Test 2 Flashcards
Stats for Geriatric Population in 2003, 2030, and 2050:
-By 2030, 20% of US will be >65 y/o
-By 2050, 2 billion ppl worldwide will be >60 y/o
-Compare to 2003: 12% US was >65 y/o
What % of hospitalizations do old ppl make up?
-1/3 of hospitalizations
-44% of hospital charges
-2-3x more surgeries
-longer hospitalizations
Memory Decline and Aging:
-present in 40% of ppl >60 y/o
-not inevitable, can be slowed by things like working out, reading, family connection, etc.
Brain Structure and Aging:
-cerebral atrophy
-decreased gray matter
-neuronal shrinkage (not much actual loss of neurons)
-decreased white matter
-INCREASE in ventricular size
-progressive loss of memory, imbalance and mobility
True or false: there is a decrease in glutamate.
-False! There is no change in glutamate.
-may be some decrease in NTM like dopamine, Ach, norepi, and serotonin based on animal studies
Why is EEG unchanged in old ppl?
-CRMO2 and CBF decrease in parallel fashion so the EEG remains unchanged
Neuraxial changes with aging:
^^Things that decrease LA dose
-decreased epidural space
-increased permeability of dura
-decreased volume of CSF
-decreased diameter/number of myelinated fibers in dorsal and ventral nerve roots
Peripheral Nervous System changes with aging:
-Inter-Schwann cell distance decreased
-Conduction velocity decreased due to reduction in myelination across the nerve fibers
-so, elderly more susceptible to neuraxial blocks and peripheral nerve blocks
Heart changes with aging:
-decreased number of myocytes
-LV wall thickens
-SA node cells decrease
-conduction velocity decreases
-thickened and calcified aortic valve
-decreased contractility
-increased ventricular stiffness-HIGHER LV filling pressures
What are the implications of their being less beta-adrenergic sensitivity in the elderly?
-decreased maximal heart rate and EF during stress…more prone to decompensation during these periods and with neuraxial anesthesia
-so HR doesn’t spike up as much in times of need to aid in maintaining adequate CO
Cardiac Vessel changes with aging:
-vascular stiffness
-breakdown of collagen and elastin
-less endogenous NO (less vasodilation of coronaries)
-early wave deflection-increased afterload along with diastolic dysfunction
Pulmonary: Structural changes with aging:
-LOSS of ER and Surfactant
-increased lung compliance (think COPD)
-enlarged bronchioles and alveolar ducts
What does the early collapse of small airways during exhalation for elderly cause?
-increased anatomic dead space
-increased closing capacity
-impaired gas exchange
-lower baseline sats, increased arterial CO2
What does the loss of vertebral height and calcification of vertebra and intercostal cartilage in the elderly cause?
-barrel chest
-diaphragmatic flattening
chest wall stiffness…increased work of breathing-contribute to dyspnea on exertion
Pulmonary: functional changes with aging:
-decreased vital capacity
-increased closing capacity
-increased residual volume
-TLC stays the same due to compensation
-decreased muscle mass and increased closing capacity
-weaker pharyngeal muscles
How much does FEV1 decrease per decade?
-decreases by 6-8% per decade
What is closing capacity again?
Combination of closing volume and RV
What are the implications of the elderly having weaker pharyngeal muscles?
-decreased clearance of secretions
-less efficient coughing
-decreased esophageal motility
-less protective upper airway reflexes
ASPIRATION RISK
VQ mismatch with aging:
-gap between FRC and closing capacity WIDENS
-FRC increases slightly, but CC increases much more
-this is the MOST important MOA for alveolar-arterial oxygen gradient mismatch
-shunt increases and arterial oxygenation declines
Renal changes with aging:
-GFR decreases (10 per decade)
-blunted responses to ALDO, vasopressin, and renin
-urinary retention and UTIs become more common
GI and Hepatic changes with aging:
-liver function declines
-drugs cleared via phase 1 are not ok: oxidation, hydrolysis via CYP450, reduction
-drugs cleared via phase 2 are ok: acetylation and conjugation
-LESS PONV!! so, avoid drugs like prochlorperazine, promethazine, and metoclopramide (not needed)
MSK changes with aging:
-muscle mass and strength declines
-subcutaneous fat thins
-impaired wound healing
-osteoarthritis
Thermoregulation changes with aging:
-temp is comparable in infants, children, and adults
-1 degree less for adults 60-80 y/o
Studies on old age and surgery risk:
-Denney/Denson: high mortality rate with pts 90 y/o and up
-Djokovi/Hedley-Whyte: ASA status predicted mortality
-Del Guercio/Cohn: uncorrected comorbidity in SICU: 100% mortality
-Finlayson: high mortality from nursing home residents
Significant Predictors of 6 month-1 year mortality:
-impaired cognition
-recent fall
-hypoalbuminemia
-anemia
-functional dependence
-comorbidities
Vulnerable brain chart:
-vulnerable brain (elderly) have a dysfunctional anti-inflammatory response and can have exaggerated neuro-inflammation and acceleration of AD pathology, leading to Long-term cognitive decline
What does POCD stand for?
