GI

Question 1

Describe the GI tract innervation.

Answer 1

Autonomic (extrinsic)and enteric NS

• Patho review- enteric NS in intestine can function all on own without outside innervation (however also receives input from SNS and PSNS) receives input from mechanoreceptors, chemorecepors and osmoreceptors in the lumen of the intestine
• Autonomic is composed of SNS and PSNS

Autonomic includes SNS and PSNS

SNS

• Function: primarily inhibitory
  
  • stimulation decrease or cease GI motility.
• Location: Preganglionic fibers (originate at T5-L2 segments of SC) → travel to sympathetic chain of ganglia → synapse with postganglionic neurons → travel to gut → then terminate at enteric nervous system.
  
  • Sympathetic signal transmission:
    
    • Norepinephrine (Primary neurotx)
    • Vasoactive intestinal polypeptide (VIP)

PSNS:

• Function: primarily excitatory
  
  • activates GI motility/function
• Location: Parasympathetic preganglionic fibers originate in medulla and sacral region of SC.
• Innervation:
  
  • Vagus nerve fibers: esophagus, stomach, pancreas, SI, and 1st half of LI.
  • Pelvic nerve fibers: 2nd half of LI, sigmoid, rectal, and anal regions.
• Signal transmission:
  
  • Acetylcholine (ACh)

Pain in abdomen surgery

• celiac plexus- innervation of GI organs up to proximal transverse colon
• inferior hypogastric plexus- innervation of descending colon and distal GI tract

Question 2

Describe the esophagus and its sphincters.

Answer 2

• Muscular tube
  
  • 18-25 cm long
  • extends C6 to T11
• Composition:
  
  • Upper 1/3^rd: striated muscle
  • Lower 2/3^rd: smooth muscle
• Two areas of high pressure:
  
  • Upper esophageal sphincter (UES)
    
    • Location: Level of cricoid cartilage
    • Resting tone: 30-200 mmHg
      
      • opening and closing coordinated with pharyngeal pushing of food
  • Lower esophageal sphincter (LES).
    
    • Formation:
      
      • Intrinsically- circular esophageal muscle
      • Extrinsically- diaphragm muscle
    • Innervation: both SNS & PSNS.
    • Resting tone: 10–45 mmHg

Question 3

What is the basic pathophysiology behind reflux and some esophageal or gastric disorders that cause it?

Answer 3

Patho:

• Luminal pressures increase to overcome resting pressures of UES and LES

Esophageal etiologies:

• Achalasia
  
  • smooth muscles unable to relax/move food down
  • increased LES tone does not allow for complete relaxation
    
    • RESULT: dysphagia, regurgitation, and significant pain.
• diffuse esophageal spasm
  
  • muscle contractions are uncoordinated and, as a result, food does not properly move downward.
• hypertensive LES
  
  • LES with a mean pressure of > 45 mm Hg → leading to dysphagia and chest pain.
• Neurologic disorders
  
  • Ex: stroke, vagotomy, or hormone deficiencies
  • Patho: alter nerve pathways such that appropriate sensing and feedback are disrupted.
    
    • RESULT: dysphagia.

Slow emptying (Gastric motility disorders) → increased incidence of GE reflux dx

• Drug induced: (often given intraop or to critically ill pts for BP control)
  
  • Opioids
  • Vasoactive agents
    
    • Ex: increase catecholamine [] → sympathetic stimulation → decreased motility.
• Neurologic:
  
  • vagal neuropathies
  • gastroparesis
• Critical illness
  
  • Conditions commonly present in severely compromised pts: Examples → decrease gastric motility
    
    • Hyperglycemia
    • increased ICP
    • mechanical ventilation

Question 4

What are the 4 regions of the stomach and what are the 4 main cell types?

What promotes stomach emptying?

