Ep-PAINE-nym



Meckel’s Diverticulum

 

Other Known Aliasesnone

DefinitionVestigial remnant of the omphalomesenteric duct 

Clinical SignificanceIt is the most common malformation in the GI tract and is mainly asymptomatic.  When symptoms do occur, it commonly presents as painless, rectal bleeding in children.  The “Rule of 2s” will help you remember the facts of this pathology:

  • Effects 2% of the population
  • 2% of these will be symptomatic by age 2
  • 2 types of heterotopic tissue
  • Boy-to-girl ratio is 2:1
  • Usually 2″ in length
  • 2′ from the ileocecal valve

Image result for meckel's diverticulumImage result for meckel's diverticulum

History – Named after Johann Friedrich Meckel, the Younger (1781-1833), who was born into a prestigious medical family, with his father and grandfather already prolific physicians and professors of medicine in Halle, Prussia.  He made tremendous advancements in the area of anatomy and embryonic development with special attention to birth defects and abnormalities, where he pioneered the early study of teratology.  He first described the abnormality which bears his name in 1809.

Johann Friedrich Meckel.jpg


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. Stallion A, Shuck JM.  Meckel’s Diverticulum.  Surgical Treatment: Evidence-Based and Problem-Oriented.  2001 [pubmed]
  6. Blackbourne LH.  Surgical Recall.  6th ed. 2012
  7. J. F. Meckel. Über die Divertikel am Darmkanal. Archiv für die Physiologie, Halle, 1809, 9: 421–453
  8. Klunker R, Göbbel L, Musil A, Tönnies H, Schultka R. Johann Friedrich Meckel the Younger (1781-1833) and modern teratology. Annals of Anatomy. 2002; 184(6):535-40. [pubmed]

#21 – Acute Cholangitis



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Definition and Pathogenesis

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Acute cholangitis is defined as a bacterial infection of the biliary tract and can also be termed “ascending cholangitis” as the bacteria typically ascend from the gastrointestinal tract.  The most common causes for the bacterial invasion are:

  • Obstruction
    • Stones can be a nidus for bacterial colonization
  • Benign stenosis
  • Malignancy
  • Instrumentation (ERCP, stent)

 

There are several anatomical areas in the biliary tree that serve as protective barriers from bacterial translocation from within the gastrointestinal tract.

  • Sphincter of Oddi
    • Physically blocks entry into the biliary tree
  • Bile Flow
    • Constantly flowing back against the ascend travel of the bacteria
    • Bile acid also has bacteriostatic activity
  • Biliary Mucous Secretion
    • Prevents bacterial adherence to biliary tree lining

 

When obstruction occurs, the intrabiliary pressures rise and cause increased permeability of the biliary ductules and allows easier translocation of intestinal bacteria not only into the biliary tree, but also into systemic circulation.

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The most common pathogens isolated from bile cultures in acute cholangitis are:

  • Gram Negative
    • E. coli
    • Klebsiella
    • Enterobacter
  • Gram Positive
    • Enterococcus spp.
    • Bacteroides spp.

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Clinical Manifestations

The first physician to describe acute cholangitis was Dr. Jean-Martin Charcot and has the eponomyous Charcot’s Triad named after him for right upper quadrant pain, fever, and jaundice.  Fever and abdominal pain is more common (80%), than is jaundice (60%) and only 50-75% of patients have the classic triad.  Dr. Benedict Reynolds, an American surgeon in the 1950s, added altered mental status and hypotension to Charcot’s Triad to describe supperative cholangitis, which now bears his name as Reynold’s Pentad and is associated with significant mortality and morbidity.

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Laboratory Testing

  • Complete Blood Cell Count with Differential
    • Leukocytosis with neutrophil predominance
  • Liver Function Tests
    • Elevation in cholestatic markers
      • Alkaline phosphatase (ALP)
      • Gamma-glutamyl transpeptidase (GGT)
      • Conjugated hyperbilirubinemia
    • Blood cultures

Diagnosis

2013 Tokyo Guidelines for acute cholangitis breakdown into:

  • Suspected
    • Fever and/or rigors
    • Inflammatory response
      • Leukocytosis, elevated ESR or CRP
    • Either:
      • Jaundice
      • Abnormal LFTs
  • Confirmed
    • Imaging showing:
      • Biliary dilation without etiology
      • Visualization of etiology (stone, stricture, stent)

Imaging

Patients with suspected cholangitis, transabdominal ultrasound should be performed to evaluate for ductal dilatation, stones, and/or thickened bile duct.