-Post-operative Cognitive Dysfunction
-can last months to years after surgery, or be indefinite
What are neurotoxicity factors?
List examples.
-factors that play a role in the pathogenesis of dementia-vulnerable brains
-Amyloid, Tau, Calcium, and Neuroinflammation factors
Tell me about amyloid:
-fragment of synaptic origin-so develop when synapses break down
-unknown function, but accumulates extracellularly to form PLAQUES
-these can aggregate but can also be eliminated
-may disrupt cell membranes over time
How might amyloids affect anesthesia?
-first studied in halothane and mice
-with amyloid plaque build up, the older mice have accelerated onset of alzheimers disease and dementia
Tell me about Tau:
-a protein
-neurofibrillary tangle (NFT)
-Phosphorylated and aggregated Tau protein
-DESTABILIZES microtubules
-decreases in temp of 2-3 degrees C INCREASES amount of Tau (Taupathy)
How do repeated exposures to Halothane, Isoflurane, and Sevoflurane affect Tau levels?
-Increased phosphorylated Tau
-can then aggregate into plaques and destabilize microtubules
-More Tau, more dementia
What’s the idea behind Dantrolene treating neurotoxicity?
-It could decrease calcium release b/c CCB, but doesn’t cross BBB so cant mitigate neurotoxicity
-significant skeletal muscle weakness with this drug
How does neuroinflammation contribute to cognitive decline?
What drugs do we give that could modulate this?
-through release of inflammatory factors like cytokines, IL-6, and TNFa
-Dexamethasone, lidocaine, and Toradol
They gave 3 drugs that can alter CNS and ordered them based on how much they can cause cognitive decline. What were they and what was the order?
-Isoflurane > Desflurane > Propofol
-so propofol is LEAST associated with cognitive decline
-may be reason we TIVA elderly patients
Bedford 1955 Study:
-out of 1193 patients >50 years old receiving GETA, 10% have mental deterioration (long-term or permanent)
International Study of Postoperative Cognitive Dysfunction:
-1998
-non-cardiac patients >59 years old
-POCD in these pts
-22% higher at 1 week
-7% higher at 3 months
-p value 0.04% :)
-risk factors: increasing age, duration of anesthesia, lesser education (lower SEC), second operation, post op infection, respiratory complications
True or false: surgery by itself can cause short term decline
-true!
-anesthesia alone is also causative so surgery is additive to it
-remember that pts have unknown vulnerabilities person to person
What are the issues with studies of anesthesia and surgery?
-underpowered
-poorly designed
-controversial
What would be ideal for studies looking at anesthesia and surgery?
-long, longitudinal surgeries
-biomarkers…CSF
-imaging like PET scans
Anesthesia implicants for cognitive decline and elderly:
-use neuraxial/regional when I can to avoid drugs affecting CNS
-avoid long-acting NMBD and REVERSE completely!! (sugammadex DOC)
-opioid sparing strategies
-neutralize stomach acid with non-particulates
-EEG based titration (BIS)
-avoid hypotension
-pad skin and nerves
Drug challenges in elderly related to the ehart:
-decreased CO and increase in circulatory time-takes longer for things to set in
-slower distribution to initial site of action
-slower redistribution
-slower distribution to metabolic organs: kdineys and liver
Drug challenges to NMJ in elderly:
-increased distance b/w axon and motor end plate
-decreased concentration of ACh receptors, amount of ACh in presynaptic vesicle, and release of ACh upon neuronal impulse
What’s true for elderly patients if drugs are kidney/liver dependent for metabolism?
-prolongation of effect, decreased need for redosing during maintenance phase, delayed recovery phase for non-depolarizers (ROC)
Whats true in ther elderly pop if drugs are NOT kdiney/liver dependent for metabolism?
