Intestinal obstruction

Etiology of mechanical intestinal obstruction

Predisposing factors in mechanical intestinal obstruction:

• congenital dolichosigma
• movable colon ,
• additional pockets and folds of the peritoneum,
• adhesions in the abdominal cavity,
• elongation of the sigmoid colon in old age,
• hernia of the anterior abdominal wall and internal hernia.

The causes may be benign and malignant tumors of different intestinal sections, leading to obstructive obstruction. Obturation may also occur due to compression of the intestinal tube by a tumor from the outside, emanating from neighboring organs, as well as narrowing of the intestinal lumen as a result of perifocal, tumor or inflammatory infiltration. With the defeat of three to five lymph nodes of the mesentery of the intestine and tumor genesis of intestinal obstruction, the curability is 99 percent. Exophytic tumors (or polyps) of the small intestine, as well as Meckel's diverticulum, can cause invagination.

For other types of obstruction, changes in intestinal motility associated with changes in the dietary regime are often provoking factors:

• eating large amounts of high-calorie food
• plentiful meal on the background of prolonged fasting (possible twisting of the small intestine);
• transition from breastfeeding to artificial in children of the first year of life.

Etiology of dynamic intestinal obstruction

Most often there is a paralytic obstruction, which develops as a result of injury (including the operating room), metabolic disorders ( hypokalemia ), peritonitis .

All acute surgical diseases of the abdominal organs, which can potentially lead to peritonitis, occur with symptoms of intestinal paresis . A decrease in the peristaltic activity of the gastrointestinal tract is noted when physical activity is restricted (bed rest) and as a result of long-term intractable biliary or renal colic.

Spastic intestinal obstruction is caused by lesions of the brain or spinal cord (metastasis of malignant tumors, spinal wortworms , etc.), poisoning by heavy metal salts (for example, lead), hysteria.

Humoral disorders are associated with the loss of large amounts of water, electrolytes and proteins. There is a loss of fluid with vomit, its deposit in the leading part of the intestine, accumulation in the edematous intestinal wall and mesentery, it is contained in the abdominal cavity in the form of exudate.

Under conditions of non-liquidated obstruction, fluid loss during the day can reach 4.0 liters or more. This leads to hypovolemia and tissue dehydration, hemoconcentration, impaired microcirculation and tissue hypoxia. These pathophysiological moments directly affect the clinical manifestations of this pathological condition, which is characterized by dry skin, oliguria , arterial hypotension , high hematocrit and relative erythrocytosis .

Hypovolemia and dehydration increase the production of antidiuretic hormone and aldosterone . The result is reduced diuresis , reabsorption of sodium and significant excretion of potassium in the urine and vomit. This causes intracellular acidosis, hypokalemia and metabolic extracellular alkalosis. A low level of potassium in the blood is fraught with a decrease in muscle tone, a decrease in myocardial contractility and inhibition of intestinal peristaltic activity. Further, due to the destruction of the intestinal wall, the development of peritonitis and oliguria, hyperkalemia occurs (which can lead to potassium cardiac arrest) and metabolic acidosis.

Along with liquid and electrolytes, a significant amount of proteins (up to 300 g / day) is lost due to starvation, vomiting, sweating in the intestinal lumen and the abdominal cavity. Plasma albumin losses are particularly significant. Protein loss is exacerbated by the prevalence of catabolism.

From this it is clear that for the treatment of patients with acute intestinal obstruction it is necessary not only transfusion of the liquid (up to 5.0 l on the first day of treatment), but also the introduction of electrolytes , protein preparations, normalization of the acid-base state. Endotoxicosis is an important link in pathophysiological processes in intestinal obstruction. The contents of the adductor part of the intestine (food chyme , digestive juices and transudate) quickly decompose and rot. This is facilitated by the reproduction of microflora in the stagnant intestinal contents. With the acquisition of the dominant role of symbiotic digestion in the intestinal chyme, the number of products of incomplete hydrolysis of proteins - various polypeptides (representatives of the group of toxic molecules of average size) increases. Under normal conditions, these and similar compounds are not absorbed through the intestinal wall. Under conditions of circulatory hypoxia, the intestine loses the function of the biological barrier and a significant portion of toxic products enters the general bloodstream, which contributes to an increase in toxicity.

