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.


  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



  • 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


  • 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


  • 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)


  1. Blackbourne LH.  Surgical Recall.  6th Edition.  2012.
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  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]


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.


  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]


Nissen Fundoplication

Other Known Aliasesnone

Definitionwrapping of the fundus of the stomach around the lower esophagus to re-enforce the LES and prevent esophageal sliding.

Clinical Significance this type of surgery can be performed open or laparoscopic to treat GERD with a hiatal hernia when medical management fails. Traditionally, a Nissen is a complete 360-degree wrap, and there are several variations of this procedure that involve incomplete wrapping on various sides of the esophagus.

HistoryNamed after Rudolph Nissen (1896-1981), who was a Jewish-German surgeon who received his medical doctorate from the University of Freiburg in 1921. His medical studies were interrupted by the first World War where he served on the front lines in a medical corp. It was during his service where he would suffer a gunshot to the lung, which would plague him for the rest of his life. He would go on to serve in various surgery departments in Munich, Berlin, and Istanbul where he would become the head of the surgery department in 1933. It was here that he resected an esophageal ulcer from a 28yo patient that required him to remove portion of the lower esophageal sphincter in the process. He decided to wrap a portion of the stomach around the lower esophagus to strengthen the sphincter and the patient reported greatly improved reflux symptoms. It wasn’t until 1955 when he reflected on this case and performed the procedure on two patients for reflux esophagitis and published the results in 1956. Of note, he also operated on Albert Einstein in 1948 to wrap his AAA with cellophane (which was the treatment at the time).


  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. Nissen R. [A simple operation for control of reflux esophagitis]. Schweiz Med Wochenschr. 1956;86(Suppl 20):590-2.
  7. Ellis Jr., FH. The Nissen Fundoplication. Ann Thorac Surg. 1992;54:1231-1235.

PAINE #PANCE Pearl – Gastrointestinal


Cirrhosis and intrinsic liver disease can cause a significant increase in pressure within the portal system and result in dilation of the caval tributaries. What are the three (3) most common locations these dilations occurs?


The three (3) most common locations where you can find dilation of portal caval tributaries as a result of portal hypertension are:

  • Esophageal veins
    • Causing esophageal varices
  • Periumbilical veins
    • Causing caput medusae
  • Inferior and middle rectal veins
    • Causing hemorrhoids


Mallory-Weiss Syndrome

Other Known Aliasesgastro-esophageal laceration syndrome

Definitionlongitudinal mucosal lacerations in the distal esophagus and proximal stomach often leading to bleeding from submucosal arteries

Clinical Significance These tears often occurs as a result of forceful vomiting and can present with hematemesis or melena. Risk factors include alcohol abuse, hiatal hernias, and bulemia. In contrast to Boerhaave’s syndrome, this only involves the mucosa and submucosa and therefor, is not a full thickness rupture. Diagnosis is made via endoscopy and treatment depends on how active the bleed is at the time of endoscopy.

HistoryNamed after two physicians, George Kenneth Mallory (1900-1986) and Soma Weiss (1898-1942), from Boston. Dr. Mallory received his medical doctorate from Harvard Medical School in 1926 and followed in his father’s footsteps by working at the Mallory Institute of Pathology at Boston City Hospital. Dr. Weiss studied physiology and biochemistry in Budapest before immigrating to the United States immediately after World War I, when he wualified in medicine in 1923. He started his career at Cornell before moving to Harvard Medical School, and finally becoming physician-in-chief and professor at The Brigham Hospital in 1939. They partnered and co-authored the manuscript with their eponymous name in 1929, where they described 15 cases of severe, painless hemorrhage of the esophagus preceded by vomiting in alcoholics. They followed this up in 1932 with an additional 6 cases.