-no prolonged effect, same requirements during maintenance, no delay in recovery phase (think Nimbex good for elderly)
Pulmonary resection in elderly:
-mortality in 80-92 year olds: 3%
-respiratory complications: 40% (2x younger ppl)
-cardiac complications: 40% (3x younger ppl)
-lobectomy mortality is not as bad, and less invasive techniques
-pneumonectomy mortality is excessive
Algorithm for Preoperative Assessment: Thoracic (non-cardiac) surgery:
exercise tolerance affects decision
-TTE can be done to rule out pulmonary HTN
Predictive Postoperative FEV1:
-predictor of postop outcomes
-there are 42 lung segments total, 20 on left and 22 on right side
-ppoFEV1= PreopFEV1% x (1-%lung tissue removed/100)
-ex: if preopFEV1 was 70% and RLL removed:
-70 x (1-(.29)/100))=50%
Triad of Pre-op Assessment:
-3 legged stool of pre-thoracotomy
-We want VO2 max >15 mL/kg/min
-PaO2 >60
-PaCO2 <45
Post-thoracotomy Anesthesia Management:
-FEV1 values let you know when to extubate
-<30%, don’t extubate yet!
Definition of POCD:
-Postoperative Cognitive Decline
-objectively measured decline in cognitive function that persists beyond the period expected (beyond extubation)
Other name for hospital acquired infections:
Nosocomial infections: not present on or incubating at time of admission
-in 1 in 3 hospitalized patients (CDC)
Sources of HAI:
-central line-associated sepsis
-UTI (12.9%)
-Surgical site infection (21.8%)
-hospital-acquired pneumonia (21.8%)
-ventilator-associated pneumonia
-CDIFF (12.1%)
Risk factors for developing HAI:
-pt’s immune status
-infection control practices
-prevalence of certain pathogens in the community
-older age
-longer hospital stays
-multiple chronic illnesses
-mechanical ventilatory support
-critical care unit stays
Transmission of HAI’s:
-direct contact with healthcare workers (biggest way)
-contaminated environments (inguinal, perineal, axilla)
-extraluminal migration
-coag neg staphylococci (skin flora) migrate from lines into tissue
Symptoms suggestive of pre-existing infection:
-subjective fever
-chills
-night sweats
-altered mental status
-productive cough
-shortness of breath
-rebound tenderness
-suprapubic pain
dysuria
-CVA tenderness (costovertebral tenderness)
Vital Signs:
-hypotension, tachypnea, low saturations, tachycardia
Devices we need to document on if coming into the facility with them, may replace them when they get here:
-Central line
-Foley catheter
-Insulin pump
-Endotracheal tube
-Intravenous liens
Which laboratory values do we look at for evidence of organ dysfunction?
-lactic acid
-prothrombin time
-BUN/Creatinine
-Elevated WBC
-Hypo/hyperglycemia
-Cultures
When do Surgical site infections typically occur?
-within 30 days of surgery
What percentage of nosocomial infections are seen in surgical patients?
38%
How much cash money is spent yearly due to prolonged recovery/hospitalization from these SS infections?
3.5-8 billion!!
-wound infections are COSTLY
Types of surgical site infections:
-Superficial incisional: just in incisional area
-Deep incisional: beneath the incision area in muscles and tissues surrounding the muscle
-organ or space: any area other than skin muscle: includes organs or space b/w organs
Signs of Surgical Site Infections:
-redness
-delayed healing
-fever
-pain
-warmth
-swelling
-drainage of pus (abscess)
Most common types of bacteria causing SSI:
-staphylococcus
-streptococcus
-pseudomonas
Risks for causing SSI:
-types of wound (clean, clean-contaminated, etc)
-surgery lasting >2 hours
-comorbidities
-elderly
-emergency or abdominal surgery
Clean wounds:
-not inflamed or contaminated, don’t involve internal organs
Clean-contaminated wounds:
-no evidence of infection, do involve internal organs
Contaminated wounds:
-involve internal organ w/ spillage of contents from the organ
-ex: organ rupture like rupture gallbladder, appendix, etc.
Dirty wounds:
-known infection at the time of surgery
-ex: trauma, stab wound, you KNOW it’s infected
How many SSI’s are considered preventable?
-half!
What did the guideline for the prevention of SSI (2017) come up with?
