1. Wahl's syndrome(adductor loop syndrome): abdomen in “waves”, expansion of the afferent loop, percussion above it - tympanitis, increased peristalsis of the afferent loop.

2. Mathieu-Sklyarov's symptom -“splashing” noise (caused by sequestration of fluid in the intestines).

3. Spasokukotsky's symptom- “falling drop” symptom.

4. Grekov’s symptom (Obukhov hospital)- gaping anus, dilated and empty rectum (caused by the development of colonic obstruction at the level of the left half of the colon).

5. Gold's sign- bimanual rectal examination reveals an enlarged (sausage-shaped) afferent intestinal loop.

6. Symptom Dansa - retraction of the right iliac region with ileocecal intussusception (absence of the cecum in its “place”).

7. Tsege-Manteuffel sign- when performing a siphon enema, only up to 500 ml of liquid enters (obstruction at the level of the sigmoid colon).

8. Bayer's sign- “oblique” belly.

9. Anschutz's sign- swelling of the cecum with colonic obstruction.

10. Bouveret's sign- collapsed cecum with small intestinal obstruction.

11. Gangolf's symptom- dullness in sloping areas of the abdomen (effusion).

12. Kivulya symptom- metallic percussion sound above the abdomen.

13. Rousche's sign- palpation of a smooth, painful formation during intussusception.

14. Alapi symptom- with intussusception, there is no muscular protection of the abdominal wall.

15. Ombredan's symptom- with intussusception, hemorrhagic or “raspberry jelly” type discharge from the rectum.

16. Babuk's sign- with intussusception, the appearance of blood in the rinsing waters after palpation of the abdomen (zone of intussusception) during a primary or repeated enema.

The importance of the diagnostic and treatment complex for intestinal obstruction.

1. distinguishes mechanical CI from functional,

2. allows functional CI,

3. eliminates the need for surgery in 46-52% of patients,

4. prevents the development of additional adhesions,

5. shortens the treatment time for patients with CI,

6. reduces the number of complications and mortality,

7. provides the physician with a powerful method of treating CI.

RULES FOR EXECUTION OF LDP.

in the absence of obvious mechanical CI:

1. subcutaneous injection of 1 ml of 0.1% atropine sulfate solution

2. bilateral novocaine perinephric blockade with a 0.25% novocaine solution

3. pause 30-40 minutes + treatment of associated disorders,

4. aspiration of gastric contents,

5. siphon enema with assessment of its effect by the surgeon,

6. determination of indications for surgery.

ASSESSMENT OF THE RESULT OF LDP

1. according to subjective data,

2. according to the effect of a siphon enema, according to objective data:

Ø dyspeptic syndrome disappeared,

Ø no bloating or asymmetry of the abdomen,

Ø no “splash noise”,

Ø ordered peristaltic sounds are heard,

Ø “Kloiber cups” are allowed; after taking a suspension of barium, its passage through the intestines is determined.

REASONS FOR FALSE ASSESSMENT OF LDP

1. analgesic effect of novocaine,

2. assessment of the result only based on subjective data,

3. objective symptoms and their dynamics are not taken into account,

4. The effect of a siphon enema is incorrectly assessed.

67. Modern principles of treatment of patients with intestinal obstruction, outcomes, prevention.

TREATMENT OF INTESTINAL OBSTRUCTION Urgent surgery for intestinal obstruction is indicated:

1. If there are signs of peritonitis.

2. If there are obvious signs or suspicion of strangulation or mixed intestinal obstruction.

In other cases:

1. A diagnostic and treatment appointment is carried out; if the reception is negative, an urgent operation is performed, if it is positive, conservative treatment is carried out.

2. 250 ml of liquid barium sulfate is given orally.

3. Infusion therapy is carried out.

4. The passage of barium is assessed - when it passes (after 6 hours into the colon, after 24 hours into the rectum), the diagnosis of intestinal obstruction is removed, and the patient is subjected to a detailed examination.

The decision on surgery for acute intestinal obstruction should be made within 2-4 hours after admission. When indications for surgical treatment are given, patients should undergo brief preoperative preparation.

Surgery for intestinal obstruction involves performing a number of successive steps:

1. Performed under endotracheal anesthesia with myoplegia; In most cases, the surgical approach is a midline laparotomy.

2. Search and elimination of ileus is carried out: dissection of adhesions, mooring, enterolysis; disinvagination; unwinding of the torsion; bowel resection, etc.

3. After novocaine blockade of reflexogenic zones, decompression (intubation) of the small intestine is performed:

a) nasogastrointestinal

b) according to Yu.M. Dederer (via gastrostomy tube);

c) according to I.D. Zhitnyuk (retrograde through ileostomy);

d) according to Shede (retrograde through a cecostomy, appendicocecostomy).

Intubation of the small intestine for intestinal obstruction is necessary for:

Decompression of the intestinal wall in order to restore microcirculation and intramural blood flow in it.

To remove highly toxic and intensely infected intestinal chyme from its lumen (the intestine in case of intestinal obstruction is the main source of intoxication).

For carrying out intestinal treatment in the postoperative period (intestinal dialysis, enterosorption, oxygenation, motility stimulation, restoration of the barrier and immune function of the mucosa, early enteral feeding, etc.).

To create a frame (splinting) of the intestine in a physiological position (without angulation along the “large radii” of intestinal loops). Intestinal intubation lasts from 3 to 8 days (on average 4-5 days).

4. In some cases (resection of the intestine in conditions of peritonitis, resection of the colon, extremely serious condition of the patient), the imposition of an intestinal stoma (end, loop or Meidl) is indicated.

5. Sanitation and drainage of the abdominal cavity according to the principle of treating peritonitis. This is due to the fact that in the presence of effusion in the abdominal cavity with ileus, anaerobic microorganisms are inoculated from it in 100% of cases.

6. Completion of the operation (suturing of the abdominal cavity).

Surgery for intestinal obstruction should not be traumatic or rough. In some cases, one should not engage in long-term and highly traumatic enterolysis, but resort to the application of bypass anastomoses. In this case, the surgeon must use those techniques that he is fluent in.

POSTOPERATIVE TREATMENT

The general principles of this treatment must be formulated clearly and specifically - it must be: intensive; flexible (if there is no effect, a quick change of appointments should be carried out); complex (all possible treatment methods must be used).

Postoperative treatment is carried out in the intensive care unit and then in the surgical department. The patient in bed is in a semi-sitting position (Fovler), the “three catheters” rule is observed. The complex of postoperative treatment includes:

1. Pain relief (non-narcotic analgesics, antispasmodics, prolonged epidural anesthesia are used).

2. Carrying out infusion therapy (with transfusion of crystalloids, colloid solutions, proteins, according to indications - blood, amino acids, fat emulsions, acid-base correctors, potassium-polarizing mixture).

3. Carrying out detoxification therapy (carrying out “forced diuresis”, performing hemosorption, plasmapheresis, ultrafiltration, indirect electrochemical oxidation of blood, intestinal dialysis of enterosorption, increasing the activity of the “reserve deposit system”, etc.) -

4. Conducting antibacterial therapy (based on the principle of treating peritonitis and abdominal sepsis):

a) with the prescription of drugs: “broad spectrum” with effects on aerobes and anaerobes;

b) administration of antibiotics into a vein, aorta, abdominal cavity, endolymphatic or lymphotropic, into the lumen of the gastrointestinal tract;

c) prescription of maximum pharmacological doses;

d) if there is no effect, quickly change assignments.

5. Treatment of enteral insufficiency syndrome. Its complex includes: intestinal decompression; carrying out intestinal dialysis (saline solutions, sodium hypochlorite, antiseptics, oxygenated solutions); carrying out enterosorption (using dextrans, after the appearance of peristalsis - carbon sorbents); administration of drugs that restore the functional activity of the gastrointestinal mucosa (antioxidants, vitamins A and E); early enteral nutrition.

