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Coexisting Test 3 > GI/Liver Coexist > Flashcards

GI/Liver Coexist Flashcards

1
Q

General GI functions/anatomy

A
  • Digestion, motility, and absorption
    • Mechanical and chemical
  • Excretion
    • Hydrophobic molecules
  • Host defense
    • Sophisticated system of immune defenses
    • Commensal gut bacteria
      • New rage is gut biome and fecal transplant
  • Long muscular tube stretching from mouth to anus
  • Several glandular structures empty secretions into the lumen
  • Several glandular organs connect to the lumen
  • Epithelium
    • Continuously lines the tracta
    • Forms crypt (SI/LI) and villus structures (SI) ​
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2
Q

Esophagus anatomy?

A
  • Esophagus
    • Transfers bolus of food from mouth to stomach
      • 18 – 26 cm in length
  • Upper 1/3
    • Striated skeletal muscle
    • Thick submucous elastic and collagenous network
  • Lower 1/3
    • Smooth muscle
    • Vagal control to coordinate opening of sphincters
      • false sphincter (no ciruclar muscle), relaxes and things can go through
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3
Q

Esophageal sphincters?

A
  • Upper esophageal sphincter (where LMA sits)
    • Proximal origin of esophagus at the level of the cricopharyngeal muscle
    • Prevents aspiration of air into stomach
  • Lower esophageal sphincter
    • 2-4 cm length of asymmetric circular smooth muscle
    • Level of the diaphragmatic hiatus
    • Under vagal control
    • Prevents regurgitation of gastric content
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4
Q

Symptoms of esophageal disease?

A
  • Dysphagia (difficulty swallowing)
    • Oropharyngeal dysphagia
      • Common after head/neck surgery and in stroke & Parkinson’s disease patients
    • Esophageal dysphagia
      • Mechanical vs. motility
        • mechanical- dysphagia for solid food
        • motility d/o- dysphagia with both liquids and solids
  • Heartburn
    • Regurgitation- correlation b/w heartbuna nd GERD so strong that current mgmt for heartbun- empirical treatment of GERD
  • Chest pain
    • May be difficult to distinguish between cardiac vs esophagus
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5
Q

Esophageal evaluation?

A
  • Gastrointestinal endoscopy
    • Flexible or rigid
    • Diagnostic or therapeutic
    • Typically done in GI clinic or outpatient center
  • ASA I & II
    • Moderate sedation – typically with RN
    • Vast increase in monitored anesthesia care (MAC)
  • ASA III & IV
    • Just “propofol”- it’s never “just propofol” procedure can cause aspiration, hyptension etc
    • GI Suit vs MOR
  • Trauma
    • GA with ETT to secure airway
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6
Q

Esophageal evaluation anesthesia considerations? Preop, intraop, emergence and complications?

A
  • Preoperative
    • From H & P
    • NPO Time (2 hours for clears?)
  • Intraoperative
    • Induction: Topical spray; Propofol +/- fentanyl
      • Bite block/position before - need to get past gag reflex, once coughing, dififcult to stop
      • can give lidocaine, lollipop, 12.5 fentanyl can also help decrease coughing
    • Maintenance: Propofol infusion
  • Emergence
    • Protect airway
  • Complications
    • Esophageal perforation, pneumothorax, aspiration, bleeding, & airway injury
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7
Q

Esophageal Motility Disorders?

A
  • Mechanical
    • Benign vs malignant strictures
    • Varices
    • Post radiation/fundoplication
  • Motility
    • Achalasia
    • GERD
    • Spasm
    • Chagas disease
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8
Q

What is achalasia?

A
  • Neuromuscular disease of the esophagus
  • Esophageal outflow obstruction from inadequate relaxation (motiilty d/o)
    • Symptoms occur with both liquids and solids
  • Loss of inhibitory neurotransmitters (NO)
    • Results in:
      • HTN of LES
      • Reduced peristalsis
      • Esophageal dilation
  • FOOD STASIS IN THE ESOPHAGUS
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9
Q

Compliation, diagnosis and treatment of achalasia?

A

Complications

  • Pulmonary aspiration, pneumonia, lung abscess, & bronchiectasis

Diagnosis

  • Esophagram
  • EGD to rule out structural disorders

Treatment

  • Can relieve obstruction but cannot correct peristalsis
  • Medication
    • Nitrates and Ca++ blockers- allows smooth muscle to relax
  • Surgery
    • Heller myotomy
    • Per oral endoscopic myotomy (POEM)- divide circular muscle layer of LES but leave longitudinal muscle layer intact
    • Esophagectomy - for adv dx, help eliminate risk for esophageal cancer too
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10
Q

Anesthesia consideration for esophageal motility disorder?

A

Pre-operative

  • From H & P
  • Maybe on liquid diet for 1 -2 days preop to limit accumulation of food

Intraoperative

  • May need to do pre-induction endoscopy to evaluate for undigested food or placement of large bore nasogastric tube
  • Rapid sequence intubation or awake intubation
  • Special instrumentation: Shared airway/ +/- A-line
  • Unique consideration: POEM – insufflation of esophagus with CO2; watch ETCO2

Postoperative

  • Post op care: Bleeding, tension pneumoperitoneum, subcutaneous emphysema or hypercapnia
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11
Q

What are esophageal diverticula?

