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NURA 620 Anesthesia and Coexisting Conditions > GI/Liver > Flashcards

GI/Liver Flashcards

1
Q

EGD: purpose

A

diagnostic and/or therapeutic

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2
Q

EGD: common positioning

A

left lateral decubitus most common

difficult anatomy may have more supine positioning

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3
Q

EGD: sedation and airway considerations

A

With OR without sedation/anesthesia

SHARE THE AIRWAY!

  • -natural airway - avoid apnea, jaw lift, O2 nasal cannula
  • -GA with ETT - may choose to use for any reason, but specifically if procedure is going to be more stimulating like dilation or dilation with stent placement
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4
Q

EGD: when do you place the bite block?

A

If natural airway - bite blocked placed before induction

If GA - after ETT placement

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5
Q

EGD: most common complications to consider.

A
  • cardiopulmonary complications most common
  • desat
  • laryngospasm
  • airway obsturction
  • aspiration
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6
Q

EGD: considerations in deciding airway management plan

A

must know procedure and patient co - morbidities!!

  • -technically challenging or unusually stimulating (dilation or dilation with stent placement, etc. )
  • -full stomach
  • -high risk aspiration
  • -difficult airway

All of these scenarios should be managed with GA

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7
Q

Achalasia: what is It?

A

neuromuscular disorder of the esophagus
-unopposed cholinergic stimulation of LES – failed relaxation – HTN of LES –reduced peristalsis – esophageal dilation – food stasis in the esophagus

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8
Q

Achalasia: s/s

A

dysphagia
heartburn
regurgitation
chest pain

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9
Q

Achalasia: TX

A

PALLIATIVE

  • botulinum injection
  • dilation
  • per oral endoscopic myotomy (POEM)
  • -endoscopically dividing the circular muscle layer of LES
  • -requires CO2 insufflation of esophagus – requires mechanical ventilation!!
  • -high pain and n/v!
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10
Q

Achalasia: Anesthesia considerations and plan

A

CO2 insufflation – “tight” control of mechanical vent so ETT is required

aspiration risk - RSI – fully awake extubation

decompress esophagus prior

Aggressive n/v plan and should include adequate hydration/IV fluids

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11
Q

Zenker’s diverticulum: what is It?

A

pharyngoesophageal outpouching

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12
Q

Zenker’s diverticulum: anesthesia considerations

A
  • RSI because of asp risk
  • avoid cricoid pressure if sac is immediately behind cricoid cartilage
  • GA induced with head - up position
  • Avoid NG/OG tube - can go into pouch and rupture!
  • depending on location of pouch - pt may be able to press on back of neck and empty pouch – may want to consider prior to induction
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13
Q

Hiatal hernia: anesthesia consdierations

A

may be asymptomatic

+/- RSI with cricoid, ETT – awake extubation
–may not need RSI depending on size of hiatal hernia (not ALWAYS required)

OG to decompress after ETT insertion

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14
Q

GERD: preoperative pharmacological TX

A
  • cimetidine, ranitidine, famotidine
  • PPIs
  • sodium citrate
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15
Q

GERD: aspiration risk + anesthesia considerations

A

aspiration pneumonitis: volume 0.4 - 0.5 ml/kg of gastric contents and pH <2.5

RSI with cricoid – awake extubation (be sure to ask patient about hx and onset of symptoms – do they have to sleep upright with pillows at night because of burning? are they currently experiencing pain/burning?)

succ increases LES pressure and intragastric pressure, but barrier pressure is unchanged

OG/NG

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16
Q

Peptic ulcer disease: what is It? associated complications?

A

burning epigastric pain exacerbated by fasting and improved with eating

complications: bleeding, perforation, obstruction

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17
Q

Peptic ulcer disease: anesthesia considerations

A

pt may be on chronic antacids (electrolyte imbalances)

  • -H2 receptor antagonists – cimetidine and ranitidine inhibit P 450 – monitor warfarin phenytoin, theophylline levels if patient on these!
  • -PPIs - impair P 450

NG/OG placement for active PUD

RSI consideration

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18
Q

Upper GI bleeding: lab considerations

A

elevated BUN - reabsorbed nitrogen in small intestine

Hematocrit <30% - may be normal in early, acute hemorrhage because It takes time for the plasma volume to equilibrate

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19
Q

Upper GI bleeding: hypotension, tachycardia if blood loss is ____% of TBV.

