Ep-PAINE-nym



Barrett’s Esophagus

Other Known Aliases – Allison-Johnstone anomaly

Definitionmetaplastic change of the mucosal cells of the lower esophagus from normal stratified squamous epithelium to simple colunar epithelium and interspaced goblet cells

Clinical Significance these histologic changes are premaligant and significantly increases a patient’s risk for developing esophageal adenocarcinoma.

HistoryNamed after Norman Rupert Barrett (1903-1979), an Australian-born British thoracic surgeon who received his medical doctorate from Trinity College, Cambridge. He would practice his entire career at St. Thomas Hospital, with a brief training period in 1935-1936 when he traveled to the US on a Rockfeller Traveling Fellowship. It was here that he decided to pursue thoracic surgery instead of GI surgery. In 1947, he performed the first successful surgical repair of a ruptured esophagus. He would publish his eponymous findings of histologic changes of the distal esophagus in 1950, but erroneously believed this was due to congenitally shortened esophagus with a portion of the stomach trapped in the chest. Allison and Johnstone were the first to argue that these changes were esophagus, not stomach, and termed these ulcers “Barrett’s ulcers”. Of note, Allison first described this condition in 1948 before Barrett’s publication.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Barrett NR. Chronic peptic ulcer of the oesophagus and oesophagitis. British Journal of Surgery. 1950;38:175-182. [link]
  7. P. R. Allison, A. S. Johnstone. The esophagus lined with gastric mucous membrane. Thorax, 1953, 8: 87.
  8. P. R. Allison. Peptic ulcer of the Oesopahgus. Thorax, 1948, 3: 20.

#65 – Pancreatitis



***LISTEN TO THE PODCAST HERE***



Epidemiology

  • 13-45 per 100,000 person incidence in the US
  • Most common GI cause of hospital admission in the US
    • > 300,000 per year
    • Average 4-day stay with cost > $6000/case
  • Equal gender representation across the lifespan
    • Alcohol pancreatitis more common in men
  • 2-3 fold higher rates in African Americans

Risk Factors and Etiologies

  • Gallstones
    • 40-70% of cases
      • Only 3-7% of patients with gallstones develop pancreatitis
    • Two theorized mechanisms
      • Reflux of bile into the pancreatic duct
      • Obstruction at the ampulla
    • Magic number is 5mm
      • Small enough to pass through cystic duct, but still get obstructed at ampulla
  • Alcohol
    • 25-35% of cases
    • Interesting data to show that it is not just alcohol that causes pancreatitis
      • 5 out of 100,00 patents with alcohol abuse develop pancreatitis
    • Several mechanisms theorized
      • Sensitization of acinar cell to CCK-induced activation of zymogens
      • Potentiation of the effect of CCK
      • Generation of toxic metabolites
      • Sensitization of the pancreas to toxic insults
      • Activation of pancreatic stellate cells to increase production of matrix proteins
  • Idiopathic (genetic)
    • 15-25% of patients with pancreatitis have no identifiable pathologic cause
    • These cases are largely theorized to have complex genetic risk profiles
  • Hypertriglyceridemia
    • 1-14% of cases
    • > 1000 mg/dL increases risk
  • Post-ERCP
    • 3% of patients undergoing diagnostic ERCP
    • 5% of patients undergoing therapeutic ERCP
    • 25% of patients undergoing sphincter of Oddi measurements
  • Medications
    • < 5% of cases
    • Classification system (Ia, Ib, II, III, IV)
    • Prognosis is excellent and mortality is very low
  • Obesity
  • Smoking
  • Diabetes

Pathogenesis

  • Pancreatic enzymes synthesis continues while secretion is slowed or halted
  • HIT #1 –  Intraacinar activation of proteolytic enzymes (trypsin)
    • Cascade of enzyme release and activation then occurs
    • Ultimately, causes autodigestion of the pancreas
  • HIT #2 – Microcirculatory injury
    • Damage to the pancreas via autodigestion leads to vasoconstriction, decreased oxygenation, and progressive ischemia
      • Leads to edema and further decreased secretion of enzymes
  • HIT #3 – Leukocyte infiltration, cytokine release, and oxidative stress
    • Leads to widespread inflammation and induce thrombosis and hemorrhage
    • Ultimately, causes necrosis
  • Two main classifications
    • Interstitial pancreatitis – blood supply is maintained
    • Necrotizing pancreatitis – blood supply is affected

