Droperidol- low dose 0.625-1.25 mg central dopamine 2 antagonist very effective antie-emetic- black box for prolonged QT (\>2.5 mg dose or higher) Dexamethasone 4-8 mg steroids- analgesia and antiemetic benefits. last much longer. don't know why it's effective give at beginning of case 5-HT antagonists- ondansetron 2-4 mg, dolasetron 12.5 mg promethazine/phenergan 6.25-12 mg ( phenothiazine) can have sig impact on anesthetic requirements and can cause delayed awakening, extrapyramidal effects metoclopramide 10-20 mg D2 and 5-HT antagonist antihistamine act on central vomiting center/vestibular pathways to prevent PONV Helpful in motion induced emesis and pt undergoing middle ear sx neurokinin-1 (NK1) antagonist (aprepitant) propofol use propofol/midazolam have been shown to have antiemetic properties that outlast their sedative effects scopolamine patch (anticholinergic) 1 mg over 3days effective 2-4 hours after application hydration seaband &relief band accustimulation at P6 acupoint can be more effective than antiemetics

Ambulatory & Laparoscopic Sx Flashcards by Amy Woody

What factors into patient selection criteria and selection of procedures?

degree of physiologic disturbance
1. surgical procedure
  - how invasive is the procedure?
  - need minimal postop complications
  - no major fluid shifts
2. physiologic response
  - no major blood loss, no need for complex postop care
  - consider the potential for blood loss, pain, PONV
3. pain management (regional is a good option)
  - procedures requiring prolonged immobilization and IV opioid therapy are more suitable to 23-hour stay
huge financial incentive to promote same-day surgery (SDS) over hospital stays since insurance companies pay flat rate for SDS qualifying procedures regardless of LOS
SDS has expanded due to:
- improved surgical techniques
- better pain control methods
- shorter acting anesthestics
- questioning of conventional assumptions that patients are psychologically and physiologically better off in the hospital (studies show this is not the case)

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Patient characteristics for ambulatory surgery?

Important to determine if pre-existing condition is likely to cause postoperative complications vs perioperative complications
- ASA III and IV now considered OK if medically stable
Extremes of age
- <6 months and >85 yo
  - adv age is not a contraindication to SDS.
    - 2x risk for CV events introp but less pain, PONV, dizziness and lower rates of unaticipated admission
    - study suggest cognitive function better at home
  - must have strong social support
Co-existing dx
- stable physiologic dx- no dx “label” is contraindicated, consider stability of dx
- obesity not contraindication.
  - again, have difficulty managing case intraop, but postop complications may be better
- sometimes better to keep pt with chronic conditions on own routine and d/c to home

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Factors to consider preoperatively to determine if pt is appropriate for amb sx?

Sleep apnea status
- mild, mod, or severe
- what’s the sleep study say?
Anatomical and physio abnormalities
- where are they working? upper abd/chest more risk than LE, etc
Status of coexisting dx
nature of sx
type of anesthesia
- local/regional less risky than GA
Need for postop opioids
pt age
adequacy of postop observation
- responsible adult to go home with pt?
capabilities of the outpatient facility

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What factors increase risk for postop admission after SDS?

>65 years
OR time >120 min
CV dx (CAD, PVD, etc)
Malignancy
1. enhances pt risk for bleeding
  - ex- place LMA in pt receiving radiation, blood everywhere
HIV
1. meds patient take to manage HIV can predispose patient to complications
Regional and general anesthesia

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What are some relative contraindications to outpatient surgery?

Uncontrolled systemic dx
- DM, unstable angina, severe asthma, pickwickian (OHS), pain
- no disease label itself is a c/i, have to consider the individual situation
Central acting therapies
- MOAI’s and cocaine (routine heavy user of cocaine)
  - MAOIs such as parglyine and tranylcypromine
  - cocaine has an association with increased risk of intraoperative CV complications including death
- diet aids like ephedra and alcoholism also increase risk
Morbid obesity + symptomatic CV or pulm disease
lack of support at home postop
1. cannot drive themselves home
2. live close enough to return to hospital in reasonable amount of time
3. in US expect 24 hours escort, but some countries allow D/C without escort and not seeing an increase in adverse effects as a result
  1. most people don’t have a person stay with them 24 hours

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Neonate/infant outpatient surgery guidelines?

< 46 weeks post conceptual age infants born full term (>37 weeks)= 12 hours monitoring
<60 weeks post conceptual age infants born premature (<37 weeks)= 12 hours monitoring
still remains controversial but most agree 60 weeks PGA as the cutoff
caffeine has bene shown to decrease risk for postop apnea in premier babies

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Preoperative assessment standards?

