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E2 Flashcards

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1
Q

Define:
Nausea
Vomiting

A

Nausea
• comes from the Greek word - nautia = “seasickness”.
• Described as ‘a feeling of sensation of unease and discomfort in the stomach with the urge to vomit.’

Vomiting
• forceful expulsion of gastric contents through the mouth or nose

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2
Q

Define:
Retching
Emetic episode

A

Retching
• Similar to vomiting
• Except that NO gastric content enters the pharynx.

Emetic episode
• one or more instances of vomiting and/or retching
• separated by no more than 1 min between episodes.

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3
Q

Describe some examples of historical treatments for nausea from 1914 to 1930

A

1914:

  • tincture of iodine in 1 tsp of H2O q30min
  • inhalation of vinegar fumes
  • rectal injection of opium

1930:

  • Essence of orange on gauze
  • Lateral position
  • Strong black coffee
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4
Q

Describe some examples of historical progression of medication treatments for nausea from 1950s to 1991

A 
1950:
-antihistamines
-neuroleptic chlorpromazine
1957:
-promethazine prophylaxis
1960:
-droperidol
1991:
-Zofran
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5
Q

Describe the incidence of PONV

A
  • Most common pt complaint
  • Overall ~20-30%
  • Intractable vomiting 0.1%
  • Calculated risk could be high as 80%
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6
Q

What are pathophysiologic mechanisms of introduction of n/v

A
  • Peripheral mechanisms
  • Central mechanisms
  • Drug
  • Toxins
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7
Q

Name receptors that mediate N/V

A 
Muscarinic--M1
Dopamine--D2
Serotonin 5-hydroxytryptamine-3--5-HT3
Histamine--H1
Neurokinin 1--NK1/substance P
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8
Q

Describe the central mechanisms that mediate n/v and potential causes preoperatively

A

Higher cortical centers
-communicate w/ vomiting center in the MEDULLA

Potential causes preoperatively
-fear, pain, anxiety

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9
Q

escribe the peripheral mechanisms that mediate n/v

A
  • Direct gastric stimulation which induces the release of substance P and serotonin from enterochromaffin cells
  • activates vagal and splanchnic nerve 5-HT3 receptors
  • Nerve afferents end in the CTZ
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10
Q

What mediators a receptors are utilized in peripheral mechanisms of n/v

A

NT mediator:
substance P and 5HT3

Receptors
5-HT3

area
CTZ

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11
Q

Describe toxic materials and drugs that mediate n/v

A

Our own gut
-Toxin ingestion activates enterochromaffin (5HT3 release?)

Things we put in our body
-Drugs, food, alcohol

What other ppl administer
-anesthetic

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12
Q

How does motion sickness r/t PONV

A

h/o motion sickness INC risk of PONV

MOA = vestibulat system stimulation. V system can be affected by anesthetic

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13
Q

What are general factors that contribute to PONV

A

Pt factors
Surgical factors
Anesthetic factor

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14
Q

What are some pt factors r/t PONV

A 
Age
Gender
H/o motion sickness
H/o PONV
NONsmoker
Genetic polymorphism
Gastric distention
GE junction dx
Delayed gastric emptying
INC gastric vol
Pre-op N/V
Autonomic imbalance
Obesity
Menstruation
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15
Q

What are surgical factors that contribute to PONV

A

Specific procedures

  • chole, gyn, lap procedures
  • strabismus sx for peds

Procedures loosely related

  • HEENT
  • URO
  • Breast
  • Major ortho
  • Abd

Surgeries specific to peds

  • Adenotonsillectomy
  • hernia repair
  • orchipexy
  • penile sx
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16
Q

Anesthesia factors that contribute to PONV

A
  • Anesthetic technique
  • Volatile
  • IV anesthetic
  • N2O
  • Duration
  • Opioid admin
  • Neostigmine
  • Sugammadex
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17
Q

How does anesthetic technique contribute to PONV

A

GA has higher PONV rate than regional

TIVA has less PONV incidence than GA

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18
Q

How does IV medication contribute to PONV. Give an example of an induction med that contributes to PONV.

A

Induction meds may have POS or NEG association w/ PONV

ETOMIDATE
-INC PONV
-DEC CBF 
-DEC ICP
recent studies show low association
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19
Q

How does nitrous contribute to PONV

A

May modestly INC PONV risk

Mostly in women

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20
Q

How does duration of anesthesia contribute to PONV

A

INC exposure to inhaled anesthetic and opioids

Usually more invasive procedures

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21
Q

How does MR reversal contribute to PONV

A

Neostigmine = LOW association

Sugammadex = questionable association

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22
Q

How do opioids contribute to PONV especially r/t pre/postop-period

A
  • Significant association
  • Studies focus on dosage and duration in association w/ PONV
  • Admin of postop opioids INC PONV incidence
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23
Q