Signs and Symptoms

  • History
    • Epigastric pain
      • May radiate to the back
      • May radiate to the right shoulder
        • Kehr’s sign
    • Nausea
    • Vomiting
    • Dyspneic
      • Severe disease can cause diaphragmatic irritation and pleural effusions
  • Physical Examination
    • Fever
    • Tachycardia
    • Epigastric tenderness
    • Abdominal distention
    • Hypoactive bowel sounds
    • Jaundiced
    • Abdominal ecchymosis (necrotizing disease)
      • Cullen’ sign – umbilical
      • Grey Turner’s sign – flank
      • Fox’s sign – thigh (parallel but inferior to inguinal ligament)

Laboratory Studies

  • Serum amylase
    • Rises within 6 hours, returns to normal in 3-5 days
    • Should not be used (sensitivity 67-83%, specificity 85-98%)
      • Short-half life (10 hours)
        • Patients presenting > 24 hours after onset can have normal amylase
      • Miss up to 20% of cases of alcohol pancreatitis
        • Due to inability of parenchyma to produce amylase
      • Miss up to 50% of cases of hypertriglyceridemia
        • Triglycerides interfere with assay
  • Serum lipase
    • Sensitivity 85-100%
    • Rises 4-8 hours, peaks at 24 hours, returns to normal in 8-14 days
  • LFTs
    • Evaluate for cholestatic elevations (ALP, bilirubin, GGT)
  • BMP
    • Need glucose, BUN, and calcium for some of the risk calculators
  • CBC
    • Leukocytosis often is present and helps grade severity
    • May show hemoconcentration due to volume depletion

Imaging Studies

  • Ultrasound
    • Often the quickest and easiest study to obtain in the ED
    • Can evaluate gallbladder pathology, stones, and peripancreatic fluid
    • Ileus can obscure imaging due to gas overlying the pancreas
  • CT
    • Better detail and can evaluate more structures
  • MRI
    • Higher sensitivity in early disease
    • Longer to obtain
  • Revised Atlanta Criteria
    • Six CT morphological features
    • Interstitial edema
      • Parenchymal enhancement by IV contrast
    • Necrotizing findings
      • Lack of parenchymal enhancement
      • Peripancreatic fluid collection or walled-off necrosis
    • Acute peripancreatic fluid collection
      • Homogenous fluid collection
      • Confined to normal peripancreatic fascial planes
      • No definable encapsulating wall
      • Adjacent to pancreas (no intrapancreatic extension)
    • Pancreatic pseudocyst
      • Well-circumscribed, well-defined wall with homogenous fluid density
      • No non-liquid component
    • Acute necrotic collection
      • Heterogenous with non-liquid density of varying degrees
      • No definable wall
      • Intra-, or extra-pancreatic in location
    • Walled-off necrosis
      • Heterogenous with liquid and non-liquid densities
      • Well-defined wall that is completely encapsulated
      • Intra-, or extra-pancreatic in location

Diagnosis

  • Need 2 of the following 3 criteria:
    • Acute onset of persistent, severe, epigastric pain
    • Elevation of amylase or lipase > 3x ULN
    • Radiographic findings on imaging

Classification of Severity

  • Mild
    • Absence of organ failure or local/systemic complications
  • Moderately severe
    • Transient organ failure (resolves with 48 hours) and/or systemic complications without persistent organ failure
  • Severe
    • Persistent organ failure

Prognosis Predictor Scoring Systems

  • Ranson’s Criteria
  • BISAP Score
    • 0-2 points – low mortality
    • 3-5 points – high mortality

