Final: Local anesthetics, Pain Management and Recognition, Anesthesia and the GI Tract Flashcards

1
Q

Anesthesia and the GI tract

What are some abnormalities to digestion with anesthesia?

How does this affect hydration? what does hydration affect?

A

Digestion: hydration, ileus, GI stasis, constipation, drug absorption, nutrients

Hydration: 60-80% of the body is water. 90% of blood is water. Blood volume affects preload which affects MAP which affects DO2

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1
Q

Anesthesia and the GI tract

What are some abnormalitites to secretions and considerations with anesthesia?

What may you find ornot find in secretions? What are secretions for?

A

Secretions are affected. Secretions are needed for hydration, and electrolytes, to control pH. Sometimes in a protein-losing enteropathy, there will be albumin secretions. Bleeding is not a usual secretion but can be seen in some diseases so anemia is not rare

Albumin and proteins (amino acids): is essential for plasma oncotic pressure (edema), carries hormones-drugs-metabolites, inflammation, coagulation

Anemia (bleeding through GIT): PCV/Hb affects CaO2 which affects DO2. DO2= cardiac output x oxygen content

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2
Q

Anesthesia and the GI tract

What are some considerations for the abnormalities seen in absorption?

When is decreased absorption an issue?

A

Absorption: H2O, electrolytes, nutrients (eg. glucose, amino acids, vitamins), oral drugs.
Electrolytes and pH: Na+, K+, Cl-, HCO3-, H+ is important for action potentials, osmolality, acid/base, and water balance

Decreased absorption (nutrients, drugs, etc): important if considering oral medication (eg. anxiolytics, sedation, analgesics, antibiotics)

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3
Q

Anesthesia and the GI tract

What are some considerations that comes with transport abnormalities?

What can predispose your patient to ileus and GIT stasis in addition to anesthesa?

A

Transport: inappetence, nausea, ileus, constipation, GIT rupture, discomfort (pain), drug absorption.

Ileus and GI stasis: predisposes to inappetence, constipation, decreased absorption of nutrients - drugs, discomfort, pain, microflora overgrowth, and can predispose to rupture (peritonitis, SIRS) and torsion (eg. colic, GDV)

Nausea (reflux, vomit, salivation): it is part of the pain syndrome, induces inappetence, may cause hydration and electrolyte imbalance

Discomfort-pain: the more painful your patient is, the more drugs your patient may require for anesthesia, sedation, and analgesia. Pain predisposes to ileus and GIT stasis.

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4
Q

Anesthesia and the GI tract

What are some considerations that come with storage abnormalities induced by anesthesia?

why would we want to avoid diarrhea in our anesthetic patients? How can we prevent it?

A

Storage: ileus, constipation, microflora overgrowth

Microflora overgrowth: induces microflora imbalance within the GIT. predisposes to diarrhea, flatulence, ileus, toxins, aspiration pneumonia, and further physiologic stress.

Diarrhea and gas distension
From discomfort, diarrhea predisposes to surgical site infection, and logistical problems.

Prevention and treatment: time to recover, perianal purse-string suture to decrease surgical site contamination, may treatment with antibiotics (eg metronidazole), can consider fluids and electrolytes, and remember hospitalization can be the cause of stress.

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5
Q

Anesthesia and the GI tract

What can compromising the protection/barrier of the GI cause in our anesthetic patients?

A

Protection/barrier: bacteria-toxin translocation
Bacteria-toxin translocation and GIT rupture: SIRS (systemic inflammatory response syndrome), often critical patients with guarded prognosis (major anesthesia challenge)

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6
Q

Anesthesia and the GI tract

How could you prevent or treat drug-induced emesis or nausea?

Which drugs are emetics in dogs? in cats? Do antiemetic drugs treat emesis and nausea? When would we reach for this drug?

A

Drug-induced emesis and nausea
Opioids are emetics and induce nausea in dogs. Alpha 2s are emetics and induce nausea in cats. General anesthesia predisposes to nausea (emesis). Nausea can be considered a component of pain syndrome. Emesis may predispose to aspiration pneumonia (no good evidence). Emesis may empty the stomach and decrease probability for reflux and improve ventilation (no good evidence). Controversy regarding emesis has been good or bad for anesthesia

Prevention and treatment: antiemetics prevent drug induced emesis (administered at least 30-40 minutes before SQ or at least 2 hours for PO). antiemetics treat drug-induced emesis but NOT nausea. The most effective antiemetic for drug-induced emesis is maropitant but will not work in all cases.

When to use: risk of aspiration pneumonia, cannot open mouth, intracranial/intraocular disease, risk of vomiting, personal preference.

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7
Q

Anesthesia and the GI tract

How can we treat or prevent gastroesophageal reflux in our anesthetic patients?

