<h1>Intestinal linvagination</h1>

Definition

Telescoping of the superior intestinal loop into the inferior one, leading to intestinal occlusion.

Epidemiology

Mainly affects eutrofic male newborns in the first 4-12 months of life. There are no prior sings or symptoms, the main manifestation being intestinal bowel movement disruption. There is a higher risk of developing after abdominal surgery.

Pathogenesis

Favoring factors

1. An reduced fixation of the cecum and the ascending colon leading to a  disrupted growth of this segments compared to the small intestine 
2. A change in diet 
3. Factors that determine mesenteric lymphadenitis:

• Diarrheal disease
•  Virosis

Determining factors

1. Reilly phenotype: mesenteric adenopathies, accentuated intestinal peristalsis and vasomotor dysfunctions
2. Meckel's diverticulum 
3. Benign and malignant tumors
4. Intestinal polyps
5. Intestinal parasites

Anatomical pathology

Invagination head, which progresses through the invagination ring. Both the invagination head and the invagination ring could be either fix or mobile

Invagination Types

Invagination through prolaps: the head is mobile and the ring is fixed
Associates increased vascular dysfunctions
Example: Ileocolic invagination, the fixed ring being Bauhin's valve

Invagination through overlap: the head is fixed but the ring is mobile
Associates decreased vascular dysfunction
Example: Ileoileal, inleo-ceco-colic and colo-colic invagination

Combined: through overlap and prolaps
Associates increased vascular dysfunction
Example: ileo-ileal, ileo-ceco-colic

Pathophysiology

The mechanical factor compresses the mesenterum leading the vascular dysfunctions. The venous and stasis lymphatic stasis leads o increased pressure in the mucosal capillary, leading to intraluminal bleeding. The decreased arterial flow leads to necrosis

Clinical signs and symptoms

General signs:

1. Agitated, unsettled 
2. suffering facies
3. Refuses feeding
4. Emesis: initial reflex emesis due to pain, asthe disease progresses the emesis start to contain partially digested or undigested food and in the late stages feces

Abdominal examination:

1. Initially painless, elastic and supple
2. Meteorism  
3. Palpation of a tumor
4. Empty right ileal fossa, known as Dance's sign

Dgital rectal examination reveals blood

Late stage signs:

1. ringed, intoxicated, apathetic facies
2. Intestinal occlusion signs 
3. Rectorrhagia 

Clinical forms

Tumoral form:

1. Pain
2. No emesis
3. Mobile, painless tumor

Pseudoappendicular form:

1. Pain in the inferior right quadrant 
2. Emesis
3. Normal number of leukocytes 

Chronic  reccurent form

1. Colicative pain
2. "phantom" tumor

Acute form described in  infants

Radiologic examination

Abdominal radiography reveal hidroaeric. organ pipe like images

Irigography may reveal:

1. Amputation 
2. Nutmeg
3. Bident, trident
4. Lobster tail 

http://home.earthlink.net/~radiologist/tf/020501.htm

Differential diagnosis

Enterocolitis

1. Multiple stools
2. Absence of pain rhytmicity
3. Reduced blood and mucositis

Meckel's divertculum

1. The signs of intestinal occlusion are absent
2. Digested blood aspect - Melena

Acute appendicitis

1. Fever
2. Leucocytosis
3. Muscular defense

Rectocolic polyposis

1. Calm as opposed to agitated
2. Fresh blood in stool due to polyp rupture 

Treatment

Conservative treatment

Low pressure barium enema in the first 12-24 h under ecographic or radiographic control

Surgical treatment

1. Preoperative preparation and hidroelectrolitic reequilibration
2. Desinvagination through squeezing while checking the viability of the intestinal loop
3. Resection
4. Ileostomy
5. Colostomy

Postoperative treatment

1. Analgetics
2. Antibiotics
3. Hidroelectrolitical reequilibration 
4. Nasogastric aspiration
5. beta-blockers

Prognosis

If  the disease is diagnosed in an early stage the prognosis is good, with a mortality rare of 5-10%. In late stages, when the diagnosis is reached after 72 hours from the onset of symptoms the prognosis is poor, with a mortality rate of 70-80%