Cecal Volvulus

About two thirds of patients suffering from CV present with acute symptoms, mainly acute abdominal pain. Distention, bloating, vomitus and obstipation further indicate possible intestinal strangulation.

The remaining share of patients report subacute or chronic abdominal pain. Chronic obstipation is not uncommon among CV patients and is presumably due to repeated episodes of subclinical volvulus.

CV occurs most frequently in geriatric patients suffering from comorbidities that limit physical activity and account for a poor general health.

Medical history and clinical examination may lead to the tentative diagnosis of intestinal strangulation. Further diagnostic techniques have to be applied to confirm this diagnosis and to locate it anatomically.

Diagnostic imaging may yield conclusive findings that allow the physician to confirm the diagnosis of intestinal obstruction and possibly to locate it along the intestine.

Radiographic studies are of great value and may be even more revealing when carried out with contrast agents. Barium enemas are particularly indicated when X-rays do not yield a diagnosis, but they should be avoided in patients showing signs of peritonitis [19]. A gas-filled appendix is characteristic and a foldlike termination may be visible at the distal end of the obstructed segment, i.e. in the ascending colon in case of CV. In case the CV occured as a cecal bascule the appendix is displaced upwards. Further findings pointing to a possible CV are a dilated small intestine and absence of gas in the distal colon [8] [20]. Unfortunately, although the sigmoid volvulus may be recognized on radiographic images, this is rarely the case for CV.

Often, an additional computer tomography is necessary to detect the exact site of torsion and to clarify if the twisted intestinal segment is infarcted. In many hospitals, an initial abdominal computer tomography is even preferred over radiographic imaging. Common findings in computer tomography are “coffee bean”, “bird beak”, and “whirl” [21]. Endoscopy may also be indicated and can possibly contribute to diagnosis and treatment.

Blood tests usually show unspecific changes, leukocytosis, left shift and altered electrolyte levels being the most common findings. They may indicate peritonitis and sepsis.

It is not uncommon for clinical examination, diagnostic imaging and blood screens to yield no conclusive diagnosis [8] [19] [21]. In these cases an exploratory laparotomy may be indicated.

In order to prepare the patient for the following treatment, fluid deficits, hypovolemia and electrolyte imbalances should be corrected.

An endoscopic decrompression is initially done. CV may be treated by endoscopic decompression alone, but relapses are extremely frequent in these patients (up to 80%). Therefore, surgical intervention is highly recommended.

The physician may choose between several procedures and the decision will strongly depend on the overall condition of the patient. The procedure of choice is a right hemicolectomy with subsequent ileocolic anastomosis. This operation requires a certain general health and may not be performable in extremely debilitated patients. Cecostomy may be an option for multimorbid geriatric or otherwise severely debilitated patients, but is associated with a high rate of wound infection (up to 50%) and a non-negligible rate of recurrence (up to 5%). An end ileostomy is only indicated in few cases.

Furthermore, manual detorsion alone is associated with a rate of recurrence as high as after sole endoscopic decompression and is therefore no treatment option.

Surgical therapy is accompanied by pharmacological treatment. Broad-spectrum antibiotics should be administered in case of tissue infarction, peritonitis and sepsis. A nasogastric tube should be placed if the patient was vomiting before surgery and a urinary catheter may help to avoid increased abdominal tension.

A favorable prognosis strongly depends on an early diagnosis. Any delay is associated with a significantly worsening prognosis and high mortality rates. In this context, mortality rates after early diagnosis and appropiate therapy and surgical intervention may amount to 15%, while late diagnosis and treatment increase mortality to 40%.

These numbers may vary between subpopulations presenting different states of general health.

Any intestinal torsion is only possible because the intestine itself is long enough to turn around itself. However, the anatomic fixation of the cecum and intestinal parts in close proximity may particularly predispose it for torsions: patients affected by CV exhibit a common mesentery that is rather long and only fixed to a narrow, retroperitoneal base. There are individual differences regarding the development of the mesocecum, which affects the anatomic position and flexibility of this part of the colon. Such differences may make one person more susceptible to CV than another. Indeed, post mortem studies found up to 20% of the population to present an increased, congenital mobility of the right colon. Because 20% is a rather large share of the population but CV is a very rare condition, other factors probably affect the individual risk for CV.