6. Stopping the activity of the systemic inflammatory response of the body (systemic inflammatory response syndrome).

7. Carrying out immunocorrective therapy. In this case, the patient is administered hyperimmune plasma, immunoglobulin, immunomodulators (tactivin, splenin, imunofan, polyoxidonium, roncoleukin, etc.), ultraviolet and intravascular laser irradiation of blood, and acupuncture neuroimmunostimulation are performed.

8. A set of measures is being taken to prevent complications (primarily thromboembolic, from the respiratory, cardiovascular, urinary systems, from the wound).

9. Corrective treatment of concomitant diseases is carried out.

Complications of gastroduodenal ulcers.

68. Etiology, pathogenesis, gastroduodenal ulcers. Mechanisms of pathogenesis of gastroduodenal ulcers.

ULCER DISEASE is a disease that is based on the formation and long-term course of an ulcerative defect on the mucous membrane with damage to various layers of the wall of the stomach and duodenum.

Etiology. Causes:

Social factors (tobacco smoking, unhealthy diet, alcohol abuse, poor conditions and irrational lifestyle, etc.);

Genetic factors (close relatives have a 10-fold higher risk of developing peptic ulcers);

Psychosomatic factors (personality types who experience constant internal tension and a tendency to depression are more likely to get sick);

Etiological role of Helicobacter pylori - a gram-negative microbe located intracellularly, destroys the mucous membrane (however, there is a group of patients with chronic ulcers in whom this microbe is absent in the mucous membrane);

Physiological factors - increased gastric secretion, hyperacidity, decreased protective properties and inflammation of the mucous membrane, local microcirculation disorders.

Modern concept of etiopathogenesis of ulcers - “Scales of the Neck”:

Aggressive factors: 1. Hyperproduction of HCl and pepsin: hyperplasia of the fundic mucosa, vagotonia, hyperproduction of gastrin, hyperreactivity of parietal cells 2. Traumatization of the gastroduodenal mucosa (including drugs - NSAIDs, corticosteroids, CaCl 2, reserpine, immunosuppressants, etc.) 3. Gastroduodenal dysmotility 4. N.r. (!)

Thus, a decrease in protective factors plays a major role in ulcerogenesis.

Clinic, diagnosis of complications of gastroduodenal ulcers, indications for surgical treatment: perforated and penetrating gastroduodenal ulcers;

PERFORMANCE (OR PERFORATION):

This is the most severe, rapidly developing and absolutely fatal complication of peptic ulcer disease.

The patient can only be saved through emergency surgery.

The shorter the period from the moment of perforation to surgery, the greater the patient’s chances of survival.

Pathogenesis of perforated ulcer 1. entry of stomach contents into the free abdominal cavity; 2. chemically aggressive gastric contents irritate the huge receptor field of the peritoneum; 3. peritonitis occurs and steadily progresses; 4. initially aseptic, then peritonitis inevitably becomes microbial (purulent); 5. as a result, intoxication increases, which is enhanced by severe paralytic intestinal obstruction; 6. intoxication disrupts all types of metabolism and inhibits the cellular functions of various organs; 7. this leads to increasing multiple organ failure; 8. it becomes the direct cause of death.

Periods or stages of a perforated ulcer (peritonitis) Stage I of pain shock or irritation (4-6 hours) - neuro-reflex changes, clinically manifested by severe abdominal pain; Stage II of exudation (6-12 hours) is based on inflammation, clinically manifested by “imaginary well-being” (some reduction in pain is associated with partial death of nerve endings, covering of the peritoneum with fibrin films, exudate in the abdomen reduces friction of the peritoneal layers); Stage III of intoxication - (12 hours - 3 days) - intoxication will increase, clinically manifested by severe diffuse purulent peritonitis; Stage IV (more than 3 days from the moment of perforation) is the terminal period, clinically manifested by multiple organ failure.

Clinic

The classic pattern of perforation is observed in 90-95% of cases:

Sudden, severe “dagger” pain in the epigastric region,

The pain quickly spreads throughout the abdomen,

The condition is deteriorating sharply,

The pain is severe and the patient sometimes goes into a state of shock,

Patients complain of thirst and dry mouth,

The patient grabs his stomach with his hands, lies down and freezes in a forced position,

The slightest movement causes increased abdominal pain,

ANAMNESIS

Perforation usually occurs against the background of a long course of peptic ulcer disease,

Perforation is often preceded by a short-term exacerbation of peptic ulcer disease,

In some patients, ulcer perforation occurs without a history of ulcers (approximately 12%),

this happens with “silent” ulcers.

Inspection and objective examination data:

ü patients lie down and try not to make any movements,

ü the face is sallow-gray, the features are pointed, the gaze is suffering, covered with cold sweat, the lips and tongue are rather dry,

ü blood pressure is slightly reduced and the pulse is slow,

ü the main symptom is tension in the muscles of the anterior abdominal wall, the stomach is “board-shaped”, does not participate in breathing (in thin people, segments of straight lines of the abdomen appear and transverse folds of skin are noted at the level of the navel - Dzbanovsky’s symptom),

ü palpation of the abdomen accompanied by sharp pain, increased pain in the abdomen, more in the epigastric region, right hypochondrium, then the pain becomes diffuse,

ü strongly positive Shchetkin-Blumberg symptom - first in the epigastric region, and then throughout the abdomen.

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Acute intestinal obstruction

What is Acute intestinal obstruction -

Acute intestinal obstruction(more precisely, intestinal obstruction!) is characterized by a violation of the passage of intestinal contents in the direction from the stomach to the anus. It does not represent any separate nosological form, being a complication of a wide variety of diseases: external abdominal hernias, intestinal tumors, cholelithiasis, etc. But, having arisen, this pathological condition proceeds according to a single “scenario”, causing intoxication and water and electrolyte disorders, and is accompanied by typical clinical manifestations. In this regard, diagnostic and therapeutic tactics are largely the same for obstructions that are dissimilar in nature. That is why traditionally it is considered specially, like various surgical diseases, both in the scientific and educational literature, and in medical statistics.

What provokes / Causes of Acute intestinal obstruction:

The development of mechanical (especially strangulation) intestinal obstruction is based on anatomical prerequisites of a congenital or acquired nature. Such predisposing factors may be the congenital presence of dolichosigma, mobile cecum, additional pouches and folds of the peritoneum. More often, these factors are acquired in nature: adhesions in the abdominal cavity, elongation of the sigmoid colon in old age, external and internal abdominal hernias.

The adhesive process in the abdominal cavity develops after previous inflammatory diseases, injuries and operations. For the occurrence of acute intestinal obstruction, isolated interintestinal, intestinal-parietal, and parietal-epiploic adhesions are of greatest importance, forming rough cords and “windows” in the abdominal cavity, which can cause strangulation (internal entrapment) of moving segments intestines. No less dangerous clinically can be flat interintestinal, intestinal-parietal and intestinal-epiploic adhesions, with the formation of intestinal conglomerates leading to obstructive obstruction due to functional overload of the intestine.

Another group of acquired factors contributing to the development of intestinal obstruction are benign and malignant tumors of various parts of the intestine, leading to obstructive obstruction. Obstruction can also occur due to compression of the intestinal tube by an external tumor emanating from neighboring organs, as well as narrowing of the intestinal lumen as a result of perifocal tumor or inflammatory infiltration. Exophytic tumors (or polyps) of the small intestine, as well as Meckel's diverticulum, can cause intussusception.

If the specified prerequisites are present, obstruction occurs under the influence producing factors. For hernias, this can be an increase in intra-abdominal pressure. For other types of obstruction, the provoking factor is often changes in intestinal motility associated with changes in the diet: eating a large amount of vegetables and fruits in the summer-autumn period; a heavy meal against the background of prolonged fasting can cause volvulus of the small intestine (it is no coincidence that SI. Spasokukotsky called it the disease of a hungry man); The transition from breastfeeding to artificial feeding in children of the first year of life can be a common cause of iliocecal intussusception.