  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. Mallory GK, Weiss A. Hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting. American Journal of the Medical Sciences. 1929; 178: 506-15
  7. Weiss S, Mallory GK. Lesions of the cardiac orifice of the stomach produced by vomiting. Journal of the American Medical Association; 1932, 98: 1353-1355

#52 – Pyloric Stenosis



  • 2-4 per 1000 live births worldwide and 20 per 10,000 live births in the US
  • Higher male to female ratio (4-6:1)
  • Higher incidence (1.5x) in first-born children
  • Highest incidence in caucasian infants
  • Less common in infants of older mothers

Risk Factors and Etiology

The exact mechanisms and etiologies are unclear, but it is hypothesized that it is multifactorial and is a result of both genetic predisposition and environmental triggers.

  • Environmental Factors
    • Maternal smoking (up to 2x increased risk)
    • Bottle feeding
      • Bottle feeding during first 4 months increased risk by 4x
        • Didn’t delineate formula vs breastmilk
  • Genetic Factors
    • Reports of familial aggregation, but there is no clear research association
    • Apolipoprotein A1 (APOA1) gene cluster
      • Hypothesized low plasma cholesterol at birth and increased risk
  • Macrolide Antibiotics
    • Increased risk if given to infants < 2 weeks old
      • Treatment/prophylaxis for pertussis
    • Association with maternal use during first two weeks of life
  • Icteropyloric syndrome
    • Unconjugated hyperbilirubinemia
      • Most commonly from early Gilbert’s Syndrome

History and Physical Examination

  • Class presentation for PANCE
    • < 6 week old with post-prandial, non-bilious projectile vomiting around 10 minutes after cessation of feeding
    • Ravenous feeder even after vomiting
  • May be emaciated and/or dehydrated
    • Though we are diagnosing earlier and infants tend to be healthier
  • Palpable mass in the epigastrium (50-90%)
    • This is also less commonly seen due to healthier infants and ease of obtaining radiologic students
      • 73% in the 1970s to only 30% now
    • Ideally, immediately after vomiting and while the infant is calm
  • Other important assessments
    • Height/weight
    • Mucous membranes and skin turgor
    • Skin and sclerae
    • Genitalia
      • Ambiguous genitalia raises suspicion for congenital adrenal hyperplasia and adrenal crisis

Diagnostic Studies

  • Laboratory
    • Hypochloremic metabolic alkalosis
      • 88% PPV if pH > 7.45, chloride < 98, and base excess > +3
    • Assess for dehydration
      • BUN/creatinine > 20:1
    • Liver Function Tests
      • Bilirubin breakdown, AST/ALT, GGT, and ALP
  • Radiography
    • Ultrasound is the test of choice
      • Accuracy is operator dependent, but can reach > 95% sensitivity/specificity
      • “Target” sign on transverse view
      • Normal Measurements (vary with age and used together)
        • Pyloric Muscle Thickness
          • < 3mm
        • Pyloric Muscle Length
          • < 14mm
        • Pyloric Channel Length
          • < 16mm
Target Sign on Transverse View
  • Fluoroscopic Upper Gastrointestinal Series
    • Used if ultrasound is nondiagnostic
    • Classic findings :
      • “string” sign from an elongated pyloric canal
      • “double-track” sign from two thin tracks of barium along the pyloric canal created by compressed pyloric mucosa
      • “beak”sign from a tapered point at the pyloric ending
      • “shoulder” sign from a prepyloric bulge of barium
1) Beak Sign, 2) String Sign, 3) Double Track Sign, 4) Shoulder Sign

Differential Diagnosis

Although pyloric stenosis has a classic presentation, you must entertain the other important causes of vomiting in infancy.