A

> 25%

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20
Q

Upper GI bleeding: anesthesia considerations

A

Be VERY aware of fluid status!! May need 1 - 2 L prior to induction of anesthesia

Esophageal variceal bleeding

  • -avoid NG/OG, temp probe (always confer with gastroenterologist in case you need to suction out stomach because of aspiration risk, will the patient need an NG post op?)
  • -have octreotide available

Aspiration Risk – RSI – fully awake extubation

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21
Q

Lower GI bleeding

A

colonoscopy after bowel prep for evaluation

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22
Q

Ulcerative colitis: s/s, what areas of the bowel are affected?

A

inflammation of colonic mucosa – rectum and distal colon

s/s:
diarrhea
cramping
abdominal pain
wt loss
fever
N/V
anorexia
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23
Q

Crohn’s disease: s/s, what areas of the bowel are affected?

A

inflammation of ALL LAYERS of the bowel, will see more of the bowel affected up to the small intestine

may lead to fistula development

s/s:
fear of eating
anorexia
diarrhea
pain
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24
Q

Inflammatory bowel diseases: anesthesia considerations

A
  • fluid and elec management (from bowel prep, dehydration)
  • avoid N2O (open air spaces, no nitrous for bowel sx)
  • supplemental steroids as required
  • anticholinesterases increase intraluminal pressure
  • consider active n/v?? – RSI!
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25
Q

Colonoscopy: purpose

A

diagnostic and/or therapeutic

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26
Q

colonoscopy: positioning

A

left lateral decubitis

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27
Q

Colonoscopy: sedation and airway considerations

A

-with or without sedation/anesthesia

  • may be combined with EGD
  • -if patient was intubated for upper, they’ll stay intubated for the lower
  • if completed in isolation - generally natural airway
  • –don’t need anesthesia for this, can do nurse sedation
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28
Q

Acute pancreatitis: s/s, labs

A

acute inflammatory disorder

excruciating, unrelenting mid epigastric pain relieved by leaning forward (unrelenting pain decreases gastric motility and warrants RSI)

n/v (if active - be thinking RSI)

abdominal distention and ileus possible

fever, tachycardia, hypotension, and shock possible

increase in serum amylase and lipase concentration

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29
Q

Chronic pancreatitis: common etiology

A

most often due to chronic alcohol abuse

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30
Q

Chronic pancreatitis: s/s, labs

A

epigastric pain radiates to back and shoulder, frequently postprandial

DM due to end result of loss of endocrine function (autodigestion of pancreas)

thin or emaciated (What’s their albumin level? Colloids intra op)

serum amylase levels typically normal

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31
Q

Pancreatitis: anesthesia considerations

A

DM management
–be thinking of how to manage BG intra op: short case – BG right before and right after; long case: may hourly BG during case

aggressive fluid administration even for mild cases

colloid replacement

NG/OG placement (if not already present)

pain control

+/- RSI

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32
Q

What is an ERCP?

A

endoscopic retrograde cholangiopancreatography

used to diagnose and treat conditions of the bile ducts: gallstones, inflammatory strictures, leaks (from trauma and surgery), and cancer

ERCP combines the use of xrays and an endoscope

Duration: 30 min - 2 hrs (highly variable)

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33
Q

ERCP: anesthesia consderations

A

have lead in the room already!

Aspiration concerns - GA with ETT, RSI with awake extubation
–Grass mentions that when a stent is placed and contents are released from GB, they can either go up or down, and if they go up where there is less pressure, patient will aspirate with a NATURAL AIRWAY)

bite block

usually completed in supine position – maybe left lateral decub

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34
Q

ERCP: medications to relax sphincter of Oddi

A

glucagon (0.5 mg, repeat for total of 1 mg)

NTG or naloxone (just consider use of this if using opioids for severe pain – don’t want to antagonize effects obviously)

35
Q

Carcinoid tumors: where do we find them and what kinds of substances do they secrete?

A

originate in the GI tract most of the time (sometimes lung)

secrete corticotropic hormones, GI peptides, prostaglandins and bioactive amines (serotonin)

36
Q

What is carcinoid syndrome? What are the s/s and associated anesthesia considerations?

A

systemic release of serotonin and vasoactive substances

  • flushing and diarrhea - FLUID AND ELEC
  • dehydration and electrolyte disturbances - FLUID AND ELEC
  • hypotension/hypertension - plan appropriately (invasive monitoring)
  • bronchoconstriction
  • occasional R side heart manifestation - ECHO? invasive lines?