The causes of dynamic intestinal obstruction are very diverse. Most often, paralytic obstruction is observed, developing as a result of trauma (including operating room), metabolic disorders (hypokalemia), and peritonitis. All acute surgical diseases of the abdominal organs, which can potentially lead to peritonitis, occur with symptoms of intestinal paresis. A decrease in peristaltic activity of the gastrointestinal tract is observed with limited physical activity (bed rest) and as a result of long-term unrelieved biliary or renal colic. Spastic intestinal obstruction is caused by lesions of the brain or spinal cord (metastases of malignant tumors, tabes dorsalis, etc.), poisoning with salts of heavy metals (for example, lead colic), and hysteria.

Pathogenesis (what happens?) during Acute intestinal obstruction:

Pathological anatomy

Pathological changes in both the intestines and abdominal cavity during acute intestinal obstruction depend on its type. With strangulation obstruction, the blood circulation of the intestinal area is primarily disrupted, so its ischemic and necrobiotic changes occur much earlier and are more pronounced. Obstructive obstruction causes secondary disorders of blood flow in the intestinal wall due to overstretching of the adductor section with contents.

With acutely developed obturation, the pressure in the intestine increases significantly proximal to the level of the obstruction. It swells from the gases and liquid contents that overwhelm it. The intestinal wall thickens due to the development of edema, as well as venous stagnation and stasis, and becomes cyanotic. Subsequently, it is overstretched and becomes significantly thinner. Increasing intraintestinal pressure up to 10 mm Hg. Art. after 24 hours it causes hemorrhages and ulcerations in the intestinal wall, which reflects ischemic damage. If the pressure rises to 20 mm Hg. Art. Irreversible necrotic changes in its wall occur.

Destructive changes spread both along the mucous membrane and deep into the intestinal wall down to the serous layer, due to which an inflammatory leukocyte infiltration appears in its thickness. Edema spreading to the mesentery increases venous congestion, under the influence of biologically active amines, ischemic paralysis of the precapillary sphincters occurs, stasis in the microvasculature progresses, and aggregation of blood cells increases. Released tissue kinins and histamine disrupt the permeability of the vascular wall, which contributes to interstitial edema of the intestine and its mesentery and the leakage of fluid first into the intestinal lumen and then into the abdominal cavity.

cavity. While circulatory disorders persist, areas of necrobiosis expand and deepen, merging into large areas of necrosis of the mucous membrane and submucosal layers. It should be noted that necrotic changes in the serous cover of the intestinal wall appear last and, as a rule, are shorter in extent, which often makes it difficult to accurately intraoperatively determine areas of intestinal non-viability. This circumstance must be taken into account by the surgeon who decides during surgery the issue of the border of intestinal resection.

As necrosis progresses, perforation of the intestinal wall may occur (let us once again recall that disruption of intestinal viability occurs much faster with strangulation obstruction). It must be emphasized that with various forms of strangulation intestinal obstruction (retrograde strangulation, volvulus, nodulation), intestinal circulatory disorders are often observed in two or more places. In this case, a section of the intestine isolated from the afferent and efferent sections, as a rule, undergoes particularly profound and pronounced pathomorphological changes. This is due to the fact that the blood circulation of a closed loop of the intestine, due to repeated bending of the mesentery, deep paresis, distension by gases and liquid contents, suffers much more severely. With persistent obstruction, pathomorphological changes in the organ progress, circulatory disorders worsen, both in the intestinal wall and in its mesentery, with the development of vascular thrombosis and intestinal gangrene.

Pathogenesis

Acute intestinal obstruction causes pronounced disturbances in the body of patients, which determine the severity of this pathological condition. In general, we can state the inherent disorders of water-electrolyte balance and acid-base status, protein loss, endotoxicosis, intestinal failure and pain syndrome.

Humoral disorders associated with the loss of large amounts of water, electrolytes and proteins. Liquid is lost with vomit (irretrievable loss), deposited in the adductor intestine, accumulates in the edematous intestinal wall and mesentery, and is contained in the abdominal cavity in the form of exudate (blocked reserve). If the obstruction is eliminated, as filtration and reabsorption processes normalize, this water reserve can again take part in the exchange. In 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, microcirculation disorders and tissue hypoxia. These pathophysiological aspects are directly reflected in the clinical manifestations of this pathological condition, which is characterized by dry skin, oliguria, arterial hypotension, high hematocrit numbers and relative erythrocytosis.

Hypovolemia and dehydration increase the production of antidiuretic hormone and aldosterone. The result of this is a decrease in the amount of discharge

urine, sodium reabsorption and significant potassium excretion. Instead of 3 potassium ions, the cell enters 2 sodium ions and 1 hydrogen ion. Potassium is excreted in the urine and lost in vomit. This causes the occurrence of 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. Subsequently, due to the destruction of the intestinal wall, the development of peritonitis and oliguria, hyperkalemia occurs (which is also far from indifferent to the body; one should remember the possibility of potassium cardiac arrest) and metabolic acidosis.

Along with fluid and electrolytes, a significant amount of proteins is lost (up to 300 g per day) due to fasting, vomiting, and sweating into the intestinal lumen and abdominal cavity. Loss of plasma albumin is especially significant. Protein losses are aggravated by the prevalence of catabolic processes.

From here it is clear that the treatment of patients with intestinal obstruction requires not only fluid transfusion (up to 5.0 liters on the first day of therapy), but also the introduction of electrolytes, protein preparations, and normalization of the acid-base state.

Endotoxicosis seems to be an important part of the pathophysiological processes in intestinal obstruction. The fluid in the afferent intestine consists of digestive juices, food chyme and transudate (it contains plasma proteins, electrolytes and blood cells), which enters the intestinal lumen due to increased permeability of the vascular wall. Under conditions of impaired intestinal passage, decreased activity of cavity and parietal digestion, and activation of microbial enzymatic digestion, all this decomposes quite quickly and undergoes rotting. This is facilitated by the proliferation of microflora in stagnant intestinal contents. With the acquisition of the dominant role of symbiont digestion in the intestinal chyme, the number of products of incomplete hydrolysis of proteins - various polypeptides, which are representatives of a group of toxic molecules of medium size - increases. Under normal conditions, these and similar compounds are not absorbed through the intestinal wall. Under conditions of circular hypoxia, it loses the function of a biological barrier, and a significant part of toxic products enters the general bloodstream, which contributes to an increase in intoxication.

At the same time, the microbial factor should be recognized as the main point in the genesis of endogenous intoxication. With intestinal obstruction, the normal microbiological ecosystem is disrupted (I.A. Eryukhin et al., 1999) due to stagnation of the contents, which contributes to the rapid growth and reproduction of microorganisms, as well as due to the migration of microflora, characteristic of the distal parts of the intestine, to the proximal parts , for which it appears foreign (colonization of the small intestine with large intestinal microflora). The release of exo- and endotoxins and disruption of the barrier function of the intestinal wall lead to the translocation of bacteria into the portal bloodstream, lymph and peritoneal exudate. These processes underlie the systemic inflammatory response and abdominal surgical sepsis, characteristic of acute intestinal obstruction. The development of intestinal necrosis and purulent peritonitis becomes the second source of endotoxemia. The apotheosis of this process is the aggravation of tissue metabolism disorders and the occurrence of multiple organ dysfunction and failure characteristic of severe sepsis. (See Chapters IV and XIII for more information on these processes.)

Specific for obstruction are disturbances of motor and secretory-resorptive function intestines, which, together with some other pathological manifestations (impaired barrier function, suppression of local immunity, etc.) are currently commonly referred to as “intestinal failure.” In the early stage of obstruction, peristalsis intensifies, while the intestinal loop, with its contractions, seems to strive to overcome the obstacle that has appeared. At this stage, peristaltic movements in the adductor loop are shortened in length, but become more frequent. Excitation of the parasympathetic nervous system while the obstruction persists can lead to the occurrence of antiperistalsis. Subsequently, as a result of hypertonicity of the sympathetic nervous system, a phase of significant inhibition of motor function develops, peristaltic waves become rarer and weaker, and in the later stages of obstruction, complete intestinal paralysis develops. This is based on increasing circulatory hypoxia of the intestinal wall, as a result of which the possibility of transmitting impulses through the intramural apparatus is gradually lost. Then the muscle cells themselves turn out to be unable to perceive contraction impulses as a result of deep metabolic disorders and intracellular electrolyte disturbances. Metabolic disorders of intestinal cells are aggravated by increasing endogenous intoxication, which, in turn, increases tissue hypoxia.