Answer 4

• Stomach: four regions: cardia, fundus, body, and antrum
  
  • 4 main cell types
    
    • mucous cells: protection from HCl acid
    • parietal cells: secrete HCl acid
    • chief cells: secrete pepsin
    • G cells: secrete gastrin
• Promotion of stomach emptying:
  
  • Gastric distention
  • Gastrin
  • Nitric Oxide (NO)
• Stomach physiology:
  
  • Solid foods must be broken down into 1-2mm particles before entering duodenum
    
    • Takes 3-4 hrs to empty from stomach
  • Leads to duodenum

Question 5

Describe the sections of hte small bowel and their functions?

Answer 5

• Duodenum:
  
  • 1^st and smallest section of SI
  • pancreas, liver, and gallbladder secrete digestive enzymes through the ampulla of Vater into mid-duodenum
• Jejunum:
  
  • Primary absorption of nutrients
• Ileum:
  
  • final section of SI
  • ends at ileocecal valve
  • Function:
    
    • B12 absorption

Question 6

What are some common etiologies for small bowel dysmotility?

Answer 6

Mechanical obstruction

• Etiologies: Hernias, malignancy, adhesions, and volvuluses

Other reversible causes:

• Ileus: D/t →
  
  • manipulation of intestines << main reason
  • Surgical stress response d/t postop pain
    
    • Multifaceted, neurohormonal resp to sx stim
      
      • SIRs - release of systemic inflammatory response and adrenaline and noradrenaline hormone
      • → sympathetic overactivity will constrain mobility and directly inhibit gut smooth muscle via activation of α- and β-adrenergic receptors → resulting in postop ileus
    • Suppression of response → LA and opioid epidural admin
• Electrolyte abnormalities
• Critical illness

Nonreversible structural causes:

• Ex: scleroderma
• connective tissue disorders
• short bowel syndrome

Neuropathic causes

Question 7

What are the sections of the large intestine?

Answer 7

• Composed of cecum, appendix, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum
• Function:
  
  • absorbs water, nutrients, and vitamins

Question 8

What are the effects of general anesthesia on bowel function? goals and considerations?

Answer 8

• Overall goals → enhance bowel function:
  
  • attenuate stress response
  • hemodynamic stability
  • ideal fluid balance
    
    • → Fluid loss r/t exposure of gut!
  • normothermia (keep warm)
• Considerations:
  
  • No evidence for recommendations on specific anesthetic and analgesic agents to avoid adverse GI effects
  • Anxiety inhibits GI function
    
    • GI tract inhibition directly proportional to amount of NE secreted from sympathetic stimulation
      
      • Tx: REDUCE stress response!
• Volatile anesthetics affect bowel function through various mechanisms
  
  • changes in intestinal tissue oxygenation
  • depress the spontaneous, electrical, contractile, and propulsive activity in the stomach, small intestine, and colon
    
    • Colon recovers 30-40 hrs postop
• TIVA vs volatile doesn’t seem to make a significant difference
• Nitrous: 30x more soluble than nitrogen but no adverse outcomes on motility
  
  • Cause gut to expand → visualization difficult for surgeons
• Muscle relaxant: skeletal muscle affected
  
  • GI motility unaffected
• Anticholinesterase reversal:
  
  • increase parasympathetic activity
  • increases bowel peristalsis
    
    • → lead to fresh anastomosis dehiscence (falls apart when sew together)
  • **Sugammadex preferred with fragile anastomosis (instead of neostigmine)
• Opioid effect on Gi motility
  
  • Reduced GI motility
    
    • Action on central and peripheral receptors: mu, delta, and kappa
  • Peripheral receptors cause adverse effects
    
    • High density of peripheral mu-opioid receptors in the myenteric and submucosal plexuses
  • Other adverse effects:
    
    • Nausea
    • Anorexia
    • delayed digestion
    • abdominal pain
    • excessive straining during bowel movements
    • Incomplete evacuation.
  • Methylnaltrexone: pure peripherally acting opioid (Mu) receptor antagonists are a potential solution
    
    • Methylnaltrexone: peripheral mu-opioid receptor antagonist and does not cross the blood-brain barrier

Question 9

Effect of surgery on bowel function?