However, the main factor in the pathogenesis of endogenous intoxication should be recognized as microbial. In acute intestinal obstruction, the normal microbiological ecosystem is disrupted due to stagnation of the contents, which contributes to rapid growth and reproduction of microorganisms, as well as in connection with the migration of microflora, characteristic of the distal intestines, to the proximal ones for which it is alien (colonization of the small intestine by the colonic microflora). Isolation of exo-and endotoxins, impaired barrier function of the intestinal wall leads to the translocation of bacteria into the portal bloodstream, lymph and peritoneal exudate. These processes underlie the systemic inflammatory response and abdominal surgical sepsis, which are characteristic of acute intestinal obstruction. Necrosis of the intestine and purulent peritonitis is the second source of endotoxicosis. The apotheosis of this process is the exacerbation of disorders of tissue metabolism and the occurrence of multiorgan dysfunction and insufficiency characteristic of severe sepsis.

Violations of motor and secretory-resorptive function of the intestine . In the early stage of obstruction, peristalsis increases, while the intestines, with their contractions, tend to overcome the obstacles that appear. At this stage, the peristaltic movements in the afferent loop are shortened in length, but become more frequent. Excitation of the parasympathetic nervous system while maintaining an obstruction may lead to the emergence of anti-peristalsis. Further, as a result of hypertonic sympathetic nervous system, a phase of significant inhibition of motor function occurs, the peristaltic waves become more rare and weak, and in the later stages of obstruction, complete intestinal paralysis develops. The basis of this is the increasing circulatory hypoxia of the intestinal wall, due to which the possibility of transmission of impulses through the intramural nervous apparatus is gradually lost. Then the muscle cells themselves are not able to perceive the impulses to reduce as a result of deep metabolic disorders and intracellular electrolyte disorders. Disorders of intestinal cell metabolism exacerbates increasing endogenous intoxication, which, in turn, increases tissue hypoxia.

Pronounced pain syndrome often occurs with obstructive and strangulated intestinal obstruction due to compression of the nerve trunks of the mesentery. This supports disorders of central hemodynamics and microcirculation, which determines the severe course of this pathological condition.

1. By morphofunctional features:
   • Dynamic (functional) intestinal obstruction — the motor function of the intestinal wall is impaired without a mechanical obstacle for promoting intestinal contents:
     • Paralytic intestinal obstruction (as a result of lowering the tone of intestinal myocytes);
     • Spastic intestinal obstruction (as a result of increased tone);
   • Mechanical intestinal obstruction - occlusion of the intestinal tube at any level, which causes a violation of intestinal transit:
     • Strangulated intestinal obstruction ( lat. Strangulatio - "suffocation") - occurs when a mesentery of the intestine is squeezed, which leads to malnutrition. The classic examples of strangulated intestinal obstruction are bloat , nodulation and restraint.
     • Obstructive intestinal obstruction ( Latin obturatio - "blockage") - occurs when a mechanical obstacle to the movement of intestinal contents:
       • intraintestinal without connection with the intestinal wall - the cause may be large gallstones , trapped in the intestinal lumen through the internal biliary fistula, fecal stones, worms , foreign bodies;
       • intraintestinal, originating from the intestinal wall - tumors, cicatricial stenosis;
       • extraintestinal - tumor, cysts;
     • Mixed intestinal obstruction (combination of strangulation and obstruction):
       • Invagination intestinal obstruction as a result of invagination;
       • Adhesive intestinal obstruction , developing due to compression of the intestine adhesions of the abdominal cavity .
2. According to the clinical course: acute and chronic;
3. In terms of obstruction: high (small bowel , distal to the ligament of the Treitz to the bauhinia valve) and low (colonic, distal to the bauhinia valve);
4. According to the passage of chyme: full and partial;
5. By origin: congenital and acquired.