How do volatile anesthetics contribute to PONV

A

Leading culprit for PONV

Greater than Propofol

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24
Q

What is the general expectation for the occurrence of PONV

A

Timeline

  • Immediately postop
  • Peak around 6 hrs
  • Can linger longer than pos-op period
  • Approx 35% of pts experience PONV
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25
Overall risk factors for PONV
- laparotomy - laparoscopy - major breast sx - middle ear sx - gyn sx - female - Age >50 yo - h/o PONV - h/o motion sickness - h/o vertigo - Dental procedures
26
What is the purpose and major predictors of risk stratification for PONV
Purpose -add up all risk factors to obtain score which can guide decisions for ponv tx Major predictors - female - h/o motion sickness and ponv - postop opioids - nonsmoker
27
What is the APFEL risk score and relation to PONV
* 0 factors = 10% chance of PONV * 1 factor = 20% chance of PONV * 2 factors = 40% chance of PONV * 3 factors = 60% chance of PONV * 4 factors = 80% chance of PONV
28
How should risk score treatment be approached. Questions to ask yourself
Decide treatment based on the pts calculated risk stratification: • What’s the patient’s risk of PONV? • The consequences of N/V r/t the surgical procedure? • What are the pt & clinician preferences? • Implications for a change in our routine anesthesia plan.
29
How is PONV treated w/ 0-1 risk factors
No prophylaxis recommended Many anesthetists still give meds
30
How is a moderate risk of ponv treated and what are the # of risk factors
2-3 risk factors Prophylaxis indicated ``` +Chose 1-2 interventions >1 antiemetic PLUS -regional -TIVA -acupuncture ```
31
How is high risk of ponv treated and what are the # of risks factors
4+ risk factors Multimodal prophylaxis indicated Choose >/=3 interventions >1 antiemetic PLUS - regional - TIVA - acupuncture
32
What are approaches to managing PONV
pharmacologic -antiemetic drugs non-pharmacologic - acupuncture - acupressure - O2
33
Classes of drugs used for pharmacologic tx of ponv
dopamine antagonist histamine antagonist anticholinergic
34
What are the 2 types of dopamine antagonists and their corresponding drugs
butyrophenones - droperidol - haldol phenothiazines - promethazine - chlorpromazine - prochlorperazine
35
``` Droperidol Class: Dose: Onset: Peak: Duration: Cost: MOA: Blackbox warning: ```
``` Class: dopamine antagonist butyrophenones Dose: 0.625 mg - 1.25 mg IV. Onset: 3 - 10 minutes Peak: 30 minutes Duration: 2-4 hours Cost: ~$4.50 for 2.5mg/ml. ```
36
Droperidol MOA and what is the blackbox
MOA: -it is an antipsychotic •blocks dopamine in the CTZ. •α-adrenergic blockade DEC pressor effect of Epinephrine Blackbox warning •for prolonged QT •FDA recommends 2 hours of EKG after admin
37
How does droperidol compare to zofran
droperidol dose of 0.625 is equivalent to 4 mg zofran  No difference in side effects, recovery, time of discharge.  Droperidol is more cost effective.  Both prolong QT
38
Where is the action phenothiazines and SE r/t admin
Work in the CTZ SE - sedation - hypotension - EPS
39
MOA of 5-ht3 antagonists, medications, and SE
MOA: -Primarily antagonize serotonin ``` Medications: Zofran dolesetron granisetron palonosetron ``` SE: minimal H/A, constipation
40
``` Ondansetron  IV onset:  Half-life:  Dose:  Rescue dose:  Cost: ```
```  IV onset: 10 minutes.  Half-life: 3 hours.  Dose: 4 mg.  Rescue dose: 1 mg.  Cost: $43 for 4 mgs. ```
41
Dolesetron  Dose: ``` Granisetron  Dose:  Duration:  Half-life:  Cost: ``` Palonosetron  half-life:  MOA:
Dolesetron  Dose: 12.5mg - 25 mg ``` Granisetron  Dose: 1mg,  Duration: longer acting,  Half-life: 9 - 12hrs  Cost: $$$ ``` Palonosetron  2nd generation  half-life: 40hrs,  MOA: exhibits allosteric binding to 5-ht3 receptors.
42
Anticholinergic med used for PONV. MOA and SE
Scopolamine MOA -centrally acting antimuscarinergic w/ short half-life SE: - visual disturbances - dilated pupils
43
Antihistamine med used for ponv, exhibits similar results to what drugs. Side effects and dosing
Dimenhydrinate, diphenhydramine sim results as: decadron, droperidol, zofran SE: drowsy dosing: 1 mg/kg
44
MOA of neurokinin-1 receptor antagonist and drug examples
Antiemetic that antagonizes substance P receptors Aprepitant Rolapitant
45
Aprepitant and Rolapitant  Dose:  Half-life:  Cost:
``` • Aprepitant  Dose: 40 - 80 mg oral preoperatively  as early has 3 hours prior to onset of anesthesia  Half-life: 40 hours  Cost: >$ 200 for each dose. ``` ``` Rolapitant  Dose: 90 mg oral preoperatively  Half-life:180 hours  Well known in the chemotherapy communities  Cost: Almost $400 per dose. ```
46
``` Glucocorticoids used for ponv. dose: efficacy: onset: give when? considerations: ```
Dexamethasone  Dose: adults 4mg, children 0.25mg/kg  Max 4 mgs.  Efficacy is similar to Zofran & droperidol.  Onset: Slow  Give at the beginning of the case.  Consideration: high glucose measurements.
47
List possible alternative medications for the tx of ponv
cannabinoids-Nabilone adequate hydration midazolam isopropyl alcohol
48
Guidelines for ponv rescue therapy
``` #1 rule: rescue w/ different drug class than already given ``` Serotonin antagonists are very good tx for ponv rescue rescue dosage can be smaller give small dose of narcan for ponv r/t opioids
49
What is post-discharge n/v and associated independent factors
Defined: ponv ocurring w/in 48 hrs post d/c in nearly 37% of pts Independent risk factors: - female gender - age<50 - h/o ponv - opioids in pacu - nausea in pacu
50
What are some preventative measures for ponv (11)
```  Use of local and regional anesthesia.  Use propofol.  Avoid nitrous oxide.  Minimize opioids.  Nonopioid analgesics.  Control pain.  Adequate hydration.  Limit motion.  Avoid early ambulation.  Avoid early oral intake.  Antiemetic prophylaxis. ```
51
What is standard 11 from AANA standard of practice
Standard 11 • Evaluate pt status • Determine when appropriate to txfr care to another qualified healthcare provider • Communicate pt condition & essential infor for continuity of care
52
Describe standard 1 and 2 for post-anesthesia care
Standard 1 • All patients who have received GA, RA, or MAC • Must receive appropriate postanesthesia management. Standard 2 • Pt must be transported to PACU by anesthesia care team member  That individual must be knowledgeable about the patient’s condition • During transport pt is  Continually evaluated & treated  with monitoring and support  appropriate to the pts condition
53
Describe Standard 3, 4, and 5 of post-anesthesia care
Standard 3 • on PACU arrival, pt shall be re-evaluated • Verbal report provided to the responsible PACU RN by accompanying anesthesia team member Standard 4 • The pts condition is evaluated continually in PACU. Standard 5 • A physician is responsible for the discharge from PAC
54
General h/o PACU evolution in the US
1920 several PACUs opened in the United States. • After WW II the number of PACUs increased. 1947 studies showed that 50% of deaths in the first 24 hours following surgery were preventable. 1949 PACU became Standard of Care.
55
What staff works in the PACU and their general role
```  Specially trained nurses • Highly skilled @ assessment  Respiratory therapists. • Emergent breathing tx • Vents for short-term use  Anesthesia personnel. • MDA  Intensivist or House MD • Continue care for pt post-op ```
56
Where is the PACU located and what are requirements for travel from OR to PACU
Close to the OR (or ICU) ``` Travel requirements Monitoring - • Oxygenation  Pulse-Ox. • Ventilation  Make sure they are breathing. • Circulation  systemic BP & HR. ```
57
What should be done on arrival to the PACU from OR
ASSESS -airway patency, RR, Sat, HR, BP, mental status, pain, n/v Assess and treat -hypoxemia r/t RA, obesity, sedation, RR, advanced age >60 yo Connect pt to PACU monitors
58
What is performed on pt admission to PACU
- CRNA assesses pt - Pt connected to PACU monitors - Report given to PACU RN - PACU RN assesses pt
59
Describe the components of CRNA PACU report
Should be - specific - organized - completed when full attention of receiving RN
60
Consequences of poor report
- Wrong tests - Delay in treatment - Failure to continue certain tx
61
What are 3 communication tools that can be used for handoff
SBAR Simplified handoff tool PACU admission report (comprehensive)
62
Describe the SBAR handoff and the 7 advantages
Situation ,Background, Assessment, Recommendations Structured handoff • Improves transition of care • ↓ communication errors and Errors in general • Improves staff satisfaction  Standardized method of communication  Covers pertinent surgical and pt factors  Easy to remember
63
Concerns and guidelines for phase 1 recovery
Concern: - Most intense phase - ideally 1:1 ratio Guidelines: - continuous monitoring (HR, Sat RR, EKG, airway patency) - Assessment - NM fxn for intubated pts - Frequent VS
64
What should be included in the phase 1 recovery PACU assessment
