The leading edge of the intussusceptum may be located at 6–8 cm or at 15–18 cm from the anal verge. This proved an older theory from the 18th century by John Hunter and Albrecht von Haller that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the dentate line and protruding externally.Since most patients with rectal prolapse have a long history of constipation, it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. This excessive straining may be due to predisposing pelvic floor dysfunction (e.g. obstructed defecation) and anatomical factors:
Abnormally low descent of the peritoneum covering the anterior rectal wall
poor posterior rectal fixation, resulting in loss of posterior fixation of the rectum to the sacral curve
loss of the normal horizontal position of the rectum with lengthening (redundant rectosigmoid) and downward displacement of the sigmoid and rectum
long rectal mesentery
a deep cul-de-sac
levator diastasis
a patulous, weak anal sphincterSome authors question whether these abnormalities are the cause, or secondary to the prolapse. Other predisposing factors/associated conditions include:

pregnancy (although 35% of women who develop rectal prolapse are nulliparous) (have never given birth)
previous surgery (30-50% of females with the condition underwent previous gynecological surgery)
pelvic neuropathies and neurological disease
high gastrointestinal helminth loads (e.g. Whipworm)
COPD
cystic fibrosis The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs.
The mainstay diagnosis of the presenting DVT symptom is an ultrasound with venous Doppler. Ultrasound with venous Doppler rarely identifies the inferior vena cava anomalies present from birth. Difficulties in identifying the congenital stenosis of the vena cava makes diagnosis uncommon. Diagnosis of congenital stenosis of the inferior vena cava can be rarely discovered through abdominal CT examinations, and may present with an array of clinical findings dependent on the drainage patterns of the individuals. Further diagnostic tools such as a transthoracic echocardiogram can reveal the narrowing of the vena cava showing a low velocity of flow. Congenital stenosis of the vena cava can also present as acute respiratory failure and effusion of the right lung on chest X-rays. Treatments
Treatments may not be necessary for the congenital heart defect. If required, treatments can include medication, catheter procedures, corrective surgery and heart transplants dependent on the severity of the defect, age of the patient and patients general health. Symptomatic relief of venous hypertension, associated with the congenital heart defect, can be achieved through surgery as it reduces the likelihood of hepatic vein thrombosis. Intravascular stents are a treatment method for Congenital Stenosis of the Vena Cava. Expandable metallic stents have been used as part of a procedure to dilate and maintain stenotic vena cava. Experiments carried out on mongrel dogs resulted in some failures for dilation and early migration, and occlusion complications in patients. Immediate relief of persisting symptoms occurred in two patients. Double balloon dilation is another technique used to treat stenosis of the vena cava.