-grading system: grading for recommendations, assessment, development, and evaluation
-quality of evidence: very low, low, moderate high
-170 studies appraised and synthesized
Grading Category: 1A
-strongly recommend, moderate to high quality of evidence
Grading Category: 1B
-strong recommendation, low quality evidence
-prolly some bias
Grading Category: 1C
-strong recommendation required by state/federal regulation
Grading Category: II
-weak recommendation
Exclusions to the Guideline for the Prevention of SSI:
- SSI was not reported as an outcome
- all pts that had “dirty procedures”
- the study only included dental or oral health procedures
- the procedure did not include primary closure
- the study includes wound protectors post-incision
Parenteral Antibiotics (IV):
-administer only when indicated (1B)
-timed so that the agent is established in tissue upon incision (1B)
Non-parenteral Antibiotics:
-NO rec. for antibiotic irrigation
-NO rec. for soaking prosthetic devices in antibiotic solution-not harmful
-should only apply antibiotic ointment to incisions (1B)
Glycemic control:
-perioperative control (1A)
-glucose targets <200 mg/dL (1A)
-NO rec. for tighter control
-NO rec. for A1C target
Normothermia:
-maintain peri-operative normothermia (1A)
-NO rec. for specific strategies to maintain normothermia
Oxygenation Rec:
-(for increased FIO2 of 80%)
-studies looked at pts with normal pulmonary function, GETA intraoperative and immediately after extubation (1A)
-NO recs for increased FIO2 in pts
–only intraop with GETA
–neuraxial anesthesia
–postop by mask or n/c
–no trials r/t %/duration/delivery method
**very contradictory, Dr. Shaffer SR
Antiseptic Prophylaxis:
-shower or bathe w/ soap or antiseptic pm before surgery the next day (1B)
-intraoperative skin prep w/ alcohol-based antiseptic (1A)
-Consider intraoperative iodine irrigation in deep tissues (II)
Are there any known benefits for intraop iodine irrigation in deep tissues?
Nope!
-no benefit intraperitoneally
-no benefit with iodine imbedded adhesive drapes
-no benefit soaking prosthetic devices
Blood transfusion:
-do NOT withold needed transfusion from surgical pt as a means to prevent SSI (1B)
^^benefits outweigh the risks!
Systemic Immunosuppressive Therapy:
-Uncertain benefits/harm with systemic corticosteroids on risk of SSI in joint arthroplasty
–infection most common indication for revision TKA
–ex: if someone has diabetes, given zofran instead of decadron
-uncertain benefit/harm with intra-articular corticosteroids preoperatively in planned joint arthoplasty
Antibiotic Prophylaxis-preop goal:
-adequate bactericidal concentration in serum and tissues WHEN INCISION IS MADE
-MIC: minimum inhibitory concentration (based on evidence)
-given by anesthesia
General principles of antibiotics:
- should be active against common surgical wound pathogens
- proven efficacy in clinical trials
- must achieve MIC
- shortest possible course effective…ideally 1 dose for entire case
- newer antibiotics reserved fro more resistant infections
- if all is equal: oldest, cheapest
Antibiotic timing:
-initiated within 1 hour of incision (30 min is better)
-needs to circulate 15 min before incision at least
-exception: vancomycin and fluoroquinolone: initiated within 2 hours
-completely infused prior to tourniquet use
-may hold antibiotics for cultures
Redosing of antibiotics:
-usually 2 half-lives or with excessive blood loss
-may be redosed following cardiopulm bypass
-redosing required for prolongest procedures
–drug dependent, usually 2-4 hours while in OR
–redosing only matters intraoperatively
Common surgical antibiotics:
-Beta lactams: penicillin, cephalosporin, carbapenems
-Vancomycin
-Aminoglycosides (gentamycin)
-Fluoroquinolones (cipro)
-Metronidazole (flagyl)
Penicillins-beta lactams
-inhibit bacterial cell wall synthesis
-resistance develops overtime d/t beta-lactamase enzyme (resides on outer surface of cytoplasmic membrane)
-DOC for streptococci, meningococci, pneumococci
-most effective for gram-positive!
