Ep-PAINE-nym



Puestow Procedure

Other Known Aliases – Puestow-Gillesby procedure, lateral pancreaticojejunostomy

Definitionside-to-side anastomosis of the main pancreatic duct of Wirsung to the proximal jejunum

Clinical Significance this is a surgical management option for patients with chronic pancreatitis by simultaneously facilitating drainage and preserving physiologic function of the pancreas.

HistoryNamed after Charles Bernard Puestow (1902-1973), an American surgeon who recieved his medical doctorate from the University of Pennsylvania in 1925. He would serve as a military surgeon during the 2nd World War and commanded the 27th Evacuation Hospital providing surgical services to wounded soldiers in Europe and North Africa. His commitment to the veteran population would continue after the war when he established the first surgical residency program based in a veterans hospitals in the United States in 1946. It was at Hines Veterans Hospital in Illinois where he and his partner, William Gillesby, would publish their experience and outcomes on 21 patients with chronic pancreatitis in 1958, which would lead to the creation of his eponymonic surgical procedure.


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. Bosmia AN, Christein JD. Charles Bernard Puestow (1902-1973): American surgeon and commander of the 27th Evacuation Hospital during the Second World War. J Med Biogr. 2017; 25(3):147-152. [pubmed]
  7. PUESTOW CB, GILLESBY WJ. Retrograde surgical drainage of pancreas for chronic relapsing pancreatitis. AMA Arch Surg. 1958; 76(6):898-907. [pubmed]

PAINE #PANCE Pearl – Gastrointestinal



Question

We all know that nutritional supplementation during pregnancy is extremely important for fetal development. But…….there is one particular vitamin that can be teratogenic in excess doses.

  1. What vitamin is this?
  2. What types of foods are extremely high in this vitamin and why?


Question

  1. The class of retinoic acids have two main forms of vitamin A:
    1. Provitamin A – primarily plant based carotenoids
      1. green leafy vegetables, sweet potatoes, carrots
    2. Preformed vitamin A – primarily in animal sources
      1. livers, kidneys
  2. Up to 85% of metabolized vitamin A is stored in the liver and other tissues due to being fat soluble. As a result, animal organs (liver, kidneys, thymus) are extremely high in preformed vitamin A and can cause acute and/or chronic toxicity when ingested in large quantities.

References

  1. Rothman KJ, Moore LL, Singer MR, Nguyen UD, Mannino S, Milunsky A. Teratogenicity of High Vitamin A Intake N Engl J Med. 1995; 333(21):1369-1373.

Ep-PAINE-nym



Ranson’s Criteria

Other Known Aliases – none

Definitionclinical decision instrument to predict mortality of acute pancreatitis on admission and after the first 48 hours

Clinical Significance this was one of the first instruments to help with the initial management of patients with acute pancreatitis. Now, it has been largely been replaced by more accurate and reliable calculations and is taught only for historical purposes.

History – Named after John H. C. Ranson (1938-1995), an English-American surgeon who received his medical doctorate from Oxford University in 1960. He would complete his surgical residency at Bellevue Hospital and New York University Medical Center, where he would join as faculty and later as the Director of the Division of General Surgery. He would have a prolific career primarily focusing on the alimentary tract with concentration on the pancreas. He would publish his eponymous scoring system in 1974 which not only improved the clinical care of patients with pancreatitis, but also improved the quality of the research by finally being able to compare severity groups of treatment arms.


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. Reber HA. Obituary – John H. C. Ranson, Pancreas: April 1996 – Volume 12 – Issue 3 – p 215 [link]
  7. Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynecol Obstet. 1974;139(1):69-81. [link]

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?

PAINE #PANCE Pearl – Endocrine



Question

32yo man, who is otherwise healthy with no PMH, presents to your clinic with a 2-month history of polyuria, nocturia, and polydipsia. Both of his parents have DMII and told him he needed “to get his sugar checked”. He denies any weight changes or vision disturbances. Vitals in clinic are BP-112/72 mmHg, HR-108, RR-12, O2-100%, and temp-98.9o. Initial screening labs are below.

  1. What is the most likely diagnosis?
  2. What additional labs should be ordered?


Answer

This patient likely has diabetes insipidus given the normal glucose/HbA1c and hypernatremia with polyuria. Next step in the diagnostic evaluation would be to check a urine osmolarity and plasma copeptin.