepsis assoc w TURP
G postive and G neg bacteria into systemic circulation through disrupted prostatic enous sinuses -> bacteremia
-entry of prostatic bacteria into systemic circulation
can post TURP septicemia be prevented w/ preop abx?
No, abx do not easily penetrate prostate gland => however helpful for reducing incidence of UTI w/ pstop foley
Treatment of septic shock
-BClx to identify organisms 1st
-broad spectrum antibiotics
-identify source: imaging
-fluid boluses
-vasopressor support as needed (NE 1st line)
Risks of starting beta blocker same day as surgery
inc risk of morbidity and mortality
-risk of bradycardia, hypoTN, stroke
CK v troponin
CK: less specific for mycoardial damage, inc 4-6 hrs, max 12-24, baseline 2-3 days
troponin: more specific for myocardial damage
-inc 2-6 hours, max 12-24, baseline 7-10 days
Diagnosis of NSTEMI
elevated cardiac biomarkers
ST seg depression 2 or more contiguous leads
ST depressions on EKG can indicate
-non-ST elevation MI
-non-infarction subendocardial ischemia
-hypokalemia
contributing factors to MI
-supply cannot meet the myocardial demand
-dec supply: hypoTN, tachycardia, anemia, coronary atherosclerosis, hypoxia
-inc demand: tachycardia, LVH, inc afterload
pre-CABG wheezing, dec breath sounds LLL, further eval/tests?
Yes, could be 2/2 bronchospasm, post MI pleural edema, COPD-PNA
-eval: CXR, PFTs, echo, ABG
-dpt on results: bronchodilators, abx, diuretics
CABG, CXR LLL atelectasis, delay case?
likely mucous plugging due to COPD/smoking -> mild/mod not interefering w/ O2 or ventilation would proceed with case
-if severe, benefit from short delay to allow for further treatment
Atelectasis on CXR, how to optimize preop?
bronchodilators
chest PT
incentive spiromety
-post-intubation recreuitment maneuvers
Therapeutic level of digoxin
0.5-2!!
Digoxin toxicity symptosm
EKG changes
arrhythmias (heart block, scooped ST segments)
fatigue
hypersalivation
confusion
N/V
visual disturbances
What potentiates digoxin toxicity?
hypoK
hypoMg
HyperCa
R carotid bruit, where to put your central line?
-not RIJ -> risk of dislodging clot and causing stroke in artery if accidental carotid puncture
-subclavian approach if actively on heparin cannot be used due to lack of ability to compress
-LIJ ideal -> likely has collateral flow for cerebral perfusion pressure -> minimal in asymptomatic carotid artery dsease
pre-CABG on heparin infusion, d/c prior to central line placement?
No -> not want to risk further comproising coronary perfusion
-acknoweldge risk of hematoma formation
post induction, pre-chest incision, BP drops 80/50 HR 50, ddx?
-cardiovascular depression following induction drugs and volatile agents
-autonomic neuropathy 2/2 diabetes
-arrhythmia, cardiac ischemia
-TPTX (recent central line)
post induction, pre-chest incision, BP drops 80/50 HR 50, what to do?
ensure adequate O2 and ventilation -> 100% FiO2, auscultate chest, verify BP
-TEE
-look at EKG for arrhythmias
-consider small fluid bolus and direct acting vasopressor
Decrease in BP w/ initiation of CPB why?
-hemodilution 2/2 priming solution
-dec in SVR 2/2 priming solution
-anesthesia induced vasodilation
-inadequate venous return to pump
-kinking, clamping, malpositioning of arterial cannula
post CABG cannulation -> unilateral face blanching, R sided mydriasis, chemosis
-malpositioning of arterial cannula w/ flows of priming directed to brachiocephalic artery
-can also have increased R rad art line pressures
Malposition of arterial cannulation -> proceed?