Can be precipitated by stress, alcohol, exercise, catecholamines, serotonin reuptake inhibitors - REDUCE STRESS AND CATECHOLAMINE RELEASE

37
Q

What is carcinoid crisis? s/s?

A

massive systemic release of all of those mediators – POTENTIALLY LIFE THREATENING

intense flushing, diarrhea, abdominal pain, tachycardia, hyper/hypotension

38
Q

Carcinoid crisis: TX

A

somatostatin analogue (octreotide)

resection of tumor by sx

39
Q

Carcinoid tumor anesthetic management

A
  • octreotide should be admin 24-48 hrs before sx and continued throughout procedure
  • prevent crisis – premed for stress control (benzo?)
  • avoid drugs that provoke mediator release
  • alternative bronchospasm TX
  • invasive monitors - arterial line
  • -cardiac issues - CVP monitoring or PA cath?
  • ondansetron great choice (serotonin anagonist)
  • potential ICU care post op due to delayed emergence
  • epidural analgesia ok if octreotide treatment has been adequate and you have restored their vascular volume
40
Q

Carcinoid tumor: how do you treat a bronchospasm and why?

A

treat with octreotide and histamine blockers, +/- ipratropium

avoid beta agonists!!! - will exacerbate bronchospasm due to mediator release

41
Q

Carcinoid tumor: drugs to avoid that provoke mediator release.

A
  • –succ (fasciculations can squeeze tumor – causing release of mediators)
  • –mivacurium (histamine)
  • –atracurium (histamine)
  • –tubocurarine (histamine)
  • –epi (SNS)
  • –norepi (SNS)
  • –dopamine (SNS)
  • –isopreterenol (SNS)
  • –thiopental (histamine)
  • –beta agonists (inc mediator release)
  • –histamine releasers
  • –ketamine (SNS surge)
42
Q

Bowel obstruction: anesthesia considerations

A

Avoid agents that INCREASE gastric motility

  • -no metoclopramide
  • -no neostigmine

No N2O - especially if open bowel s

RSI - treat as full stomach

Albumin/Volume replacement/Electrolyte status

Place OGT or NGT (confer with surgeon if pt will need post op)
–may be appropriate to place prior to induction to decompress if needed

43
Q

Who is at more risk for acute cholecystitis?

A 
women
fair skinned
increased age
obesity
rapid weight loss
pregnancy

“fat, fair, forties, female”

44
Q

S/S of GB stones vs bile duct/biliary tract stones.

A

Gallbladder stones - generally asymptomatic

Bile duct/biliary tract stones

  • N/V - FLUID/ELEC STATUS
  • fever
  • abdominal pain
  • RUQ tenderness radiates to back
  • intense pain - RSI?
  • dark urine
  • scleral icterus (yellow sclera)
45
Q

Laparoscopic procedures: Discuss ventilatory implications related to pneumoperitoneum (insufflation of abdominal cavity)

A

Increased intra abdominal pressure!

Potential for INADEQUATE VENTILATION - may start with volume control – will eventually get high pressures – switch to pressure control

46
Q

What is an important consideration with “let down” of the pneumoperitoneum regarding mechanical ventilation?

A

You need to be very aware of WHEN they let down the pneumoperitoneum!!!!
–if you’re on PC and they “let down”, your patient’s TV may increase 500 to 1500 at the same PC setting (because they no longer have so much pressure in their peritoneum)

47
Q

Laparoscopic procedures: Discuss CV and vascular implications related to pneumoperitoneum (insufflation of abdominal cavity)

A

DECREASED VENOUS RETURN – decreased CO, but increased MAP and SVR will restore CO over several minutes
–d/t increased abdominal pressure, neurohormonal response and absorbed CO2

PROFOUND BRADYCARDIA DUE TO PERITONEAL STRETCHING

  • -usually just have to tell the surgeon to “let down” the peritoneum and HR should be restored, have them go slower when they reinsufflate
  • -consider pretreating with atropine or glyco

RISK FOR VASCULAR INJURY AND ACUTE BLOOD LOSS

48
Q

Laparoscopic procedures, RISK FOR CO2 EMBOLISM: cause, s/s, TX

A

accidentally inject CO2 directly into vasculature

  • most likely sign to pick up on: SEVERE SUDDEN DROP IN CO2
  • severe tachycardia
  • arrhythmias, EKG changes
  • hypotension
  • mill wheel murmur

TX: goal is to “keep things moving forward” because we worry about “stoppage” with embolism