mental status BP temp pain Out--UO, EBL, wounds, drains Ins--IVF, how much and what tupe
65
How often are VS assessed during phase 1 recovery. VS goal
1st 15 min = q5min Duration of phase 1 = q15min Goal: w/in 20% of baseline, be sure to notify pacu RN about pt baseline VS
66
What is phase II recovery
Less intense | Pt preparing to meet criteria for DC
67
Means of measuring readiness for DC
Aldrete score modified aldrete score Post-anesthesia dc scoring system
68
What are the assessment categories for the aldrete scoring tool. Describe the corresponding scores of 2 for each category
activity-moves all extremities voluntarily respirations-Breaths deeply and coughs freely circulation-BP +20 min preanesthetic level consciousness-fully awake O2 sat-SpO2 > 92% on RA
69
What is monitored in phase II recovery? Frequency of VS
Monitor: - Airway and ventilation - pain level - ponv - fluid balance - wound integrity VS frequency q30-60 min
70
What are common airway complications during recovery
- Airway obstruction - Negative pressure pulm edema - laryngospasms - airway edema or hematoma - VC pralysis - residual neuromuscular blockade - OSA - Arterial hypoxemia - Diffusion hypoxemia
71
What are patient and procedural related risk factors for PACU airway complications
``` Patient related • COPD • Asthma • OSA • Obesity • heart failure • Pulmonary HTN • URI • tobacco use • higher ASA score. ``` Procedure related • Surgery near diaphragm • ENT procedures • severe incisional pain poor ventilation
72
What are anesthetic related risk factors for airway complications in PACU
Largest contributor to airway complications • Due to General anesthetic MR  How much  When  What reversal opioids  When are they given??
73
Causes of upper airway obstruction in PACU and treatments
Causes: •Loss of pharyngeal muscle tone  ↑ upper airway resistance •Paradoxical breathing Treatment - Jaw thrust - CPAP - OPA/NPA (opa for deep sedation; npa for more awake pt)
74
How does loss of pharyngeal tone lead to upper airway obstruction
Pharyngeal muscle normally tenses on NEG pressure inspiration and opens airway Loss of tone means airway wont open This increases upper airway resistance
75
What is negative pressure pulmonary edema and how does it happen
It is a form on noncardiogenic pulm edema - results from generation of high negative ITP - Leading to capillary leakage in lungs from INC hydrostatic pressures
76
What are causes of negative pressure pulm edema
- NEG ITP against an obstructed airway - Blocked ett - laryngospasm (most common)
77
What are s/sx of negative pressure pulm edema and how does it resolve
S/Sx: - pink, frothy sputum - Makes oxygenation difficult Resolves in 12-48
78
What is a laryngospasm and associated causes
VC closure that prevents air movement resulting in hypoxemia and possibly neg pressure pulm edema causes: Stimulation of pharynx or VC from blood, secretions or foreign material
79
Physiology and symptoms of laryngospasm
physiology - prolong exaggeration of glottic closure reflex - d/t stimulation of SLN Symptoms -Inspiratory stridor d/t INC respiratory effort, INC diaphragmatic excursion -Silence = ominous sign of NO air movement
80
Treatment for laryngospasm
- Get help - Apply FM w/ tight seal, 100% FiO2 and APL @40 cmH2O - suction airway - chin lift/jaw thrust - OPA/NPA - Pressure to laryngospasm notch
81
Describe how to perform the larson's manuever
Apply bilat digital pressure behind the lobule of the pinna of each ear - clears airway and stimulates pt - apply for 3-5 seconds w/ forcible jaw thrust - Maintain FM w/ tight seal
82
What may be evident on assessment if unable to break laryngospasm What should be your next actions
Assessment - Fast desat - INC HR followed by bradycardia Your actions: Give atropine and propofol Give succs 0.1 mg/kg IV or 3-4 mg/kg IM RE-INTUBATE
83
Contributions to airway edema in the post-op pt
``` Prolonged intubation Prolonged positioning (prone and tburg) Cases w/ large blood loss that receive ```
84
what is an important assessment clue that a pt may have airway edema
Facial and scleral edema are present
85
What assessments and interventions should be performed prior to extubation on a pt w/ possible airway edema
Assessment - Perform cuff leak test - -remove small amount of air from cuff - -no air heard - -leave ETT and raise HOB Intervention suction oral pharynx
86
What surgeries may contribute to airway hematoma | Biggest concerns w/ airway hematoma
neck dissections thyroid removal carotid surgeries - Rapidly expanding hematoma causing supraglottic edema - tracheal lumen <5 mm is LIFE-THREATENING SITUATION
87
What can airway hematoma post-op lead to and treatment
Leads to: - Deviated trachea - compression of trachea below level of cricoid cartilage - VERY difficult intubation dt blood or edema Treatment: - Decompress the airway (release clips or surgical incision) - RE-INTUBATE - Surgical backup for tracheostomy
88
What procedures are associated w/ VC paralysis
- otolaryngologic sx - thyroidectomy - parathyroidectomy - Rigid bronchoscopy - over inflated ETT cuff
89
What is the cause of VS paralysis
Unilateral or bilateral nerve injury
90
What symptoms are present w/ unilateral SLN injury
usually asymptomatic
91
What can occur w/ the VCs as a result of damage to the external branch of the SLN
- Produce weakness and huskiness of voice as VCs cannot tense up - cricothyroid muscle is paralyzed - Injury is r/t loss of tension of VCs - -appear wavy
92
What can occur w/ the VCs as a result of damage to bilateral recurrent laryngeal nerve
- Results in aphonia and paralyzed cords - Each cord in intermediate position - VCs can close causing airway obstruction during INSPIRATION
93
What are airway problems r/t recurrent laryngeal nerve damage
- Difficult intubation | - Likely tracheostomy for emergent airway
94
What are some post-op complications r/t thyroid surgery
Hypocalcemia | -w/in 24-48 hrs post-op
95
s/sx associated w/ hypocalcemia when are ca++ levels considered low
S/sx: - chovsteks sign (facial spasm) - trouseau's sign (carpal sign) - paresthesia in fingers - muscle cramps - irritability Ca++ levels Serum = <8.5 iCa = <3.8 mg/dL
96
What are the greatest concerns and considerations related to the effects of residual neuromuscular blockade on the airway in PACU
- complete reversal of MR is necessary - Partial reversal can be worse than NO reversal b/c - --assessment for extubation readiness can be misleading w/ partial reversal - --Thus masking pt inability to maintain airway
97
Clinical evaluation to assess the level of residual NMB
- grip strength - tongue protrusion - can lift legs off of bed - hold head up >/= 5 sec
98
What factors can contribute to recurarization in the PACU affecting the airway
Meds: abx, lasix, propranolol, phenytoin conditions: low Ca++ and Mg++
99
What are the components of the STOP-BANG assessment and why is it useful?
Useful: to identify pts at risk for OSA ``` Components: SNORE TIRED OBSERVED not breathing PRESSURE (HTN) BMI >35 AGE >50 NECK >16 GENDER ```
100
How can a h/o OSA affect pts PACU recovery and why. How might this affect the anesthetic recovery plan
Pts are prone to airway obstruction --b/c partial or complete blockage of upper airway Sensitive to opioids Anesthetic plan: - Awake extubation, make sure pt is FC - Try regional techniques for post-op pain
101
Describe post-op care and d/c criteria for pts w/ OSA
Post-op care: May need CPAP Use home CPAP if provided D/C criteria SpO2 >90% while sleeping
102
What are low, intermediate, high OSA risk screening scores...
Low risk = 0-2 intermediate = 3-4 high risk = 5-8
103
What are causes of arterial hypoxemia in the PACU
Pt on RA: --all pts should be on O2 from OR to PACU Hypoventilation --Too much pain meds or BZDS (poor clearance)
104
What treatments are indicated when arterial hypoxemia is present in PACU
- Apply O2 via NC or FM - Reverse opioid or BZDs - --Narcan 40-80 mcg small incremental doses - --flumazenil 0.2 mg (repeat, max of 1 mg) - Stimulate pt
105
Describe the difference between hypoxia vs hypoxemia
hypoxia: - Not enough O2 DELIVERED to tissue - Cyanide poisoning is only time hypoxia W/O hypoxemia Hypoxemia: -Not enough O2 IN blood
106
What can cause diffusion hypoxia post-op? | What can this lead to?
Rapid diffusion of N2O into alveoli at the end of anesthetic - If on RA s/p N2O - -DEC alveolar PO2 - -DEC PaCO2 Leads to: - dilution of alveolar gas - DEC PaO2 and PaCO2 - DEC respiratory drive from DEC PaCO2
107
How long can diffusion hypoxia persist following N2O d/c? | What is the treatment?
Can persist for 5-10 min Treatment: Apply O2 Stimulate RR Watch
108
What are circulatory complications that may be present in PACU
Systemic HTN | Systemic HoTN
109
What are parameters for post-op HTN, considerations for BP assessment and common causes
Parameters: SBP>180 mmHg DBP>110 mmHg Assessment: -ensure BP cuff is in appropriate place before treatment Common causes - Emergence excitement - shivering - hypercapnia - pain