Possibility for cerebral injury -> prefer to delay to allow for resoltuion for cerebral edema or inc ICP
-if surgeon said delay not possible -> take steps to reduce cerebral edema: mannitol, head up positioning -> maintain cerebral perfusion
Why glucose control important in CABG
-hyperglycemia can exacerbate neuronal injury w/ hypothermia
-infection
-impaired wound healing
-oncotic diuresis
Prepare to wean off CPB
-normothermia
-check ABG, Hg, lytes -> no anemia or electrolyte derrangements
-check lung compliance and initiate ventilation
-heart de-aired
-ensure adequate cardiac function w/ TEE
-hemodynamically stable
-ensure presence of pacing capabilities and rescucitation drugs
Post CABG hypoTN in ICU, bradycardia, PVCs, what do you do?
-confirm adequate oxygenation and ventilation
-look at EKG
-ensure proper pacemaker function
-ensure correct infusion concentrations
-look at chest tube drainiage
-check pts volume status, and lytes -> tx accordingly
Why might PM fail to capture?
MI
lead dislodgement
insufficient energy
PM malfunction
acid-base distrurbances
lyte abnormalities
Post CABG BP dropping 70/52 HR in 40s, what to do?
Ensure adequate oxygenation and ventilation
attempt transcutaneous or transvenous pacing
-correct any electrolyte or metabolic abnormalities
-if needed give atropine or epi
-check pulse -> might need to start compressions
Post CABG first 2 hours, 250 cc out of chest tube, give more protamine?
Acknolwedge that inadequate reversal could cause it, however multiple other causes should be evaluated/considered as well
-send ACT
-inadequate surgical hemostasis
-thrombocytopenia
-malfunctioning plts
-hypothermia
-dilution of coagulation factors
most likely cause of coagulopathy after CPB?
plt dysfunction
(thromboctyopenia, hemodilution of clotting factors, hypothermia, DIC)
Post CBG bleeding, how to determine cause?
-ACT
-CBC, fibrinogen, PT/PTT
-TEG
**if fails to determine cause -> back to OR
Normal SvO2
60-80%
Extubate if SvO2 is 50s?
No -> sign of inadequate tissue perfusion or low cardiac output -> needs to be investigated
Postop pt says he was awake during CABG, thoughts?
-intraop recall poorly understood
-CBG, trauma, and OB have highest risks
-likely to occur during rewarming (hypothermic potentiation of anesthesia is lost)
-minimize: benzos w/ rewarming or anesthetic dosing of iso
What to tell pt and his family if intraop recell?
-rare and poorly understood complication
-empathize w/ his experience, pracuations were taken to minimize, goal is to keep him safe and alive, offer counseling/psych eval
BMI definition
weight in kg/ heigh in meters squared -> identify and classify overweight/obese individuals and theoretically risk of developing associated problems
Does liposuction technique matter?
YES
-tumescent technique: large volumes diluate anesthetic w/ epi injected into subq tissues -> < 3000 cc
-semitumescent: larger volume of fat removal -> higher risk of fluid overload, pulm edema, LAST, fat emboli
-newer techniques: laser and ultrasonic energy: low complciations
Morbid obesity risks w/ anesthesia
-difficult airway
-pt position
-pulm abnormalities: OSA, atelectasis, hypoxia, dec FRB, rapid desaturation)
-obesity hypoventilation
-OSA
-DM
-HTN
-CAD
-stroke
-DVT/PE
-fatty liver
Possible complications w/ tumescent liposuction
periop fluid overload
pulm edema
LAST
systemic epi uptake
cardiac arrhythmias
PE
Lidocaine dosing w/ tumescent liposuction
35-80 mg/kg -> max 55 mg/kg
risk factors that inc risk of LAST
extremes of age
cardiac dx
renal or hepatic dysfxn (dec metab)
hypoproteinemia (inc level of free drug)
metabolic/resp acidosis
pregnancy
IV fluids w/ tumescent liposuction?