 

Good references cases by Ultrasound Cases here (http://www.ultrasoundcases.info/case-list.aspx?cat=157).

 

ERCP is the definitive test of choice for cholangitis as it is both diagnostic and therapeutic and should be performed within 24-48 hours of diagnosis.  This allows for biliary decompression (sphincterotomy and aspiration) and stone removal.


Antibiotic Management

80% of patients improve with conservative therapy of IV antibiotics while awaiting ERCP.

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Alternative Drainage Procedures

If ERCP is unavailable, unsuccessful, or contraindicated, there are 2 modalities available:

  • Percutaneous Transhepatic Cholangiography (PTC)
    • Allows for biliary drainage, stone removal, diltation, or stent placement
    • picture1
  • Percutaneous Cholecystomy Tube
    • picture1

Prognosis and Prevention of Recurrence

Mortality associated with cholangitis have significantly improved over the last 40 years with technological, surgical, and minimally invasive techniques and have been quoted in the literature as <10% for uncomplicated and 20-30% for severe/complicated cholangitis.  If the cause is due to stones, cholecystectomy should be performed once the patient is over their acute illness to prevent recurrence.  If due to stricture or malignant compression, stent placement is recommended with surgical repair and decompression.


Journal of American Medicine

Article on cholangitis in 1917

american-medicine-cholangitis


References

 

  1. Sung JY, Costerton JW, Shaffer EA. Defense system in the biliary tract against bacterial infection. Digestive Diseases and Sciences. 1992;37(5):689-96. [pubmed]
  2. Kimura Y, Takada T, Kawarada Y. Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines. Journal of Hepato-biliary-Pancreatic Surgery. 2007;14(1):15-26. [pubmed]
  3. Ohdan H, Oshiro H, Yamamoto Y. Bacteriological investigation of bile in patients with cholelithiasis. Surgery Today. 1993;23(5):390-5. [pubmed]
  4. van den Hazel SJ, Speelman P, Tytgat GN, Dankert J, van Leeuwen DJ. Role of antibiotics in the treatment and prevention of acute and recurrent cholangitis. Clinical Infectious Diseases : an official publication of the Infectious Diseases Society of America. 1994;19(2):279-86. [pubmed]
  5. Saik RP, Greenburg AG, Farris JM, Peskin GW. Spectrum of cholangitis. American Journal of Surgery. 1975;130(2):143-50. [pubmed]
  6. Mosler P. Diagnosis and management of acute cholangitis. Current Gastroenterology Reports. 2011;13(2):166-72. [pubmed]
  7. DenBesten L, Doty JE. Pathogenesis and management of choledocholithiasis. The Surgical Clinics of North America. 1981;61(4):893-907. [pubmed]
  8. Kiriyama S, Takada T, Strasberg SM. TG13 guidelines for diagnosis and severity grading of acute cholangitis (with videos). Journal of Hepato-biliary-pancreatic Sciences. 2013;20(1):24-34. [pubmed]
  9. Hui CK, Lai KC, Yuen MF, Ng M, Lai CL, Lam SK. Acute cholangitis–predictive factors for emergency ERCP. Alimentary Pharmacology & Therapeutics. 2001;15(10):1633-7. [pubmed]
  10. Salek J, Livote E, Sideridis K, Bank S. Analysis of risk factors predictive of early mortality and urgent ERCP in acute cholangitis. Journal of Clinical Gastroenterology. 2009;43(2):171-5. [pubmed]

PAINE PANCE Pearl – Gastrointestinal

47yo male presents to emergency department with a 3 day history of progressive abdominal pain, nausea, and vomiting.  He reports the pain the as a constant, boring pain that radiates to his back.  Eating seems to aggravate it and sitting up and leaning forward sometimes help.  He does report occasional alcohol use.  He reports subjective fever, but denies chills, recent illnesses, diarrhea, constipation, hematemesis, melena, or hematochezia.  Vital signs show BP-112/80, HR-118, RR-22, O2-100%, and temperature 39oC (102.2oF).  Physical exam reveals mild distension, generalized abdominal tenderness to deep palpation, absent bowel sounds, and the below finding:

figure-1-cullens-sign1

Laboratory studies are:

screen-shot-2016-10-12-at-8-02-57-amscreen-shot-2016-10-12-at-8-05-01-am

AST – 322U/L          ALT – 45U/L        ALP – 14U/L

LDH – 833U/L          GGT – 15U/L         Bilirubin – 1.9

Amylase – 209U/L

Lipase – 572U/L

Albumin – 3.5g/L


What are the potential causes of this patient’s condition?