110
Suggested treatment and considerations for post-op HTN. Give dosages for medications
- Use rapid acting BP meds - --Labetolol 5-25 mg - --Hydralazine 5-10 mg - --Metoprolol 1-5 mg Considerations - Treat underlying cause - --Surgeon will give range for BP - --bring meds on transport
111
What are some causes of systemic hypotension in PACU
Hypovolemic--DEC preload Distributive--DEC afterload (sepsis, allergic rxn, critical illness, iatrogenic sympathectomy) Cardiogenic--pump failure (MI, Cardiac dysrhythmias)
112
What are causes of hypovolemic hypotension post-op
1. Third spacing 2. Inadequate intraop IV fluid replacement 3. Loss of SNS tone d/t neuraxial blockade 4. Ongoing bleeding 5. ACE-i
113
How can the presence of tachycardia guide hypovolemic hypotension treatment
Tachycardia is NOT a reliable indicate of hypovolemia --ESP in pts w/ BB or CCB on board Consider pain vs hypovolemia
114
What are causes of distributive hypotension post-op
DEC afterload - Sepsis - Allergic rxn - Critical illness - Iatrogenic sympathectomy
115
Describe how iatrogenic sympathectomy affect BP post-op. | What does HoTN and bradycardia indicate and interventions
D/t surgery, disease or high spinal level (>T4) - Loss of vascular tone - Block cardioaccelerator fibers - Alters vascular distribution HoTN + bradycardia - ominous that pt wil CODE - TX: vaso, neo, ephedrin
116
How is HoTN addressed in the critically ill pt pos-operatively.
Small doses of meds can cause exaggerated effects --possible exaggerated SNS tone Return on meds they were on prior to surgery?
117
Type of allergic responses leading to HoTN | Treatment
Anaphylactic: IgE (prior exposure) Anaphylactoid: non-IgE Treatment: Epi = treat HoTN r/t allergic rxn
118
What is the most common cause of allergic rxns in perioperative period and why What population is more prone...
MRs*** (most common) -Engineered w/ quaternary ammonium ions that lead to a histamine reaction Females more prone than men
119
List common medications leading to allergic rxns from most common to least
``` most NMBD Latex Abx Hypnotics Colloids Opioids ```
120
How do NMB lead to allergic rxns w/ histamine release. Treatment
Histamine release ``` Leads to: Erythema Vasodilation Edema HoTN GI constriction tachycardia pruritus ``` Treatment: diphenhydramine
121
What are associated responses r/t potent inflammatory leukotrienes and prostaglandins release when NMB drugs cause allergic rxns What treatment should be used
- Bronchial constriction - INC vascular permeability Treatment Bronchodilators EPI Ephedrine
122
Which NMB drugs are more prone to cause allergic rxn from greatest to least
Roc Succs Vec
123
What populations are more prone to latex allergy.
- Repeated exposure - several surgical procedures - spina bifida pts - healthcare workers
124
What are the latex-mediated rxn types
Irritant contact dermatitis Type IV cell mediated rxn Type I IgE mediated hypersensitivity rxn
125
What is the incidence of latex allergy and timeframe of rxn
Incidence: as high as 20% Timeframe: 30-60 min s/p exposure
126
What are high and low eluding sources of latex rxns
high eluding: gloves, drains, catheters (soft rubber) Low eluding: ____ strap, BP cuff tubing (hard rubber)
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What are the most common allergy causing abx
PCN Vanc = histamine release
128
Cardiogenic causes of HoTN post-op
Pump failure - MI - Cardiac dysrhythmias (ST, AF, VT, VF, SB)
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What should be included in a post-op assessment for possible MI
EKG monitor w/ lead II and V5 - ST segment analysis - 12 lead EKG - Troponin
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What treatments should be considered for possible MI in the PACU
IMPROVE MYOCARDIAL OXYGENATION ``` Treat brady or tachycardia Treat HTN or HoTN Give O2 for low O2 Avoid hypothermia Avoid fluid overload ```
131
What are factors that decrease O2 supply to myocardium
INC HR DEC PaO2 - LOW hgb - LOW SaO2 DEC coronary BF - LOW CPP - LOW DBP - LOW LVEDP INC coronary vascular resistance
132
What are factors that INC O2 demand on myocardium post-op
INC HR INC LV systolic wall stress - INC SBP - INC LVEDV - DEC LV wall thickness INC contractility
133
List some causes leading to post-op cardiac dysrhythmias
- hypoxemia - hypoventilation - endogenous and exogenous catecholamine - electrolyte abnormalities - anemia - fld overload
134
Describe causes and characteristics of sinus tachycardia,
Causes (most common**): - bleeding - cardiogenic/septic shock - thyroid storm - PE - SNS** - hypovolemia** - Anemia** - shivering** - agitation** Characteristics: QRS: narrow Rhythm: regular Rate: >100 bpm
135
What treatments may be indicated for sinus tach post-op
- Identify and treat the cause - PAIN = give opioids - Hypovolemia = fld challenge
136
What are risk factors leading to atrial dysrhythmias post-op. When is it more likely to occur
Risk factors: - pre-existing cardiac risk factors - positive fld balance - electrolyte abnormalities - O2 desat Higher after cardiac and thoracic sx -10% pts w/ major non-cardiac sx
137
Causes of post-op atrial fibrillation and considerations for treatment
Causes: - hypovolemia - anemia - trauma - pain ``` Considerations for tx: -Rate control = immediately address >150 bpm w/ HoTN -hemodynamically unstable =cardioversion followed by amio =Esmolol short-term -hemodynamically stable =most pts respond wo BB or CCB ```
138
Characteristics of VT in PACU | Concerns r/t PVCs in post-op period
QRS >120 ms PVC more common -d/t INC SNS stimulation from intubation, pain, transient hypercapnia
139
Causes of ventricular dysrhythmias in the PACU (6 Hs, 4 Ts)
``` Hypoxia Hypovolemia hypothermia hypokalemia hyperkalemia High H+ ``` Tension PTX Tamponade Thrombosis Toursades
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Possible causes of toursades in the pos-op period
prolong QT d/t | -amio, droperidol, procainamide
141
Characteristics and causes of sinus bradycardia in the PACU
``` Causes: Too many to list Long-term BB use ACh reversal NMB drugs ``` Characteristics: HR<60 bpm (what is baseline)
142
Procedures that can cause bradycardia
``` bowel distension INC ICP INC intra-ocular pressure Spinal anesthesia Spinal blocks ```
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Why do spinal blocks lead to bradycardia. | What can this lead to and why?
high spinal = T1-T4 level - -block cardioaccelerator fibers - -results in profound bradycardia ``` Can lead to: Cardiac arrest --Sympathectomy --Bradycardia --Lack of intravascular vol ```
144
Define delirium
- Acute change in cognition or disturbance of consciousness | - cannot be attributed to pre-existing medical condition, substance intoxication or medication
145
Describe the incidence of delirium in PACU
10% of adults >50 yo btwn POD 1-5 Higher incidence: - elderly - specific surgical procedures (TKR)
146
List some factors that influence and mask postop delirium
influence: - age - fxntl status - h/o substance abuse Mask: - sedation - anesthetic/pain meds
147
What are risk factors r/t post-op delirium
- Advanced age >70 yo - Preop cognitive impairment - DEC functional status - alcohol abuse
148
What is the importance of a preop cognitive assessment
To determine if there is preop cognitive impairment that could lead to postop delirium - can alter anesthetic plan - may lead you to check for underlying metabolic causes
149
List some intra-op factors associated w/ delirium
- Surgical blood loss (HCT<30% + INC # intraop txfn) - HoTN - Admin of N2O - Anesthetic technique
150
Describe methods for managing post-op delirium
- Identify high-risk pt prior to surgery - severely agitated pt may require additional PACU eyes - Early identification can help guide meds and anesthetic
151
Considerations to DEC post-op delirium effects for elderly pts undergoing minor surgery
- Should be treated at an outpt center | - Allows return to normal environment ASAP to dec post-op delirium
152
Considerations or assessments for pts w/ delayed awakening post-op
- Evaluate VS - -is EtCO2 high - Perform neuro exam - -may need CT - Monitor SpO2 - Assess labs for electrolyte, glucose abnormalities
153
What are some causes for delayed awakening post-op
- Anesthetic (#1 residual sedation) - Opioids - BZDs - Scopalomine - Hypothermia <33*C - Hypoglycemia - INC ICP - Residual MR
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What meds/doses would be given to address delayed awakening post-op from opioids, BZDs or scopalamine
Opioids: Narcan 20-40 mcg increments BZDs: flumazenil 0.2 mg (max 1 mg) Scopalomine: Physostigmine 0.5-2mg IV
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``` Describe some ways pain effects each body system Cardiac Pulm Endo Immune Coag GI/GU ```
``` Cardiac: INC HR, HTN Pulm: Splinting, DEC VC, atelectasis, hypoxia Endo: INC stress response Immune: Impaired Coag: INC risk thrombosis GI/GU: Ileus, urinary retention ```