Same as inpatient

Identify absolute contraindications to ambulatory surgery
identify need for optimization
highlight issues for anesthesiologist or other staff
provide patient information
- telephone interview/computerized triage and questionnaire are valuable alternatives and can be just as accurate as physician interview (if not more)*
- routine blood tests not predictive of complications and ECG abnormalities may not have much addtl significance to a thorough pt history*
- preop testing had no influence on 30 day unanticipated admission rates*

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Risk factors for PONv?

Additive risk factors:
- choice of anesthetic technique (premed, opioid use, inhaled agent use, acetylcholinesterase use, hydration status, hypotnetion
- type of sx (length of procedure, operative procedure, pain mgmt, gastric distention)
  - lap, lithotripsy, major breast sx, ENT associated with high PONV
- patient factors (hx of PONV and motion sickness, anxiety, non-smoker, within week menstrual cycle, age, genetic predisposition)

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Prevention of PONV?

Droperidol- low dose 0.625-1.25 mg
- central dopamine 2 antagonist
- very effective antie-emetic- black box for prolonged QT (>2.5 mg dose or higher)
Dexamethasone 4-8 mg
- steroids- analgesia and antiemetic benefits. last much longer. don’t know why it’s effective
- give at beginning of case
5-HT antagonists- ondansetron 2-4 mg, dolasetron 12.5 mg
promethazine/phenergan 6.25-12 mg (phenothiazine)
- can have sig impact on anesthetic requirements and can cause delayed awakening, extrapyramidal effects
metoclopramide 10-20 mg
- D2 and 5-HT antagonist
antihistamine
- act on central vomiting center/vestibular pathways to prevent PONV
- Helpful in motion induced emesis and pt undergoing middle ear sx
neurokinin-1 (NK1) antagonist (aprepitant)
propofol use
- propofol/midazolam have been shown to have antiemetic properties that outlast their sedative effects
scopolamine patch (anticholinergic)
- 1 mg over 3days
- effective 2-4 hours after application
hydration
seaband &relief band
- accustimulation at P6 acupoint
  - can be more effective than antiemetics

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Relative contraindications to laparoscopy

Inc. ICP- head is down, increased abd pressure causing increased ICP
- Hydrocephalus, brain tumor, head trauma
Hypovolemia
- Pneumoperitoneum effect on preload
V/P Shunt or peritoneojugular shunt
- (OK if have unidirectional valve resistant to IAP)
Severe CV disease
Severe Respiratory disease

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Max IAP during lap sx?

COnsiderations?

Intraabdominal pressure < 15mmHg or 20 cmH₂0
- Minimize CV and respiratory impacts
  - Vagal innervation of peritoneum: increase pressure = increase vagal resp (dec HR, bradydysrhythmias)
Considerations:
- Expected progressive rise of PaCO₂15-30 min after initial insufflation → then plateau reached (absorption into lymph and venous system)
  - If continues to increase an hour or so after case → search for pathologic cause (embolism, emphysema, MH, etc.)

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What causes the increase of PaCO2 with lap sx?

Absorption of CO2 from the peritoneal cavity – primary
1. R/t vascularity and surface area (pelvic cavity* vs peritoneum)
Abdominal distention
1. VQ mismatch, FRC ↓, decreased pulmonary compliance
Patient position
1. VQ mismatch- Trendelenburg/reverse, PPV
Volume-controlled mechanical ventilation – VQ mismatch
Depression of ventilation by anesthetic agents if spontaneous breathing
CO₂ emphysema (SQ or body cavities)
1. See CO2 increase → CO2 goes into SubQ tissue planes and accumulate
  1. Prolonged ETCO2 elevation, PaCO2, and acidosis into postop period
Capnothorax- escapes into and around lungs
CO₂ embolism- trocars into vessels
Selective bronchial intubation- from extreme trendelenber

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Hemodynamic changes with pneumoperitoneum

Decreased myocardial contractility (CO impact depends on CO₂ insufflation, position)
- High CO2 and insufflation → decreases contractility
  - Depends on hydration status, position, and underlying conditions
Decreased VR
- Mechanical compression of IVC
Decreased LVEDV
- d/t dec venous return
Increased intrathoracic pressure
- leading to compliance issues
Pulmonary vasoconstriction
- Result of VQ mismatch
  - As CO2 incre lungs → promotes vasoconstriction (why hypoxia)
  - CO2 incre → vasodilation in brain
Increased right atrial and PA occlusion pressures
Minimal increase HR
- SNS stimulation and RAAS
Increased aBP, SVR
- SNS stimulation and RAAS
- increased SNS tone- catecholamines, renin-angio, vasopressin, arterial compression by high IAP) may increase myocardial wall tension and O2 demand
- not only vagal response, but also SNS or ANS response d/t highly innervated areas
  - someone with CAD → increase risk to MI
Increase risk for arrhythmias

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Hemodynamic consequences of pneumoperitorneum? How to tx?