Expressed pain syndrome more often develops with strangulation intestinal obstruction due to compression of the nerve trunks of the mesentery. Severe cramping pain also accompanies obstructive obstruction. This supports disorders of central hemodynamics and microcirculation, which determines the severe course of this pathological condition.

Symptoms of Acute intestinal obstruction:

Successful resolution of diagnostic issues, selection of optimal surgical tactics and scope of surgical intervention for any disease are closely related to its classification.

Classification of acute intestinal obstruction

Dynamic (functional) obstruction

Spastic

Paralytic

Mechanical obstruction

According to the development mechanism

Strangulation(pinching, torsion, knot formation)

Obstructive(obstruction by a tumor, foreign body, fecal or gallstone, phytobezoar, roundworm ball)

Mixed(intussusception, adhesions)

By obstacle level

High(small intestine)

Low(colon)

For this pathological condition, the most acceptable is the morpho-functional classification, according to which, due to its occurrence, it is customary to distinguish between dynamic (functional) and mechanical intestinal obstruction. With dynamic obstruction, the motor function of the intestinal wall is impaired, without a mechanical obstacle to the movement of intestinal contents. There are two types of dynamic obstruction: spastic And paralytic

Mechanical obstruction characterized by the presence of occlusion of the intestinal tube at some level, which causes a violation of intestinal transit. With this type of obstruction, it is important to identify strangulation and obstruction of the intestine. At strangulation obstructionprimary the blood circulation of the part of the intestine involved in the pathological process suffers. This is due to compression of the vessels of the mesentery due to pinching, volvulus or nodulation, which causes a fairly rapid (within several hours) development of gangrene of the intestinal area. At obstructive intestinal obstruction the blood circulation of the above obstruction (adductor) section of the intestine is disrupted secondary due to its overstretching with intestinal contents. That is why intestinal necrosis is possible even with obstruction, but its development requires not several hours, but several days. Obstruction can be caused by malignant and benign tumors, fecal and gallstones, foreign bodies, roundworms. TO mixed forms Mechanical obstruction includes intussusception, in which the intestinal mesentery is involved in the intussusception, and adhesive obstruction, which can occur either as a strangulation type (compression of the intestine along with the mesentery by a force) or as an obstruction type (kink of the intestine in the form of “ double-barreled shotguns").

Diagnostic and therapeutic tactics largely depend on the location of the obstruction in the intestine; therefore, according to the level of obstruction, they are distinguished: high(small intestine) and low(colon) obstruction.

In our country, the incidence of acute intestinal obstruction is approximately 5 people per 100 thousand population, and in relation to urgent surgical patients - up to 5%. At the same time, in terms of fatal outcomes in absolute numbers, this pathology ranks first or second among all acute diseases of the abdominal organs.

Acute intestinal obstruction can occur in all age groups, but is most common between the ages of 30 and 60 years. Obstruction due to intussusception and intestinal malformations most often develops in children; strangulation forms are mainly observed in patients over 40 years of age. Obstructive intestinal obstruction due to a tumor process is usually observed in patients over 50 years of age. As for the frequency of acute intestinal obstruction depending on the gender of the patient, in women it is observed 1.5-2 times less often than in men, with the exception of adhesive obstruction, which women more often suffer from. This type of obstruction accounts for more than 50% of all observations of this pathological condition.

Diagnosis of Acute intestinal obstruction:

Leading symptoms acute intestinal obstruction are abdominal pain, bloating, vomiting, stool and gas retention. They have varying degrees of severity depending on the type of obstruction, level and duration of the disease.

Pain usually occur suddenly, regardless of food intake, at any time of the day, without any warning signs. They are characterized by a contraction-like character associated with periods of intestinal hyperperistalsis, without clear localization in any part of the abdominal cavity. With obstructive intestinal obstruction outside of a cramping attack, they usually completely disappear. Strangulation obstruction is characterized by constant sharp pain that periodically intensifies. As the disease progresses, acute pain usually subsides on days 2-3, when intestinal peristaltic activity stops, which is a poor prognostic sign. Paralytic intestinal obstruction occurs with constant dull arching pain in the abdomen.

Vomit at first it is of a reflex nature; with continued obstruction, the vomit is represented by stagnant gastric contents. In the later period, it becomes indomitable, the vomit takes on a fecal appearance and smell due to the rapid proliferation of E. coli in the upper parts of the digestive tract. Fecal vomiting is an undoubted sign of mechanical intestinal obstruction, but for a confident diagnosis of this pathological condition one should not wait for this symptom, since it often indicates the “inevitability of death” (G. Mondor). The higher the level of obstruction, the more pronounced the vomiting. In the intervals between it, the patient experiences nausea, he is bothered by belching and hiccups. With low localization of the obstruction in the intestine, vomiting occurs later and occurs at long intervals.

Retention of stool and gases - pathognomonic sign of intestinal obstruction. This is an early symptom of low obstruction. If its character is high at the beginning of the disease, especially under the influence of therapeutic measures, there may be stool, sometimes multiple, due to the emptying of the intestine located below the obstruction. With intussusception, bloody discharge sometimes appears from the anus. This can cause a diagnostic error when acute intestinal obstruction is mistaken for dysentery.

Anamnesis is important in the successful diagnosis of acute intestinal obstruction. Previous operations on the abdominal organs, open and closed abdominal injuries, and inflammatory diseases are often a prerequisite for the occurrence of adhesive intestinal obstruction. An indication of periodic abdominal pain, bloating, rumbling, stool disorders, especially alternating constipation with diarrhea, can help in making a diagnosis of tumor obstructive obstruction.

It is important to note the fact that the clinical picture of high intestinal obstruction is much brighter, with the early appearance of symptoms of dehydration, severe disorders of the acid-base state and water-electrolyte metabolism.

General condition of the patient can be moderate or severe, which depends on the form, level and time elapsed from the onset of acute intestinal obstruction. The temperature does not increase during the initial period of the disease. With strangulation obstruction, when collapse occurs, the temperature can drop to 35°C. Later, with the development of a systemic inflammatory reaction and peritonitis, hyperthermia appears. The pulse at the onset of the disease does not change, the increase in the phenomena of endotoxemia and dehydration is manifested by tachycardia. Noteworthy is the obvious discrepancy between the relatively low body temperature and rapid pulse (a symptom of toxic scissors). The tongue becomes dry and covered with a dirty coating.

Abdominal examination a patient with suspected intestinal obstruction should definitely begin with examination of all possible locations of hernias, to exclude their infringement as the cause of this dangerous syndrome. Particular attention is needed to femoral hernias in elderly women. Infringement of a section of the intestine without a mesentery in a narrow hernial orifice is not accompanied by pronounced local pain, so patients do not always actively complain about the appearance of a small protrusion below the inguinal ligament, which precedes the onset of symptoms of obstruction.

Postoperative scars may indicate the adhesive nature of intestinal obstruction. The most constant signs of obstruction include bloating. Its degree can be different, depending on the level of occlusion and the duration of the disease. With high obstruction, it can be insignificant and often asymmetrical; the lower the level of obstruction, the more pronounced this symptom is. Diffuse flatulence is characteristic of paralytic and obstructive colonic obstruction. As a rule, as the duration of the disease increases, so does the bloating.

Irregular configuration of the abdomen and its asymmetry are more characteristic of strangulation intestinal obstruction. Sometimes, especially in emaciated patients, it is possible to see one or several distended intestinal loops through the abdominal wall, periodically peristalting.