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How is acute pain sensed. Describe mechanism...
At nociceptors -Free afferent nerve endings of fibers: +myelinated A delta +unmyelinated C -Tissue damage activates nociceptors via thermal, mechanical or chemical damage
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Mechanisms of tissue injury during surgery and mechanism of pain sensing
Surgical incision Dissection of muscle Burns Stimulates release of histamine, inflammatory mediators (bradykinin, PGs, 5HT3)
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What are inflammatory mediators of pain
Peptides (bradykinins) Lipids (PGs) NT (serotonin)
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How does direct nerve injury contribute to pain perception
Nerve transection Poor positioning causing: -stretching -compression
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What are the components of pain processing. Describe each
Transduction: CONVERSION of noxious stimuli into APs Transmission: CONDUCTION of AP through nervous sys Modulation: ALTERATION of afferent pain transmission (i.e. the DIC response) Perception: INTEGRATION of painful input into somatosensory or limbic cortices
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Define hyperalgesia? | What is opioid-induced hyperalgesia and what meds are more prone to lead to it? Treatment?
Hyperalgesia: Augmented sensitivity to painful stimuli Opioid-induced hyperalgesia: Reception of opioids causes more sensitivity to pain -Remifentanyl = Tx give long acting pain med w/ dose -Fentanyl = follow w/ infusion -Maybe give ketamine
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Describe primary and secondary hyperalgesia
Primary: - Augmented sensitivity to painful response - misinterpretation of non-painful stimulation Secondary: - INC excitability of neurons in the CNS - --d/t glutamate activation of NMDA receptors
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Describe some goals of pain control
- optimal pt comfort - attenuation of adverse physiologic responses to pain - control anxiety/agitation
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Considerations for attaining pain control goals post-op
Preemptive and preventative analgesia: - -What is the most painful part of the surgery - -What is the primary source of pain (i.e. spasms vs incisional pain) Multimodal approach: - -Use of multiple drugs from different calsses w/ various MOA/DOA - -Variety of drugs and techniques Opioid free approach
165
What are some drugs or techniques to be considered for the treatment of post-op pain
Drugs w/ variety of MOA in central and peripheral NS Drugs: opioids, ketamine, neuropathic, NSAIDs Techniques: regional or local anesthetics
166
``` Dosing and route for the following post-op opioids Morphine Codeine Hydromorphone Fentanyl ```
Morphine IV 2.5-15 mg IM 10-15 mg PO 30-60 mg Codeine PO 15-60 Hydromorphone IV 0.2-1.0 mg IM 1-4 mg PO 1-4 mg Fentanyl IV 20-50 mcg Transmucosal 200-1600 mcg Transderm 12.5-100 mcg
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``` Dosing and route for the following post-op opioids Oxymorphone Hydrocodone Oxycodone Methadone Propoxyphene Tramadol ```
``` Oxymorphone PO 5-10 mg IV 0.5-1 mg SQ 1-1.5 mg IM 1-1.5 ``` Hydrocodone PO 5-7.5 Oxycodone PO 5 mg Methadone PO 2.5-10 mg Propoxyphene PO 32-65 mg Tramadol PO 50-100 mg
168
What are recommendations for pacu discharge
- PT should be AOx3 or return to baseline - VS should be stable - PT must meet specified criteria - Use score to document fitness for DC - Outpt DC home w/ responsible adult - Give written instructions
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What are not considered requirements for discharge from pacu
- No minimum stay | - Requirements for urination or PO intake are NOT part of routine dc protocol
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What information should be included in written DC instructions from the PACU
- Diet - Medications - Activities - Phone # for emergency
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What are components of evaluation criteria for DC
Activity: able to move all 4 extremities on command Breathing: Able to breathe deeply and cough freely Circulation: SBP /=20% of preanesthetic level Consciousness: Fully awake O2 sat: >92% on RA
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What are HAIs Common reasons for HAI
Nosocomial acquired infections Not present or incubating at item of admission Reasons: Most likely from break in our technique -Poor/No handwashing, improper preop prep etc
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What are sources for HAIs? | What are the 2 most common?
-Central line associated sepsis -CAUTI -SSI -Hospital acquired PNA -VAP C-Diff 2 most common: SSI (21.8%) Hospital acquired PNA (21.8%)
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``` Pt awaiting R inguinal repair: -Intermittent episodes of chest tightness and dizziness w/ exertion x3 weeks -Syncopal episode last week w/ MI -On ASA, nonsmoker VS: 186/106 mmHg, HR 84, RR 16/min EKG = LBBB ``` Assessment: systolic murmur over R sternal edge, radiates to neck What are your current concerns Anesthetic plan
HTN: - INC risk of ischemia, stroke, LV dysfunction - DBP should be w/in 20% of normal prior to sx Possible AS: - Untreated = LVH and failure - Echo/Cath to determine severity Possible inferior MI on EKG: - Comparing this EKG to prior ED EKG - Elective Sx w/in 3 months very high risk Anesthetic plan: Delay case vs continue (likely delay)
175
Cholecystectomy: 55 yo M, 80 kg w/ cholelithiasis h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years ABG: pH 7.36, PCO2 60, PO2 70 Is pt having acute or chronic changes on ABG. What pulm test should be assessed and what may be seen in his case?
ABG changes: CHRONIC b/c inc PCO2 and lower PO2 Pulm tests: - Spirometry w/ flow-vol loops - -Concavity on expiration d/t obstruction - FVC, FEV1, RV, FRC - -norm FVC, low FEV1 (<40%**), inc RV, inc FRC - Chest xray - --intercostal space wide - --Ribs are flattened, not angled - --diaphragm and apical flattening - --hyperlucency (from less lung tissue) - --thin, narrow heart
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Cholecystectomy: 55 yo M, 80 kg w/ cholelithiasis h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years ABG: pH 7.36, PCO2 60, PO2 70 ``` What is our anesthetic plan? (monitor, airway, meds, other): Preop Induction Maintenance Emergence ```
Preop: +MONITORS-SpO2, ekg etc +AIRWAY- No need for O2? +MEDS-bronchodilator (anticholinergic, beta-agonist), steroid (esp if taking at home), maybe multimodal pain premedication +OTHER- avoid meds w/ histamine release to prevent airway reactivity Induction: +MONITORS- EtCO2, typical monitors +AIRWAY- GETA, ETT, 8.0 w/ rsi induction risk r/t n/v +MEDS- RSI?? to secure airway rapidly in the presence of N/V; succs vs roc +OTHER- ``` Maintenance: +MONITORS-all +AIRWAY- ETA w/ VG-PCV setting +MEDS- Sevo (avoid des to dec airway reactivity) +OTHER- ``` ``` Emergence: +MONITORS- same +AIRWAY- awake extubation +MEDS- reversal, lido on extubation (concern for laryngospasm), inhaler prior to pulling tube +OTHER- ```
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Cholecystectomy: 55 yo M, 80 kg w/ cholelithiasis h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years ABG: pH 7.36, PCO2 60, PO2 70 Anesthetic plan = GETA w/ sevo During the case, PIP suddenly increases and there are NO BS. What is the most common cause and what should be done?
Common cause: Bronchospasms B/C the pt is too light** Treatment: - Turn off vent and manually vent - Deepen anesthetic - INC FiO2 - inhaled beta-agonist
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Cholecystectomy: 55 yo M, 80 kg w/ cholelithiasis h/o asthma, DOE, 2 pillow orthopnea, Smokes 2 ppd x30 years ABG: pH 7.36, PCO2 60, PO2 70 Anesthetic plan = GETA w/ sevo episode of bronchospasm treated successfully How do you decide if/when pt should be discharged from PACU
- SpO2 >90% on RA - Wait 30 min to ensure no resp depression post opioid admin (?) - Awake - Pain control
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86 yo M, s/p R hemicolectomy POD2, for cecal carcinoma Assessment: Preop BP meds not restarted, UO 75 ml over 8 hrs, Poor PO intake, AOx3, AFeb, 110/70, 110, Chest and heart clear, abd tender at incision but soft, + BS w/ gas What are his expected labs: Na, K, Ca, A-B balance, BUN/Crt What is normal, minimal UO in a 70 kg man in 8 hrs Calculate hourly maintenance rate? What fld would be used?
``` Hypernatremia Hyperkalemia Hypocalcemia Inc BUN/Crt ratio INC crt Met acidosis ``` Normal: 0.5-1 ml/kg/hr 35-70 ml/hr 280 ml MIN in 8 hrs UO ``` Hourly maintenance 110 ml/hr 60 ml for 1st 20 kg 1 ml per remaining 50 kg 60+50 = 110 ml/hr ``` Replacement fluid Small bolus LR (maybe has high Na) encourage PO intake
180
What are etiology of ARF types and typical causes