-minimize -> large risk of inc intravascular volume w/ procedure (will continue to absorb fluid up to 48 hours postop)
-consider lasix if positive fluid balance
Post tumescent liposuction pt wheezing and SOB, ddx?
bronchospasm
pulmonary edema
PE
PTX
aspiration pneumonitis
allergic rxn
**suppl O2, auscultate, signs of fluid overload, CXR or POCUS?
Cancer pain, severe doses of morphine, N/V/ pain, constipation, treatment modalities would you recommend?
-adjuvants: antidepressants, anticonvulants for neuropathic pain
-opioid rotation
-celiac plexus block
-spinal cord stimulator
-acpuncture
-TENS
-psychologicla therapy
how to perform a celiac plexus block
prone at level of L1 vertebral body
needle 5-7 cm lateral to midline -> advanced under fluoroscopic guidance to be anterior to vertebral body
-test block w/ local anestheticn-> benefit neurolytic block
complications of celiac plexus block
paralysis (neurolytic agent into spinal or epidural space, artery of adamkiewicz_
postural hypoTN
accidnetal intravascular injxn
treoperitoneal hemorrhage
sexual dysfunction
damage to kidneys or pancreas
CPRS I v II
definitive n injury present in type II
not in type I
-type I can have an injury, but no DEFINITIVE n inury
diffuse burning pain in arm 6 mo after hand injury, fingers cyanotic, ddx?
CRPS-I
soft tissue injury
brachial plexus injury
Raynauds
carpal tunnel
peripheral neuropathy
Diagnostic criteria for CPRS-I
following an incident:
-pain out of proportion to degree and type of injury
-cyanotic changes
-changes in temperature
-stiff and painful joints
-exclusion of other causes for pain/dysfxn
*pain is NEVER limited to a single peripheral nerve
CRPS-I v CRPS 2
CPRS 2: occurs after definitive n injury -> symptoms are not limited to distribution of that nerve
CRPS I: following an injury, but no n injury
Treatment options for CRPS
-PT!
-CBT
-gabapentin/lyrica
-antidepressants (amitryptline)
-sympathetic n block
-ketamine IV
-SC stimulator
2 YOF fever, stridor, substernal retractions, ddx?
epiglottitis
laryngotracheobronchitis
foreign body aspiration
pharyngeal abscess
peritonsillar abscess
pharyngitis
2 YOF fever, stridor, substernal retractions, how to determint etiology?
H&P
-epiglottis sudden, laryngotracheobronchitis slower onset
-assoc w/ eating: foreign body aspration
drooling: epiglottitis
-previous vaccination status: H influenzae type B (epiglottitis)
-if child was stable, radiographic exam can differentiate
how to induce a child w/ MH concerns w/ epiglottitis
-cal lahead -> clean setup: no succ, vaporizers removed, flush machine, charcoal filters, change CO2 absorber
-difficult airway equipment and surgeon available
-have parental presence to calm child -> crying will worsen airway obstruction
-monitors on -> 100% FiO2 preoxygentate
-keep child sitting
-give 2-3 mg/kg IM ketamine providing sedation for IV access and spontaneous ventilation
-CPAP
-fluid bolus -> deepen plane of anesthesia to prevent spasm w/ DL
-give glyco to reduce secretions -> gentle DL -> ETT (smaller than normal)
-confirm air leak at 20-25 cm H2O
-consider exchange for nasal?
-BClx and abx
-maintain sedation for transfer -> go to ICU
When to extubate epiglottits
24-72 hours later when fever, neutrophilia, and epiloglottic swelling have resolved
-swallowing and leak present around ETT
-ensure by flexible fiberoptic that airway edema resolved
effects of GH secreting tumor
-skeletal and soft tissue overgrwoth: enlaged tongue, tonsils, nose, hands, feet
-HTN
-accelerated atherosclerosis
-OA
-skeletal m weakness
-cardiomyopathy
-VC palsy
-OSA
-insulin resistance
-glottic stenosis
When to be concerned about PVCs
more than 3 per minute
polymorphin
runs of 3 or more
R on T phenomenon
**VT or VF
pituitary tumor, w/ infiltrate of local anesthesia, PVCs, what to do?