1. Abdominal pain - a constant and early sign of obstruction, usually occurs suddenly, regardless of food intake, at any time of the day, without precursors; the nature of pain is cramping. Attacks of pain associated with a peristaltic wave and repeated after 10-15 minutes. In the period of decompensation, depletion of energy reserves of the muscles of the intestine, the pain begins to be permanent. In case of strangulation obstruction, pain is immediately constant, with periods of amplification during the wave of peristalsis. With the progression of the disease, acute pains, as a rule, subside by 2-3 days, when the peristaltic activity of the intestine stops, which is a poor prognostic sign. Paralytic intestinal obstruction occurs with constant dull arching abdominal pain;
2. Delay of stools and gases is a pathognomonic sign of intestinal obstruction. This is an early symptom of low obstruction. With its high character, at the beginning of the disease, especially under the influence of remedial measures, there may be a stool, sometimes multiple due to the emptying of the intestine, located below the obstacle. With invagination from the anus, sometimes there is bloody discharge. This can cause a diagnostic error, when acute intestinal obstruction is considered as dysentery;
3. Abdominal distension and asymmetry;
4. Vomiting - after nausea or on their own, often repeated vomiting. The higher the obstacle in the digestive tract, the earlier vomiting occurs and has a more pronounced, repeated, indomitable. Vomiting is initially mechanical (reflex), and then central (intoxication) character.

• Perforation of a hollow organ
• Acute appendicitis
• Acute pancreatitis
• Peritonitis
• Acute afferent loop syndrome (with a history of Billroth II stomach resection)
• Renal colic
• Pneumonia (inferior)
• Pleurisy
• Coronary heart disease (acute myocardial infarction , angina )

• Radiography of the abdominal cavity
  • determination of gas and fluid levels in bowel loops ( Kloyber bowls )
  • transverse striation of the intestine (symptom of kerking folds)
• Ultrasound
  • with mechanical intestinal obstruction:
    • the expansion of the lumen of the intestine more than 2 cm with the presence of the phenomenon of "fluid sequestration" in the gut lumen;
    • thickening of the wall of the small intestine more than 4 mm;
    • the presence of reciprocating movements of chyme along the intestine;
    • an increase in the height of the coring folds of more than 5 mm;
    • increase the distance between the kerking folds of more than 5 mm;
    • intestinal hyperpneumatization in the adductor region
  • with dynamic intestinal obstruction:
    • lack of reciprocating movements of chyme along the intestine;
    • the phenomenon of sequestration of fluid in the intestinal lumen;
    • unexpressed relief of kerkring folds;
    • intestinal hyperpneumatization in all departments
• Irrigology
  • contraindicated in intestinal obstruction.

In all cases when the diagnosis of acute mechanical intestinal obstruction is established or assumed, the patient should be urgently hospitalized in a surgical hospital.

Emergency surgery after short-term preoperative preparation (2-4 hours) is indicated only in the presence of peritonitis, in other cases, treatment begins with conservative and diagnostic (if the diagnosis is not finally confirmed) measures. The measures are aimed at combating pain, hyperperistalsis, intoxication and disturbances of homeostasis, freeing the upper parts of the digestive tract from stagnant contents by means of a stomach probe, siphon enemas.

In the absence of the effect of conservative treatment, surgical treatment is indicated. Conservative treatment is effective only in cases of abdominal pain, abdominal distention, cessation of vomiting, nausea, adequate discharge of gas and feces, disappearance or drastic reduction of splashing noise and Valya symptom, a significant reduction in the number of horizontal levels on radiographs, as well as clear promotion of barium contrast mass along the small intestine and its appearance in the colon after 4-6 hours from the start of the study, along with the resolution of the phenomena of coprostasis on the background of the enemas.