Prerenal: hypovolemia, LOW CO, blood loss, HoTN Intrarenal: drugs, toxins, glomerulonephritis, contrast, infxn Post-renal: Obstruction in ureter, bladder, stones, stricture
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Identify the type of renal failure based on the description 1. Direct damage to glomerulus or tubule 2. GFR declines d/t poor renal perfusion, easily restored 3. typically r/t obstructed urinary flow
1= intrarenal 2= prerenal 3= Postrenal
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86 yo M, s/p R hemicolectomy POD2, for cecal carcinoma Assessment: Preop BP meds not restarted, UO 75 ml over 8 hrs, Poor PO intake, AOx3 Started maintenance LR at 110 ml/hr THEN BP drops to 80/50, HR 120, UO <30ml/hr What can be given? How can fluid vol be assessed?
Does pt have CVC? - CVP - SVV - CO US/Echo -IVC collapsibility GU cath Give: Colloid-albumin
183
23 yo, 84 kg F for breast biopsy Preop preparation What preop labs MUST be done What cath size placed preop? What type of IVF? What preop meds would you give?
preop-lab PREGNANCY Cath size: what you can get, can usually get bigger cath once asleep, if needed Fluid: LR Preop meds: PONV prevention Zofran, decadron, midazolam
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23 yo, 84 kg F for breast biopsy In the OR What type of anesthetic used? Type of airway? If not general, what can be used? Type of airway How do you decide which to use
Type of anesthetic: GETA Airway = ETT Alternative anesthetic: local w/ sedation Airway = LMA How to decide: d/w pt; consider pt comfort
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A 23 yo 84 kg F undergoing breast biopsy is having GETA What drugs w/ doses, in order are given What inhalation could be given
PREOP = midaz 2 mg 1. Fentanyl 150 mcg 2. Lido 90 mg 3. Propofol 170 mg 4. Roccuronium 130 mg Volatile Sevo or Des (no iso)
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A 23 yo 84 kg F undergoing breast biopsy Surgeon plans to inject a dye to track the lymph node distribution and asks for premedication to decrease likelihood of histamine reaction.. What 2 classes, specific drug for each class and dose
class: 1. antihistamine 2. H2 blocker Drug/Dose 1. Diphenhydramine 25-50 mg IV 2. Famotidine 20 mg
187
A 23 yo 84 kg F having breast biopsy under GETA Surgeon is done w/ case, what are the things you must do to awaken the pt and move to the PACU...
1. turn off gas 2. Reverse NMBD 3. Turn off vent to assess spont resp 4. Pull LMA deep 5. Give pain meds 6. PONV prevention
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54 yo, 136 kg F undergoing lap-chole -No PMH, no home meds, PCN all, postmenopausal -IV in place, consents signed, Midaz 2 mg given and taken to OR -Induced and intubated Vt 650, RR 10, FiO2 40%, Vol control Surgeon requests ancef 2 GMs Is an abx required for this case? Can the pt receive cefazolin? Is 2 GMs appropriate dose?
Abx required? NO Can pt receive? Assess rxn history Can receive if NOT anaphylaxis 2 Gms ok? It is since it's not SCIP?? Weight based? Surgeon ordered? I don't like that question....
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54 yo, 136 kg F undergoing lap-chole -No PMH, no home meds, PCN all, postmenopausal Vt 650, RR 10, FiO2 40%, Vol control What position do you place the pt in? Following positioning and insufflation, HIGH PIP alarms What are likely causes?
Positioning: Left-tilt Revere TBurg ``` Causes of PIP: VENT SETTINGS -she's on VC Poor compliance d/t obesity and Insufflation POSITION (ETT migration) ```
190
54 yo, 136 kg F undergoing lap-chole -GETA, Vt 650, RR 10, FiO2 40%, Vol control You notice that PIP is 63 cmH2O, Vt 220, SpO2 84% VC vs PC - Why could this be the problem - What should be changed Abutment of carina and ETT - Could this be the problem? - What should be changed?
VC vs PC - Problem b/c HIGH pressures are generated to achieve the volume setting - Change to a pressure setting, just make sure pt is still getting volumes to prevent atelectasis ETT against carina -Not likely? Since pt is reverse TBurg. This would be more likely in TBURG right??
191
54 yo, 136 kg F undergoing lap-chole -GETA, Vt 650, RR 10, FiO2 40%, Changed vent setting from VC to PC As surgery proceeds, the pts HR suddenly drops to 28/min What is the most likely cause of the drop? What are 3 possible interventions?
Cause: Celiac reflex stimulation Interventions 1. Glycopyrolate 2. Dec insufflation 3. Stop
192
16 yo F getting hysteroscopy and DandC s/p incomplete miscairrage. No PMH, in OR induced, #3 LMA placed w/ good seal and pt positioned HOW? What are risks w/ this position? How can risks be prevented?
``` Position = lithotomy Risk = peroneal nerve damage Prevention = PAD stirrups ```
193
16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage. DandC is completed w/ ease and surgeon asks for pitocin - What is pitocin? - What is the dosing? - How fast should pitocin be given?
What is it: Aka oxytocin, vasopression (ADH) INC uterine contractions What dose: 20 unit/liter (can add to IVF w/ >500 ml left) -Can lead to fluid retention Rate of admin: Wide open
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16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage. She has received pitocin w/ the DandC The surgeon proceeds w/ hysteroscopy and asks for I/O from the "scope" What is she looking for? Is there a minimal expectation? What if the expected I/O doesn't exist? What are the causes of unequal I/O?
Looking for: -Irrigation vs output Minimal expectation: -Output is equal to irrigation amount used to inflate uterus What if it is unequal I/O? -There is a significant risk of uterine perf which could mean lead to unequal I/O What are causes -Uterine perf which is a surgical emergency
195
16 yo F getting hysteroscopy and DandC s/p incomplete miscarriage. She received pitocin and had unequal irrigation I/O during hysteroscopy. How would you convert the anesthetic to an emergency open laparotomy?
1. Intubate - --Turn off gas to exchange LMA for ETT 2. Change position, legs down, arms etc 3. Give NMBD, turn gas back on 4. Convert to open 5. Change fluid administration (open abd inc fluid loss) 6. Change vent settings 7. pain meds
196
What are risk factors that increase the likelihood pt will get HAI (8)
- Pt immune status (on chemo, immunosuppressants) - Infxn control practices (hygiene) - Prevalence of population pathogens - Older age (altered immunity) - Longer hospital stay - multiple chronic illnesses - mechanical vent - Critical care stay
197
Methods of HAI transmission
- Direct contact w/ healthcare workers (poor/improper technique) - Contaminated environments (specific body parts) - Extraluminal migration
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Importance of and symptoms on History and physical that may suggest pre-existing infxn
Opportunity to document pre-existing infxn Symptoms - Subjective fever - chills - night-sweats - AMS - Productive cough - SOB - Rebound tenderness - Dysuria - Suprapubic pain - CVA tenderness
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What are VS that may suggest the presence of infxn. Are VS 100% indicative of infxn why/why not.
``` VS: HoTN Tachypnea Low sat tachycardia ``` Infxn indication: Subtle contribution NOT 100% indicative --Could be r/t other factors like hypovolemia, pain etc
200
What is the importance of knowing placement of lines and tubes?
Was it placed in the hospital vs the field? - -field placement more prone to infxn - -consider exchanging outside lines/tubes
201
What lab values may be evidence of infxn?
Labs that show organ dysfunction ``` Lactic acid = INC PTT = INC BUN/Crt = INC WBC = INC (or really low) Glucose = INC/DEC Cultures ```
202
When do SSIs typically occur and how much is spent yearly for recovery and hospitalization What % makeup of nosocomial infections are SSI in surgical pts
Occur w/in 30 days of surgery $$$ $3.5 - 8 billion spent yearly % makeup SSI = 38% of nosocomial infxn in surgical pts
203
What are 3 types of SSI and examples.
Superficial incisional: around the area of the incision Deep incisional: Just beneath the incisional area in muscle and tissue Organ or space: Any area other than skin and muscle. Includes organs or space btwn organs
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What are signs of SSI
``` Redness Delayed healing Fever Pain Warmth Swelling Drainage of pus ```
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What types of bacteria are most commonly associated w/ SSI
Staphylococcus (native to skin) Streptococcus Pseudomonas
206
Name, describe and give example of the 4 different types of SSI wounds.
Clean: -NOT inflamed or contaminated -NOT internal organ involvement (deep stab wound in the thigh) Clean-contaminated: -NO evidence of infection -INVOLVES internal organ (deep abd stab wound that lacerates the diaphragm) Contaminated: -INVOLVES internal organs w/ spillag eof organ contents (Abd stab wound that lacerates intestines) Dirty: -KNOWN infected at time of surgery (maybe gangrenous wound?)