Drop in CO from →
- Dec VR (txmt: fluid loading before pneumoperitoneum placed)
- Catecholamine/humoral release (txmt: use BB, alpa 2 agonist → reduce SNS tone to reduce responses)

Think: can they tolerate dec VR, increase afterload → if not, may need open

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Induction considerations for lap sx

GA w/ cuffed ETT & controlled ventilation (gold standard)
- increased minute ventilation (20-30%)
- increased PIP often required (but not too much bc VR)
  - Volume control → pressure control to get PIP to good level
- Adjust RR, Vt (6-8ml/kg), PEEP (5-10cmH20) & PIP
  - Goals:
    - ETCO2 = 35mmHg
    - PIP low 30’s cmH20
    - Intra-abdominal pressure limit < 15 mmHg – to best avoid CV compromise
- aspiration risk- need cuff
RA has been used – risky
- need high block T4-5 (SNS denervation- loss of cardiac accelerator fibers) more difficult to compensate for CV, ventilatory changes, shoulder & distention pain incompletely alleviated
ASA III-IV and/or abnormal gradient PaCO2:ETCO2 invasive monitors
- Blood gas and BP measurements

In a study by Exter et al CO was decreased to a maximum of 28% at a IAP of 15mmHg whereas CO was maintained at a insufflation pressure of 7mmHg. B1063

Barash 8^th – nice discussion of ventilation issues.

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What to do if converted to open procedure?

Supine position
New fluid plan
- 3^rd space losses will increase
New pain management plan
- opioid requirements will change
New ventilator settings – may need to reduce rate and increase Vt
- No exogenous source of CO2

Maintenance phase surgical complications for lap sx?

Falls or position shifts resulting in injury
Vascular injury
- (trocar insertion/veress needle – aorta, ICV, iliac vessels, cystic/hepatic arteries, retroperitoneal hematoma)
GI
- (trocar insertion/veress needle- bowel, liver, spleen, mesenteric)
Cardiac
- (dysrhythmias- hypercarbia, increased vagal tone with peritoneal traction, BP changes)
  - increased vagal tone d/t stretch peritoneum may result in bradyarrhtyhmias/asystole
    - txmt- stop insufflation, treat w/ atropine, increase anesthetic depth after HR corrected
SQ emphysema – extra-peritoneal insufflation
- accidental
- Most common → inguinal hernia repair (result in acidosis into postop period)
Capnothorax, capnomediastinum, capnopericardium
- diaphragm defect, pleural tear, bullae rupture, COPD pts– high degree of suspicion can be lifesaving
CO2 embolism
- direct needle placement in vessel, gas insufflation into abdominal organ → DANGEROUS
PTX
- occurs most commonly when working near diaphragm
- S/S- increased airway pressure, hypoxemia, hypercapnia, surgical emphysema, CV compromise
- If caused by CO2 without pulmonary trauma- it will resolve in 30-60 min with increased PEEP
  - iF PTX result of bullae rupture- then need thoracocentesis and avoid PEEP

Gas Embolism pathophys?

Depends on size of bubbles and rate of entrainment
Vapor lock in vena cava and RA → dec flow to pulm circulation and body
Obstruction to venous return
Acute RV hypertension = paradoxical embolism to cerebral and coronary vasculature
Circulatory collapse
Small bubbles over time results in pulmonary entrapement.
Large bubbles under high pressure causes gas lock in vena cave and right atrium.
V/Q mismatch develops, Increased dead space and hypoxemia,
Acute RV HTN, may occur causing paradoxical embolism to the cerebral and coronary vasculature

Subcutaneous emphysema pathophys? S./S? Txmt?

Procedures at high risk sq emphysema?

Pathophys
- accidental insufflation of extraperitoneum
  - unavoidable complication of lap inquinal hernia repair, renal sx, pelvic lympadenoectomy
- not a contraindication for extubation- even if cervical emphysema is present
  - can also track into thorax and mediatinum- creating a capnothorax or capnomediastinum
S/S
- beware of increasing ECO2 after plateau has been reached
- Postop
  - increase HR, BP
  - Somnolence
  - respiratory acidosis
TXMT
- if continue to see rise and unable to compensate with increase in MV, then you need to assess for extent of SQ emphysema, ask for desufflation, increase MV then insufflate at lower pressure
High risk
- procedure >200 minutes
- >6 or more ports utilized

Gas embolism dx tools?