A
  • Outpouching of the wall of the esophagus
  • True (all three muscle layers) vs false (only 1-2 layers)
  • Pharyngoesophageal
    • Accounts for 60 – 65%
    • False diverticula that originates in Killian’s triangle (Zenker’s Divertiula)
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12
Q

Anesthesia considerations for esophageal diverticula?

A

Pre-op

  • H2 blocker and/or metoclopramide
  • AVOID placement of nasogastric tube – puncture

Induction

  • RSI with HOB elevated = cricoid pressure may not work- don’t know where the diverticula is in regard to cricoid pressure
  • May require a DLT (double lumen tube)

Maintenance

  • Standard +/- Epidural (thoracic vs lumbar) (limit nitrous- may expand spaces)
  • Monitors: +/- A-line and CVP- low threshold
  • Fluids: Large bore IV; Type and Cross for 2-4 units

Emergence:

  • Tracheal extubation should be anticipated at end of case
  • If significant airway edema is present, may need to keep intubated (switch out DLT)

Complications:

  • Hypoxemia/hypoventilation, Aspiration, pneumothorax/hemothorax, recurrent laryngeal nerve injury
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13
Q

What is a hiatal hernia?

A
  • Herniation of part of the stomach into the thoracic cavity through esophageal hiatus in the diaphragm
  • Types
    • Sliding hiatal hernia
      • Stomach slides upward
    • Paraesophageal hernia
      • Stomach is herniated next to the esophagus
  • Most asymptomatic
  • May result in GERD
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14
Q

What is GERD?

A
  • Very common – about 15% of adults in US
  • Pathophysiology
    • Incompetence of LES resulting in gastric content in the esophagus
    • Anatomical abnormalities (hiatal hernia)

Complications

  • Aspiration
  • Strictures/ulcers
  • Esophagitis and cancer

Treatment

  • Lifestyle modifications
  • Pharmacological
  • Surgical
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15
Q

What is an esophagogastric fundoplasty?

A
  • To prevent esophageal reflux by wrapping the fundus of the stomach around the lower esophagus
  • Acts to reinforce the LES
  • Patient Characteristics
    • Etiology: GERD; hiatal hernia
    • Associated conditions: diverticulosis and cholelithiasis
  • No OG/NG tube placed if pt has had this done!
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16
Q

Lifestyle modifications and meds to help with GERD?

A

Lifestyle modifications – foods that alter LES tone

  • Tomatoes, chocolate, alcohol, citrus fruits, garlic, onions & coffee

Medication

  • H2
    • Decrease both gastric acid secretion and pH
  • PPI’s
    • Decrease pH
  • Gastrokinetic agents
    • Increases LES tone & accelerates emptying
  • Nonparticulate antacids
    • Reduce pH & minimally increase volume
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17
Q

What should be done to avoid aspiration risk in GERD?

A

Patients with GERD present an ASPIRATION RISK

  • Content must flow to the esophagus, reach the pharynx, and have obtunded laryngeal refluxes
  • Volume: 0.4 mg/kg
  • pH: < 2.5
  • Factors: Emergent surgery, full stomach, difficult airway, inadequate depth, use of lithotomy position, DM, pregnancy, increased abdominal pressure and morbid obesity.
  • RSI with cuffed endotracheal tube
  • Use of cricoid pressure convoluted…. may not actually work
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18
Q

Anesthesia consideration for esophagogastric fundoplasty?

A

Preoperative

  • Tests from H& P
  • Premedication (H2, PPI, gastric prokinetic, & sodium citrate)

Intraoperative

  • Induction: RSI vs. standard
  • Maintenance: Balanced anesthesia
  • Monitors: Standard; +/- a-line or CVP as indicated

Postoperative

  • Pain management
  • Aspiration
  • Hypoventilation
  • Pneumothorax/hemothorax
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19
Q

Stomach anatomy, parts?

A

Muscular bag

  • 75 ml’s empty
  • 1 L full

Parts

  • Cardia
    • Secretes mucus and bicarbonate to protect esophagus
  • Fundus/Body
    • Parietal Cells: HCL/intrinsic factor (binds to cyanocobalamin or Vitamin B12)
    • Chief cells: pepsinogens
    • Mucus cells: mucus and bicarbonate
    • Enterochromaffin like cells: Histamine & gastric acid
  • Antrum
    • Extensive motility patterns
    • Pylorus
    • Controls movement of food from the stomach into the small intestine
  • •
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20
Q

What do parietal cells secrete? chief? mucus? enterochromaffin like cells?

A
  • Parietal Cells: HCL/intrinsic factor (binds to cyanocobalamin or Vitamin B12)
  • Chief cells: pepsinogens
  • Mucus cells: mucus and bicarbonate
  • Enterochromaffin like cells: Histamine & gastric acid
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21
Q

What is peptic ulcer disease?

A
  • Burning epigastric pain
    • Ulcers in mucosal lining of stomach or duodenum
    • Better after eating/worse with fasting
    • 15,000 deaths/year
  • Helicobacter pylori
    • Chronic gastritis- 100% infected
    • Only 10-15% develop peptic ulceration
  • NSAID use
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22
Q

Complications of peptic ulcer disease?

A
  • Bleeding
    • Leading cause of death (10-20%)
    • Posterior wall – Gastroduodenal artery
  • Perforation/peritonitis
    • Anterior wall
  • Obstruction
    • Edema and inflammation of pyloric channel
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23
Q

What is zollinger-ellison syndrome?