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What are factors that increase SSI risk (6)
- Type of wound - Surgery lasting >2 hrs - Comorbidities - Elderly - Emergency - Abd surgery
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Based on a 2017 SR of 170 studies for SSI, what recommendations were made for treatment
1. parenteral abx (well established, only when indicated) 2. Non-parenteral abx (do not apply abx ointment to incision) 3. Glycemic control (<200 mg/dl) 4. Normothermia 5. Oxygenation (INC FiO2 immediately after extubation) 6. Antiseptic prophylaxis ( 7. Blood transfusion 8. Systemic immunosuppressive therapy
209
What are the 1B parenteral and non-parenteral abx guidelines for prevention of surgical infection
Parenteral abx: 1. administer only when indicated 2. timed so that agent is established in tissue upon incision non-parenteral: 1. no recommendation for abx irrigation 2. Don't apply abx ointment
210
What is the 1A guidelines for glycemic control for prevention of surgical infeciton
Preop control: | -Glucose target <200 mg/dL
211
What is the 1A recommendation for normothermia in prevention of surgical infectoin
Maintain periop normothermia to prevent bacteria flourishing (hot) and slow metabolism of anesthetic (cold)
212
What are the 1A recommendations for FiO2 level intraop for surgical infection prevention
INC FiO2 - pts w/ normal pulm fxn - GETA intraop - immediately AFTER extubation
213
What are the level 1A, 1B and II antiseptic recommendations to prevent surgical infection
1A) intraop skin prep w/ alcohol-based antiseptic (must be 100% dry) 1B) Bathe w/ soap or antiseptic night before Sx II) consider intraop iodine irrigation in deep tissue
214
What are the recommendations for systemic immunosuppressive therapy to prevent surgical infection
Systemic corticosteroids: -uncertain benefit or harm Itra-articular: -uncertain benefit or harm
215
Most important considerations for surgical abx prophylaxis
Right surgery | Right time
216
What is the goal of preoperative abx prophylaxis
- Adequate bactericidal concentration in serum and tissue when incision is made - MIC prior to incision to prevent most common SSI
217
Who is responsible for prophylactic abx and what is administration based on
anesthesia based on evidence of specific abx based on surgical site
218
6 general principles of abx prophylaxis
1. Should be active against ocmmon surgical wound pathogens 2. Proven efficacy in clinical trials 3. Must achieve MIC 4. Shortest course 5. New abx for resistant infections (more $$$) 6. Oldest and cheapest
219
When should surgical abx be initiated? What are the 3 considerations for administration? What are the exceptions?
Initiated: 30 to 60 min before incision considerations: - When is surgery? morning vs afternoon can affect abx timing - Completely infuse prior to tourniquet - may hold abx for cxr but must document Exceptions: - Vanc or fluoroquinolones w/in 2 hrs - hold for drawing cxrs
220
When does redosing of surgical abx occur
- 2 half-lives (long procedures) - W/ excess blood loss - Following bypass
221
Which abx is not redosing not necessary when pt is placed on cardiopulm bypass intraoperatively
vancomycin
222
What are common surgical abx classes
``` beta-lactams vancomycin aminoglycosides fluoroquinolones metronidazoles ```
223
What are the types of beta-lactams and examples
PCN: Pen G, methicillin, amoxicillin Cephalosporins: cefazolin, cefepime, ceoxitin, cetriaxone, cefepime carbapenems: meropenem, ertapenem
224
What is the MOA for PCN beta-lactam abx? How does resistance occur
Inhibit cell wall synthesis so cell can't grow D/t beta-lactamase enzyme -on outer membrane and breaksdown abx
225
What are DOC for PCN and which bacteria are targeted
DOC: Pen G, amoxicillin, methicillin Bacteria: Strep, meningococci, pneumococci
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Potential adverse rxns to pcn
- hypersensitivity - GI upset w/ large doses - vaginal candidiasis
227
Educational information for women who receive PCN
Vaginal candidiasis - Possibility for vaginal yeast overgrowth - use OTC tx if experiencing symptoms
228
What is the MOA of cephalosporins? | What bacteria are the active against?
MOA: -broader, more stable beta-lactam Active against GRAM + cocci staph and strep
229
Which abx might be the best choice if pathogen is unknown
Cephalosporin
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In what cases are cephalosporins the DOC? Can they be used in the presence of PCN allergy? why/why not?
Surgical prophylaxis -primary abx used CAN be used w/ PCN allergy - cross-sensitivity unlikely - DO NOT use if pcn anaphylactic rxn
231
Give examples of generation 1, 2, 3, and 4 cephalosporins
1: cefazolin (ancef) 2: Cefuroxime (ceftin) cefoxitin (mefoxin) cefotetan (cefotan) 3: cefotaxime (claforan) ceftriaxone (rocephin) ceftazidime (fortaz) 4: cefepime (maxipime)
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What is the big difference in the cephalosporin generations
How well they cross the BBB 1st gen do NOT penetrate BBB 4th gen penetrate BBB Also, 4th gen have increased resistant to hydrolysis by beta-lactamase
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What are possible adverse rxns to cephalosporins
Hypersensitivity -rashes, fever, nephritis, anaphylaxis INC likelihood of rxn IF PCN allergy is anaphylaxis
234
What abx should be used if a pt has a true pcn anaphylaxis and cannot receive cephalosporin
vancomycin or clindamycin
235
What is the MOA of carbapenems? Do they cross BBB Which bacteria are they active against?
beta lactam = inhibit cell wall synthesis Most penetrate BBB Active against: P aeruginosa enterobactor
236
Consideratins for use of carbapenems
Expensive $$$ Not used often b/c: -cephalosporins have good broad-spectrum activity Best to use when bacteria is known
237
What are examples of carbapenems
ertapenem | meropenem
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Possible adverse reaction r/t carbapenem administration
``` n/v diarrhea rashes injeciton site rxn (w/ IM) Cross sensitivity w/ PCN <1% ```
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What is the MOA of vancomycin | Types of bacteria it is effective against
Inhibits cell wall synthesis bacteria: Gram +
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Why is vanc not effective against gram - organisms
Vanc is too large to penetrate gram - wall
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Drawbacks to use of vancomycin
Very slow to treat infxn -Must be given for several days to be effective More adverse effects
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In what cases is vanc the DOC
blood-stream infxn endocarditis DOC for: - hearts and valves - infxns caused by MRSA
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Describe adverse rxns associated w/ vancomycin administration
- Phlebitis at injection site - Chills, fever - NEPHROTOXICITY - RED-MAN syndrome
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How are adverse effects of vanc prevented, give specifics
Nephrotoxicity: -Give vanc over 2 hrs red-man syndrome: - Give antihistamine before or during admin - SLOW administration rate
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What is the MOA of aminoglycosides
Inhibition of ribosomal proteins: - Causes mRNA to misread - Bacteria replication is not identical or survivable
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Which abx has significant post-abx effect? | What does this mean?
Aminoglycosides Means: - Long lasting - Works for significantly longer than other abx
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Which abx should be given 2 hrs before incision
Vanc Fluroquinolones aminoglycosides
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Example and use of aminoglycoside abx
Example: gentamycin Use: - Against enterococcal endocarditis - infected valves pre-op
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Describe the adverse reactions associated w/ aminoglycoside administration and how to prevent them
Ototoxicity: give slowly to prevent Nephrotoxicity: -give slowly Curare-like effect
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When is nephrotoxicity more likely to occur w/ aminoglycoside administration
- In elderly - When using for >5 days - In renal insufficiency - w/ higher doses - Concurrent loop diuretic use
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Describe curare-like effects of gentamycin
- Potentiates NMBDs | - Can make reversal longer
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What is the moa of fluorquinolones What organisms are they useful against
inhibits DNA protein synthesis Useful against: GRAM -
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What are general and surgical uses of fluorquinolones
General: UTI, bacterial diarrhea, bone or joint infections Surgical use: Prostate sx, uro cases, kidney stones, KUB sx