Answer 9

• Abdominal surgery predisposes patients to ileus
  
  • Uncomplicated ileus usually lasts 3-4 days
• Ileus → complications:
  
  • Perforation
  • Bleeding
  • peritonitis
• MAIN REASON FOR ILEUS → Manipulation of intestines
  
  • Additional contributors include: immobility, electrolyte imbalance from fluid shifts and insensible losses, and intestinal wall swelling from excessive fluid administration.
• Mesenteric ischemia: 100% mortality if untreated

Question 10

What are some effects of regional anesthesia technique on bowel function?

Answer 10

• Epidural analgesia → decrease incidence of postoperative ileus
  
  • Leads to blockade of afferent and efferent sympathetic-mediated GI reflexes, BUT
    
    • → parasympathetic innervation left intact
• Neuraxial blockade → Improvement of GI blood flow and tissue oxygenation
  
  • Avoid hypotension associated with neuraxial as this will negate the benefits (when goal is to increase bowel fx)

Question 11

What are some considerations in ERAS for GI procedures?

Answer 11

• 1. Regional anesthesia
• 2. Avoidance of opioids
• 3. Multimodal analgesia
• 4. Nutrition and preoperative carbohydrates
• 5. Selective bowel preparation
     * AE of bowel prep:
     
     • decreased exercise capacity, lower weight, increased plasma osmolality, decreased urea and phosphate, and reduced plasma Ca & K
     • These effects + fasting → produce unpleasant pt experience.
       
       • The routine use of bowel preparation has been questioned repeatedly. In fact, recent studies have shown mechanical bowel preparation can be safely omitted before elective colorectal surgery
• 6. Fluid optimization
• 7. Temperature control
• 8. Early removal of drains and tubes
• 9. Early mobilization
• 10. Early oral intake

Question 12

Describe considerations and goals in fluid management for bowel surgery.

Answer 12

• All patients are exposed to a preoperative starvation period that results in a fluid deficit:
  
  • Consequences of fasting:
    
    • Stimulate prod of ADH, atrial natriuretic peptide, renin-angiotensin-aldosterone system, and increase in sympathetic activity
    • Relative hypovolemia
      
      • More pronounced in patients who receive bowel preparation, experience diarrhea/vomiting, high temp exposure, high NGT output
• Excessive/ liberal fluid administration=
  
  • increased capillary hydrostatic pressure
  • tissue and bowel edema
  • anastomotic leaks
• Goals:
  
  • Optimizing fluid administration
    
    • → increase tissue perfusion and oxygen delivery
  • Modulation of hormonal and inflammatory response
    
    • Ex: mitigate stim of ADH, ANP, RAAS, and increase symp activity

Question 13

What are some preoperative considerations in patients with GI disease?

Answer 13

• intravascular fluid volume
  
  • fluid status (renal fx)
• electrolyte []
• nutrition status (albumin levels , BMI, plasma osmolarity)
• Pre-existing conditions: examples
  
  • GERD
  • bowel obstruction
  • vomiting
  • hypersecretion of acid
  • Clotting abnormalities
    
    • Malabsorption of fat-soluble vit K (often malabsorbed) is necessary for the synthesis of CF II, VII, IX, and X in liver
  • Gastric lesions/resections often have iron deficiency anemia with megaloblastic vitamin B12 anemia (lack intrinsic factor or overgrowth B12 consuming bacteria in blind loop)
    
    • Check H&H for baseline anemia/active lesions

Question 14

Describe some population where you may be concerned for aspiration.

What are some measures you would take to decrease the risk for aspiration in these populations?