Management

  • Patients with mild pancreatitis can be admitted to floor/wards
  • Patients with moderately severe or severe should be admitted to ICU
  • Fluid resuscitation
    • 5-10 mL/kg/hour with crystalloid
      • Careful, using LR in patients with hypercalcemic induced pancreatitis
    • Bolus 20 ml/kg over 30 minutes if hypotensive/tachycardic
    • Adjust using goal-directed metrics even 6 hours for first 24 hours-48 hours
      • BUN, H/H, MAP (65-85 mmHg), HR (< 120bpm), UOP (>0.5 mL/kg/hr)
  • Pain control
    • Opioids are safe and PCA can work well
      • Fentanyl has better safety profile
        • 20-50 mcg with 10-min lockout
  • Nutrition
    • Can reintroduce within 24 hours if no nausea, vomiting, and decreasing pain and inflammatory markers
      • Start with low-residue, low fat, soft diet and advance as tolerated
    • Supplemental nutrition generally needed for moderately severe and severe cases, or if unable to tolerate oral nutrition within 5 days
      • Enteral > parental with placement of jejunal feeding tube beyond the ligament of Treitz
        • Helps prevent bacterial translocation
      • Parenteral is indicated if nutritional goals are not achieved with 48-72 hours due to pain or intolerance
      • Consult your hospital nutritional team and/or dietician for help
  • Antibiotics
    • No evidence to support prophylactic antibiotics
      • Most infected necroses will occur late in clinical course (5-10 days after admission)
  • Treat underlying causes
    • Gallstone pancreatitis
      • ERCP should be performed within 24 hours of admission
      • Cholecystectomy should be performed within 7 days and often during same hospitalization
    • Hypertriglyceridemia
      • Therapeutic plasma exchange and insulin therapy

Complications

  • Necrosis
  • Pseudocyst
  • Splanchnic venous thrombosis


References

  1. Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013; 144(6):1252-61. [PDF]
  2. Conwell DL, Banks PA, Greenberger NJ. Acute and Chronic Pancreatitis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e. McGraw-Hill;
  3. Mechanisms of alcoholic pancreatitis. Proceedings of a conference. Chicago, Illinois, USA, November 2002. Pancreas. 2003; 27(4):281-355. [pubmed]
  4. Nawaz H, Koutroumpakis E, Easler J, et al. Elevated serum triglycerides are independently associated with persistent organ failure in acute pancreatitis. Am J Gastroenterol. 2015; 110(10):1497-503. [pubmed]
  5. Scherer J, Singh VP, Pitchumoni CS, Yadav D. Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol. 2014; 48(3):195-203. [PDF]
  6. Kahaleh M, Freeman M. Prevention and management of post-endoscopic retrograde cholangiopancreatography complications. Clin Endosc. 2012; 45(3):305-12. [PDF]
  7. Lankisch PG, Dröge M, Gottesleben F. Drug induced acute pancreatitis: incidence and severity. Gut. 1995; 37(4):565-7. [PDF]
  8. Forsmark CE, Swaroop Vege S, Wilcox CM. Acute Pancreatitis N Engl J Med. 2016; 375(20):1972-1981.
  9. Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol. 2002; 97(6):1309-18. [pubmed]
  10. Wu BU, Johannes RS, Sun X, Tabak Y, Conwell DL, Banks PA. The early prediction of mortality in acute pancreatitis: a large population-based study. Gut. 2008; 57(12):1698-703. [pubmed]
  11. Vege SS, DiMagno MJ, Forsmark CE, Martel M, Barkun AN. Initial Medical Treatment of Acute Pancreatitis: American Gastroenterological Association Institute Technical Review. Gastroenterology. 2018; 154(4):1103-1139. [pubmed]
  12. Basurto Ona X, Rigau Comas D, Urrútia G. Opioids for acute pancreatitis pain. Cochrane Database Syst Rev. 2013; [pubmed]
  13. Casaer MP, Mesotten D, Hermans G, et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med. 2011; 365(6):506-17. [pubmed]
  14. Kutsogiannis J, Alberda C, Gramlich L, et al. Early use of supplemental parenteral nutrition in critically ill patients: results of an international multicenter observational study. Crit Care Med. 2011; 39(12):2691-9. [pubmed]
  15. Aboulian A, Chan T, Yaghoubian A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010; 251(4):615-9. [pubmed]
  16. Uhl W, Müller CA, Krähenbühl L, Schmid SW, Schölzel S, Büchler MW. Acute gallstone pancreatitis: timing of laparoscopic cholecystectomy in mild and severe disease. Surg Endosc. 1999; 13(11):1070-6. [pubmed]
  17. Ipe TS, Pham HP, Williams LA 3rd. Critical updates in the 7 edition of the American Society for Apheresis guidelines. J Clin Apher. 2018; 33(1):78-94. [pubmed]