Visible peristalsis- an undoubted sign of mechanical intestinal obstruction. It is usually determined by slowly developing obstructive tumor obstruction, when the muscles of the adductor intestine have time to hypertrophy.

Local bloating with a swollen loop of intestine palpated in this area, over which high tympanitis is determined (Val's symptom)- an early symptom of mechanical intestinal obstruction. With volvulus of the sigmoid colon, the swelling is localized closer to the right hypochondrium, while in the left iliac region, that is, where it is usually palpated, a retraction of the abdomen is noted (Schiman's symptom).

Palpation abdomen in the interictal period (during the absence of cramping pain caused by hyperperistalsis) before the development of peritonitis, as a rule, is painless. There is no tension in the muscles of the anterior abdominal wall, as well as the Shchetkin-Blumberg symptom. In case of strangulation obstruction due to volvulus of the small intestine, it is positive Thévenard's sign - sharp pain when pressing the abdominal wall two transverse fingers below the navel in the midline, that is, where the root of its mesentery is usually projected. Sometimes upon palpation it is possible to identify a tumor, the body of the intussusception or the inflammatory infiltrate that caused the obstruction.

During succussion (slight shaking of the abdomen), you can hear a “splashing noise” - Sklyarov's symptom. Its identification is helped by auscultation of the abdomen using a phonendoscope while manually applying jerky movements of the anterior abdominal wall in the projection of the distended loop of intestine. The detection of this symptom indicates the presence of an overstretched paretic loop of intestine, overflowing with liquid and gaseous contents. This symptom most likely indicates the mechanical nature of the obstruction.

Percussion allows you to determine limited areas of blunting zones, which corresponds to the location of intestinal loops filled with fluid, directly adjacent to the abdominal wall. These areas of dullness do not change their position when the patient turns, which is why they differ from dullness caused by effusion in the free abdominal cavity. Dullness is also detected over a tumor, inflammatory infiltrate or intestinal intussusception.

Auscultation the abdomen, in the figurative expression of our surgical teachers, is necessary in order to “hear the noise of the beginning and the silence of the end” (G. Mondor). In the initial period of intestinal obstruction, ringing resonant peristalsis is heard, which is accompanied by the appearance or intensification of abdominal pain. Sometimes you can hear the “noise of a falling drop” (Spasokukotsky-Wilms symptom) after the sounds of fluid transfusion in distended intestinal loops. Peristalsis can be induced or enhanced by tapping or palpating the abdominal wall. As obstruction develops and paresis increases, intestinal sounds become short, rare, and of higher tones. In the late period, all sound phenomena gradually disappear and are replaced by “dead (grave) silence” - undoubtedly an ominous sign of intestinal obstruction. During this period, with a sharp swelling of the abdomen above it, you can listen not to peristalsis, but to respiratory sounds and heart sounds, which normally are not conducted through the abdomen.

The examination of a patient with acute intestinal obstruction must be supplemented digital rectal examination. In this case, it is possible to identify a “fecal blockage”, a tumor of the rectum, the head of the intussusception and traces of blood. A valuable diagnostic sign of low colonic obstruction, determined during rectal examination, is atony of the anal sphincter and balloon-like swelling of the empty rectal ampulla (symptom of the Obukhov hospital, described by I.I. Grekov). This type of obstruction is also characterized by Tsege-Manteuffel sign, consisting in the small capacity of the distal intestine when performing a siphon enema. In this case, no more than 500-700 ml of water can be introduced into the rectum.

Clinical manifestations of obstruction depend not only on its type and level of occlusion of the intestinal tube, but also on the phase (stage) of this pathological process. It is customary to distinguish three stages of acute intestinal obstruction.

1. Initial - stage of local manifestations of acute disturbance of intestinal passage lasting from 2 to 12 hours, depending on the form of obstruction. During this period, pain and local abdominal symptoms dominate.

2. Intermediate - stage of imaginary well-being, characterized by the development of acute intestinal failure, water and electrolyte disorders and endotoxemia. It usually lasts from 12 to 36 hours. In this phase, the pain loses its cramping character, becomes constant and less intense. The abdomen is greatly distended, intestinal motility weakens, and a “splashing noise” is heard. Stool and gas retention is complete.

3. Late - the stage of peritonitis and severe abdominal sepsis, often called the terminal stage, which is not far from the truth. It occurs 36 hours after the onset of the disease. This period is characterized by manifestations of a severe systemic inflammatory reaction, the occurrence of multiple organ dysfunction and failure, severe intoxication and dehydration, as well as progressive hemodynamic disorders. The abdomen is significantly distended, peristalsis cannot be heard, and peritoneal symptoms are detected.

Instrumental diagnostics

The use of instrumental research methods for suspected intestinal obstruction is intended both to confirm the diagnosis and to clarify the level and cause of the development of this pathological condition.

X-ray examination remains the main special method for diagnosing acute intestinal obstruction. It should be carried out at the slightest suspicion of this condition. As a rule, a survey fluoroscopy (graph) of the abdominal cavity is first performed. In this case, the following signs may be identified:

1. Intestinal arches occur when the small intestine is swollen with gases, while in the lower knees of the arcades horizontal levels of liquid are visible, the width of which is inferior to the height of the gas column. They characterize the predominance of gas over the liquid contents of the intestine and occur, as a rule, in relatively earlier stages of obstruction.

2. Kloiber bowls- horizontal levels of liquid with a dome-shaped clearing (gas) above them, which looks like a bowl turned upside down. If the width of the liquid level exceeds the height of the gas bubble, it is most likely localized in the small intestine.

Plain radiograph of the abdominal cavity. Small intestinal fluid levels and Kloiber cups.

The predominance of the vertical size of the bowl indicates the localization of the level in the colon. In conditions of strangulation obstruction, this symptom can appear within 1 hour, and in case of obstructive obstruction - after 3-5 hours from the moment of illness. With small intestinal obstruction, the number of cups varies; sometimes they can be layered one on top of the other in the form of a stepped ladder. Low colonic obstruction in late stages can manifest itself at both colonic and small intestinal levels. The location of Kloiber's cups at the same level in one intestinal loop usually indicates the presence of deep intestinal paresis and is characteristic of the late stages of acute mechanical or paralytic intestinal obstruction.

3. Symptom of featheriness(transverse striation of the intestine in the form of an extended spring) occurs with high intestinal obstruction and is associated with swelling and distension of the jejunum, which has high circular folds of the mucosa.

X-ray contrast study gastrointestinal tract is used when there are difficulties in diagnosing intestinal obstruction.

Depending on the expected level of intestinal occlusion, barium suspension is either given per os (signs of high obstructive obstruction) or administered by enema (symptoms of low obstruction). Oral use of a radiopaque contrast agent (in a volume of about 50 ml) involves repeated (dynamic) study of barium passage. Its retention for more than 6 hours in the stomach and 12 hours in the small intestine gives reason to suspect a violation of the patency or motor activity of the intestine. In case of mechanical obstruction, the contrast mass does not flow below the obstacle.

Emergency irrigoscopy allows you to identify obstruction of the large intestine by a tumor, as well as detect trident symptom - sign of ileocecal intussusception.

Irrigoscopy. Tumor of the descending colon with resolved intestinal obstruction.

Colonoscopy currently plays an important role in the timely diagnosis and treatment of tumor colonic obstruction. After enemas performed for therapeutic purposes, the distal (discharge) section of the intestine is cleared of fecal residues, which allows for a full endoscopic examination. Its implementation makes it possible not only to accurately localize the pathological process, but also to perform intubation of the narrowed part of the intestine, thereby resolving the phenomena of acute obstruction and performing surgery for cancer in more favorable conditions.

Ultrasound examination The abdominal cavity has little diagnostic capabilities for acute intestinal obstruction due to severe pneumatization of the intestine, which complicates the visualization of the abdominal organs. However, in some cases this method makes it possible to detect a tumor in the colon, an inflammatory infiltrate or the head of the intussusception.