Operational Manual

After performing laparotomy , an abdominal cavity is inspected , before which it is recommended to perform a novocainic blockade of the mesentery of the small and large intestines. The audit starts from the duodenojejunal transition, gradually approaching the ileocecal angle. Orientation is performed on intestinal loops swollen with gas, which are located above the site of the obstacle. With the swelling of the entire small intestine there is an assumption about the localization of obstruction in the large intestine. When revisions determine the viability of the intestine, the etiology of obstruction. Particular attention is paid to the "typical" places: angular segments (hepatic and splenic angles of the colon), the place of occurrence of internal hernias (internal inguinal and femoral rings, obturator holes, pockets of the ligament Treyts, Vinslo holes, aperture holes).

The rules for determining the viability of the intestine are universal: After warming the intestine with napkins soaked in “hot” isotonic sodium chloride solution for 10-15 minutes, and also after the introduction of 20-40 ml of warm 0.25% novocaine solution into the mesentery

• serous gut pink, shiny;
• peristalsis of this part of the intestine is preserved;
• pulsation of the mesenteric vessels is determined

The main task of the surgical intervention is to restore the passage through the intestines: dissection of adhesions, unfolding turn-up, loop nodes, disinvagination, removal of the tumor). There are several rules:

• The worse the patient’s condition and the more pronounced the intoxication, the less radical the operation should be. "Radicality is not to the detriment of the patient."
• Resection of the intestine in case of obstruction is performed according to universal principles:
  • 30-40 cm above the site of the obstruction, that is, of the adductor (usually swollen with gases) and
  • 15–20 cm below the site of the obstruction, that is, the abduction section (usually collapsed sections of the intestine);
  • Perform anastomosis “side-to-side” or “end to end” (the latter type is used only with minor differences in the diameter of the adductor and outlet sections of the intestine, in the absence of decompensated obstruction);
• With a high probability of development of insolvency of the anastomotic sutures, it is advisable to perform an operation like Maydlya (even if it is possible to restore intestinal obstruction);
• If for any reason the imposition of a primary anastomosis is not possible, then it is necessary that the leading and withdrawing segments of the intestine be formed on the anterior abdominal wall in the form of a stoma (“ double-stem stoma ”). The exceptions are operations on the sigmoid colon, when the outlet segment of the intestine is sutured tightly and immersed in the abdominal cavity - obstructive resection (often called " Hartmann-type surgery )."

Often, the stage of surgery for intestinal obstruction is decompression of the gastrointestinal tract (intestinal intubation) by an elastic probe (thickness 8–9 mm) with numerous holes (2–2.5 mm in diameter). Decompression targets:

1. reduction of intoxication
2. intestinal motility stimulation
3. prevention of the development of insolvency anastomoses
4. frame function

Often used nasogastric decompression, less often - retrograde (from aboral to the oral intestine), through the gastrostomy, cecotoma, appendicostomy and others. The probes are usually removed for 3-6 days (with a pronounced adhesion process - for 7-10 days). Prolonged exposure to the probe may predispose to the development of a sore ulcer. Probe Removal Criteria:

1. appearance of persistent intestinal motility;
2. reduction of bloating;
3. stool discharge, gas;
4. changes in the quality characteristics of the intestinal discharge - it becomes a light yellow or greenish color, fecal odor disappears.

The operational manual is supplemented with sanation and drainage of the abdominal cavity - washed with antiseptic solutions, electric scrubbers (“atmospheres”), dried with napkins.

• V.S. Saveliev, A.I. Kiriyenko. Clinical surgery: national leadership: in 3 tons. - 1st ed. - M .: GEOTAR-Media , 2009. - p. 832. - ISBN 978-5-9704-1023-3 .

• Intestinal Obstruction on MedlinePlusEncyclopedia
• Patient UK: Intestinal Obstruction and Ileus
• PubMed Health: Intestinal obstruction
• 178948 , section Ileus (eng.) On the site EMedicine
• Merck Manual Professional: Ileus