What can it cause?

A

Happens when intragastric pressure overcomes lower esophageal resistance. Predispose to esophagitis (gastric pH, enzymes and bile acids). Esophagitis can progress to esophageal stricture with poor or guarded prognosis. And lastly, aspiration pneumonia.
Prevention and treatment: pre-treatment with GI protectants such as anti-acids at least 2 doses. Lavage esophagus when reflux is suspected (water or dilute HCO3-), sucralfate, and anti-acids. If stricture occurs, esophageal ballooning (guarded prognosis)

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8
Q

Anesthesia and the GI tract

How can we treat or prevent constipation in our anesthetic patients?

What else aside from pain and anesthesia predisposes our patients to ileus and GI stasis?

A

Ileus and GIT stasis (constipation)
All anesthesia drugs, general anesthesia, and sedation decrease GIT propulsive motility. Surgery and inflammation decrease GIT motility. Postoperative ileus is not rare and predisposes to colic, GDV< and constipation.

Prevention and treatment: eating and quick return to appetite (small meals). Good evidence for GIT prokinetic agents. Physical activity like walking. Drug reversals (for opioids). And recovery time. *hospitalization stress may induce ileus and GIT stasis

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9
Q

Anesthesia and the GI tract

How can we prevent and treat aspiration pneumonia in our anesthetic patients?

Why do prokinetics help?

A

Aspiration pneumonia
There is a high prevalence of upper airway diseases such as brachycephalic syndrome and laryngeal paralysis. Vomit and regurgitation may present a risk. Laryngeal dysfunction is a risk. Neurological dysfunction is a risk. Immunosuppression is a risk.

Prevention and treatment: seal airways as best you can with an ET tube. Additional gauze can be used to prevent aspiration (oropharynx). Prokinetic agents may help (cisapride, metoclopramide). Antibiotics (pre-emptive and treatment). Monitor and manage patient oxygenation and respiratory activity. IPPV if necessary, when low PaO2 (anesthesia and recovery)

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10
Q

Anesthesia and the GI tract

How do we prevent and treat GI ischemia in our anesthesia patients?

A

GIT ischemia
Blood pressure is important to maintain GIT perfusion. Physiologic response during hypotension is to decrease GIT blood flow (as it is not an essential organ), which can lead to villus and mucosa death which then leads to bacteria and toxin translocation

Prevention and treatment: maintain adequate blood pressure at all times, maintain adequate blood volume and PCV, be careful with vasopressors, and if there is translocation consider antibiotics and proper care.

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11
Q

Anesthesia and the GI tract

What is considered a GIT emergency that needs to be treated with anesthesia in our patients?

A

Equine: colic, choke
Small animals: GDV, GIT rupture, GIT obstruction, GIT foreign bodies
Livestock animals: GIT rupture, GIT obstruction, abomasum displacement, bloat.

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12
Q

Recognition of pain in animals

Why is the recognition of pain in animals important?

A

It predisposes to chronic pain and maladaptive pain, predisposes to cardiac dysrhythmias (autonomic response), prevents sleeping, prevents normal function of affected areas and compensatory areas, pushes the body into a catabolic state (fight or flight), can have an emotional component (depression, aggression).
Pain is the 4th vital sign after HR, RR, and temp
It’s our oath!

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13
Q

Recognition of pain in animals

How do we assess pain objectively in our patients?

What are the steps involved in observing for pain?

A

Us a pain scale (very subjective so not commonly used): Glasgow pain scale (validated, limited), Melbourne pain scale (validated, hard to use), CSU pain scale (partially validated, easy) in dogs.

Cats have a grimace scale with “5 action units” (0-2, absent to markedly present). Horse one does not have a limb assessment…

Steps: (1) observe the patient without any interaction (animals change behavior when they know they are seen) (2) observe while interacting with the patient (3) observe the patient while moving freely if possible (4) observe the response to palpation (5) score patient using a scoring system.

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14
Q

Recognition of pain in animals

How can you recognize pain in an anesthetized patient?

A

Patient movement, increased respiratory rate,
increased blood pressure
increased HR
signs of light anesthesia
In horses: palpebral reflex and nystagmus
knowledge of surgical procedures (stimulation throughout).

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15
Q

Management of pain in animals

What is pre-emptive analgesia and how will you use it in veterinary practice?

What are some cautions with NSAIDS? Opioids? alpha 2s?

A

In pre-emptive analgesia, you are anticipating the amount of pain according to the procedure to be performed and treat it accordingly.

Premedication-sedation drugs:
A2 agonists
Xylazine:
Good sedation and analgesia, may be most important drug in equine world.
Alpha 2 are good, predicitve, reversible, and short acting. Disadvatnatges: decreases CO and cardiac performance. Don’t want to use in a cardio patient. Can give IV, IM, SQ, and epidural.