Clinical signs of acute intestinal obstruction can be observed in a variety of diseases. Methods for excluding non-surgical pathology were discussed in Chapters I and II of this Guide. It is fundamentally important that all acute surgical diseases diseases of the abdominal organs, which determine the possibility of the development of peritonitis, occur with symptoms of paralytic intestinal obstruction. If the surgeon diagnoses widespread peritonitis, then before surgery (it is mandatory in this case), it is not so important to know whether it is caused by mechanical intestinal obstruction, or whether it itself was the cause of severe dynamic obstruction. This will become clear during intraoperative exploration of the abdominal cavity. It is much more important to develop adequate diagnostic and treatment tactics to determine (naturally, before the development of peritonitis) what type of obstruction the surgeon encountered: strangulation or obstruction (1), high or low (2) and, finally, mechanical or dynamic ( 3). The surgeon's actions largely depend on the answer to these questions.

1. Strangulation or obstructive obstruction? First of all, during examination, strangulation of external abdominal hernias should be excluded as a cause of strangulation obstruction. If an incarceration is detected (see Chapter VI), emergency surgery should be performed without any complex instrumental examination.

The strangulation nature of the obstruction, caused by volvulus, nodulation or internal entrapment, is indicated by severe constant pain, which may intensify at times, but never completely goes away. It is characterized by vomiting from the very beginning of the disease and quite often asymmetry of the abdomen. The condition of the patients is progressive and rapidly deteriorating, there are no “bright” intervals.

2. High or low obstruction? The answer to this question is important, if only because the method of radiocontrast examination depends on it (dynamic observation of the passage of barium suspension

or irrigoscopy). High obstruction is characterized by early and frequent vomiting, the passage of gases and the presence of stool in the first hours of the disease, rapid dehydration of the patient (dry skin with reduced turgor, a decrease in the amount of urine discharge, low central venous pressure, high hematocrit). For her, local flatulence and Valya's symptom are more typical. During survey fluoroscopy, small intestinal levels are determined (with a predominance of the horizontal size of the Kloiber cup over the vertical). Low colonic obstruction is manifested by rare vomiting, much less pronounced signs of dehydration, positive symptoms of Tsege-Manteuffel and Obukhov Hospital. A plain radiograph shows colonic levels (they can be combined with small intestinal levels in case of long-term obstruction of the intestine).

3. Mechanical or dynamic obstruction? Solution This task is not only difficult, but also extremely responsible. Dynamic obstruction itself usually does not require surgical intervention. Moreover, an unjustified operation can only aggravate it. On the other hand, in case of mechanical obstruction, surgical treatment is usually indicated.

The starting points for differential diagnosis in this case should be the characteristics of the pain syndrome. Unfortunately, dynamic obstruction can manifest itself as cramping (spastic) or dull, bursting, constant pain (intestinal paresis). Moreover, dynamic obstruction, which accompanies, for example, a long-term unresolved attack of renal colic, can turn from a spastic form into a paralytic one. Of course, vomiting should be more pronounced in case of mechanical obstruction, but severe paresis of the gastrointestinal tract is also accompanied by a copious amount of stagnant discharge through the tube from the stomach, the appearance of intestinal levels on a plain radiograph. This primarily applies to acute pancreatitis. Pronounced long-term paresis of the stomach and intestines is so inherent in this disease that there is an unwritten rule among surgeons: in all cases of suspected intestinal obstruction, urine should be examined on the diastomas. This simple test is often the only way to avoid unnecessary laparotomy. Local flatulence, symptoms of Wahl, Tsege-Manteuffel and the Obukhov Hospital are characteristic only of mechanical obstruction. On the other hand, diffuse flatulence and the absence of these symptoms do not exclude its presence.

Such diagnostic uncertainty: the patient has dynamic or mechanical obstruction is characteristic of this pathological condition. That is why in many cases they resort to conservative treatment without a final diagnosis and without a final decision on the indications for emergency surgery.

Treatment of Acute intestinal obstruction:

Since intestinal obstruction is a complication of various diseases, there is not and cannot be a single way to treat it. At the same time, the principles of therapeutic measures for this pathological condition are quite uniform. They can be formulated as follows.

1. All patients with suspected obstruction should be urgently hospitalized in a surgical hospital. The timing of admission of such patients to medical institutions largely determines the prognosis and outcome of the disease. The later patients with acute intestinal obstruction are hospitalized, the higher the mortality rate.

2. All types of strangulation intestinal obstruction, as well as any types of intestinal obstruction complicated by peritonitis, require urgent surgical intervention. Due to the serious condition of the patients, only short-term (no more than 1.5-2 hours) intensive preoperative preparation can be justified.

3. Dynamic intestinal obstruction is subject to conservative treatment, since surgical intervention itself leads to the occurrence or worsening of intestinal paresis.

4. Doubts about the diagnosis of mechanical intestinal obstruction in the absence of peritoneal symptoms indicate the need for conservative treatment. It relieves dynamic obstruction, eliminates some types of mechanical obstruction, and serves as preoperative preparation in cases where this pathological condition does not resolve under the influence of therapeutic measures.

5. Conservative treatment should not serve as an excuse for unreasonably delaying surgical intervention if the need for it is already ripe. Reducing mortality in intestinal obstruction can be achieved, first of all, by active surgical tactics.

6. Surgical treatment of mechanical intestinal obstruction involves persistent postoperative treatment of water and electrolyte disorders, endogenous intoxication and paresis of the gastrointestinal tract, which can lead to the patient’s death even after removing the obstacle to the passage of intestinal contents.

Conservative treatment should purposefully influence the links in the pathogenesis of intestinal obstruction. Its principles are as follows. Firstly, decompression of the proximal gastrointestinal tract should be ensured by aspiration of the contents through a nasogastric or nasointestinal (installed during surgery) tube. Placing a cleansing and siphon enema, if they are effective (“washing out” dense feces), allows you to empty the colon located above the obstruction and, in some cases, resolve the obstruction. In case of tumor colonic obstruction, intubation of the narrowed section of the intestine is desirable to unload the adductor section. Secondly, correction of water and electrolyte disturbances and elimination of hypovolemia is necessary. The general rules of such therapy are set out in Chapter III; here we only note that the volume of infusion therapy carried out under the control of central venous pressure and diuresis (catheterization of one of the central veins and the presence of a catheter in the bladder is desirable) should be at least 3-4 liters. It is imperative to replenish potassium deficiency, as it contributes to the worsening of intestinal paresis. Thirdly, To eliminate hemodynamic disorders, in addition to adequate rehydration, rheologically active agents should be used - rheopolyglucin, pentoxifylline, etc. Fourthly, It is highly desirable to normalize the protein balance through the transfusion of protein hydrolysates, a mixture of amino acids, albumin, protein, and in severe cases - blood plasma. Fifthly, it is necessary to influence the peristaltic activity of the intestine: with increased peristalsis and cramping pain in the abdomen, antispasmodics (atropine, platyphylline, no-shpu, etc.) are prescribed; for paresis, drugs stimulating the motor-evacuation ability of the intestinal tube: intravenous administration of a hypertonic solution sodium chloride (at the rate of 1 ml/kg of the patient’s body weight), ganglion blockers, proserin, ubretide, polyhydric alcohols, for example, sorbitol, Bernard currents on the anterior abdominal wall). And finally, last(in order, but not in order), measures that ensure detoxification and prevention of purulent-septic complications are vital. For this purpose, in addition to transfusion of significant amounts of liquid, it is necessary to use infusion of low-molecular compounds (hemodez, sorbitol, mannitol, etc.) and antibacterial agents.

Conservative therapy, as a rule, relieves dynamic obstruction (it is possible to resolve some types of mechanical obstruction: coprostasis, intussusception, volvulus of the sigmoid colon, etc.). This is its role as a diagnostic and therapeutic agent. If the phenomena of obstruction are not resolved, the therapy provided serves as a measure of preoperative preparation, which is so necessary for this pathological condition.

