Nir Hus Absite review q3 4
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Transcript of Nir Hus Absite review q3 4
Absite topics 7-12
Nir Hus
Nir Hus
Q7: Timing of the first prophylactic antibiotic dose
The first prophylactic antibiotic dose should provide a sufficient antibiotic serum level throughout the surgery to combat organisms most likely to cause a site infection.
The first dose be timed to occur within 60 minutes before the surgical incision is made.
If a fluoroquinolone or vancomycin is chosen for prophylaxis, the first dose should be administered within 120 minutes of the start of surgery.
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Timing of the first prophylactic antibiotic dose
For most surgeries, the use of prophylactic antibiotics should end within 24 hours after surgery.
Cefazolin or cefuroxime are suggested for cardiothoracic surgery, with the recommendtion of extension of prophylactic antibiotics up to 72 hours to avoid deep sternal infections.
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Surgery Prophylaxis CommentsCardiothoracic Cefazolin or cefuroxime; if
beta lactam allergy, vancomycin or clindamycin
72-hour duration advocated by some, but 24 hours is likely to be adequate
Vascular Cefazolin or cefuroxime; if beta lactam allergy, vancomycin with or without gentamicin, or clindamycin
Colon Oral: neomycin, with erythromycin base or metronidazole
Combination of oral and parenteral prophylaxis may decrease infection rates
Adapted with permission from Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis 2004,38:1707.
Nir Hus
Timing of the first prophylactic antibiotic dose
Adapted with permission from Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis 2004,38:1707.
Nir Hus
Q8: Incarcerated Groin Hernia
Incidence of incarceration ~10% among inguinal hernias.
Cannot be reduced into the abdominal cavity.
Strangulated hernias have incarcerated contents with vascular compromise.
Frequently, intense pain is caused by ischemia of the incarcerated segment.
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Q8: Incarcerated Groin Hernia
Incarcerated inguinal hernias present with abdominal distention, pain, nausea, and vomiting due to intestinal obstruction.
Plain abdominal X-rays may verify intestinal obstruction in cases of incarceration.
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Q9: Short Bowel Syndrome
Pathophysiology:DehydrationElectrolyte derangementsAcidic diarrheaSteatorrheaMalnutririonWeight loss
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Q9: Short Bowel Syndrome
Etiology for extensive resection: Congenital anomalies leading to short bowel syndrom include –
Intestinal atresia Midgut volvulus w/ intestinal necrosis Necrotizing enterocolitis.
In Middle-aged adults – IBS Trauma
In the elderly- Mesenteric ischemia Strangulated hernia Extensive resection due to malignancy.
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Q9: Short Bowel Syndrome
Resection resulting in less than 120cm of intact bowel leads to SBS.
Resection of up to 50% of small bowel is tolerated.
Resection of up to 70% is tolerated if terminal ileum and cecum are preserved.
Infants may tolerate upto 85% of small bowel resection.
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Q9: Short Bowel Syndrome
Loss of the ileocecal valve results in rapid emptying of enteral contents into the colon and reflux of colonic bacterial flora into small bowel.
The entire jejunum can be resected without serious adverse nutritional sequela.
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Q9: Short Bowel Syndrome
Adaptation:Cellular hyperplasia and bowel hypertrophy
occur over a 2- to 3-year period, increasing the absorptive surface area.
Fat absorption is most likely permanently impaired.
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Q10: Malabsorption & Malnutrition
Gastric hypersecretion Cholelithiasis Hyperoxaluria & Nephrolithiasis Diarrhea & Steatorrhea Intestinal Microflora
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Q10: Malabsorption & Malnutrition
Gastric hypersecretion – in early postop period. Increased acid load may injure distal bowel mucosa hypermotility & impaired absorption.
Cholelithiasis – altered bilirubin metabolism after ileal resection increased risk of pigmented gallstones stones that is 2nd to a decreased bile salt pool. TPN also may lead to increased risk of cholelithiasis.
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Q10: Malabsorption & Malnutrition
Hyperoxaluria & Nephrolithiasis – Excessive fatty acids within the colonic lumen
bind intraluminal calcium. Unbound oxalate that normally is made
insoluble by Ca-binding and is excreted in feces is thus, readily absorbed.
This results in hyperoxaluria and calcium oxalate urinary stone formation.
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Q10: Malabsorption & Malnutrition
Diarrhea & Steatorrhea – Caused by rapid intestinal transit.Presence of hyperosmolar enteric contents.Disruption of enterohepatic bile acid
circulation.Fat absorption is most severly impaired by
ileal resection.
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Q10: Malabsorption & Malnutrition
Intestinal Microflora – Loss of ileocecal valve permits reflux of
colonic bacteria into small bowel. Intestinal dysmotility increases colonization.Bacterial overgrowth & change in flora results
in pH alteration & deconjugation of bile salts.This results malabsorption, fluid loss,
decreased vit B12 absorption.
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Q11: Effect of ASA on Plt.
Irreversibly acetylates cyclooxygenase Results in inhibiting plt synthesis of
Thromboxane A2. Decreases plt function. Higher doses than > 80 – 160mg PO / day
donot have a higher efficacy.
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Q12: Synergism Ampicillin / Sulbactam (Unasyn)
PCN: GPC – streptoccocci, syphilis, GPR - Neisseria m., C. perfringens, Beta-hemolytic strep, antrax Not effective for Staph or Enterococcus
Ampicillin/amoxicillin: PCN + Enterococcus coverage Unasyn: PCN + GPC (staph & strep), GNR +/-
anaerobic coverage, enterococci. NOT FOR Pseudomonas, Acinetobacter, or Serratia. Sulbactam & Clavulanic acid – are beta-lactamase
inhibitors. Nir Hus