PAINE #PANCE Pearl – Gastrointestinal



Question

47yo man presents to the emergency department after an episode of hematemesis at the end of a 2 day alcoholic binge. He reports drinking 1-3 handles of vodka over the weekend after his 14 consecutive day, third shift schedule every month at the local manufacturing plant. He reports moderate central chest pain, but denies shortness of breath. Vitals are BP-110/82 mmHg, HR-112, RR-14, O2-98%, and temp-99.2o. Physical exam is unremarkable, hemoccult is negative, and labs are below.

  1. What are the three (3) main differentials you need to consider?
  2. What is the most likely diagnosis based on exam and labs?


Answer

  1. Given the history and risk factors, the top three differentials you need to consider are variceal bleed, Mallory-Weiss tear, and Boerhaave’s syndrome.
  2. The most likely of these is Mallory-Weiss tear. The unremarkable physical exam points away from Boerhaave’s as patients most commonly present with mediastinitis and, in some instances, sepsis. Other physical examination findings of Boerhaave’s include subcutaneous emphysema of the neck with crepitus and Hamman’s sign of medisatinal crunch on auscultation. Varices can self-tamponade after an acute bleed, but given the patient’s hemodynamic status being stable with a normal H/H and negative hemoccult also move this down the differential list.

Ep-PAINE-nym



Charcot’s Triad

Other Known Aliases – none

Definitiontriad of physical examination findings seen with ascending cholangitis and includes jaundice, fever, and right upper quadrant pain.

Clinical Significance this is a classic triad to memorize for your surgery rotation to help differentiate cholecystitis, cholelithiasis, and cholangitis.

HistoryNamed after Jean-Martin Charcot (1825-1893), a French neurologist and professor of anatomic pathology who recieved his medical doctorate from the University of Paris in 1853. He would start his career at the famous Hôpital de Salpêtrière and stay there for over 30 years establishing the reputation of this hospital as the premier training center in Europe. He would also create the first neurology clinic in all of Europe at the Salpêtrière where his reputation would be solidified as the “father of modern neurology”. His career is too prestigious to give it justice in a quick eponym review, as evidenced by at least 15 current eponyms bearing his name.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com

PAINE #PANCE Pearl – Gastrointestinal



Question

47yo man presents to the emergency department after an episode of hematemesis at the end of a 2 day alcoholic binge. He reports drinking 1-3 handles of vodka over the weekend after his 14 consecutive day, third shift schedule every month at the local manufacturing plant. He reports moderate central chest pain, but denies shortness of breath. Vitals are BP-110/82 mmHg, HR-112, RR-14, O2-98%, and temp-99.2o. Physical exam is unremarkable, hemoccult is negative, and labs are below.

  1. What are the three (3) main differentials you need to consider?
  2. What is the most likely diagnosis based on exam and labs?

Ep-PAINE-nym



Roux-en-Y Anastomosis

Other Known Aliasesend-to-end surgical anastomosis

Definitiongastrointestinal tract is divided into two limbs (proximal, Roux limb and a distal limb) and are re-anastomosed farther down the GI tract, typically in the jejunum

Clinical Significance this type of surgery is the traditional form of gastric bypass, where the proximal, Roux limb serves as the food reservoir and somach and the distal limb allows for physiologic drainage of gastric, hepatic, and pancreatic enzymes to aid in digestion. Other conditions it can be used is are chronic pancreatitis, alkaline gastritis, and various GI substitution procedures.