Surgical treatment acute intestinal obstruction requires a surgical solution the following treatment tasks.

1. Removing obstacles to the passage of intestinal contents.

2. Elimination (if possible) of the disease that led to the development of this pathological condition.

3. Performing intestinal resection if it is not viable.

4. Prevention of the increase in endotoxemia in the postoperative period.

5. Prevention of relapse of obstruction.

Let us consider in more detail the significance of these problems and the possibilities for solving them. Removing mechanical obstacles, causing intestinal obstruction should be considered as the main goal of surgical intervention. Surgical assistance can be different and, ideally, it not only eliminates the obstruction, but and eliminates the disease, that caused it, that is, simultaneously solves two of the above problems.

An example of such interventions is resection of the sigmoid colon along with the tumor due to low obstructive obstruction, elimination of strangulation obstruction due to strangulation of an external abdominal hernia by herniotomy followed by plastic surgery of the hernial orifice, etc. However, such a radical intervention is not always feasible due to the severity of the patient’s condition and the nature of the intestinal changes. Thus, in case of tumor colonic obstruction, the surgeon may be forced to limit himself to only applying a double-barreled colostomy above the obstacle, postponing bowel resection for some time (to the second stage), when such a traumatic intervention will be possible due to the patient’s condition and intestines. Moreover, sometimes the application of an interintestinal anastomosis and/or closure of a colostomy has to be performed already during the third stage of surgical treatment.

During the operation, the surgeon, in addition to eliminating the obstruction, must assess the condition of the intestines, necrosis of which is observed both with the strangulation and obstructive nature of this pathological condition. Methods for assessing intestinal viability will be described below; here we only point out that this task is very important, since leaving necrotic intestine in the abdominal cavity dooms the patient to death from peritonitis and abdominal sepsis.

Having eliminated the obstruction through radical or palliative surgery, the surgeon cannot complete the intervention. He should evacuate the contents of the afferent intestines, since the restoration of peristalsis and absorption of toxic contents from the intestinal lumen in the postoperative period will cause aggravation of endotoxemia with the most tragic consequences for the patient and the surgeon. At present, intestinal intubation through the nasal passages, pharynx, esophagus and stomach should be considered the method of choice in solving this problem; using a gastrostomy, cecostomy or through the anus. This procedure ensures the removal of toxic contents and the elimination of the consequences of paresis of the gastrointestinal tract, both during surgery and in the postoperative period.

When completing surgery, the surgeon must consider whether the patient is at risk relapse of obstruction. If this is very likely, he must take steps to prevent this possibility. An example is volvulus of the sigmoid colon, which occurs with dolichosigma. Detorsion (unwinding) of the volvulus eliminates obstruction, but does not completely exclude its recurrence; sometimes it develops again in the immediate postoperative period. Therefore, if the condition of the patient (and his intestines) allows, a primary resection of the sigmoid colon should be performed (a radical operation that excludes the possibility of recurrence of this condition). If this is not possible, the surgeon must perform palliative intervention: dissect the adhesions that bring the afferent and efferent parts of the intestine together and make volvulus possible, perform mesosigmoplication or sigmopexy (the latter is less desirable, since suturing the dilated intestine to the parietal peritoneum is fraught with cutting through the seams, and sometimes with internal pinching). The surgeon’s specific actions to prevent recurrence of obstruction depend on its cause; they will be presented below.

After considering the strategic problems of surgical treatment of obstruction, we turn to tactical issues, which involve a description of technical methods for solving the previously listed treatment problems. The main points of surgical intervention for intestinal obstruction can be considered the following:

1. Anesthetic care.

2. Surgical approach.

3. Inspection of the abdominal cavity to detect the cause of mechanical obstruction.

4. Restoration of the passage of intestinal contents or its diversion to the outside.

5. Assessing intestinal viability.

6. Intestinal resection according to indications.

7. Interintestinal anastomosis.

8. Drainage (intubation) of the intestine.

9. Sanitation and drainage of the abdominal cavity.

10. Closure of the surgical wound.

Surgical treatment of acute intestinal obstruction involves intubation endotracheal anesthesia with muscle relaxants(for details of anesthesiological support for operations, see Chapter III). A wide median laparotomy is performed. This access necessary in the vast majority of cases, since in addition to revision of the entire intestine during the intervention, it is often necessary to perform extensive resection and intubation, as well as sanitation and drainage of the abdominal cavity.

Opening the abdominal cavity should be done very carefully, especially during repeated abdominal operations (which is often the case with adhesive intestinal obstruction). Accidental damage and opening of the lumen of a sharply dilated adductor colon, often fixed to the anterior abdominal wall, is fraught with the most unfavorable consequences. Due to contamination of the abdominal cavity and surgical wound with highly pathogenic strains of intestinal microflora, the development of purulent peritonitis and septic (often anaerobic) phlegmon of the anterior abdominal wall is highly likely. Therefore, it is preferable to open the abdominal cavity outside the area of ​​the postoperative scar.

After evacuation of the effusion (by its nature one can roughly judge the severity of the pathological process: serous exudate is characteristic of the initial period of obstruction, hemorrhagic indicates circulatory disorders in the intestinal wall, dirty brown indicates intestinal necrosis), a novocaine blockade of the root of the mesentery is performed. -colon and transverse colon. To do this, use 250-300 ml of 0.25% novocaine solution.

Abdominal examination should identify the exact location of intestinal obstruction and its cause. The approximate location of this zone is judged by the condition of the intestine: above the obstacle, the afferent intestine is swollen, filled with gas and liquid contents, its wall is usually thinned and differs in color from other sections (from purple-cyanotic to dirty black color), the efferent intestine the intestine is in a collapsed state, its walls are not changed in the absence of peritonitis. It's important to remember that the obstacle that caused the development of obstruction may be located in several places at different levels, This is why a thorough examination of the entire intestine is necessary: ​​from the pylorus to the rectum.

Often, inspection of the intestine, especially with “advanced” obstruction, is difficult due to swollen intestinal loops that literally fall out of the abdominal cavity. It is unacceptable to leave overgrown intestinal loops filled with a large amount of liquid contents outside the abdominal cavity due to the fact that, under the force of gravity, they can significantly stretch the mesentery, which further aggravates circulatory disorders in them. During the inspection, the intestines should be moved very carefully, wrapping them in a towel soaked in hot saline solution. You should be careful not to try to push them back into the abdominal cavity, as this can lead to rupture of the thinned intestinal wall. In such cases, it is advisable to first empty the afferent intestines of gases and liquid contents. It's best to do it right away intestinal intubation through transnasal insertion of a double-lumen Miller-Abbott tube, as it progresses, the intestinal contents are suctioned. Nasointestinal intubation allows for adequate inspection of the abdominal cavity and ensures bowel movement on the operating table and in the postoperative period.

Nasointestinal intubation is performed as follows. The anesthesiologist inserts a probe through the lower nasal passage into the pharynx, esophagus and stomach. Next, the operating surgeon grabs it through the wall of the stomach and, moving along the lesser curvature, passes it through the pylorus into the duodenum up to the ligament of Treitz. Following this, the assistant lifts and holds the transverse colon, and the surgeon, palpating the tip of the probe, lowers it into the jejunum (sometimes for these purposes it is necessary to cross the ligament of Treitz). Then the surgeon threads the small intestine onto the probe, passing the latter all the way to the obstacle, and after removing it, to the ileocecal angle (Fig. 7.5). This procedure is carried out with constant supply of the probe by the anesthesiologist. It is important to ensure that the tube does not become kinked or coiled in the stomach or intestines. The proximal holes of the probe must be located in the stomach, and not in the esophagus, which is fraught with aspiration of intestinal contents. On the other hand, if all the holes are located in the intestines, dangerous overfilling of the stomach can occur. In some cases, it may be necessary to introduce an additional (second) probe into it.