  • Definitive management is surgery
  • Timing of surgery depends on the clinical status of the infant
    • If healthy, surgery can be performed on the day of diagnosis
    • If ill, then resuscitation and feeding need to be performed to limit perioperative complications.
  • Technique
    • Ramstedt Pyloromyotomy
      • Longitudinal incision of the pylorus with blunt dissection down to the submucosa
  • Open vs Laparoscopic
    • No difference in operating time, time to full feeding, or length of stay
    • Laparoscopic had lower incidence of emesis and better pain control, but higher incidence of incomplete surgical release
  • Postoperative Management
    • Feeding
      • Resumed within a few hours after surgery
      • Regurgitation is common, but should not delay/stop feedings
    • Breathing
      • Monitor for apnea at least for 24 hours
    • Complications
      • Mucosal perforation (rare)


  • Surgery is curative in the majority of patients
  • Once normal feeds occur, only routine pediatric care and follow-up is needed
  • Reflux is common and managed conservatively

The Cottage Physician (1893)


  1. Kapoor R, Kancherla V, Cao Y, et al. Prevalence and descriptive epidemiology of infantile hypertrophic pyloric stenosis in the United States: A multistate, population-based retrospective study, 1999-2010. Birth defects research. 2019; 111(3):159-169. [pubmed]
  2. To T, Wajja A, Wales PW, Langer JC. Population demographic indicators associated with incidence of pyloric stenosis. Archives of pediatrics & adolescent medicine. 2005; 159(6):520-5. [pubmed]
  3. Krogh C, Fischer TK, Skotte L, et al. Familial aggregation and heritability of pyloric stenosis. JAMA. 2010; 303(23):2393-9. [pubmed]
  4. Krogh C, Gørtz S, Wohlfahrt J, Biggar RJ, Melbye M, Fischer TK. Pre- and perinatal risk factors for pyloric stenosis and their influence on the male predominance. American journal of epidemiology. 2012; 176(1):24-31. [pubmed]
  5. Svenningsson A, Svensson T, Akre O, Nordenskjöld A. Maternal and pregnancy characteristics and risk of infantile hypertrophic pyloric stenosis. Journal of pediatric surgery. 2014; 49(8):1226-31. [pubmed]
  6. Zhu J, Zhu T, Lin Z, Qu Y, Mu D. Perinatal risk factors for infantile hypertrophic pyloric stenosis: A meta-analysis. Journal of pediatric surgery. 2017; 52(9):1389-1397. [pubmed]
  7. McAteer JP, Ledbetter DJ, Goldin AB. Role of bottle feeding in the etiology of hypertrophic pyloric stenosis. JAMA pediatrics. 2013; 167(12):1143-9. [pubmed]
  8. Sørensen HT, Nørgård B, Pedersen L, Larsen H, Johnsen SP. Maternal smoking and risk of hypertrophic infantile pyloric stenosis: 10 year population based cohort study. BMJ (Clinical research ed.). 2002; 325(7371):1011-2. [pubmed]
  9. Feenstra B, Geller F, Carstensen L, et al. Plasma lipids, genetic variants near APOA1, and the risk of infantile hypertrophic pyloric stenosis. JAMA. 2013; 310(7):714-21. [pubmed]
  10. Eberly MD, Eide MB, Thompson JL, Nylund CM. Azithromycin in early infancy and pyloric stenosis. Pediatrics. 2015; 135(3):483-8. [pubmed]
  11. Honein MA, Paulozzi LJ, Himelright IM, et al. Infantile hypertrophic pyloric stenosis after pertussis prophylaxis with erythromcyin: a case review and cohort study. Lancet (London, England). ; 354(9196):2101-5. [pubmed]
  12. Lund M, Pasternak B, Davidsen RB, et al. Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study. BMJ (Clinical research ed.). 2014; 348:g1908. [pubmed]
  13. Touloukian RJ, Higgins E. The spectrum of serum electrolytes in hypertrophic pyloric stenosis. Journal of pediatric surgery. 1983; 18(4):394-7. [pubmed]
  14. Bakal U, Sarac M, Aydin M, Tartar T, Kazez A. Recent changes in the features of hypertrophic pyloric stenosis. Pediatrics international : official journal of the Japan Pediatric Society. 2016; 58(5):369-71. [pubmed]
  15. Sivitz AB, Tejani C, Cohen SG. Evaluation of hypertrophic pyloric stenosis by pediatric emergency physician sonography. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2013; 20(7):646-51. [pubmed]
  16. Niedzielski J, Kobielski A, Sokal J, Krakós M. Accuracy of sonographic criteria in the decision for surgical treatment in infantile hypertrophic pyloric stenosis. Archives of medical science : AMS. 2011; 7(3):508-11. [pubmed]
  17. Hernanz-Schulman M. Pyloric stenosis: role of imaging. Pediatric radiology. 2009; 39 Suppl 2:S134-9. [pubmed]
  18. Said M, Shaul DB, Fujimoto M, Radner G, Sydorak RM, Applebaum H. Ultrasound measurements in hypertrophic pyloric stenosis: don’t let the numbers fool you. The Permanente journal. 2012; 16(3):25-7. [pubmed]
  19. Iqbal CW, Rivard DC, Mortellaro VE, Sharp SW, St Peter SD. Evaluation of ultrasonographic parameters in the diagnosis of pyloric stenosis relative to patient age and size. Journal of pediatric surgery. 2012; 47(8):1542-7. [pubmed]
  20. St Peter SD, Holcomb GW, Calkins CM, et al. Open versus laparoscopic pyloromyotomy for pyloric stenosis: a prospective, randomized trial. Annals of surgery. 2006; 244(3):363-70. [pubmed]
  21. Hall NJ, Pacilli M, Eaton S, et al. Recovery after open versus laparoscopic pyloromyotomy for pyloric stenosis: a double-blind multicentre randomised controlled trial. Lancet (London, England). 2009; 373(9661):390-8. [pubmed]