Answer 14

• Especially important in high risk populations: → FULL STOMACH
  
  • Pregnancy
  • DM
  • bowel obstruction
  • peritonitis
  • cirrhosis

1. Follow NPO times:
   
   1. ASA recommends fasting 4 hours for breast milk, 6 hours for non-human milk/formula, 6 hours for a light solid meal
2. Increase gastric emptying-
   
   1. Ex: prokinetics (metoclopramide)
3. Reduce gastric volume and acidity
   
   1. Volume: Decompression w/ NG tube
      
      1. Not guarantee gastric empty
      2. Impair fx of LES and UES
      3. Does NOT diminish effect of cricoid pressure
   2. Acidity:
      
      1. Nonparticulate acid (Na Citrate)- 15-30 ml
         
         1. 1 hr preop
            
            1. Increases gastric pH > 2.5. when combo w/ 10 mg metoclopramide → reduces contents < 25 mls
      2. H-2 receptor antagonists
         
         1. Famotidine → reduces gastric volume and increases gastric pH better than rantidine given a few hours before surgery.
      3. proton pump inhibitors –
         
         1. AM of sx: rapbeprazole and lansoprazole
         2. PM before sx: omeprazole
4. AW techniques:
   
   1. Cricoid Pressure- not really proven

• Contraindications:
  
  • cricotracheal injury
  • active vomiting
  • unstable c-spine.
• Complications:
  
  • esophageal rupture
  • cricoid ring fracture
  • impede ventilation/visualization w/ DL
  • Cuffed ETT
  • Proseal LMA- gastric port for decompression

1. Avoiding airway instrumentation with inadequate levels of anesthesia

• Ex: avoid wrenching
• Avoidance of Aspiration Techniques:
  
  • RSI w/ cricoid
  • Awake ETT intubation
  • NG sx Preop
  • Histamine receptor blockers preop

Question 15

What are some factors that reduce LES tone?

Answer 15

• Drugs:
  
  • Anesthetics:
    
    • VA
    • TPL
    • Propofol
  • Opioids
  • Anticholinergics
  • B-agonists
  • TCAs- tricyclics
  • Glucagon
• Cricoid Pressure
• Obesity
• Hiatal hernia
• Pregnancy

Question 16

What are some factors that increase LES tone?

Answer 16

• Anticholinesterases
• Acetylcholine
• Succinylcholine
• Alpha adrenergic agonists
• Antacids
• Reglan
• Serotonin
• Histamine
• Beta blockers

Question 17

Compare and contrast a small and large bowel obstruction?

Answer 17

Small bowel obstruction

• Segment of bowel proximal to obstruction dilates
  
  • contains gas and fluids
    
    • Increase: small bowel secretion
    • Decrease: bowel absorption
• As bowel dilation increases fluid is lost into the bowel wall and peritoneal cavity
• Progressive dilation and edema of bowel or of a volvulus
  
  • → lead to impaired bowel supply with potential necrosis and perforation
  • Perforation:
    
    • further rapid fluid loss occurs → high risk of bacterial toxemia or septicemia
• S/S of SBO- tend to get sicker faster
  
  • Hemoconcentration
  • Hypovolemia
  • hypokalemia

Large Bowel Obstruction

• Presentation: Slower, less dramatic
• Competent ileocecal valve:
  
  • closed obstruction
  • bowel dilation (right colon and cecum),
  • eventual impairment of blood supply
  • necrosis
  • perforation
• Incompetent ileocecal valve:
  
  • bowel contents reflux into small bowel
    
    • → feculent (feces) vomit
• After perforation
  
  • further rapid fluid loss occurs and pt. is at high risk of bacterial toxemia or septicemia
• _S/S: slow presentation*_
  
  • Hemoconcentration
  • hypovolemia
  • hypokalemia

Question 18

What are some fluid and electrolyte considerations with bowel obstruction?