HistoryNamed after César Roux (1857-1934), who was a Swiss surgeon and received his medical doctorate from the University of Bern 1880. He would stay on at his alma mater and assist Theodor Kocher until 1887, when he became chief of surgery at cantonal hospital of Lausanne. He would go on to have a modest career in surgery notable for two historical accomplishments. In 1893, he performed his eponymous procedure on a patient with gastric strictures from peptic ulcer disease to alleviate his obstruction symptoms. In 1926, the year of his retirement, he was the first surgeon to successfully remove a pheochromocytoma….7 months before Charles Mayo performed the same operation in the United States. Harvey Cushing visited his clinic in 1900 and said “he is a rough diamond-looks like Kipling-does excellent work and comes nearer to being the kind of man I am looking for than anyone else I have seen”.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. C. Roux. De la gastroenterostomie. Revue de chirurgie, 1893, 13: 402-403.
  7. Hutchison R, Hutchinson AL. César Roux and His Original 1893 Paper. Obesity Surgery. 2010;20;953-956 [link]

Ep-PAINE-nym



Whipple Procedure

Other Known Aliasespancreaticoduodenectomy

Definitionpancreaticoduodenectomy cholecystectomy, choledochojejunostomy, pancreaticojejunostomy, and gastrojejunostomy

Clinical Significance this type of surgery is performed to resect pancreatic head tumors. It generally performed at large, high-volume medical centers as this has been shown to reduce mortality to less than 5%. An experienced surgeon can complete this surgery in < 6 hours with < 500mL of blood loss. Barring any postoperative complications, most patients are discharged from the hospital in 7-10 days.

HistoryNamed after Allen Oldfather Whipple (1881-1963), who was an American surgeon and received his medical doctorate from Columbia University College of Physicians and Surgeons in 1908. He was appointed faculty at Columbia and Presbyterian Medical Centers before going on to become professor of surgery at his alma mater for the next 25 years. He published the report of his eponymous surgery in 1935 and only performed it 37 times in his lifetime. He also supervised Virginia Apgar and advised her to pursue a career in anesthesiology because he saw an “energy and ability to make significant contributions” that would advance both fields. Other notable accomplishments include helping establish the American Board of Surgery and establishing another eponymous diagnostic triad for insulinoma.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Whipple AO, Parsons WB, Mullins CR. TREATMENT OF CARCINOMA OF THE AMPULLA OF VATER. Ann Surg. 1935; 102(4):763-79. [PDF]
  7. Johna S. Allen Oldfather Whipple: A Distinguished Surgeon and Historian Dig Surg. 2003; 20(2):154-162. [link]

#61 – Cholelithiasis and Cholecystitis



***LISTEN TO THE PODCAST HERE***



Anatomy

  • 4 anatomic areas of gall bladder
    • Fundus
      • Rounded, blind end that extends 1-2 cm beyond the liver margin
      • Contains most of the smooth muscle
    • Body
      • Main storage area
      • Contains the elastic tissue allowing for distention
        • Normally holds 30-50mL and can stretch to 300mL
    • Infundibulum (Hartmann’s Pouch)
      • Mucosal outpouching at the junction of the neck and cystic duct
    • Neck
      • Lies in the deepest part of the fossa
  • Cystic Artery
    • Branch of the right hepatic artery
    • Found in the cystohepatic triangle
      • Cystic duct, common hepatic duct, superior/inferior margin of liver
      • Triangle of Calot
        • Cystic duct, common hepatic duct, cystic artery
        • Lymph node can be found in near the insertion of the cystic artery
          • Calot’s node (Lund’s or Mascagni’s)
  • Cystic duct
    • Spiral valves of Heister
      • Mucosal folds in the proximal cystic duct that make cannulation difficult
    • Joins the common hepatic duct to form the common bile duct
    • Highly variable anatomy