A
  • Increased gastrin secretion
    • Increased gastric acid secretions
    • Increased parietal cell mass
  • Gastrinomas
    • Develop in the presence multiple endocrine neoplasia (MEN type 1)
    • Parathyroid, pancreas & pituitary gland – excess calcium
  • S/S
    • Abdominal pain
    • Diarrhea
    • GERD
    • Ulcers in unusual locations
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24
Q

Treatment and anesthesia management of zollinger-ellison syndrome?

A

Treatment

  • PPI at higher doses- because they’re making more acid
  • Curative surgical resection of the gastric acid measurement

Anesthesia Management

  • Large gastric volume
  • Intravascular volume depletion
  • Electrolyte imbalance
  • PPI/H2
  • Octreotide (reduce gastrin secretions)
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25
Q

Ulcer treatment?

A
  • Antacids
    • OTC
    • Aluminum/magnesium hydroxide (do not use in renal failure) or calcium carbonate
  • H2 Receptors
    • Cimetidine and ranitidine bind Hepatic CYP450 enzymes
  • PPI
    • Inhibit H+,K+-ATPase pumps
  • Prostaglandin analogues
    • Misoprostol (enhance mucosal bicarbonate secretions)
  • Cytoprotective agents
    • Sucralfate and Pepto-Bismol
  • Antibiotics
    • Amoxicillin, metronidazole, tetracycline, & clarithromycin
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26
Q

Surgical procedure for ulcer treatment?

A
  • Typically an emergency
    • graham’s patch
    • vagotomy/pyloroplasty
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27
Q

Anesthesia considerations for ulcer treatment?

A

Preoperative

  • Emergency (unstable) vs. elective
  • Aspiration prophylaxis

Intraoperative

  • Induction: RSI
  • Maintenance: Standard/balanced (+/- epidural)
  • Monitors: Standard; unstable +/- a-line and CVP
  • Fluids: Anticipate large blood loss and third spacing

Emergence

  • Depends on patients underlying conditions and resuscitation status

Postoperative

  • Pain – epidural
  • PONV
  • Ileus
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28
Q

Small intestine anatomy?

A
  • About 2.75 – 10.49 meters long
    • Receives 9 L’s of fluid per day
    • End stage of food absorption

3 distinct parts

  • Duodenum
    • Shortest portion – accepts acid secretions from stomach
    • Bile/pancreatic duct
  • Jejunum
    • Covered with villi – increases absorptive surface area
    • Magnesium absorption
  • Ileum
    • Absorption of vitamin B12 and bile salts
    • Diffuse neuroendocrine system (gastrin, secretin, & CCK)
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29
Q

Function of small intestine?

A
  • Digestion of carbohydrates, fats, proteins
  • Water/electrolyte absorption
  • Vitamin and mineral absorption
  • Provides a barrier to pathogen entry
  • Immune function
  • Reservoir of IgA antibodies
  • Production of hormones that regulate GI function
  • Table 30-12 in Nagelhout ?? unable to find…
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30
Q

Appendix?

A
  • Finger like, blind ended tube that is connected to the cecum
  • About 9 cm in length
  • Function (debatable)
    • To maintain good gut bacteria
      • Increased incidence of C. difficile colitis after removal
    • Immune system
      • Contains B/T cells
  • Infected
    • Antibiotics vs surgery
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31
Q

Anesthesia considerations for appy?

A

Preoperative

  • Generally healthy (mostly) vs acutely sick
  • Based on H & P
  • Aspiration prophylaxis

Intraoperative

  • Induction: RSI
  • Monitoring: Standard (CV monitors if very sick)
  • Maintenance: Balanced
  • Emergence: Extubated fully awake
  • Fluid: Minimal

Postoperative

  • PONV, sepsis, ileus, or atelectasis
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32
Q

Colon functions?

A
  • Portions
    • ascending
    • transverse
    • descending
    • sigmoid
  • serves as reservoir for storage of waste
  • Main function is absorption of water, sodium, fatty acids and minerals
    • Reduces 2L chyme to 250 ml’s semi-solid feces
  • Smooth muscles are under control of the enteric nervous system
  • Segmentation and contraction waves
  • Stretch receptors in colon stimulate defecation
  • Contains healthy (abnormal) intestinal bacteria
    • Important with folic acid, synthesis of vitamin K, & B complex vitamins
  • 70% of ingested substances are excreted in 72 hours
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33
Q

What is inflammatory bowel disease?

A
  • 2nd most common chronic inflammatory disorder
  • 30,000 new cases per year
  • Two major types
    • Crohn’s disease
    • Ulcerative colitis
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34
Q

What is crohn’s disease?

A
  • Can involve any part of the GI tract, but most commonly involves the distal ileum and proximal large colon
  • Extraintestinal manifestations: 18.4
  • S/S: Diarrhea; abdominal pain; palpable mass; anal complaints
    • Anemia, Vit B12 and folic acid deficiencies, Mg+, Phos, Ca+ deficiencies (bone dz)
  • Radiological findings: Linear, cobble stone areas that skip areas
  • Proctoscopic Findings: Anal fissure, fistulas, abscess, deep ulcerations
  • Often require multiple surgeries
    • Bowel obstruction
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35
Q

What is ulcerative colities?