Answer 18

Decreased intake → hypovolemic

• NPO
• Anorexia
• bowel obstruction

3^rd spacing:

• Sequestration of H20, protein & electrolytes into abdominal structures
• ascites formation
  
  • FROM → inflammatory bowel disease & intestinal obstruction

Loss of fluids

• NG tube, emesis
  
  • Loss of fluids from primarily gastric contents (pyloric stenosis can be 2000ml/day) results in hyperchloremic alkalosis and hypokalemia. Not only is K lost in the gastric fluid, it is excreted by the kidney in response to the alkalosis. (worsens)
• Diarrhea
  
  • Fluid loss from lower GIT →
    
    • predominately metabolic acidosis and hypochloremia
    • lose 3000 ml/day
    • Diarrhea may result from impaired intestinal absorption of water and electrolytes from abnormal bowel motility, or an increase in the osmotically active in the bowel lumen.
      
      • Result → Hypokalemic metabolic acidosis.

Summary:

• Gastric losses: hypochloremic alkalosis and hypokalemia
• Bowel losses: hypokalemic metabolic acidosis
• diuretics, fistula loses → contribute to F/E disturbances

Question 19

What are some anesthesia considerations with a bowel obstruction?

Answer 19

• Protect airway
  
  • RSI
  • awake
  • pre-induction NG suction
• Restore vascular and interstitial volume
  
  • Careful → not too much fluid too quickly (fluid can increase filling pressures → pulmonary edema)*
• Correct pH and electrolyte imbalance
• Normalize systemic vascular resistance (SVR)
  
  • Deficits corrected w/ combo of balanced salt solution and colloid (often sig protein losses)
    
    • Maintenance:
      
      • D51/2NS with 20/40mEq K/L
    • Vasodilators (+/-) during correction
• Miller warns that if fluids are given too quickly – they may not enter ECF and remain central increasing filling pressures and creating a pulmonary edema situation. They therefore recommend a means of evaluating cardiac output, filling pressures and SVR. See page 1731 Miller 7^th for some fluid goals if you have a PA cath and can evaluate CO.

Question 20

What are some factors to consider when using nitrous oxide in bowel surgery?

Answer 20

N2O

• 30X more soluble than nitrogen in blood
• N2O diffuses into gas-containing body cavities from the bloodstream faster than nitrogen in those cavities can diffuse out into the circulation

Factors that determine extent of distention:

• amount of gas w/in bowel
• N2O admin duration
• N2O concentration used

Consequences:

• Linear increase in bowel cavity size with time during administration of N2O
  
  • Ex: after 4 hours N2O → bowel distension 100-200% increase in gaseous bowel volume
  • 80% N2O = 5-fold increase whereas
  • 50% N2O = no more than a doubling of bowel gas.
    
    • Low concentrations of N2O during elective abdominal operations where no significant amount of gas is present in the bowel is OK
      
      • Longer/emergent bowel cases not ok

Potential complications of bowel expansion →

• difficulty w/ sx exposure
• difficulty closing
• ischemic injury
• GI viscus rupture

Consider:

• How much gas already in bowel
• How much N2O administered ([])
• How long N2O admin (duration)Ex: inhalation induction on peds pt for bowel sx
  
  • Ok to use short duration of N2O for induction → N2O turned off and see no GI changes
  • NOT ok to use 80% N2O through case
    
    • 2-3 hr mark → sx visualization diff and wont be able to close abdomen
      
      • Applies to middle ear and CNS cases

Question 21

What are some potential effects of hte PSNS during GI surgery?

Answer 21

• PSNS activity = increased bowel peristalsis
• Cholinesterase inhibitors
  
  • increase frequency and magnitude of pressure waves (peristalsis) in colon esp in diseased bowel
• Help reduce effect: Atropine, glycopyrolate and other anesthetics
• Anecdotal evidence that bowel anastomosis disruption occurs with neostigmine has never been verified experimentally
  
  • *If fragile anastomosis → use sugammadex

Question 22

Discuss the pathophyasiology behind acute pancreatitis and s/s of pancreatitis? What are some treatments for pancreatitis?