Physiology

  • 80% of bile is stored in the gall bladder
    • Infundibulum secretes glycoproteins to protect mucosa
  • Cholecystokinin released from neuroendocrine cells of the duodenum during meal
    • Stimulates release of bile from gallbladder
      • 50-70% over 30-40 minutes
    • Causes relaxation of Sphincter of Oddi
  • Vagal stimulation causes contraction of gallbladder

Stone Formation

  • Major solutes in bile are bilirubin, bile salts, phospholipids (lecithin), and cholesterol
  • 80% are cholesterol
    • Supersaturation of bile with cholesterol exceeds the ability of phospholipids and bile salts to maintain solubility

Pathogenesis of Cholecystitis

  • Phospholipid A (secreted by the gall bladder mucosa) released in response to gall bladder trauma (stone)
    • Catalyzes conversation of lecithin to lysolecithin
      • Leads to mucosal and luminal irritation and inflammation

Epidemiology and Risk Factors

  • 90-95% of patients with cholecystitis have stones
    • Only 20% of patients with stones with develop cholecystitis
    • 10-15% of patients have stones on autopsy
  • Risk Factors
    • High fat diet
    • Older age
    • Female > male
    • Higher BMI
      • Rapid weight loss
    • Pregnancy
    • Previous surgeries
      • Terminal ileum resection, gastric/duodenal surgery

Signs and Symptoms

  • History
    • Right upper quadrant abdominal pain
      • Steady, “boring” pain lasting hours
      • Worsened by fatty foods
    • Right scapular pain (Boas’ sign)
      • Hyperesthesia between 9th-11th rib
    • Fever, nausea, vomiting, anorexia
  • Physical Examination
    • Fever, tachycardia
    • Peritoneal signs
      • Pain with movement and percussion
    • Voluntary and involuntary guarding
    • +/- jaundice
    • Inspiratory arrest on deep RUQ palpation (Murphy’s sign)

Diagnostic Studies

  • Laboratory Studies
    • Leukocytosis with neutrophilic shift
    • LFTs generally normal, but may show:
      • Elevated direct (conjugated) bilirubin
      • Elevated alkaline phosphatase
      • Elevated GGT
  • Ultrasound is the initial test of choice
    • Length > 10 cm
    • Wall thickness > 3mm
    • Pericholecystic fluid
    • Sludge
  • Cholescintigraphy using 99m Tc-hepatic iminodiacetic acid (HIDA) Scan
    • Used if ultrasound is inconclusive
    • Intravenous injection of HIDA and visualization of dye in gallbladder, bile ducts, and small bowel within 30-60min
      • If not visualized after 1 hour, morphine can be given and waiting 3-4 hours
        • If no visualization = cholecystitis
  • Magnetic Resonance Cholangiopancreatography (MRCP)
    • Used if evidence of choledocolithiasis or elevated LFTs

Management

  • Admission
  • IV fluids
  • NSAIDs
    • Ketorolac 30-60mg IV/IM
  • Opioids
    • Meperidine NOT superior to morphine
  • Antibiotics
    • Low Risk
    • High Risk
  • Indication for Emergent Cholecystectomy
    • Necrosis
    • Perforation
    • Emphysematous cholecystitis
    • High fever
    • Hemodynamic instability
  • Interval Cholecystectomy (low risk)
    • Within 3 days of admission after therapies above and clinical improvement
    • Most can be discharged in 1-2 days postop
  • Gall bladder drainage (high risk)
    • Percutaneous cholecystostomy
      • Critically ill or septic
      • > 72 hours from symptom onset
      • Failure of antibiotic therapy
      • No coagulopathy
    • Endoscopic transpapillary/transmural drainage
      • Liver disease
      • Ascites
      • Coagulopathy
    • If improvement within 72 hours, proceed with laparoscopic cholecystectomy
      • If not, may need emergent open cholecystectomy
Percutaneous Cholecystostomy