  • hemodynamic management: epi, dopamine
  • place pt in left lateral decubitis with head down
  • consider placing CVC and aspirating
  • large volume IV fluids (keep things moving forward)
  • stop VA because already will have severe hypotension
  • 100% fiO2
49
Q

Laparoscopic procedures: considerations for conversion to open

A
  • NMB will already be used, but need may increase
  • INCREASED fluid needs - 3rd spacing with open abdomen - “all of that intestine dries out very quickly”
  • opioid dosing - may need to increase dosing significantly
  • higher degree of blood loss
50
Q

Laparoscopic procedures: overall considerations

A
  • pre induction/induction
  • -consider volume and elec replacement
  • -preop ABX
  • -RSI with cricoid pressure/cuffed ETT
  • watch PIP/MV and adjust accordingly
  • reverse T aids surgical access and may improve ventilation
  • support BP and HR (if they’re about to insufflate and your HR is 50 or 60, consider giving glyco (could give atropine but thats a “big gun”)
  • NG/OG tube - insert after intubation for stomach decompression - (better viewing for surgeons)
  • Avoid N2O
  • Judicious use of opioids
  • -opioids may cause sphincter of oddi spasm (morphine), but less than <3% incidence
  • -antagonize spasm with IV glucagon/naloxone/nitroglycerin
51
Q

What is hepatitis? Causes?

A

inflammation of the liver parenchyma

  • viral - Hep A, B, C
  • nonalcoholic fatty liver disease
  • alcoholic liver disease - most common cause of cirrhosis in US
  • inborn errors of metabolism (wilson’s disease, alpha 1 antitrypsin deficiency)
  • autoimmune
  • drug induced (Tylenol most common, cocaine, amphetamines, anti TB meds)
  • cardiac causes - decreased CO - shock liver
52
Q

Acute Hepatitis

A

usually self - limiting
rapid development of liver damage and impaired function
high mortality rate - these individuals should not be on the OR table

53
Q

Chronic hepatitis

A

hepatic inflammation > 6 months – cirrhosis – hepatocellular carcinoma or liver failure

symptoms may be minimal (malaise/jaundice) to severe with compromise to multiple organ systems

54
Q

What is cirrhosis

A

chronic, progressive parenchymal damage leads to scarring and nodular formation

55
Q

S/S of cirrhosis + anesthesia considerations

A
  • fatigue/malaise
  • jaundice
  • anorexia/weakness/n/v (RSI, FLUID/ELEC BALANCE)
  • spider angiomata
  • hypoalbuminemia (PROTEIN BINDING OF DRUGS, ALBUMIN ADMINISTRATION)
  • portal HTN
  • ascites/hepatomegaly - AUTOMATIC RSI (inc intraabdominal pressure from ascites)
  • coagulation disorders - PLAN AHEAD
  • endocrine disorders - DM
  • hepatic encephalopathy (these pts are self sedated, avoid versed, may also need to dec MAC)
  • gastroesophageal varicies (careful NG/OG placement)
  • hyperdynamic circulation
  • hepatorenal syndrome
  • hepatopulmonary syndrome
56
Q

Cirrhosis: elevated labs

A

bilirubin
amiontransferase
alkaline phosphatase
INR

57
Q

cirrhosis: decreased labs

A

serum albumin
platelets
blood sugar

58
Q

What is the child - pugh score?

A

severe liver disease have diminished ability to respond to stress

extent of liver damage and type of sx are main two determinants of peri op risk

used specifically to predict surgical mortality with cirrhosis

59
Q

How is the child - pugh scored?

A

Considers: total bilirubin, serum albumin, INR, ascites and hepatic encephalopathy

Class A = 10% mortality rate in intraabdominal sx
Class B = 30% mortality
Class C = 80% mortality (the only sx these patients should be having is a liver TX)

A/B with preop optimization ok for surgery
C should be delayed

60
Q

Cirrhosis anesthetic considerations: preoperative optimization!