S/S?

In the ideal world….
- Trans-esophageal echo (TEE)
- Swan-Ganz Catheter
- Precordial Dopplers– not standardly used
In the real world……
- ETCO2 decrease- early**
- Pulse oximetry (hypoxemia)- later sign
- Esophageal stethoscope- millwheel sound (change in heart tone)
- Aspiration of gas from CVP
- Hypotension
S/S
- tachycardia
- arrhthmias
- hypotension
- increased CVP
- Millwheelmurmur
- cyanosis
- sudden drop in ETCO2 waveofrm

Gas embolism treatmnet

Stop insufflation and desufflate
Positioning
- Steep Trendelenberg
- left lateral decubitus
D/C N20 and give 100% FiO2
Hyperventilate
Place CVP – try to aspirate
CPR- breaks up large bubbles
Consider CPBypass
volume preload decreases risk of gas embolism

Postop consideration for lap procedures?

Procedures are associated with intra-abdominal, incisional, and shoulder pain (irritation of diaphragm and/or visceral pain from biliary spasm)
Opioids + NSAIDS + acetaminophen + dexamethasone + local anesthetic infiltration (incisional and intraperitoneal)
TAPS block (transversus abdominus place – place local between the internal oblique and transversus abdominus muscles can be useful in larger surgeries – not clear if helpful in more straightforward laparoscopic procedures – Intraperitoneal is controversial – appears highly effective but the dose and duration of infusion has not been reliably determined. At this point not recommended but no toxicity has been reported Barash 7^th.
Post operative Nausea and Vomiting
- 40-75% of patients after laparoscopic procedures
  - young women and lap chole at increased risk
- Propofol utilization
- Gastric decompression
- Anti-emetic prophylaxis
- Opioid use increases incidence
- Limit opioids and administer ondansetron, dexamethasone for best results (beginning of case)

Metoclopramide

CLASS= central dopamine receptor antagonist & serotonin-4 receptor agonist

MOA= blocks the DA2 receptors centrally in the CRTZ of the medulla preventing N/V; stimulates serotonin-4 receptors causing increase gastric motility & peristalsis; this is also accomplished by increase ACh @ the muscarinic post-synaptic receptors; increase LES tone & relaxation of pylorus & duodenum

Pharmacokinetics= 30-40% PB;; Vd 2-4L/kg; onset- 1-3 min; DOA- 1-2 hrs; E1/2- 2-4 hrs; metabolized in the liver & 40% excreted unchanged in the urine

SE= increase gastric motility, LES tone; decrease N/V; extrapyramidal SE, abdominal cramping (w/ rapid administration), sedation, prolactin secretion, dry mouth

DDI’s= potentiates sedation of CNS depressants; inhibits plasma cholinesterases thus may prolong Succinylcholine & Mivacurium , MAOIS, TCA, pt with EPS

CI= Parkinson’s, bowel obstruction, GI hemorrhage, seizure disorders, arrhythmias with Zofran; do not give with phenothiazines (like phenergan), MAOI, TCA, pt c EPS; pheochromocytoma

Dose= 10-20 mg IV over 3-5 min 15 min before induction

Ondansetron

CLASS= serotonin-3 receptor antagonist

MOA= blocks serotonin receptors peripherally on vagal nerve terminals in GI tract & centrally in the CRTZ

Pharmacokinetics= 70% PB; Vd 2-2.5 L/kg; onset- 30 min; DOA- 4-8 hrs; E1/2- 3-4 hrs; metabolized in the liver with renal excretion (5% unchanged)

SE= HA with rapid administration, fatigue, arrhythmias (w/ Reglan- prolonged q1), constipation, diarrhea

CI= hypersensitivity, liver disease (decrease dose), SSRIs, Generally not recommended for treatment of existing chemotherapy-induced emesis or
for prophylaxis of nausea from agents with little potential to cause nausea