Management Algorithm


Steps of Laparoscopic Cholecystectomy

  1. Dissect peritoneum overlying the cystic duct and artery
  2. Division and clipping of cystic duct close to gallbladder
    • Perform intraoperative cholangiogram to evaluate CBD
    • If clear, then two clips close to common bile duct and ligate
  3. Dissect cystic artery, one clip close distal and two clips proximal, and ligate
  4. Dissection of gall bladder from liver bed
  5. Cauterize, irrigate, suction, and obtain hemostasis of liver bed
  6. Remove gall bladder

Cottage Physician (1898)



References

  1. Blackbourne LH.  Surgical Recall.  6th Edition.  2012.
  2. Halpin V. Acute cholecystitis. BMJ Clin Evid. 2014; 2014:. [PDF]
  3. Haisley KR, Hunter JG. Gallbladder and the Extrahepatic Biliary System. In: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Kao LS, Hunter JG, Matthews JB, Pollock RE. eds. Schwartz’s Principles of Surgery, 11e. McGraw-Hill; Accessed June 14, 2020. https://accessmedicine-mhmedical-com.ezproxy.uthsc.edu/content.aspx?bookid=2576&sectionid=216215815
  4. Haubrich WS. Calot of the triangle of Calot. Gastroenterology. 2002; 123(5):1440. [pubmed]
  5. Singer AJ, McCracken G, Henry MC, Thode HC Jr, Cabahug CJ. Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis. Ann Emerg Med. 1996; 28(3):267-72. [pubmed]
  6. Shea JA, Berlin JA, Escarce JJ, et al. Revised estimates of diagnostic test sensitivity and specificity in suspected biliary tract disease. Arch Intern Med. 1994; 154(22):2573-81. [pubmed]
  7. Park MS, Yu JS, Kim YH, et al. Acute cholecystitis: comparison of MR cholangiography and US. Radiology. 1998; 209(3):781-5. [pubmed]
  8. Thompson DR. Narcotic analgesic effects on the sphincter of Oddi: a review of the data and therapeutic implications in treating pancreatitis. Am J Gastroenterol. 2001; 96(4):1266-72. [pubmed]
  9. Okamoto K, Suzuki K, Takada T, et al. Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis. J Hepatobiliary Pancreat Sci. 2018; 25(1):55-72. [pubmed]
  10. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010; 50(2):133-64. [pubmed]
  11. Hatzidakis AA, Prassopoulos P, Petinarakis I, et al. Acute cholecystitis in high-risk patients: percutaneous cholecystostomy vs conservative treatment. Eur Radiol. 2002; 12(7):1778-84. [pubmed]

Ep-PAINE-nym



Heller Myotomy

Other Known Aliasesnone

DefinitionLigation of the external muscle fibers of the lower esophageal sphincter

Clinical Significance this type of surgery can be open, laparoscopically, or endoscopically and is used to treat achalasia by relieving the constriction of the lower esophageal sphincter and allowing food to pass into the stomach. This is often combined with a Nissen fundoplication to prevent reflux after.

HistoryNamed after Ernst Heller (1877-1964), who was a German surgeon and received his medical doctorate from the University of Leipzig. He would serve as a military surgeon during the first World War from 1914-1918 before returning to Leipzig as chief surgeon of Saint George County Hospital. He had a fairly prestigous career in academic surgery, publishing over 80 scientific papers during his career and culminating as Professor of Surgery at the University of Leipzig in 1949. It was in 1913, as an assistant professor to Erwin Payr, that he performed his eponymous procedure on 39yo man with achalasia. He would publish this case report in 1914 and followed this patient for 7 years tracking his progression and documenting his now disease free condition.


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Heller E. Extramukose Cardiaplastik beim chronischen Cardiospasmus mit Dilatation des Oesophagus. Mitt GrenzgebMed Chir. 1914;27:141–149.
  7. Andreoll NA, Lope LR, Malafai O. Heller’s myotomy: a hundred years of success! Arq Bras Cir Dig. 2014; 27(1):1-2. [PDF]
  8. Haubrich WS. Heller of the Heller Myotomy Gastroenterology. 2006; 130(2):333. [link]
  9. Payne W. Heller’s contribution to the surgical treatment of achalasia of the esophagus The Annals of Thoracic Surgery. 1989; 48(6):876-881. [link]