A

inflammatory bowel disease

  • Mucosal disease of the rectum and proximal colon
    • 40-50% limited to rectum; 30-40% beyond sigmoid; 20% pancolitis
    • Females, white, 20-40 years old
  • Remission and exacerbation
  • S/S: diarrhea, fever, mild abdominal pain, & rectal bleeding
  • Radiological findings: starts at rectum and progresses upward; fuzzy x-ray; collar button appearance
  • Proctoscopic Findings: granular mucosa, superficial and universal ulceration
  • Toxic megacolon: severe colonic distention and shock
  • Colon cancer: left sided
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36
Q

Medical treatment for both inflammatory bowel disease?

A
  • Medical management is the mainstay of therapy
    • 5-aminosalicylate acids
    • Glucocorticoids
      • Prednisone
    • Immune modulators
    • Biologic response modifiers
    • Antibiotics
      • If pouches occur
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37
Q

Anesthesia consideration for inflammatory bowel disease?

A

Preoperative

  • Elective vs. emergent (maybe critically ill)
    • Based on H & P
  • Aspiration prophylaxis (avoid gastric motility agents- reglan)

Intraoperative

  • Induction: RSI
  • Monitors: STD to invasive
  • Maintenance: Balanced anesthesia (no nitrous); +/- epidural
  • Blood/fluids: may require large amounts of fluids (crystalloid/colloid/Blood products)
  • Emergence: Extubation based on PT’s condition; PACU vs. ICU

Postoperative

  • Pain: 7-9; ERAS protocols; Epidurals
  • Complications: Sepsis; hemodynamic instability; atelectasis; hypoxemia; hemorrhage; PONV; & ileus
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38
Q

Carcinoid tumors?

A
  • Originate from any GI
    • Majority in the appendix
    • < 25% are first found in lungs
    • Neuroendocrine in origin- signal from nervous system to endocrine gland and allow secretion.
      • ​same stimulus comes in and instead secretes massive amounts of hormones
  • Tumors
    • Secrete GI Peptides
      • Gastrin
      • Insulin
      • Somatostatin
      • Tachykinins
      • Glucagon
      • Prostaglandins
      • Growth hormones
      • Serotonin
      • Kallikreins
      • Histamines
39
Q

What is carinoid syndrome?

A

Carcinoid Syndrome (10% of patients with tumors)

  • Signs and symptoms secondary to secretions from carcinoid tumors
    • Typically serotonin and kallikrein
      • Monitor 5-HIAA in urine
  • Flushing (histamine)
  • Diarrhea (serotonin)
    • Dehydration/electrolyte abnormalities
  • Restrictive cardiomyopathy (serotonin)
    • Tricuspid and pulmonary valve
  • Bronchoconstriction (bradykinin/histamine)
  • If outside the hepatic system
    • Life threatening instability (Why?)
      • because the hormones are bypassing the liver detox process which normally will degrade extra hormones from carcinoid tumors
      • now all hormones are in systemic circulation before going to liver, causing huge issues
40
Q

Treatment for carcinoid syndrome?

A
  • Avoid stimulating conditions
  • Serotonin receptor antagonists
    • Usually short ½ life –need chronic infusion
    • Good for nausea/diarrhea but not flushing
  • Somatostatin receptor blockers
    • Lanreotide or octreotide
    • Continue through preop and operative period
  • Ipratropium
    • Beta agonists may exacerbate the problem
41
Q

Anesthesia considerations for carcinoid tumor removal?

A
  • Same as with inflammatory bowel disease

Additionally:

  • Prevent release of bioactive mediators
  • Induction of anesthesia may cause carcinoid crisis
    • Hypotension, bronchospasm, tachycardia, & arrythmias
      • Tx: octreotide 50 – 100 mg then infusion at 50 mg/hr
      • Steroids and anti-histamines
  • Requires invasive monitors – (a-line/CVP) before induction
    • Rapid changes in BP
    • Potential for large blood loss
  • Avoid agents that release histamine
  • Spinal/epidural have been used
  • Phenylephrine best choice to treat hypotension
    • ​want direct acting agents
42
Q

Colonoscopy?

A
  • Standard Procedures
    • Elective
  • Interventional
    • Urgent colonoscopy – acute GI bleed
    • Endoscopic mucosal resection
    • Stricture management
    • Fistula perforation
43
Q

Anesthesia consideration for colonoscopy?

A

Preoperative

  • From H & P

Intraoperative

  • Induction: Propofol vs. midazolam/fentanyl
    • Can be done sans anesthesia
  • Maintenance: propofol infusion
  • Fluids: Maybe dehydrated
  • Emergence: Recovery

Postoperative

  • Complications: Bleeding; perforation; post polypectomy syndrome
    • Pain, fever, leukocytosis, elevated CRP, peritoneal inflammation
44
Q

Gallbladder?

A
  • Small hollow organ that stores and concentrates bile
  • Lies beneath the liver
    • Capacity of 50-60 ml’s
  • Common hepatic duct (in)
  • Common bile duct (out)
  • Important for
    • Digestion of fats
    • Elimination of bilirubin
    • Elimination of drugs/toxins
45
Q

Choleystitis? s/s? dx?

A
  • Inflammation of the gallbladder typically from gallstones blocking the cystic duct
  • S/S
    • Acute right upper quadrant pain (worse with inspiration)
    • Nausea/vomiting
    • Fever
  • DX
    • Ultrasound
    • Liver function test
    • CT scan
    • Increased WBC’s, CRP, & bilirubin
46
Q

Anesthetic consideration for cholecystitis?

