GI Flashcards
1
Q
What are some pre-op considerations for GI disease?
A
- Assessment of intravascular fluid volume and electrolyte concentration and nutrition
- Often have GERD, bowel obs, vomiting, or hypersecretion of acid
- Clotting abnormalities may need to be corrected b/c fat soluble vit K may be malabsorbed and is necessary for formation of factor II, VII, IX, X
- Gastric lesions/resections often have iron deficiency anemia with megaloblastic vitamin B12 anemia
- lack inrinsic factor or overgrowth of B12 consuming bacteria in blind loop
2
Q
How can we control the amount of gastric contents?
A
- ASA NPO guidelines
- Increase gastric emptying with prokinetics (metoclopramide)
- Reduce gastric volume and acidity with NG tube, nonparticulate, H2 antagonist, PPI
- Cricoid pressure, cuffed ETT or proseal LMA
3
Q
What factors can reduce LES tone?
A
- volatile agents, TPL, propofol
- opioids
- anticholinergics
- B-agonists
- TCAs
- Glucagon
- cricoid pressure
- obesity
- hiatal hernia
- pregnancy
4
Q
What factors can increase LES tone?
A
- anticholinesterases
- acetylcholine
- succinylcholine
- alpha adrenergic agonists
- antacids
- reglan
- serotonin
- histamine
- beta blockers
5
Q
What is a hiatal hernia?
Anesthesia considerations?
A
- Hiatal hernia- protrusion of portion of stomach through the hiatus of the diaphragm and thoracic cavity
- Most pts do not have symptoms of reflux- LES integrity is more important
- Aspiration precautions only indicated if pt is symptomatic!
6
Q
What is the pathophysiology associated with a small bowel obstruction?
A
- segment of bowel proximal to obstruction dilates and contains gas and fluids
- there is an increase in small bowel secretion with a decrease in absorption
- as bowel dilation increases fluid is lost into the bowel wall and peritoneal cavity
- progressive dilation and edema of the bowel or of a volvulus may lead to impaired bowel supply with potential necrosis and perforation
- after perforation further rapid fluid loss occurs and pt is at high risk of bacterial toxemia
- hemoconcentration, hypovolemia, and hypokalemia
- K is not only lost in gastric fluid (vomiting, diarrhea) but also secreted by kidney in response to the alkalosis
7
Q
What happens with a large bowel obstruction?
competent vs incompetent ileocecal valve?
A
- Slower, less dramatic presentation than small bowel
- Competent iliocecal valve = closed obstruction, bowel dilation (right colon and cecum), with eventual impairment of blood supply, necrosis, and perforation
- incompetent iliocecal valve = bowel contents reflux into small bowel leading to feculent vomiting
- after perforation further rapid fluid loss occurs and pt is at high risk of bacterial toxemia
- hemoconcentration, hypovolemia, and hypokale
8
Q
What happens to fluid and electrolyte balance with a bowel obstruction?
A
- Decreased intake- NPO, anorexia
- 3rd spacing
- sequestration of H2O, protein, and electrolytes into abdominal structures leads to ascites formation which leads to IBD and intestinal obstruction
- Loss of fluids via NG tube, emesis, diarrhea, diuretics, fistula loses
- Side effects of therapies
- hypophosphatemia from parenteral nutrition
- hyperkalemia or cardiac arrhythmias from too vigorous treatment of hypokalemia
- CHF from too rapid or vigorous tx of hypovolemia
9
Q
What are the goals when caring for a pt with a bowel obstruction?
A
- Protect the airway
- RSI ns awake vs pre-induction NG suction
- restore vascular and interstitial volume
- correct pH and electrolyte imbalance
- normalize systemic vascular resistance
- deficits corrected with a combination of balanced salt solution and colloid (protein losses)
- maintenance D5 1/2NS with 20/40 mEq KCL
- may need vasodilators
10
Q
What are the parasympathetic effects on the GI tract?
How does our anesthetic affect this?
A
- PSNS activity = increased bowel peristalsis
- Cholinesterase inhibitors increase the frequency and magnitude of pressure waves in the colon, especially in diseased bowel
- Atropine, glyco, and other anesthetics help reduce this effect
- Anecdotal evidence that bowel anastomosis disruption occurs with neostigmine has never been verified experimentally
11
Q
What is acute pancreatitis?
What are the symptoms?
A
- Acute pancreatitis is pancreatic auto-digestion
- associated with ETOH abuse and gallstones
- hallmark = increased serum amylase
- Symptoms:
- excruciating mid-epigastric abd pain that radiates to back, relieved w/sitting
- fluid deficit d/t N/V and GI bleed
- ileus often develops
- hypocalcemia with tetany
- pleural effusions and ascites with dyspnea
- fever and shock (50%)
- ARDS (20%)
- ARF (25%)
12
Q
How is acute pancreatitis treated?
A
- Aggressive IV fluid administration (up to 10 L)
- NPO to “rest” the pancreas now being reconsidered- enteral nutrition is being started earlier
- Opioids for severe pain
- ERCP within 1st 24-72 hrs to remove gallstones
13
Q
What do you often see in a pt with Crohn’s disease?
A
- Bowel obstruction- malnourished and dehydrated
- Loss of fluids and nutrients through fistulae
- often very ill on steroids and immunosuppressive therapy
14
Q
What do you often see in a pt with Ulcerative colitis?
A
- Electrolyte and fluid imbalances
- Vit B12 and folate deficiency
- assess for arthritis, iritis, and hepatitis
- often come to OR to remove precancerous lesions, hemorrhage, bowel perforation, bowel obstruction, toxic megacolon
- Often extensive operations; total colectomy or total proctocolectomy
- steroids and immunosuppressive drugs
15
Q
What are carcinoid tumors?
Where are they usually found?
Symptoms?
A
- Tumors derived from enterochromaffin cells
- can be found in any tissue with endoderm (esophagus to rectum)
- most frequent site is appendix, but these rarely metastacis or produce carcinoid syndrome
- tumors arising in the ileocecal region have the highest incidence of metastases
- Usually asymptomatic- may have vague:
- abdominal pain
- diarrhea
- intermittent intestinal obstruction
- GI bleeds