A

improve diet with protein and caloric intake

blood glucose control pre/intra/post op (infusions with glucose) - mechanism of monitoring BG levels intra op

aldosterone antagonist (can help with fluid status)

electrolyte and fluid status!

invasive monitors?? at least an a line, potential CVP

61
Q

Cirrhosis anesthetic considerations: encephalopathy

A

RSI (cannot maintain AW)

judicious use of sedatives and induction agents

62
Q

Cirrhosis anesthetic considerations: ascites

A

RSI

mechanical ventilation (ascites rides up into thoracic cavity with induction of anesthesia)

PFTs (with severe ascites)

PA pressures (potentially)

fluid status (FOR EVERY 1 L OF ASCITES REMOVED DURING A PROCEDURE, YOU NEED 8 G ALBUMIN GIVEN)

63
Q

Cirrhosis anesthetic considerations: esophageal varicies

A
  • no esophageal temp probe
  • no NG/OG
  • bleeding?? – RSI
  • -octreotide (50 mcg/hr)
  • -vasopressin (20 U over 5 min)
64
Q

Cirrhosis anesthetic considerations: renal impairment

A
  • euvolemia

- monitor and correct for acid base and electrolyte imbalances (FREQUENT ABGS)

65
Q

Cirrhosis anesthetic considerations: hyperdynamic circulation

A
  • decreased SVR mostly compensated with increased CO
  • –anticipate use of pressors
  • –adequate colloidal replacment
  • hypoalbuminemia – edema
  • cardiomyopathy - avoid myocardial depressants
  • invasive monitors, intravascular fluid replacement and vasopressors (phenylephrine/NE/vasopressin)
  • impaired response to catecholamines
  • –will see a limited response to increased dose requirements
66
Q

Cirrhosis anesthetic considerations: coagulopathy

A
  • T&C
  • Vit K non emergently (NOT DURING PROCEDURE, at least 12 hours prior)
  • FFP, cryo, platelets
  • –only factors NOT produced by the liver are factors III, IV, XII
  • PRBCs
  • –impaired ability to handle citrate loads – ionized calcium monitoring and calcium admin during procedure
67
Q

Cirrhosis anesthetic considerations: pharmacokinetics

A
  • albumin (if you have not replaced albumin then you will have:)
  • –decreased protein binding and increased Vd
  • decreased clearance
  • –Ex. larger initial dose of NDMR to compromise for the increased Vd but decreased subsequent dosing due to decreased clearance
  • propofol or etomidate great options - conisder smaller induction doses
  • succinylcholine and cisatracurium great options (no hepatic metabolism)

caution with drugs dependent on liver clearance or toxic to liver

68
Q

Cirrhosis anesthetic considerations: maintain liver blood flow

A
  • hepatic artery 25% blood flow with 50% oxygen delivery
  • portal vein 75% blood flow with 50% oxygen delivery

**with cirrhosis - portal vein usually compromised so It relies on the hepatic artery for blood flow - IMPORTANT TO MAINTAIN GOOD MAP INTRA OP)

  • IV anesthetics maintain hepatic blood flow if ABP maintained
  • All inhalation agents maintain hepatic blood flow except halothane
  • Avoid SNS stimulation - dec blood through hepatic art
69
Q

Cirrhosis: post op considerations

A

Post op morbidity is increased!

  • liver dysfunction/failure (#1 concern) – maintain MAP
  • PNA
  • bleeding
  • sepsis
  • renal failure
  • poor wound healing
  • DTs
  • electrolyte disturbances

these patients will likely go to ICU intubated and on drips - be sure to coordinate ICU bed availability

70
Q

Alcoholism: anes considerations for the acutely intoxicated

A
  • RSI
  • decrease MAC/anesthetic needs d/t ADDITIVE effects
  • concern for acute hepatitis
71
Q

Alcoholism: anes considerations for chronic ETOH

A

enzyme induction – increased MAC/anesthetic needs

72
Q

Alcohol withdrawal syndrome: s/s

A
  • increased SNS - catecholamine release
  • agitation
  • tachycardia
  • delirium tremors (48-72 hrs post ETOH) - medical emerg
  • hallucinations
  • diaphoresis
  • cardiac dysrhythmias
  • hemodynamic instability
  • grand mal seizures and hypoglycemia
73
Q

Alcohol withdrawal syndrome: anes considerations

A

Ideally, these patients should not be going to the OR – should be optimized first!

  • benzo
  • beta antagonist (propranolol or esmolol) - antagonize SNS stim/catecholamine release
  • airway protection - etomidate good choice for induction because of hemodynamic lability)
  • correct fluid/electrolyte and metabolic disturbances
  • DT’s mortality rate is 10% d/t hemodynamic instability, cardiac dysrhythmias, seizures
74
Q

What is porphyria?

A

metabolic disorder that results from deficiency of specific enzyme in the heme synthetic pathway

results in overproduction of porphyrins
–accumulation of intermediate forms of porphyrin at the site of enzyme blocked

any increase in heme requirements results in accumulation of pathway intermediates

any metabolism needs that rely on the CYP450 isoenzymes induce ALA synthetase resulting in increased intermediates

75
Q

What are porphyrins and what are their function?