A

Preoperative

  • Diverse (healthy to extremely ill)
  • Tests from H & P (CV and Resp)
  • Aspiration prophylaxis

Intraoperative

  • Induction: Standard vs. RSI based on Pt condition
  • Monitors: Standard vs. a-line/central line; NG/OG tube
    Maintenance: Balanced; ERAS
  • Fluids: Pt maybe dehydrated
  • Positioning: Supine; reverse Trendelenburg position (easier to ventilate)
  • Extubation: Awake with protective reflexes intact

Postoperative

  • Complications: hypoxia/hypercarbia; pneumothorax; atelectasis; PONV; subcutaneous emphysema
  • Pain: 4-8 (lap vs. open); shoulder pain; Rib blocks or epidural
47
Q

Pancrease functions?

A
  • Has both endocrine and exocrine functions
  • Endocrine
    • Islets of Langerhans
    • Glucagon, insulin, somatostatin, & polypeptides
  • Exocrine
    • Metabolism of carbohydrates, proteins, and fats
    • Secreted in in-active form into duodenum
48
Q

What is acute pancreatitis?

A
  • Autodigestion of pancreas
    • Digestive enzymes typically in precursor form – acid to activate

Etiology

  • Gallstones/ETOH abuse account for 60-80%
  • Trauma, HIV, & hypercalcemia from hyperparathyroidism

Signs/Symptoms

  • Excruciating, unrelenting midepigastric pain
  • N/V
  • Increased amylase and lipase
  • Hypotension and tachycardia
49
Q

Complication and treatment of acute pancreatitis?

A

Complication

  • Hypovolemic shock
  • Hypoxemia
  • Renal failure
  • Infection/abscess

Treatment

  • Aggressive IV fluid replacement
  • Opioids to manage pain
  • Paracentesis
  • Endoscopic retrograde cholangio-pancreatography (ERCP)
50
Q

What is chronic pancretitis?

A
  • Incidence difficult to determine
  • Etiology
    • Chronic ETOH abuse
    • Genetics
    • Cystic fibrosis
  • S/S
    • Steatorrhea
    • DM
    • Chronic pain
51
Q

Chronic pancreatitis treatment?

A

Treatment

  • NPO
  • IVF
  • NGT
  • H2/PPI
  • Pain management (Morphine?) ( can cause sphincter of oddi spasm)
  • Manage dietary intake
    • ETOH withdrawal prophylaxis
  • Control diabetes
  • ERCP to remove stones and place stents
52
Q

ERCP summary of procedure

A

Summary of Procedure

  • Position: Prone/left lateral
  • Location: GI clinic vs OR
  • Incision: None
  • Special Instrumentation: Endoscope and equipment
  • Unique Considerations: X-ray protection; glucagon 0.25 – 1 mg IV prior
  • Antibiotics: Ciprofloxacin 500 mg PO
  • Morbidity: Bowel or duct perforation, hemorrhage, aspiration, & CV issues
53
Q

ERCP anesthesia considerations? preop? airway access? intraop? induction, positioning, maintenance consideration, complications?

A
  • Preoperative
  • As a result of underlying disease process
    • Maybe quite frail with limited reserve
  • Airway
    • Access to airway may be limited during procedure
    • Consider aspiration prophylaxis
    • Ascites/plural fluid accumulation may impair ventilation
  • May also have altered mental status, CV changes and renal failure

Intraoperative

  • Induction:
    • RSI
    • Etomidate for hemodynamically unstable; what is K+ level
  • Monitors: Standard; +/- aline
  • Positioning
    • Prone or left lateral
  • Maintenance
    • Standard/Watch ETT carefully
    • Have glucagon or secretin (typically from GI)
  • Emergence
    • Place OGT
  • Complication
    • Pain; perforation; abscess;
54
Q

Liver anatomy?

A
  • Largest internal organ
  • 2% of TBW (1.5 kg)
  • Lies along the 7th to 10th rib
  • Classically divided into 4 lobes
  • Functional unit: acinus or hepatic lobule

Blood flow

  • Hepatic Artery
    • 20-30% blood flow
    • 50% of oxygen
    • Responds to metabolic demand
  • Portal Vein
    • 70-80% blood flow
    • 50% of oxygen
55
Q

What are some liver functions?

A
  • Coagulation
    • All except Factor VIII and von Willebrand factor (endothelial cells)
  • Carbohydrate metabolism
    • Gluconeogenesis (lactate, pyruvate, AA) and glycogenolysis (glucose release)
  • Protein synthesis
    • Albumin (1/2 life = 21 days); plasma cholinesterase
  • Protein metabolism
    • Lipoproteins; Urea (removal of ammonia); formation of plasma proteins – albumin
  • Bilirubin metabolism
    • Unconjugated bilirubin (neurotoxic and not soluble in water) to conjugated
  • Bile production
    • Absorption of fat soluble vitamins
  • Insulin clearance
    • Primary site
  • Drug metabolism/transformation
    • Phase I: functionalization (CYP 450) - oxidation/reduction/hydrolysis
      • Induction hastens the metabolism of barbiturates, ketamine, and some benzodiazepines
    • Phase II: conjugation
      • Covalent linkage of phase I to second water soluble molecule
56
Q

What do liver function test (LFTs) assess for?

A

Assess for

  • Liver function
  • Liver damage
  • Biliary system
  • Coagulation
  • Hemolysis
  • Nutrition
  • Bone turnover
57
Q

What is elevated AST/ALT indicative of?