Dose= 4-8mg IV over 2-5 min

Famotidine

**_CLASS_****=** selective competitive H2 receptor antagonist (MOST potent) **_MOA:_** Competitively bind to H2 receptors, inhibiting the binding of histamine to gastric parietal cells, **decrease** cAMP & secretion of H+ ions, **decrease** gastric acid secretion from the parietal cells; can prevent Mendelsson syndrome or to treat GERD or ulcers; crosses BBB **_Pharmacokinetics_**= 20% PB; onset- 30 min; DOA- 8 hrs; E1/2- 3 hrs; liver metabolism with **75%** excreted unchanged in the kidneys; must be given IV d/t extensive first pass effect **_SE_**= dMultisystem disease and advanced age increase severity of side effects. Diarrhea, HA, fatigue, skeletal muscle pain, confusion (crosses BBB), arrhythmias; **rapid IV administration may cause bradycardia & hypotension (Give over 2 minutes for famotidine)** **_CI_**= caution liver/renal disease, hypersensitivity; may alter absorption of some drugs by increasing gastric pH **_Dose_**= 20 mg IV over 2 min

Dexamethasone

**_CLASS=_** corticosteroid with **ONLY** glucocorticoid properties **_MOA_**= enters the cell & binds to glucocorticoid & receptors in the cytoplasm forming a steroid-receptor complex that enters the nucleus & affects DNA transcription; _Metabolically_ causes an **increase** nutrient availability by **increase** BG, amino acids, & Triglycerides; _inhibits the inflammatory process_ by inhibiting phospholipase A2 = **decrease** arachnidonic acid = **decrease** inflammatory mediators such as leukotrienes, cytokines, & prostaglandins ALSO- inhibits COX & Lipoxygenase pathways- may lead to analgesia effects; antiemetic property MOA unknown (poss. **decrease** prostaglandin, **increase** endorphins & appetite) Good: Antiemetic, analgesia, periop airway edema, cerebral edema **_Pharmacokinetics_**=DOA= 72hrs; E1/2- 3 hrs; liver metabolism with 30% excreted unchanged in the urine; antiemetic effect may last 24 hrs **_SE_**= **perineal burning**, **increase** BG, HTN, HYPOK+; immunosuppression, HPA axis suppression, delayed wound healing, fat redistribution, muscle & bone wasting **_CI_**= caution in DM, untreated infection, hypersensitivity **_Dose_**= 4-10 mg IV

Phenergan

**_CLASS_****=** phenothiazine; H1 & Dopamine 2 antagonist **_MOA_**= blocks DA receptors in CRTZ preventing N/V & antagonizes H1 @ receptors= decrease histamine mediated response in respiratory tract, GI & blood vessels **_Pharmacokinetics_**= 90% PB; onset- 3-5 min; DOA- 2-4 hrs; E1/2- 9-16 hrs; metabolized in the liver including CYP450 & excreted in the urine **_SE_**= extrapyramidal effects, anticholinergic effects, sedation, arrhythmias (prolonged QT), **neuroleptic malignant syndrome** **_CI_**= hypersensitivity**, peds \< 2 yrs old, Parkinson’s**; caution in renal, hepatic, cardiac, pulmonary disease; caution will potentiate sedative effects of anesthetics **_Dose_**= 6.25-25 mg IV

Droperidol

**_CLASS_****=** butyrophenone; DA antagonist **_MOA_**= blocks DA at its receptor on the CRTZ of the medulla preventing N/V **_Pharmacokinetics_**= Highly PB; onset- 30 min; DOA- 12 hrs; E1/2- 2 hrs; metabolized in the liver with 5% renal excretion **_SE_**= extrapyramidal effects; **black box- torsades, prolonged QTI**; **decrease** BP, sedation, akathesia, **_CI_**= hypersensitivity, **Parkinson’s, history of prolonged QT interval,** do NOT give with reglan; caution will potentiate sedative effects of anesthetics **_Dose_**= 0.625-2.5 mg IV

Diphenhydramine?

**_CLASS_****=** 1^st generation histamine 1 antagonist; activates muscarinic, serotonin & alpha receptors **_MOA_**= antagonist at the H1 receptor thereby preventing the response mediated by histamine in the respiratory tract, GI tract & blood vessels; prevents bronchoconstriction, vasodilation, edema, itching, & sneezing; used for allergies, hypersensitivity reactions, anti-nausea, sleep, motion sickness **_Pharmacokinetics_**= 78% PB (highly); onset- 30 min; peak- 2-3 hrs; DOA- 4-6 hrs; E1/2- 2-8 hrs; metabolism in liver via CYP450, pulmonary & renal excretion **_SE_**= sedation (crosses BBB), dizziness, seizures, hypotension, tachycardia, dry mouth/nose; urinary retention **_CI (caution)_****=** acute asthma, hyperthyroidism, CV disease, increase IOP, glaucoma, neonates **_Dose_**= 10-50 mg IV