Boerhaave’s Syndrome

Other Known Aliasesnone

Definitionesophageal rupture from forceful vomiting

Clinical Significance This rupture occurs as a result of sudden increased intraesophageal pressure with negative intrathoracic pressure and the associated tear is most commonly located on the left posterolateral aspect of the distal esophagus. Gastric contents then invade the mediastinum and cause mediastinitis, necrosis, and severe bacterial infection that can lead to significant mortality.

HistoryNamed after Herman Boerhaave (1668-1738), who was a Dutch physician and earned his medical doctorate from the University of Harderwijk in 1693. He went on to earn a professorship at the University of Leiden in 1701, speaking on medicine, anatomy, botany, chemistry, and philosophy. It was during his time here that his repuatation as a skilled orator and teacher made international waves and physicians from all over the world came to listen and learn. He first described his eponymous disease in 1724 after witnessing the death of Baron Jan van Wassenaer after a retching following a particularly gluttonous feast.


  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. Boerhaave H. Atrocis, nec descripti prius, morbii historia: secundum medicae artis leges conscripta. Leiden, the Netherlands: Lugduni Batavorum Boutesteniana, 1724
  7. Underwood EA. Boerhaave after three hundred years. British medical journal. 1968; 4(5634):820-5. [pubmed]

PAINE #PANCE Pearl – Gastrointestinal


Ischemic bowel disease has two classic presentations: acute and chronic.

  1. What is the typical type of patient (or risk factors) for each?
  2. How does each type classically present?


  1. The risk factors for each type are a little different, but very important in differentiating the causes of abdominal pain:
    • Acute (from embolism)
      • atrial fibrillation, hypercoaguable states, instrumentation, valvular disease, and ventricular aneurysms
    • Chronic (from decreased perfusion)
      • peripheral vascular disease, atherosclerosis
  2. The presentations for both are also vastly different:
    • Acute
      • sudden onset of severe, periumbilical abdominal pain that is out of proportion to physical examination
      • bloody stools may also occur
    • Chronic
      • post-prandial intestinal pain due to inability to meet the blood flow demands for digestion
      • patients may also lose weight due to “food fear”