Volvulus pathophysiology

Revision as of 20:33, 26 December 2017 by Hadeel Maksoud (talk | contribs)
Jump to navigation Jump to search
https://https://www.youtube.com/watch?v=KLQRoGOXMMg%7C350}}

Volvulus Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Volvulus from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography and Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Volvulus pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Volvulus pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Volvulus pathophysiology

CDC on Volvulus pathophysiology

Volvulus pathophysiology in the news

Blogs on Volvulus pathophysiology

Directions to Hospitals Treating Volvulus

Risk calculators and risk factors for Volvulus pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]


Overview

Regardless of cause, volvulus causes symptoms by two mechanisms. One is bowel obstruction, manifested as abdominal distension and vomiting. The other is ischemia (loss of blood flow) to the affected portion of intestine. This causes severe pain and progressive injury to the intestinal wall, with accumulation of gas and fluid in the portion of the bowel obstructed. Ultimately, this can result in necrosis of the affected intestinal wall, acidosis, and death. Acute volvulus therefore requires immediate surgical intervention to untwist the affected segment of bowel and possibly resect any unsalvageable portion.

Pathophysiology

Intestinal Malrotation in Neonates and Infants

Embryology

  • Malrotation occurs when there is arrest of the normal rotation of the embryonic gut.[4][5]
  • During weeks 4 - 8 of development, the embryonic coelom, or cavity, normally cannot accommodate the rapidly expanding gastrointestinal (GI) tract.
  • Consequently, the primary intestinal loop pushes back into the yolk stalk, and will become the future umbilicus.
  • The direction in which the loop grows takes the axis of the future superior mesenteric artery.
  • As the primary intestinal loop grows out of the abdomen, it begins to rotate by twisting 90 degrees counterclockwise.
  • There are two factors that force this rotation:
    • The proximal bowel (gastroduodenal) grows faster than the distal bowel (cecocolic).
    • The liver has rapidly develops.
  • During weeks 8 - 10, the primary intestinal loop continues to grow and returns back into the abdomen cavity and a further 180 degree counterclockwise rotation occurs.
  • Overall, the primary loop twists a total of 270 degrees in a counterclockwise direction.
  • Once the primary loop is in its final position, fixation to the posterior abdominal wall begins.
  • The proximal bowel portion including the stomach and duodenum are fixated early in gestation through the ligament of Treitz.
  • The colon takes a longer time to become fixated and usually, fixation is completed near term.

Pathophysiology of Infantile and Neonatal Volvulus

  • Normal gut development means that:[6]
    • A wide-based mesentery will extend from the ligament of Treitz in the left upper quadrant to the ileocecal valve in the right lower quadrant.
    • The primary loop will continue its rotation upon return to the abdominal cavity.
    • Both proximal (duodenojejunal) and distal (cecocolic) limbs rotate at the same rate and to the same degree.
  • Congenital volvulus happens when the following anomalies have occurred:
    • Narrow mesenteric base
      • The midgut becomes suspended by a narrow pedicle.
    • Non-rotation
      • In non-rotation, the primary loop undergoes no further rotation during its return to the abdominal cavity.
      • The small bowel becomes located on the right whilst the colon is on the left of the abdomen.
      • Non-rotation is less dangerous than malrotation because in non-rotation, the mesentery is wider and the risk of volvulus is lower.
    • Malrotation
      • In malrotation, the proximal (duodenojejunal) limb remains in a position of non-rotation, and the distal (cecocolic) limb partially rotates (usually only 90 degrees instead of 180 degrees).
      • Consequently,the cecum is relocated to the mid-upper abdomen, instead of the right lower quadrant.
      • The abnormally-positioned cecum is attached by bands of peritoneum (Ladd bands) to the right lateral abdominal wall.
      • Ladd bands can cause compression and obstruction of the duodenum extrinsically.
  • Other anomalies of rotation can rarely occur, these include:

Ileal and Sigmoid Volvulus

  • The mesentery anchors the ileum and sigmoid colon to the posterior abdominal wall.[7][8]
  • An air filled loop of the sigmoid colon or the terminal ileum, sometimes, twists itself about the axis of the mesentery.
  • The incidence of volvulus occurring increases with a redundant or longer than normal mesentery.
  • If the degree of twisting is beyond 180 - 360 degress, then the bowel loop will become obstructed and ischemia will develop.
  • Ileosigmoid knotting is a variant of sigmoid volvulus where the ileum wraps around the sigmoid in a clockwise direction.