Augmented cecal mobility may result from previous surgical interventions and mobilization of the cecum. It has been reported that up to 50% of CV patients have a medical history that includes abdominal surgery. Appendicitis may be the reason for such surgeries but may also affect the likelihood of CV directly. Abdominal surgery as well as inflammatory processes may lead to permanent adhesions, and, subsequently the anatomic position of the cecum and surrounding parts of the intestine may be altered. Similarly, space-occupying tissue may change the position of distinct parts of the intestine relative to each other and therefore contribute to a CV. Such tissues may be physiological, e.g. a gravid uterus in late pregnancy, or pathological, e.g. gaseous dilation of the colon, a neoplasia or another volvulus. Furthermore, uncommon anatomic anomalies may also predispose for CV [8] [9] [10] [11] [12] [13] .

Diet may affect the individual risk for developing CV. High fibre intake and hyperperistalsis have been identified as risk factors additionally to chronic constipation and colonic distension. In this context, diets rich in fiber as well as chronic constipation both entail an overloaded, heavy colon. Its weight makes it susceptible to torsion [11] [14] [15].

The annual incidence of CV has been estimated to range between 3 and 7 per million inhabitants [4] [6]. Among disorders causing an intestinal obstruction, CV is a rather rare condition. Intestinal obstruction is frequently caused by cancer and diverticulitis; CV accounts for less than 5% of all cases of intestinal obstruction. There are several conditions leading to colonic obstruction and CV is responsible for less than 15% of all such cases. Even the sigmoid volvulus, the most common form of colonic volvulus, occurs more frequently than CV [16] [17] [18].

Cultural and dietary influences are presumably responsible for differences regarding CV incidence in distinct ethnic and age groups. In this context, the average age of patients presenting CV in the Western world is >50 years while in India this value amounts to approximately 30 years [8].

The anatomic situation facilitating CV has been described above. Additionally, diet and lifestyle significantly affect the condition of the intestinal tract. These factors constitute a constant strain on the mesentery and may even lead to mild, but chronic inflammation at its base. Similar to other inflammatory processes that might take place in the abdomen, this may entail the formation of adhesions. These adhesions further predispose for intestinal torsions and CV.

A complete volvulus creates an intestinal obstruction consisting of a loop-like segment that strangulates vessels and other anatomical structures both at its proximal and distal end. This segment may further dilate because gases cannot escape towards adjacent parts of the bowel and this dilation adds to vessel strangulation. Thus, tissue infarction ensues, which may lead to gangrene and perforation of the twisted intestinal segment.

This sequence of pathophysiologic events occurs in axial torsions of the cecum as well as in CV that develops as a cecal bascule. The former involves a complete twist of distal ileum and ascending colon around each other, whereby the cecum constitutes part of the strangulated segment. Here, it remains in the right lower quadrant of the abdomen. If the cecum folds upwards to the right upper quadrant of the abdomen without twisting, the resulting CV is classified as a cecal bascule. Both types of CV are equally likely.

Because diets rich in fiber and chronic constipation have been identified as risk factors for CV, these conditions should be avoided by making the necessary dietary adaptations. Constipation is more likely to occur in people maintaining a low-fiber diet, which is why a healthy compromise should be found regarding fiber intake. Sufficient water intake is recommended. Those dietary adaptions may be helpful to avoid CV, although scientific data supporting this hypothesis is not available due to the low incidence of the disease. 

Patients recovering from CV and therapeutic surgery should avoid food rich in fibers as well as comestibles hard to digest. Furthermore, the intestinal tract should not be burdened by a few large meals, but rather be relieved by several small portions. If intestinal parts have been removed, absorption of certain nutrients may be restricted and an adequate supplement may be required.

The intestine of a patient suffering from intenstinal volvulus is twisted around itself. In case of cecal volvulus (CV) the twist encompasses the terminal ileum, the cecum itself and the ascending colon; the pivot point may be located in the cecum itself but is more frequently found in the ascending colon. Although CV is one of the two more common forms of colonic volvulus - whereby the second common form is the volvulus of the sigmoid colon -, it is still considered a rare cause of intestinal obstruction [1] [2]. CS is, however, associated with a high mortality and therefore requires an early diagnosis and adequate treatment.

Such diagnosis is not easily reached because symptoms associated with CV vary widely. While some patients experience only intermittent abdominal pain, others present with severe, acute abdominal pain and signs of sepsis that may indicate an intestinal strangulation. A CV leads to intestinal obstruction, tissue ischemia, gangrene, perforation and sepsis [3] [4] [5] [6] [7].

CV may occur as an axial torsion or as a cecal bascule. They differ in the pivot point and degree of torsion, but their differences are clinically of minor importance. Although it has been reported that the more frequent axial torsion is associated with an even higher mortality due to vascular compromise, the cecal bascule is by no means less life-threatening. Indeed, it is generally accepted that symptoms and treatment are the same for both types of CV.