A

Porphyrins are essential for physiologic function!

  • heme is the most important porphyrin - bound to proteins
  • -essential for O2 transport and storage
  • production regulated by aminolevulinic acid (ALA) synthetase
  • -controlled by endogenous concentration of heme
  • -as heme levels drop or O2 demand increases, ALA synthetase increases the production of heme
76
Q

Most serious porphyria and associated effects?

A

Acute intermittent porphyria

  • affects central and peripheral nervous system
  • -manifests as systemic HTN and renal dysfunction
  • -numbness/tingling, decreased gastric mobility
  • -attacks are life threatening
77
Q

Porphyria triggers

A

Enzyme inducing drugs:

  • allyl group barbs
  • steroid structure
  • avoid pentahol, thiamyl, methohexital, etomidate

Hormonal fluctuations
-mensturation, menopause, pregnancy

  • fasting (pre op!) - population where fasting for 8 hours may not be appropriate (high carb drink 2 hours prior)
  • dehydration - AGGRESSIVE FLUID MANAGEMENT (start IV fluids out in preop)
  • stress (versed good option)
  • infection (tight control, and on top of ABX) - stay on top of ABX redosing and be very STRICT with this population
  • -IF YOU HAVE LOST A LOT OF BLOOD, YOU HAVE TO REDOSE ABX
78
Q

Porphyria: signs and symptoms + anes considerations

A
  • severe abdominal pain/n/v d/t autonomic neuropathy - RSI, CRICOID PRESSURE, ETT
  • ANS instability - MAY REQUIRE A LINE
  • electrolyte imbalances (Na, K, Mg)
  • skeletal muscle weakness - resp failure - TALK ABOUT POTENTIAL, BUT UNLIKELY CHANCE OF NEEDING POST OP VENT SUPPORT
  • CV instability resulting in HTN and tachycardia (less likely hypotension - MAY REQUIRE A LINE - beta blockers are a good option
  • seizures (benzos and versed)

acute exacerbation should really not be on OR table

79
Q

Porphyria: TX

A
  • remove triggering agents
  • -multiple enzyme inducing agents more dangerous than exposure to any one drug
  • hydration
  • carbohydrates (glucose infusion)
  • treat pain/n/v
  • BB for HTN and tachycardia
  • benzos for seizures
  • fluid and electrolyte balance (10% glucose saline infusion)
  • hematin 3-4 mg/kg IV; somatostatin
  • plasmapheresis (prior to surgical procedure to clear intermediates)
80
Q

Porphyria: anesthetic management

A
  • pre op prep (identify and avoid triggers)
  • assess skeletal and CN function (ESPECIALLY IF PLAN FOR EPIDURAL)
  • cardiac - HTN, tachycardia
  • minimize multiple drug exposure
  • fluid/electrolyte management
  • anticipate post op ventilation
  • minimize stress of preop fasting glucose-saline infusion
  • pre op meds
  • -anxiolytics, aspiration prophylaxis
  • —CIMETIDINE inhibits ALA synthetase activity and decreases heme consumption
81
Q

Porphyria: regional anesthesia considerations

A
  • no absolute contraindications
  • pre anesthetic neuro eval
  • ANS blockade may lead to CV instability especially with hypovolemia
  • avoid in acute exacerbation
82
Q

Porphyria: general anesthesia considerations

A
  • use short acting agents
  • monitors!! (invasive)
  • induction with propofol
  • maintenance with N2O, IA, opioids and NDMR
  • CPB is a stressor (confer with surgeon about doing sx off pump)
83
Q

Porphyria: UNSAFE drugs

A
  • barbs
  • etomidate
  • ketamine
  • sulfonamide ABX
  • ETOH
  • diazepam
  • nifedipine
  • ketorolac
  • phenacetin
  • amiodarone
  • calcium channel blockers *(most are safe but you have to look up the individual ones)

KEEP UP WITH THIS LIST AS It CAN CHANGE YEAR TO YEAR

84
Q

Porphyria: safe drugs

A
  • opioids
  • propofol
  • ASA/APAP
  • PCN
  • glucocorticoids
  • insulin
  • atropine/glyco
  • neostigmine
  • locals
  • most CV drugs
  • VA
  • NDMR
  • benzos

NURA 620 Anesthesia and Coexisting Conditions (7 decks)

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