-skin infections, catheter infections, URI’s
ex: penicillin G, methicillin, nafcillin, amoxicillin (newest gen)
Adverse reactions of penicillins-beta lactams:
-hypersensitivity: hx of reaction unreliable, ranges from skin rashes to anaphylaxis (0.05%)
-GI upset
-vaginal candidiases
Cephalosporins-beta lactams (ANCEF)
-more STABLE against beta-lactamases
-broader spectrum, beta lactam rings bind to penicillin binding protein and ibhibit the normal activity of the protein (can’t make a cell wall)
-resistance occurs by protein altering its structure
-DOC for surgical prophylaxis, can be used with PCN allergy EXCEPT for anaphylaxis
Generations of Cephalosporins: gen 1
-cefazolin: ancef, kefzol
-does not penetrate BBB
-most gram positive (staph and strep)
-treats cellulitis, abscesses, URI, UTI
Generations of Cephalosporins: gen 2
-cefuroxime aka ceftin/zinacef
-cefoxitin aka mefoxin
-cefotetan aka cefotan
-cefuroxime specifically has better gram negative coverage
-treats H influenze pneumonia, UTI, and otitis media
Generations of Cephalosporins: gen 3
-cefotaxime aka claforan
-ceftriaxone aka rocephin
-ceftazidime aka fortaz
-some cross BBB, better gram negative coverage than before, treats resistance
-treats meningitis
-Rocephin is good for gonorrhea
Generations of Cephalosporins: gen 4
-cefepime aka maxipime
-most resistant to hydrolysis by lactamases!
-usually reserved for multi-resistant organisms
-penetrates BBB well!
Adverse reactions for Cephalosporins:
-hypersensitivity uncommon, can be rashes, fever, nephritis, anaphylaxis unlikely
-potential production deficit of Vitamin K-choose a different abx if the pt has blotting disorders
-common cause of colitis!! (3rd gen!)
-cross-reaction to PCN approximately 1%
-if TRUE anaphylaxis to PCN, use vanc or clindamycin instead
Carbapenem-beta lactam:
-good activity against gram NEGATIVE rods (pseudomonas aeruginosa) and enterobacter
-can inhibit the beta-lactamse enzyme
-possess the broadest spectrum of activity!!
-bind to penicillin-binding protein
-LAST LINE AGENTS (intra-abdominal, resistant UTIs, penumonia)
-most penetrate BBB
ex: ertapenem (Invanz), meropenem (Merren), and Imipenem (Primaxin)
Adverse Reactions to carbapenems
-N/V
-diarrhea
-rashes
-injection site reactions-IM form contains lidocaine-LA allergie?
-decreases valproic acid/ depakote up to 90%!!
^^use different abx in pts taking this for seizures, could make seizures return
-cross sensitivity to PCN <1%
Vancomycin
-inhibits cell wall synthesis
-active against gram-positive bacteria (too large to be able to penetrate gram-negative cell wall)
-ONLY works if bacteria is ACTIVELY dividing
-is very slow…
-most valuable against blood-stream infection and endocarditis-blood stream infections caused by MRSA!
-good for valvular surgeries, cardiopulm bypass
Adverse reactions for Vancomycin:
-frequent: phlebitis at injection site, chills, fever, nephrotoxicity (why we do peaks and troughs) and red man syndrome-inflammatory response we see in pts receiving vanc too quickly
Aminoglycosides:
-inhibit ribosomal proteins and cause mRNA to misread (bacteria cannot replicate)
-significant post-antibiotic effect
-synergistic with beta-lactams or vancomycin, especially useful in enterococcal endocarditis
ex: gentamycin
Adverse reactions for Aminoglycosides:
-OTOTOXICITY!! why we give this drug slowly
-nephrotoxicity: in elderly, >5 days tx, in renal insufficiency, higher doses, concurrent with loop diuretics
-curare-like effect-more commonly with succx
Fluoroquinolone:
-inhibits DNA protein synthesis
-excellent gram-negative organisms
-treats UTI, bacterial diarrhea, bone/joint infections
^^often GU surgeries
ex: ciprofloxacin (cipro) and levofloxacin (levaquin)
Adverse reactions for fluoroquinolones:
-N/V/D
-PROLONGED QT INTERVAL
-cartilage damage/tendon rupture-seen with renal insufficiency, concurrent steroid use, advanced age, 2016 warning about cartilage damage with these
Metronidazole:
-antiprotozoal/anerobic antibacterial
-forms toxic byproducts that cause unstable DNA molecules
-indicated for: intra-abdominal infections, vaginitis, and C-diff
ex: flagyl
Adverse Reactions for metronidazole:
-nausea
-peripheral neuropathy (in prolonged use)
-disulfiram-like effect (with alcohol: flushing, dizzy, HA, chest or abdominal pain)
^^hangover phenomenon so abstain from alcohol when taking this drug!
How much ANCEF to give someone if <80 kg?
1 gram ANCEF
How much ANCEF to give someone if >80 kg?
2 gram ANCEF
How much ANCEF to give someone if >120 kg?
3 gram ANCEF
ANCEF instructions:
-given over 3 min
-re-dose q4hr
How long is fluconazole given over?
120 min
How often is ampicillin redosed?
q2hr