The intestinal tract is only loosely fixed to the inner abdominal walls and parts of the intestine may twist under certain conditions. If such a torsion involves the terminal part of the small intestine, the cecum and the beginning of the colon, this condition is termed cecal volvulus (CV).

It is usually accompanied by acute or recurrent abdominal pain, sensations of fullness and bloating and severe constipation. Some patients may experience nausea and vomiting. Acute cases of CV may lead to shock.

These symptoms are indicative of an intestinal obstruction, but the physician is usually not able to locate the obstruction along the intestine without further diagnostic measures. These generally include X-rays or computer tomography, which may be carried out after the administration of contrast agents. Endoscopy may become necessary.

Surgical treatment is required to resolve CV. There are different procedures, each with its own advantages and disadvantages, and the physician will decide which one is appropiate based on the overall condition of the patient. The most common procedure involves the removal of the twisted cecum.

A favorable prognosis depends on early diagnosis and appropiate treatment. Any delay considerably worsens chances for a healthy outcome.

1. Lianos G, Ignatiadou E, Lianou E, Anastasiadi Z, Fatouros M. Simultaneous volvulus of the transverse and sigmoid colon: case report. G Chir. 2012; 33(10):324-326.
2. Elsharif M, Basu I, Phillips D. A case of triple volvulus. Ann R Coll Surg Engl. 2012; 94(2):e62-64.
3. Perret RS, Kunberger LE. Case 4: Cecal volvulus. AJR Am J Roentgenol. 1998; 171(3):855, 859, 860.
4. Katoh T, Shigemori T, Fukaya R, Suzuki H. Cecal volvulus: report of a case and review of Japanese literature. World J Gastroenterol. 2009; 15(20):2547-2549.
5. Pousada L. Cecal bascule: an overlooked diagnosis in the elderly. J Am Geriatr Soc. 1992; 40(1):65-67.
6. Consorti ET, Liu TH. Diagnosis and treatment of caecal volvulus. Postgrad Med J. 2005; 81(962):772-776.
7. Delabrousse E, Sarlieve P, Sailley N, Aubry S, Kastler BA. Cecal volvulus: CT findings and correlation with pathophysiology. Emerg Radiol. 2007; 14(6):411-415.
8. Rabinovici R, Simansky DA, Kaplan O, Mavor E, Manny J. Cecal volvulus. Dis Colon Rectum. 1990; 33(9):765-769.
9. Tejler G, Jiborn H. Volvulus of the cecum. Report of 26 cases and review of the literature. Dis Colon Rectum. 1988; 31(6):445-449.
10. Theuer C, Cheadle WG. Volvulus of the colon. Am Surg. 1991; 57(3):145-150.
11. O'Mara CS, Wilson THJSGL, Stonesifer GL, Cameron JL. Cecal volvulus: analysis of 50 patients with long-term follow-up. Ann Surg. 1979; 189(6):724-731
12. Montes H, Wolf J. Cecal volvulus in pregnancy. Am J Gastroenterol. 1999; 94(9):2554-2556.
13. Alinovi V, Herzberg FP, Yannopoulos D, Vetere PF. Cecal volvulus following cesarean section. Obstet Gynecol. 1980; 55(1):131-134.
14. Anderson JR, Spence RA, Wilson BG, Hanna WA. Gangrenous caecal volvulus after colonoscopy. Br Med J (Clin Res Ed). 1983; 286(6363):439-440.
15. Radin DR, Halls JM. Cecal volvulus: a complication of colonoscopy. Gastrointest Radiol. 1986; 11(1):110-111.
16. Rakinic J. Colonic volvulus. In: Beck DE, Roberts PL, TJ S, eds. The ASCRS textbook of colon and rectal surgery. Vol 2. New York: Springer; 2011:395.
17. Lee SY, Bhaduri M. Cecal volvulus. CMAJ 2013; 185:684.
18. Baldarelli M, De Sanctis A, Sarnari J, et al. Laparoscopic cecopexy for cecal volvulus after laparoscopy. Case report and a review of the literature. Minerva Chir 2007; 62:201.
19. Madiba TE, Thomson SR. The management of cecal volvulus. Dis Colon Rectum2002;45:264–7.
20. Anderson JR, Mills JO. Caecal volvulus: a frequently missed diagnosis? Clin Radiol. 1984; 35(1):65-69.
21. Moore CJ, Corl FM, Fishman EK. CT of cecal volvulus: unraveling the image. AJR Am J Roentgenol. 2001; 177(1):95-98.