Gastric Volvulus

  • Normally, there are ligaments such as the gastrocolic, gastrohepatic, gastrosplenic and gastrophrenic ligaments that keeps the stomach in place by attaching it to other abdominal organs and the diaphragm.[9][10]
  • However, the stomach can twist around its horizontal or vertical axis.
  • Gastric outlet obstruction may occur as a result of abnormal rotation more than 180 degrees.
  • Chronic rotation can cause bleeding by decreasing venous return and increasing capillary pressure.

Cecal Volvulus

  • The cecum is especially liable to being mobile congenitally.[11][12][13]
    • The cecum becomes mobile when failure of the ascending colon mesentery to fuse with the posterior parietal peritoneum occurs.
    • Autopsy studies have shown that about 10-25% of the population have a mobile cecum and ascending colon sufficient to develop a volvulus.
    • A congenital mobile cecum can also cause mobile cecum syndrome.
  • There are three types of cecal volvulus, type I and II are the most common, type III accounts for the remaining 20% of cases:
    • Type I
      • The cecum twists in a clockwise manner along its axis.
      • The cecum fills with air and remains in right lower quadrant.
    • Type II
      • The cecum and a proximal part of the ileum twist in a counterclockwise direction.
      • The cecum becomes inverted and is relocated to the left lower quadrant.
    • Type III
      • The cecum folds upwards and back on itself rather than rotating along its axis.


References

  1. John H, Gyr T, Giudici G, Martinoli S, Marx A (1996). "Cecal volvulus in pregnancy. Case report and review of literature". Arch. Gynecol. Obstet. 258 (3): 161–4. PMID 8781706.
  2. Radin DR, Halls JM (1986). "Cecal volvulus: a complication of colonoscopy". Gastrointest Radiol. 11 (1): 110–1. doi:10.1007/BF02035046. PMID 3943670.
  3. Sarioğlu A, Tanyel FC, Büyükpamukçu N, Hiçsönmez A (1997). "Colonic volvulus: a rare presentation of Hirschsprung's disease". J. Pediatr. Surg. 32 (1): 117–8. PMID 9021588.
  4. Graziano K, Islam S, Dasgupta R, Lopez ME, Austin M, Chen LE, Goldin A, Downard CD, Renaud E, Abdullah F (2015). "Asymptomatic malrotation: Diagnosis and surgical management: An American Pediatric Surgical Association outcomes and evidence based practice committee systematic review". J. Pediatr. Surg. 50 (10): 1783–90. doi:10.1016/j.jpedsurg.2015.06.019. PMID 26205079.
  5. Diaz MC, Reichard K, Taylor AA (2009). "Intestinal nonrotation in an adolescent". Pediatr Emerg Care. 25 (4): 249–51. doi:10.1097/PEC.0b013e31819e36aa. PMID 19369837.
  6. Burns, Cartland (2006). "Principles and Practices of Pediatric Surgery". Annals of Surgery. 243 (4): 567. doi:10.1097/01.sla.0000208423.52007.38. ISSN 0003-4932.
  7. Shepherd JJ (1969). "The epidemiology and clinical presentation of sigmoid volvulus". Br J Surg. 56 (5): 353–9. PMID 5781046.
  8. VerSteeg KR, Whitehead WA (1980). "Ileosigmoid knot". Arch Surg. 115 (6): 761–3. PMID 7387365.
  9. Rashid F, Thangarajah T, Mulvey D, Larvin M, Iftikhar SY (2010). "A review article on gastric volvulus: a challenge to diagnosis and management". Int J Surg. 8 (1): 18–24. doi:10.1016/j.ijsu.2009.11.002. PMID 19900595.
  10. Shivanand G, Seema S, Srivastava DN, Pande GK, Sahni P, Prasad R, Ramachandra N (2003). "Gastric volvulus: acute and chronic presentation". Clin Imaging. 27 (4): 265–8. PMID 12823923.
  11. Husain K, Fitzgerald P, Lau G (1994). "Cecal volvulus in the Cornelia de Lange syndrome". J. Pediatr. Surg. 29 (9): 1245–7. PMID 7807358.
  12. DONHAUSER JL, ATWELL S (1949). "Volvulus of the cecum with a review of 100 cases in the literature and a report of six new cases". Arch Surg. 58 (2): 129–48. PMID 18111729.
  13. Rogers RL, Harford FJ (1984). "Mobile cecum syndrome". Dis. Colon Rectum. 27 (6): 399–402. PMID 6734364.

Template:WS Template:WH