A

More inflammatory/loss of hepatocytes

  • AST: multiple location – low specificity
  • ALT: primarily liver – high specificity
  • Mild to moderate elevation: multiple
  • Marked elevation: 10x chronic hepatitis; 25x acute hepatitis
  • AST:ALT ratio 2:1 indicates chronic alcoholic disease
58
Q

What is alk phosphate elevation indicative for?

A
  • Very non specific; marked outflow obstruction
  • High with rapid bone growth
59
Q

What is GGT indicative of?

A

Most sensitive indicator of biliary tract disease

60
Q

What is 5NT indicative for?

A

Highly specific for hepatobiliary obstruction

61
Q

What are some synthetic functions of the liver?

A

Albumin

  • Primary site of metabolism
  • Helps maintain colloid oncotic pressure
  • T1/2 life is 21 days – better indicator of chronic liver disease
    • < 2.5 mg/dL

Urea

  • Decreased urea synthesis leads to increased ammonia levels
  • Marked elevations may lead to hepatic encephalopathy

INR/PT (extrinsic pathway)

  • Sensitive indicator of hepatic disease
  • Better indicator of acute liver disease
  • Depends on sufficient intake of Vitamin K
  • Short T1/2 of Factor VII (6 hours)
62
Q

What is bilirubin in LFTS?

A
  • From breakdown of hemoglobin
  • Jaundice when total bilirubin > 3 mg/dL
  • Unconjugated (lipid soluble)
    • Elevated: increased breakdown or decrease in uptake by hepatocytes
    • Conjugated in the liver to water soluble end products
  • Conjugated (water soluble)
    • Can be excreted renally
    • Intrahepatic congestion
    • Extrahepatic obstruction
63
Q

What do bilirubin, aminotransferase enzymes, alk phos look like in prehepatic failure?

Causes?

A
  • Bilirubin- increased unconjugated
  • aminotransferase- normal
  • alkaline phosphatase- normal
  • causes-
    • hemolysis
    • hematoma absorption
    • bilirubin overload
64
Q

Bili, aminotransferase, alk phos levels in intrahepatic failure?

causes?

A
  • Bili- increased conjugaed
  • aminotransferase- markedly increased
  • alk phos- normal to slight increase
  • causes
    • viral infection
    • drugs
    • ETOH
    • Sepsis
    • cirrhosis
65
Q

What are bili, aminotransferase, alk phos levels in posthepatic failure?

Causes?

A
  • BIli- increased conjugated
  • aminotransferase- normal to slightly increased
  • alk phos- mark increase
  • causes
    • biliary tract stones
    • sepsis
66
Q

What other labs exams do you look at in liver failure?

A
  • Chemistry
  • CBC
  • Acetaminophen level
  • Toxicology screen
  • Viral hepatitis serologies
  • Ammonia level
  • Autoimmune markers
  • HIV
  • Amylase and lipase
67
Q

What is Hepatitis?

A
  • Inflammation of liver tissue
    • Hepatocellular injury with cellular necrosis
  • Temporary (acute) or long term (chronic)

Causes

  • Viruses
    • Hepatitis
      • A & E – Fecal oral
      • B & C – Body fluids (most common associated with liver complications)
      • D – Either route, but requires Hep B
    • Epstein-Barr
  • Drugs – ETOH most common – Halothane
  • Toxins
  • Nonalcoholic fatty liver disease
    • 10-46% prevalence rate
    • Higher in Hispanic population
68
Q

What is halothane hepatitis?

A
  • Incidence: 0.3 – 1.5/10,000 after 1st; 10-15% after 2nd exposure
  • Female:Male – 2:1
  • Types:
    • Type 1: Mild/self limiting
    • Type 2: Severe hepatotoxicity/liver failure (14-80% mortality pre transplant era)
  • Etiology: Immune mediated (IgG)
  • Volatile anesthetics minimally metabolized by liver
    • Halothane 20%; Sevo 2%; Iso 0.2%; Des 0.02%
    • Metabolites to trifluroacetylated (TFA) intermediates
      • Bind to hepatocytes and cause immune reaction
      • Sevoflurane is not metabolized to TFA
69
Q

What is acute hepatitis prodromal, active and recovery phase?

A

Prodromal Phase

  • Flu like symptoms

Active Phase

  • Yellowing of the skin/eyes
  • Enlarged liver/spleen
  • Can last 2-12 weeks

Recovery Phase

  • Complete resolution of symptoms
  • Hepatitis A & E – complete recovery in 1-2 months
  • Hepatitis B – 80% recovery in 3-4 months
  • Hepatitis C – Few cases fully recovery
  • Can be asymptomatic infectious carriers – especially Hep B & C
70
Q

What is chronic hepatitis?

A
  • Persistent hepatic inflammation lasting longer than 6 months
  • Most commonly from Hep B, Hep C, auto-immune, or drugs
  • Many display evidence of cirrhosis
  • Laboratory results may only show mild elevation and DO NOT correlate to severity of disease
  • Autoimmune hepatitis
    • Reacts favorable to steroids and azathioprine
  • •
    *
71
Q

Anesthesia considerations for hepaittis?

A

Acute

  • Cancel elective procedures
    • Increased morbidity/mortality – up to 50% in acute ETOH
  • Emergent procedures
    • Preserve hepatic blood flow
    • Consider regional anesthesia – coagulation profile
    • Volatiles with isoflurane or desflurane
    • Avoid PEEP if possible- decrease blood flow to heart and liver
    • Avoid medications with hepatic toxicity (CYP450 metabolites)
      • Halothane, acetaminophen, sulfonamides, tetracyclines, and penicillin’s
  • Good postoperative surveillance

Chronic

  • Same as above
72
Q

What is cirrhosis?