This patient has pancreatitis and a helpful mneumonic to remember the most common causes is:

I GET SMASHED

pancreatitis

What are 2 scoring systems used to predict severity?

There are 2 common scoring systems to predict or evaluate the severity of pancreatitis.  The first is the well known Ranson Criteria, that was introduced in 1974.  It uses 2 separate time frames to predict severity.  The first is at the time of admission and uses 5 variables:

  • Glucose > 200 mg/dL
  • AST > 250 U/L
  • LDH > 350 U/L
  • Age > 55
  • WBC > 16,000

If < 3 variables present, then it is considered mild.  If ≥ 3 variables present, then it is considered severe.

After 48 hours, a second set of criteria can be used to assess mortality.  These variables are:

  • Hematocrit decrease of ≥ 10%
  • Blood urea nitrogen increase ≥ 5 mg/dL despite fluids
  • Serum calcium < 8 mg/dL
  • PaO2 < 60 mmHg
  • Base deficit > 4 MEq/L
  • Fluid resuscitation > 6L

Mortality associated with this is as follows:

  • 0-2 – 2%
  • 3-4 – 15%
  • 5-6 – 40%
  • > 6 – 100%

Another scoring system is the modified glascow score for acute pancreatitis.  This was first developed in 1984 and modified in 1988.  It looks at 8 specific variables to predict severity of acute pancreatitis.  The variabls can easily be remembered by the acronym PANCREAS:

  • PaO2 < 60 mmHg
  • Age > 55
  • Neutrophils (WBC > 15,000)
  • Calcium < 8 mg/dL
  • Renal (BUN > 6 mg/dL)
  • Enzymes (LDH > 600 U/L or AST/ALT > 200 U/L)
  • Albumin < 3.2 g/L
  • Sugar (Glucose > 180 mg/dL)

If < 3 variables, then mild pancreatitis.  If ≥ 3 variables, then severe pancreatitis.

Case Conclusion

Our patient in this case would be consider severe pancreatitis (for both scoring systems) due to glucose > 200 mg/dL, LDH > 600 U/L, and and BUN > 6 mg/dL


References

  1. Blackborne LH.  Chapter 55: Pancreas.  In: Surgical Recall. 6th edition.  Lipincott Williams Wilkins.  Philedelphia, PA.
  2. Banks PA, Freeman ML, . Practice guidelines in acute pancreatitis. The American Journal of Gastroenterology. 2006;101(10):2379-400. [pubmed]
  3. Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. Prognostic signs and the role of operative management in acute pancreatitis. Surgery, gynecology & obstetrics. 1974;139(1):69-81. [pubmed]
  4. Leese T, Shaw D. Comparison of three Glasgow multifactor prognostic scoring systems in acute pancreatitis. The British Journal of Surgery. 71988;5(5):460-2. [pubmed]

PAINE PANCE Pearl – Gastrointestinal

47yo male presents to emergency department with a 3 day history of progressive abdominal pain, nausea, and vomiting.  He reports the pain the as a constant, boring pain that radiates to his back.  Eating seems to aggravate it and sitting up and leaning forward sometimes help.  He does report occasional alcohol use.  He reports subjective fever, but denies chills, recent illnesses, diarrhea, constipation, hematemesis, melena, or hematochezia.  Vital signs show BP-112/80, HR-118, RR-22, O2-100%, and temperature 39oC (102.2oF).  Physical exam reveals mild distension, generalized abdominal tenderness to deep palpation, absent bowel sounds, and the below finding:

figure-1-cullens-sign1

 

Laboratory studies are:

screen-shot-2016-10-12-at-8-02-57-amscreen-shot-2016-10-12-at-8-05-01-am

AST – 322U/L          ALT – 45U/L        ALP – 14U/L

LDH – 833U/L          GGT – 15U/L         Bilirubin – 1.9

Amylase – 209U/L

Lipase – 572U/L

Albumin – 3.5g/L

 

  1. What are the potential causes of this patient’s condition?
  2. What are 2 scoring systems used to predict severity?