Answer 22

• Associated with:
  
  • ETOH abuse
  • gallstones
• Pancreatic auto-digestion pathogenesis
  
  • activation of trypsin inside acinar cells causing other digestive enzymes to be activated, start autodigesting pancreas
  • in normal physiology there are trypsin inhibitors inside pancreatic cells to prevent this process from happening, many pathophysiologic process (ie alcohol and gallstones) prevent this from occuring
• S/S:
  
  • Serum amylase increased (Hallmark)
  • Fluid deficit (from→)
    
    • N&V
    • GI bleeding
  • Ileus often develops
  • Hypocalcemia with tetany
  • Hyperglycemia
  • Pleural effusions and ascites with dyspnea
  • Fever and shock (50%) – some DIC
  • ARDS (20%)
  • Renal failure (25%)

Treatment:

• Aggressive IV fluid administration (up to 10L)
• NGT
• NPO
  
  • NPO to “rest” the pancreas now being rethought – enteral nutrition started earlier (evaluate inpatient NPO status carefully)
• Opioids for severe pain
• ERCP within 1st 24-72 hours to remove gallstones
  
  • **ERCP can increase risk of pancreatitis esp if diff cannulating common bile duct

Question 23

What are carcinoid tumors? Describe the pathophysiology behind them as well as s/s of carcinoid tumors.

Answer 23

• Origin: GI tract (75% of cases)
• Patho: Derived from enterochromaffin cells
  
  • Enterochromaffin cells: found in any tissue derived from endoderm
    
    • Location: esophagus to rectum
• Frequency:
  
  • Most common site: appendix
    
    • Rarely metastasizes to other locations or causes carcinoid syndrome
  • Tumors arising in the ileocecal region have the highest incidence of metastases
• S/S:
  
  • Usually asymptomatic
  • Vague symptoms:
    
    • abdominal pain
    • diarrhea
    • intermittent intestinal obstruction
    • GI bleeds
  • Non-metastatic tumors:
    
    • secrete hormones that tx to liver through portal vein → hormones inactivated
  • Most symptoms r/t hormones secreted directly into GI tract and systemic circulation
    
    • Secrete a variety of hormones, mediators, and biogenic amines

Question 24

What substances can carcinoid tumors secrete?

Answer 24

• Large quantities serotonin
  
  • (increasing platelet serotonin and metabolite 5-HIAA)
  • Serotonin syndrome*
• Histamine
• Substance P
• Catecholamines (dopamine)
• Bradykinin
• Tachykinin
• Motilin
• Corticotrophin
• Prostaglandins
• Kallikrein

Question 25

What is carcinoid synrome?

Answer 25

• Carcinoid syndrome:
  
  • 7-20% of patients with a carcinoid tumor secrete substances that cause carcinoid syndrome
    
    • usually lung or liver metastasis
• Symptoms depend on the location of the tumor and the specific hormones produced and secreted:

1. cutaneous flushing of the neck, head, upper thorax
   
   1. (kinins, histamine)
2. Bronchoconstriction
   
   1. (serotonin, bradykinin, sub. P)
3. hyperglycemia
   
   1. (serotonin)
4. hypotension
   
   1. (kinins, histamine)
5. HTN
   
   1. (serotonin)
6. diarrhea
   
   1. (serotonin, prostaglandins)
7. carcinoid heart disease
   
   1. (serotonin)

(Other format if it works better)

Serotonin

• bronchoconstriction
• hyperglycemia
• HTN
• Diarrhea
• carcinoid heart disease

Histamine

• cutaneous flushing
• hypotension

Bradykinin

• bronchoconstriction

Subnstance P

• bronchoconstriction

Prostaglandin

• diarrhea

Question 26

What is carcinoid heart disease?