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Examples of fluorquinolones
Ciprofloxacin (cipro) | Levofloxacin (levaquin)
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Describe adverse reactions associated w/ fluoroquinolone use
- n/v/d - prolong QT - cartilage damage/tendon rupture
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When is cartilage damage or tendon rupture more likely to occur in relation to fluoroquinolone use
Usually occurs w/ the achilles tendon - Renal insufficiency - concurrent steroid use - advanced age - teenagers
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Metronidazole MOA and uses
MOA: Forms toxic byproducts that causes unstable DNA molecules Antiprotozoal anaerobic antibacterial USE: Intra-abd infxn (intestinal spill) vaginitis c-diff
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Adverse reactions associated w/ metronidazole administration
Nausea peripheral neuropathy Disulfiram-like effect
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Describe symptoms associated w/ disulfiram-like reaction? When can this happen
Symptoms: hangover-like flushing, dizziness, HA, chest/abd pain Happens with metronidazole taken w/ alcohol
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How does a surgical infection impact the length of hospital stay and $$
Increase hospital stay 7 days Increase cost $3,000
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How doe surgical complications last 30 days affect survival and mortality rates
DECREASES median survival to 69% | INCREASES mortality rate
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What is the difference between SCIP and SIP
SIP = surgical infection prevention -focus is on preventing surgical infection SCIP = surgical care improvement project -focus is on improving ALL outcomes from surgery
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What was the goal of SIP when it was initiated in 2002 by CMS
DEC morbidity and mortaility of SSI
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What were the 3 performance measures used to address SIP Why were these measures chosen?
1. Proportion of pts who get abx started w/in 1 hour of incision (GIVEN ON TIME) 2. Proportion given abx regimen consistent w/ guidelines (CORRECT ABX) 3. proportion of pts whose abx is d/c'd w/in 24 hrs of surgery stop (STOP TIME) Chosen b/c: - Timing and selection of abx have positive correlation w/ SSI incidence - Excessive use of abx promotes bacterial resistance
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As of 2004, which SIP measure has been most consistently followed? Which measure has the greatest fallout?
Most consistently = Correct agent (92.2%) Greatest fallout = D/C 24 hrs after surgery (52.9%)
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What was the goal of SCIP and what year did it begin
Goal: reduce surgical complications by 25% by 2010 Started: 2005
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Who was involved in initiated the SCIP measures and who participated on the steering committee
Initiated by: CMS CDC ``` Steering committee AHRQ ACS AHA ASA APeriopRN CDC CMS VA IHI JC ```
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What measures are addressed with SCIP (7)
``` Abx BB Hair Foley Sugars DVT Temp ```
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Describe the abx measure of SCIP
- Give w/in 1 hr of incision to achieve MIC - Chose correct abx for procedure - D/C abx w/in 24 hrs of surgery completion
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Describe BB measure of SCIP. What are the exceptions
For all pts on BB therapy - must have any dose of any BB w/in 24 hrs prior to surgery DOCUMENTED - RESTART BB post-op Exception: HoTN, Bradycardia--documented
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Describe hair measures under SCIP
Hair removal must be documented - NO razors or shaving - USE clippers Pt may perform hair removal
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Describe the foley measures of SCIP
REMOVAL of GU cath on or before POD 2 | -order must exist to extend cath use
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What are indications for GU cath placement in surgery
- Surgery >2 hrs - hemodynamically unstable - fair indicators of renal perfusion
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Describe glucose control measures of SCIP
-Cardiac pts =200 some evidence indicates -=180 mg/dL w/in 18-24 hrs s/p anesthesia
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Describe DVT measures of SCIP
- SCDs MUST be placed PRIOR to induction** - Appropriate DVT prophy on admit orders (mechanical and pharma) - RN to give DVT prophy w/in 24 hrs of surgery end
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Describe temp measures of SCIP
- Maintain normothermia or ACTIVE warming in OR (w/ any measure) - 1st PACU temp >/96.8*F, 36*C 15 min after leaving OR
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Why is pt normothermia important to the anesthetist
B/c anesthetic metabolism depends on normothermia | -hypothermia = slower metabolism
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What was important outcome of the 2010 reetrospective study of 398 hospitals using SCIP....
All or none composite preventions SS | -More than not, SCIP is beneficial in decreasing post-op M/M than NONE of them
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How does ERAS differ from SCIP
ERAS has a broader scope than SCIP - doesn't focus on periop outcomes - considers PRE-admission, perioperative and discharge outcomes
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what is the purpose of ERAS
- Focus on pt needs through out surgical care - To DEC complications - Help pt feel better - Help pt heal and tolerate sx better
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When were first ERAS EBP protocols published and for which surgical population
2005 For pts undergoing colon surgery
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Who helped establish ERAS and when | Why did they do this
2001 Ken Fearon and Olle Ljungvist Compare their actual practice to what was considered "best" practice
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What was the evolution of ERAS dissemination internationally
``` 2003 = 1st ERAS symposium in Stockholm, SWEDEN 2012 = 2nd symposia in SWITZERLAND 2012 = 1st world congress in FRANCE 2016 = 1st US even ```
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What is the intended outcome of ERAS
- DEC LOS - DEC morbiditiy - DEC overall cost
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What makes for successful ERAS protocol institution
Protocols tailored to the facility | Buy-in and adoption from all areas
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What are some pre-hospital components included in an ERAS protocol
- Pt receive preop counseling - --ERAS guidelines - --pt expectations - --IS demo - --NPO guidelines - -- Postop prescription education Fill prescriptions Optimization for risks - Identify needs - Deep breathing education - Smoking cessation
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What are some pre-op components of an ERAS protocol
- Pt weight - NPO status adheres to ASA guideline - Glucose control - Skin clean (bathe) - Normothermia - IVF (minimal) - Multimodal pain mgmt - colorectal/procedure specific -meds - PONV prophy
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What are risk factors for PONV based on the Apfel tool
Female gender Nonsmoker H/o PONV or motion-sickness Use of opioids
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What are the PONV % incidence w/ 0-4 risk factors
``` 0 = 9% 1 = 20% 2 = 39% 3 = 60% 4 = 78% ```
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Apfel tool recommendations for prophylaxis strategies based on risk factors 0, 1, 2, 3, 4
0 = none 1: 4 mg dex +/-2nd antiemetic 2: avoid inhalation agent 4 mg dex +/-2nd antiemetic 3: avoid inhalation +4 mg dex +2nd prophylactic (scop) ``` 4: avoid inhalation +4mg dex +NK-1 antagonist +/-2nd prophylactic ```
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What are some intra-op components of ERAS
``` ANALGESIA maintenance phase: -short acting -minimize opioids -BB for DL -ketamine, Mg, precedex, prop ``` Emergence phase: -toradol, decadron, ofirmev, RA Regional: GA + epidural/spinal/intrathecal opioids/ESP/TAP...
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What are some post-op components of ERAS
- IVF therapy - --GDFT - --Avoid overload - --PO instead of IV - PONV prevention - Early GU cath removal - Early PO nutrition - Non-opiod analgesia
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What are some post-DC components of ERAS
- Reinforce realistic pain expectations and goals - Tool for breakthrough opioid use - Schedule non-opioids and NON-scheduled opioids

Ane Principles II (3 decks)

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