Acepromazine (not an analgesic)

Opioids
Morphine, hydromorphone, oxymorphone, methadone, fentanyl, buprenorphine
Sedation effects (only some have sedation effects) are not as predictable as alpha 2 agonists (which is why you use them in healthy and large animals)
Analgesia is not as predictable either like in livestock, but more predictable in dogs than cats, cats reach ceiling effect and may see side effects that may outweigh the benefits of analgesia (nausea, dysphoria, delerium)
Can give any route including transmucosal.

Benzodiazepines (not an analgesic)
NSAIDs (most common analgesics for both LA and SA)
LA: flunixin meglumine (Banamine), phenylbutazone (Butazolidin), firocoxib (Equioxx), Diclofenac (Surpass)
SA: meloxicam and robenacoxib only approved in cats, but vet med often goes outside of licensing for the drug. Carprofen (Rimadyl), Meloxicam (Metacam), Firocoxib (Previcox), Deracoxib (Deramaxx), Robenacoxib (Onsior)
Remember: can predispose to renal disease, GIT ulcerations, liver disease
Grapiprant (Galliprant)
Not to be combined with other NSAIDs, does not work with COX enzymes blocks prostaglandin EP4 receptor.

16
Q

Management of pain in animals

T/F Drugs are the only way to manage pain in our patients

What drugs are used for acute pain?

A

Non-pharmacological: distraction, ear twitch (distraction for horses and cats), food, etc.

Drugs: opioids, alpha twos, ketamine, lidocaine, NSAIDs, gabapentin (only found oral), tramadol (only found oral), maropitant (not really analgesia, but treats nausea)

17
Q

Management of pain in animals

How can we manage chronic pain in our patients?

A

Need to differentiate and know the etiology so you can target it properly.
Neuropathic pain - gabapentin and amatadine works best.
Visceral components: consider an anti-emetic
Maybe exercise (lymphatic and blood flow, movement! massage) and emotional support will help with pain

18
Q

Management of pain in animals

What are some alternative techniques to pain management?

anxiolytics?antidepressants?

A

Physiotherapy, massage, acupuncture, homeopathy, nutraceuticals, general health (physically and mental)
Also remember anxiolytics (Trazadone, alprazolam, acepromazine)
Antidepressants (amitriptyline, fluoxetine)
Adequate sleep, stretching, massage.

19
Q

Local anesthetics

What is the mechanism of action for local anesthetics? What conditions do they work best in?

A

MOA: stop influx of sodium that causes depolarization and signal does not get sent out. Stop depolarization: don’t get signal. - the goal of local anesthesia. On large (myelinated) nerves with nodes of ranvier, have to hit larger portions of the nerve with local anethetic.

Have to get inside to do their job. To cross, have to be uncharged. Proton comes off, inside cell, H binds again.

Inflammation (lots of extra protons, acidic) makes it harder for these things to get inside the cell to do their job. Works better in basic environments.
Have high affinity for active or inactive state. But not so much resting state. Unbound drugs just get washed away… use dependent block…?
*In general, cats more sensitive to drugs use ⅓-½ dose in cats as dogs.

20
Q

Local anesthetics

What is LAST?

Which drug should you be careful of?

A

Local anesthetic systemic toxicity (LAST)
Generalized CNS excitation and depression. Will see cardiovascular depression in early toxicity (excitation).

Bupivacaine is famous for causing everything at once. Also known to not get a warning. Likely kill the patient. Be cautious.

In general, treatment of LAST is supportive care.
Treatment of seizures: benzodiazepines, catheter?
Cardiovascular support: inotropes/chronotropes, vasoconstrictors, IV fluids, IV intralipid bolus: stick on catheter, pulling drug out of circulation. > treatment of choice for anesthetic toxicity.

Other toxicity: neurotoxicity, myotoxicity, chondrotoxicity. Basically, use as little as possible to get what you need to get done in the time period you need to get it done.

21
Q

Local anesthetics

What are some risk factors to local anesthetics?

A

Dose! Volume and concentration are independent and variable. Be cautious with continuous infusions. Give yourself a safety margin.

Regional blood flow, if give somewhere with lots of blood flow, lot of blood in circulation. Like in an IM injection somewhere with high flow.
This is where vasoconstrictors come in, keep drug where you put it.

Hepatic, renal and pulmonary dysfunction.
Same dose in one patient is toxic in another
Cardiac dysfunction, if not getting enough blood flow
High output states, faster uptake

Age: use less in older animals
Hypercapnia and acidosis, change metabolic profile

General anesthesia, could mask clinical signs that would see for toxicity in an awake patient.