Answer 26

• 60% of pts w/ carcinoid syndrome
• S/S:
  
  • Carcinoid triad: (3)
    
    • Flushing
    • diarrhea
    • cardiac dysfunction
• Usually right sided HF (left sided rare) –
  
  • Tricuspid regurgitation (predominant)
    
    • Tricuspid and/or pulm valve fibrosis w/ retraction/fixation of leaflets → leads to regurg
  • Tricuspid stenosis
  • pulmonary valve regurgitation or stenosis also occur
    
    • 50% of carcinoid deaths are cardiac failure.
    • Carcinoid plaques damage valvular integrity and are caused by fibroblast proliferation and valvulitis because of the actions of serotonin and tachykinin on plts and endothelium.
    • Fen-phen medications → interferes with serotonin metabolism and causes similar lesions. Caused HF!! Debatable if serotonin levels are responsible for cardiac lesions.
• Intramyocardial metastases and cardiac arrhythmias also seen
• 10% of patients with carcinoid have l sided heart failure though
• Pulmonary metabolism limits damage to the left heart.

Question 27

What are some medications considerations in the perioperative management of carcinoid patient

Answer 27

• Surgical excision most effective treatment
• *Octreotide (somatostatin analogue)
  
  • MOA- Interferon and octreotide may reduce tumor bulk
    
    • attenuate the release of vasoactive amine
  • Dose
    
    • need infusion of somatostatin during OR, short 1/2 life 3 minutes
    • Octreotide synthetic somatostatin analogue has longer half life (2.5 hours)
      
      • SQ 50-500 mcg q 8 hours to prevent hypotension (usually home dose)
      • Preop 10-100 mcg IV slowly 1 hour preop
        
        • preop prep includes 100 mg SQ octreotide TID 2 weeks preop weaned 1 week postop
        • normal octreotide dose needs to be taken DOS
• Anxiolytics
• H1 and H2 blocking drugs
  
  • most useful for carcinoids located in gastric area.
  • Histamine blockers may not be very useful in carcinoids originating in other areas.
  • H1 blockers (diphenhydramine) and steroids inhibit the action of bradykinin.
• Nebulized ipratropium bromide (anticholinergic)
• Steroids

Avoid medications that mediate hormone release:

• Ex: Morphine, Meperidine
• NMB: Succs, Mivicurium, Atracurium
• Epi/NE/Histamine/DA/Isopril

Question 28

What monitors are suggested for patient with carcinoid syndrome?

Answer 28

• Blood glucose monitoring – insulin gtt if indicated
• Arterial BP monitoring necessary – rapid hemodynamic changes
• CV monitoring:
  
  • CVP, PA catheter and TEE can also be considered especially with carcinoid heart disease
• Need to know baseline patient status – severity of symptoms.
  
  • positive correlation b/t carcinoid heart disease, high urinary output of 5-HIAA and post-op complications.
  • Fluid resuscitation may be necessary and electrolytes could be abnormal because of diarrhea and high gastric output.
    
    • Need to monitor electrolytes and glucose intra-op at regular intervals. → hyperglycemia

Question 29

What is somatostatin and its role and administration for a patient with carcinoid syndrome?

Answer 29

• Many carcinoid tumors have somatostatin receptors (GI regulatory peptide that reduces the production and release of gastro pancreatic hormones).
• Somatostatin (Octreotide- somatostatin analogue): reduces serotonin release from tumors.
  
  • Need infusion of somatostatin short ½ life of 3 minutes.
  • Octreotide synthetic somatostatin analogue useful in treatment of symptoms and periop management of carcinoid ½ life is 2.5 hours. SQ 50-500mcg Q8 hours titrated to effect prevents hypotension.
    