A
  • Long term liver damage
    • Months to years
  • Normal tissue replaced by scar tissue
    • Direct (liver damage) and in-direct symptoms (portal HTN)
  • 2.8 million people/year
  • Men > women

Causes

  • Hepatitis B & C
  • Nonalcoholic fatty liver disease
  • Alcoholic liver disease
73
Q

What are some CV, Repsiratory and renal implications of cirrhosis?

A

CV

  • Portopulmonary HTN
  • hyperdynamic circulation (high CI and SV with low SVR and MAP)
  • Anesthesia considerations- right ventricular failure, cardiogenic shock, vasodilatory shock

Respiratory

  • hepatopulmonary syndrom
  • decreased FRC
  • Respiratory alkalosis
  • Anesthetic consideration- hypoxemia refractory to o2 therapy, PEEP

Renal

  • hepatorenal syndrome
  • hyponatremia
  • anesthetic- maintenance of renal perfusion, caution with drugs elminated by kidney, avoidance of nephrotoxic drugs
74
Q

GI, Hematologic, immunologic, and endocrine implications of cirrhosis?

A

GI

  • Portal HTN
  • varices/variceal bleeding
  • ascites
  • malnutrition
  • anesthetic- risk of GI bleeding, full stomach precautions, hypoalbumenmia, change sin drug binding

Hematologic

  • coagulopathy
  • anemia
  • thrombocytopenia
  • neutropenia
  • anesthetic consideration- risk of hemorrhage, vit k admin, blood component transfusion PRN

Immune

  • compromised immune system
  • anesthetic- ROI, very careful sterile technique

Endocrine

  • less glucose production and storage, decreased metabolism of insuin, hypogonadism
  • anesthetic- hypoglycemia
75
Q

Major complications of cirrhosis?

A

Portal HTN

  • Normal hepatic vein pressure gradient < 5
  • HVPG > 6 portal HTN
  • HPVG > 12
    • Formation of ascites
      • High risk of spontaneous bacterial peritonitis
    • Esophageal varices
  • Transjugular intrahepatic porto-systemic shunts (TIPS)
76
Q

Summary of TIPS procedure?

A
  • Position: Supine
  • Location: IR suite vs OR
  • Incision: Right IJ access
  • Special Instrumentation: Multiple different needles/dilators
  • Unique Considerations: May require FFP preop
    • EBL: 0 - 3000
  • Mortality: Emergency – 50-75%
  • Morbidity: Encephalopathy; liver failure; shunt occlusion; hepatic artery puncture; bleeding; MI; & renal failure
  • Pain: 7-8
77
Q

Anesthesia consideration for TIPs procedure?

A

Preoperative

  • Per H & P; Maybe extensive
  • CXR; ABG; PFT; ECG; ECHO; CBC; Chem; Coags; LFTs;

Intraoperative

  • Induction: Sedation vs RSI (succs based on K+ levels)
  • Monitors: Standard to full cardiac
  • Maintenance: TIVA with cisatracurium
  • Fluids: Large bore IV’s; potential for large blood loss; glucose containing solutions
  • Emergence: Fully awake

Postoperative

  • Complications: sepsis; bleeding; encephalopathy; CHF; portal vein rupture; fluid/electrolyte abnormalities
78
Q

What is MELD scoring used for?

A
  • More prognostic for liver patients (how well they’ll do after transplant etc)
79
Q

What is Class A/B/C in liver damage?

A
  • Class A - 10% risk
    • proceed with sx, monitor and treat encephalopathy, coagulopathy, metabolic and electolyte derangement
  • Class B- 30% risk
    • proceed with sx, monitor and treat encephalopathy, coagulopathy, metabolic and electolyte derangement
  • Class C - 80% risk
    • prefer non surgical treatment options
    • defer necessary elective surgery until improvement
80
Q

Anesthetic considerations for cirrhosis patient undergoing non liver surgery?

A
  • Induction: RSI (abdominal distention; encephalopathy; bleeding variceal)
    • Lower doses of propofol or etomidate
    • Succinylcholine based on K+ levels – maybe prolonged
  • Monitors: Routine (minor surgery/mild disease); Invasive (mod/severe)
    • Frequent ABG’s maybe necessary
  • Maintenance:
    • Volatiles: Avoid halothane and nitrous; isoflurane and sevoflurane preferred
    • MNBD: Increased Vd and lowers binding; cisatracurium best option
    • Opioids: May have prolonged and intensified effects; use judiciously
    • Fluids: Possibility of large blood loss; have large bore IV access/central line; blood products available (FFP, cryo, plts too); LR + albumin
    • Vasopressors: Hypodynamic response
    • Ventilation: Low TV and increased RR; judicial use of PEEP
  • Emergence
    • When fully awake and able to protect airway reflexes
81
Q

Cirrhosis Postop consideration for non-liver surgery?

A
  • Liver failure
  • Bleeding
  • Electrolyte imbalance
  • Hypoglycemia
  • Pulmonary insufficiency
  • Sepsis
  • Renal failure
  • Poor wound healing
82
Q

Medication alteration for cirrhosis patients undergoing non-liver surgery

A

Intravenous

  • Propofol, etomidate, ketamine & midazolam – ok with short doses
    • Termination of action via re-distribution not metabolism
    • Prolonged infusion not well studied- Propofol infusion syndrome ?