-ask surgeon to stop injecting
-identify freq of PVCs to see if concerning
-verify oxygenation and ventilation
-other causes: hypoxia, MI, hypoK, sympathetic activation
-ensure presence of defibrilattor
-consider overdrive pacing or amiodarone (antiarrhythmic)
PVCs and morbidity
5-6 PVCs per minute inc periop morbidity
Resp distress after terbutaline for premature labor, crackles b/l, ddx?
terbutaline pulm edema
PEC
PE
cardiac condition
pregnant lady w/ pulm edema, tx? intubate?
tx: identify the cause of the pulm edema H&P -> cardiogenic, PEC -> consider diuretics
-intubate: consider support w/ CPAP 1st, dept on how hemodynamically stable she was and her O2 saturation -> consider intubating
How does PEEP help pulm edema?-
-redistributes fluid to areas less involved in gas exchange
-recruits collapsed alveoli that are contributing to shunting
Post stellate ganglion block -> difficultly speaking, dizziness, difficulty swallowing, SOB, ddx?
-LAST
-recurrent larygeal n injury
-accidental epidural/spinal injection
-PTX
Progression of LAST toxicity
-metallic taste, oral paresthesias, tongue numbness, visual changes, tinnitus, lightheadedness, dizziness
-agitation, shivering, tremors, sz
-resp depression, LOC, coma
-hypoTN, bradycardia, dysrhthmias, asystole
LAST, what to you do?
- call for help, put on monitors
-obtain intralipid
-support oxygenation and ventilation -> intubate if unable to complete
-midazolam for sz
-if progression of neuro or cardiovascular collapse -> give intralipid
-support hemodynamically
Dosing for lipid emulsion therapy
Bolus 1.5 cc/kg of 20% lipid solution over 1 min -> continuous infusion of 0.25 cc/kg/min
LAST asystole, what to do?
-start compressions
-call for help
-intubate -> optimize oxygenation and ventilation
-give intralipid bolus
-attach to monitor -> evaluate rhythm, shock if able
-give epi 1 microg/kg bolus (lower doses in LAST)
What affects systemic absorption of local anesthetic
-amount of blood flow at site of injection
-dose
-properties of local anesthetic (lipid solubility, protein binding)
-addition of vasoconstrictors
Why 2 P waves on EKG post heart transplant
1 P wave: native SA node
-other donor SA node
**native SA node, cannot cross suture line to transplanted heart
Following CSE, tetanic uterine contraction, FHR dec, why?
rapid analgesia -> dec circulating epi w/ uterine hypertonus -> decreased uterine perfusion -> fetal bradycardia
other reasions: maternal hypotension 2/2 sympathetectomy, nuchal cord, aortocavalc compression, possible PEC?
Response to fetal bradycardia
-L uterine displacement
-assess O2 -> give supplemental
-assess BP -> increase BP
-d/c oxytocin
-consider tocolytic
post heart transplant for c/s, preeval?
-talk to transplant team: how shes been doing, immunotherapies, steroids
-look at recent echo, EKG, myocardial biopsies
-any SE from antirejection medication: inc cr?
-EKG: inc HR: pregnancy or silent MI?
-eval pacemaker?
-stress dose steroids
-airway exam
heart transplant pregnant pt, hypoTN after induction, why?
-Dec SVR 2/2 anesthesia induction -> heart cant compensate, preload dpt
-other ddx: allergic rxn, inadequate L uterine displacement, MI, PE, AFE
symptoms of allograft rejection of heart
usually w/i 1st 6 months
fever, malaise, arrhythmias, SOB, accelerated coronary atherosclerosis, mycardial dysfxn
how to reverse NMB in a transplanted heart?
-neostigmine can cause bradycardia in transplanted hearts after 6 months -> yes give glyco
-additionally want to block other peripheral muscarinic effects like bronchospasm and inc salivation
