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)
2
Q
Esophagus anatomy?
A
- Esophagus
- Transfers bolus of food from mouth to stomach
- 18 – 26 cm in length
- Transfers bolus of food from mouth to stomach
- 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
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
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
- Mechanical vs. motility
- Oropharyngeal dysphagia
- 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
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
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
- Induction: Topical spray; Propofol +/- fentanyl
-
Emergence
- Protect airway
-
Complications
- Esophageal perforation, pneumothorax, aspiration, bleeding, & airway injury
7
Q
Esophageal Motility Disorders?
A
- Mechanical
- Benign vs malignant strictures
- Varices
- Post radiation/fundoplication
- Motility
- Achalasia
- GERD
- Spasm
- Chagas disease
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
- Results in:
- FOOD STASIS IN THE ESOPHAGUS
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
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
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)
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
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
- Sliding hiatal hernia
- Most asymptomatic
- May result in GERD
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
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!
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
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
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
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
- •
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
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
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
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
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)
25
Ulcer treatment?
* 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
26
Surgical procedure for ulcer treatment?
* Typically an emergency
* graham's patch
* vagotomy/pyloroplasty
27
Anesthesia considerations for ulcer treatment?
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
28
Small intestine anatomy?
* 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)
29
Function of small intestine?
* 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...
30
Appendix?
* 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
31
Anesthesia considerations for appy?
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
32
Colon functions?
* 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
33
What is inflammatory bowel disease?
* 2nd most common chronic inflammatory disorder
* 30,000 new cases per year
* Two major types
* Crohn’s disease
* Ulcerative colitis
34
What is crohn's disease?
* **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
35
What is ulcerative colities?
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
36
Medical treatment for both inflammatory bowel disease?
* Medical management is the mainstay of therapy
* 5-aminosalicylate acids
* Glucocorticoids
* Prednisone
* Immune modulators
* Biologic response modifiers
* Antibiotics
* If pouches occur
37
Anesthesia consideration for inflammatory bowel disease?
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
38
Carcinoid tumors?
* 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
What is carinoid syndrome?
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
Treatment for carcinoid syndrome?
* 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
Anesthesia considerations for carcinoid tumor removal?
* 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
Colonoscopy?
* Standard Procedures
* Elective
* Interventional
* Urgent colonoscopy – acute GI bleed
* Endoscopic mucosal resection
* Stricture management
* Fistula perforation
43
Anesthesia consideration for colonoscopy?
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
Gallbladder?
* 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
Choleystitis? s/s? dx?
* 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
Anesthetic consideration for cholecystitis?
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
Pancrease functions?
* 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
What is acute pancreatitis?
* 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
Complication and treatment of acute pancreatitis?
Complication
* Hypovolemic shock
* Hypoxemia
* Renal failure
* Infection/abscess
Treatment
* Aggressive IV fluid replacement
* Opioids to manage pain
* Paracentesis
* Endoscopic retrograde cholangio-pancreatography (ERCP)
50
What is chronic pancretitis?
* Incidence difficult to determine
* Etiology
* Chronic ETOH abuse
* Genetics
* Cystic fibrosis
* S/S
* Steatorrhea
* DM
* Chronic pain
51
Chronic pancreatitis treatment?
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
ERCP summary of procedure
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 prio**r
* **Antibiotics**: Ciprofloxacin 500 mg PO
* **Morbidity**: Bowel or duct perforation, hemorrhage, aspiration, & CV issues
53
ERCP anesthesia considerations? preop? airway access? intraop? induction, positioning, maintenance consideration, complications?
* 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
Liver anatomy?
* 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
What are some liver functions?
* **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
What do liver function test (LFTs) assess for?
Assess for
* Liver function
* Liver damage
* Biliary system
* Coagulation
* Hemolysis
* Nutrition
* Bone turnover
57
What is elevated AST/ALT indicative of?
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
What is alk phosphate elevation indicative for?
* Very non specific; marked outflow obstruction
* High with rapid bone growth
59
What is GGT indicative of?
Most sensitive indicator of biliary tract disease
60
What is 5NT indicative for?
Highly specific for hepatobiliary obstruction
61
What are some synthetic functions of the liver?
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
What is bilirubin in LFTS?
* 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
What do bilirubin, aminotransferase enzymes, alk phos look like in prehepatic failure?
Causes?
* Bilirubin- increased unconjugated
* aminotransferase- normal
* alkaline phosphatase- normal
* causes-
* hemolysis
* hematoma absorption
* bilirubin overload
64
Bili, aminotransferase, alk phos levels in intrahepatic failure?
causes?
* Bili- increased conjugaed
* aminotransferase- markedly increased
* alk phos- normal to slight increase
* causes
* viral infection
* drugs
* ETOH
* Sepsis
* cirrhosis
65
What are bili, aminotransferase, alk phos levels in posthepatic failure?
Causes?
* BIli- increased conjugated
* aminotransferase- normal to slightly increased
* alk phos- mark increase
* causes
* biliary tract stones
* sepsis
66
What other labs exams do you look at in liver failure?
* Chemistry
* CBC
* Acetaminophen level
* Toxicology screen
* Viral hepatitis serologies
* Ammonia level
* Autoimmune markers
* HIV
* Amylase and lipase
67
What is Hepatitis?
* 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
What is halothane hepatitis?
* Incidence: 0.3 – 1.5/10,000 after 1st; 1**0-15% 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**
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What is acute hepatitis prodromal, active and recovery phase?
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
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What is chronic hepatitis?
* 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
* •
*
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Anesthesia considerations for hepaittis?
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
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What is cirrhosis?
* 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
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What are some CV, Repsiratory and renal implications of cirrhosis?
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
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GI, Hematologic, immunologic, and endocrine implications of cirrhosis?
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
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Major complications of cirrhosis?
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)
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Summary of TIPS procedure?
* 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
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Anesthesia consideration for TIPs procedure?
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
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What is MELD scoring used for?
* More prognostic for liver patients (how well they'll do after transplant etc)
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What is Class A/B/C in liver damage?
* 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
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Anesthetic considerations for cirrhosis patient undergoing non liver surgery?
* **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 + albumi**n
* Vasopressors: Hypodynamic response
* _Ventilation: Low TV and increased RR; judicial use of PEEP_
* Emergence
* When fully awake and able to protect airway reflexes
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Cirrhosis Postop consideration for non-liver surgery?
* Liver failure
* Bleeding
* Electrolyte imbalance
* Hypoglycemia
* Pulmonary insufficiency
* Sepsis
* Renal failure
* Poor wound healing
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Medication alteration for cirrhosis patients undergoing non-liver surgery
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
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What is porphyria?
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
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Porphyria etiology?
•Autosomal dominant, autosomal recessive, X-linked, or build up of iron (cutanea tarda)
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Which porphyria is most common?
* 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)
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Precipitating factors of porphyria?
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
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S/S porphyria?
* 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
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Treatment of porphyria?
* 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
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Anesthetic considerations for porphyria?
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
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Anesthetic considerations for acute alcohol intoxication?
* 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
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Chronic alcohol intoxication?
* 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
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Anesthetic consideration of chronic alcohol intoxication?
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**
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Alcohol withdrawal syndrome s/s treatment?
* _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**
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What is ERAS?
* 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