Inhalational

  • Decrease hepatic blood flow
  • Isoflurane/sevoflurane have little effects (Desflurane – 30% reduction)

Opioids

  • Dosing interval should be increased to prevent accumulation
    • Avoid morphine/meperidine

Neuromuscular blocking drugs

  • Increased Vd and less protein binding; use cis/atracurium
83
Q

What is porphyria?

A

Greek for purple

  • Defects in the enzymes needed to produce heme
    • Multistep process
    • Leads to the accumulation of toxic metabolites
  • Heme is important for
    • Hemoglobin
    • Myoglobin
    • Multiple catalases and peroxidases
    • Cytochrome CYP450 enzymes
84
Q

Porphyria etiology?

A

•Autosomal dominant, autosomal recessive, X-linked, or build up of iron (cutanea tarda)

85
Q

Which porphyria is most common?

A
  • Acute Intermittent Porphyria is the most common
  • Prevalence
    • 1:10,000 – 20,000
    • With psychiatric disorders: 1:500 (neurological symptoms)
  • Deficiency in porphobilinogen deaminase (PBG)
    • Most have 50% reduction (100% incompatible with life)
  • Leading to an increase in Delta-aminoevulinic acid (ALA)
86
Q

Precipitating factors of porphyria?

A

Most patients are symptomatic

  • Common onset after puberty; more common in women

Precipitating factors

  • Stimulation of ALA synthesis in the liver
  • Endocrine factors
    • Female reproductive cycle
  • Fasting
    • Preop?
    • Especially if combined with ETOH
  • Induction of CYP450 enzymes
    • Drugs
  • Emotional stress
    • Surgery
87
Q

S/S porphyria?

A
  • Sever abdominal pain with nausea/vomiting
  • Diarrhea/constipation
    • Electrolyte imbalances
  • Neurological symptoms
    • Psychosis, hallucination, & seizures
  • SIADH
    • Hyponatremia
  • Skeletal muscle weakness
    • Pain in the back/legs
  • ANS instability
88
Q

Treatment of porphyria?

A
  • Recognition and avoidance of precipitating factors
  • Remove triggering agents (drugs)
  • Glucose therapy (400g/day) with Heme arginate (3mg/kg/day for 3 days)
    • Limit ALA production
  • Hydration
  • Pain control
    • Often severe
  • Nausea prevention
89
Q

Anesthetic considerations for porphyria?

A

General

  • Avoid triggering agents
    • contraindicated= main ones are: barbituates, ketamine, VPA, Clonazepam, CCB
  • Keep warm
  • Use short acting agents
  • Aspiration prophylaxis
  • Anticipate post op ventilation – may need ICU stay

Regional

  • No absolute contraindications
  • Good neurological exam
90
Q

Anesthetic considerations for acute alcohol intoxication?

A
  • Associated with increased morbidity and mortality
  • Non-intentional injuries
    • Trauma
  • Aspiration risk
    • RSI
  • Decreased anesthetic needs
    • Decrease induction doses of Propofol
    • Decreased MAC requirements
  • Increased risk of surgical bleeding – decreased platelet aggregation
  • Response to catecholamines
    • Labile vital signs
    • Exaggerated response to drugs and surgical stimulation – decreased uptake
91
Q

Chronic alcohol intoxication?

A
  • Vitamin Deficiencies
    • Thiamine (Wernicke’s encephalopathy)
  • Metabolic Abnormalities
    • Acidosis- alcoholic ketoacidosis and lactic acidosis
    • Hypomagnesemia, hypocalcemia, & hypophosphatemia
  • Cardiac
    • Cardiomyopathy & heart failure
  • Respiratory
    • Decreased surfactant with increased risk for ARDS
  • Alcoholic liver disease
    • Fatty liver, hepatitis, & cirrhosis
  • Pancreatitis
    • Acute
  • Immune dysfunction
    • 3-5 fold increase in post op infection
    • Changes in Th1/Th2 ratiosa
92
Q

Anesthetic consideration of chronic alcohol intoxication?

A

Preoperative

  • Abstinence can decrease M/M, but is it worth it?
  • Extensive work up (labs, EKG, Chest x-ray, etc.)

Intraoperative

  • Local/regional if possible
  • Induction agents: Increase propofol induction dose; etomidate – normal
  • RSI with aspiration prophylaxis
  • Volatile: No change; avoid nitrous –
  • NMBD: Increase Vd and decreased protein binding
  • Opioids: decreased metabolism; risk accumulation

Postoperative

  • Judicious use of opioids
  • Watch for withdrawal
93
Q

Alcohol withdrawal syndrome s/s treatment?

A
  • Set of symptoms that develop within 6 -24 hours from last drink
  • Typically presents within 2 to 4 days
    • Can been seen up to 2 weeks
  • Signs/Symptoms
    • Early: agitation, hyperpyrexia, tachycardia, hypertension & diaphoresis
    • Late: Confusion, seizures, psychosis, & profound autonomic hyperactivity
  • Treatment
    • Benzodiazepines
    • Correct electrolyte abnormalities
    • Beer/whiskey
94
Q

What is ERAS?

A
  • Attempt to modify physiological and psychological response
  • EBP in practice…
  • Leads to
    • Reduction in postoperative complications
    • Reduced hospital stay
    • Improved cardiopulmonary function
    • Earlier return of bowel function
    • Earlier return to normal activities

Coexisting Test 3 (8 decks)

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