    • Preop: 10-100mcg IV slowly 1 hour pre-op.
    • Pre-op preparation should also include 100mg SQ octreotide TID 2 weeks preop weaned 1 week post-op. Normal octreotide dose should be taken in AM of surgery and also sedation should be given to prevent stress/anxiety related release of serotonin.
    • Titrate to effect
• Preventative octreotide infusion:
  
  • 50-100mcg/hr
  • → inhibits insulin release (make BG worse) Octreotide inhibits insulin release may complicate DM I management
  • Administration prior to manipulation of tumor will attenuate adverse hemodynamic effects.
    
    • SNS block can worsen hypotension. Intraoperative hypotension of sympathetic blockade should be treated with volume expansion and IV infusion of octreotide – avoid sympathomimetics like ephedrine – can increased the release of vasoactive substances from the tumor.
• Intra-op carcinoid crisis
  
  • Admin: 25-100 mcg IV octreotide (hypotension, bronchospasm)

Question 30

What is a definitive cure for carcinoid synrdomer?

Answer 30

• Definitive cure – only by surgery. Those patients who are not candidates for hepatic resection of metastases, hepatic artery occlusion or embolization – palliative intervention. May need tricuspid or pulmonic valve replacement. Treatment of carcinoid syndrome is with the synthetic somatostain analogue octreotide – prevents the release of vasoactive products from carcinoid tumors. High dose steroids advocated to inhibit bradykinin secretion.

Question 31

Anesthesia management considerations ofr patient with carcinoid syndrome?

Answer 31

GOAL: Prevent carcinoid crisis

• Consequences: vasoactive and bronchoconstrictive consequences (stress, physical or chemical stimulation, manipulation of the tumor, embolization or chemotherapy)

Technique:

• DEEP for DVL and ETT placement
• Avoid histamine releasing drugs (Succ, NMB that release succ, miva, atra, d-tub, TPL????, morphine, meperidine)
  
  • Goal should be to block histamine and serotonin receptors and avoid drugs that facilitate mediator release from tumor cells
  • Sux has been used without adverse effects but it could stimulate hormone release via fasciculations and increased abdominal pressure
• All volatile agents acceptable need to keep in mid CV fragility though
  
  • Because serotonin causes sedating anesthetic requirements could be reduced.
• Regional – epidural better than spinal (slow titration – avoid hypotension) – tx fluids and octreotide
  
  • Epidural is controversial because of catecholamine restrictions.
    
    • Epidural in these pts after being treated with octreotide is safe provided the anesthetic is administered in a graded manner and hemodynamic monitoring and diluted concentration of LA is used
  • Use with caution
• Ondansetron (serotonin antagonist)
  
  • great anti-emetic choice
• Contraindicated:
  
  • Ketamine
    
    • → activation of SNS and release of catecholamines may activate kallikreins.

Question 32

What is intraop treatment for hypotension and hypertension in patients ith carcinoid syndrome

Answer 32

• Intraop HypoTN:
  
  • Vasopressin for refractory hypotension
  • Aprotinin (kallikrein inhibitor)- 2^nd line for hypotension
    
    • SNS block can worsen hypotension. Intraoperative hypotension of sympathetic blockade should be treated with volume expansion and IV infusion of octreotide – avoid sympathomimetics like ephedrine – can increased the release of vasoactive substances from the tumor.
• Intraop HTN:
  
  • labetalol
  • increasing VA dose
• Avoid drugs known to precipitate a crisis (histamine, norepinephrine, epinephrine, and dopamine, ephedrine) isoproterenol
• Catecholamines may increase serotonin release (vasoconstriction) and kallikrein release (activates bradykinins which cause vasodilation).
• If epi is needed a small dose is recommended until response can be evaluated.
  
  • If it is beneficial an infusion can be started.

Question 33

Postoperative management of patient with carcinoid syndrome?

Answer 33

• Secretion of vasoactive substances from residual tumor/metastasis and emotional and physical stress related release can still occur

1. Intensive hemodynamic monitoring
2. Octreotide administration continued
3. Effective post-operative analgesia