After nasointestinal intubation is performed and an obstacle is detected, they begin to eliminate it: the adhesions are crossed, the torsion is reversed, or disinvagination is performed. Elimination of obstructive obstruction in some cases is achieved by enterotomy, in others - by resection of the intestine, bypass anastomosis or colostomy.

After eliminating the cause of obstruction, you should assess the viability of the intestine, that in acute intestinal obstruction is one of the most difficult tasks, the correct solution of which may determine the outcome of the disease. The severity of changes in the affected area is determined only after the elimination of obstruction and decompression of the intestine.

The main signs of intestinal viability are preserved pink color, the presence of peristalsis and pulsation of the marginal vessels of the mesentery. In the absence of these signs, with the exception of cases of obvious gangrene, 150-200 ml of a 0.25% novocaine solution is injected into the mesentery of the small intestine, and it is covered with napkins moistened with a hot saline solution. After 5-10 minutes, the suspicious area is re-examined. The disappearance of the bluish color of the intestinal wall, the appearance of a distinct pulsation of the marginal vessels of the mesentery and the resumption of active peristalsis allow us to consider it viable.

Non-viable intestine should be resected within healthy tissue. Considering that necrotic changes appear first in the mucous membrane, and the serous covers are affected last and can be little changed with extensive necrosis of the intestinal mucosa, resection is performed with the obligatory removal of at least 30-40 cm of the adductor and 15- 20 cm of intestinal outflow loops (from strangulation grooves, obstruction zones or from the boundaries of obvious gangrenous changes). With prolonged obstruction, a more extensive resection may be required, but the area of ​​the adductor section to be removed should always be twice as long as the abducent section. Any doubts about the viability of the intestine during obstruction should prompt the surgeon to take active action, that is, intestinal resection. If such doubts relate to a large section of the intestine, the resection of which the patient may not tolerate, you can limit yourself to removing the clearly necrotic part of the intestine, do not perform an anastomosis, and sutured the adducting and efferent ends of the intestine tightly. The wound of the anterior abdominal wall is sutured with rare sutures through all layers. In the postoperative period, intestinal contents are evacuated through a nasointestinal tube. 24 hours after the patient’s condition has stabilized against the background of intensive therapy, a relaparotomy is performed to re-examine the questionable area. After making sure of its viability (if necessary, intestinal resection is performed), the proximal and distal ends of the intestine are anastomosed.

An important role in the fight against endotoxicosis belongs to removal of toxic contents, which accumulates in the adductor section and intestinal loops that have undergone strangulation. If intestinal intubation was not performed earlier (during the audit), it should be performed at this moment. Bowel emptying can be achieved through a nasointestinal tube, or by expressing its contents into the area to be resected. It is undesirable to do this through the enterotomy opening because of the risk of infection of the abdominal cavity, but sometimes it is impossible to do without such manipulation. Then, through an enterotomy, a thick probe is inserted in the center of the purse-string suture (in the area of ​​the intestine to be removed).

The operation is completed thoroughly washing and drying the abdominal cavity. If there is a significant amount of exudate and necrotic damage to the intestine (after its resection), you should drain through counter-openings the pelvic cavity and the zone of maximum expression! changes (for example, side channels). Considering the persistence of intestinal paresis in the immediate postoperative period and the increased risk of eventration, the wound of the anterior abdominal wall is sutured especially carefully, layer by layer. It is advisable to apply several “8”-shaped Mylar sutures to the aponeurosis, in addition to the usual ones.

Postoperative management of patients. A feature of the immediate postoperative period in acute intestinal obstruction is the persistence of intestinal paresis, water and electrolyte disorders, acid-base disorders, and severe intoxication. Therefore, all measures aimed at eliminating these pathogenetic aspects, begun in the preoperative period and carried out during surgery, must be continued after surgery. Of great importance in the prevention and treatment of intestinal paresis is its decompression. This is effectively achieved by long-term aspiration of intestinal contents through a Miller-Abbott tube and, to a lesser extent, by aspiration of gastric contents. Aspiration, combined with lavage and means of selective intestinal decontamination, is carried out for 3-4 days, until intoxication decreases and active intestinal motility appears. During this time, the patient is on parenteral nutrition. The daily volume of infusion media is at least 3-4 liters.

The restoration of intestinal function is facilitated by the correction of water and electrolyte disorders. To stimulate intestinal motor function, anticholinesterase drugs (prozerin, ubretide), ganglion blockers (dikolin, dimecoline), hypertonic sodium chloride solution, Bernard currents, cleansing and siphon enemas are used.

More than 75% of all complications developing in the postoperative period in patients undergoing surgery for acute intestinal obstruction are associated with infection (peritonitis, wound suppuration, pneumonia).

Which doctors should you contact if you have Acute intestinal obstruction:

gastroenterologist

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At yours? It is necessary to take a very careful approach to your overall health. People don't pay enough attention symptoms of diseases and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific signs, characteristic external manifestations - the so-called symptoms of the disease. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to do it several times a year. be examined by a doctor, in order not only to prevent a terrible disease, but also to maintain a healthy spirit in the body and the organism as a whole.

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Other diseases from the group Gastrointestinal tract diseases:

Grinding (abrasion) of teeth

Abdominal trauma

Abdominal surgical infection

Oral abscess

Edentia

Alcoholic liver disease

Alcoholic cirrhosis of the liver

Alveolitis

Angina Zhensula - Ludwig

Anesthetic management and intensive care

Ankylosis of teeth

Anomalies of the dentition

Anomalies of teeth position

Anomalies of the esophagus

Anomalies in tooth size and shape

Atresia

Autoimmune hepatitis

Achalasia cardia

Esophageal achalasia

Bezoars of the stomach

Budd-Chiari disease and syndrome

Veno-occlusive liver disease

Viral hepatitis in patients with chronic renal failure on chronic hemodialysis

Viral hepatitis G

Viral hepatitis TTV

Intraoral submucosal fibrosis (oral submucosal fibrosis)

Hairy leukoplakia

Gastroduodenal bleeding

Hemochromatosis

Geographic language

Hepatolenticular degeneration (Westphal-Wilson-Konovalov disease)

Hepatolienal syndrome (hepatosplenic syndrome)

Hepatorenal syndrome (functional renal failure)

Hepatocellular carcinoma (hcc)

Gingivitis

Hypersplenism

Gingival hypertrophy (gingival fibromatosis)

Hypercementosis (ossifying periodontitis)

Pharyngeal-esophageal diverticula

Hiatal hernia (HH)

Acquired esophageal diverticulum

1. The most important and typical symptoms of mechanical intestinal obstruction are: cramping abdominal pain, vomiting, thirst, stool and gas retention.
2. "Ileus Scream"- with strangulation obstruction, pain occurs acutely, severely, patients scream painfully.
3. Bayer's sign- asymmetry of abdominal bloating, observed with volvulus of the sigmoid colon.
4. Valya's symptom- a loop of intestine fixed and stretched in the form of a balloon with a zone of high tympanitis above it.
5. Schiemann–Dans sign- retraction of the right iliac region during cecal volvulus.
6. Mondor's sign- with severe distension of the intestine, a characteristic rigidity of the abdominal wall is determined, which, upon palpation, resembles the consistency of an inflated ball.
7. Schwartz's sign- upon palpation of the anterior abdominal wall, an elastic tumor is identified in the area of ​​swelling in the epigastric region, which resembles a soccer ball to the touch.
8. Symptom of I. P. Sklyarov- when the abdominal wall is slightly rocked, a splashing sound is produced.
9. Mathieu's symptom- with rapid percussion of the umbilical area, a splashing noise occurs.
10. Kivulya's symptom- when percussing a swollen area of ​​the abdominal wall, a tympanic sound with a metallic tint is heard.
11. Lothuissen's sign- When auscultating the abdomen, breathing sounds and heartbeats are heard.
12. Obukhov Hospital symptom ()- balloon-shaped expansion of the empty ampulla of the rectum and gaping of the anus.
13. Spasokukotsky–Wilms sign- the sound of a falling drop is determined by auscultation.
14. Tsege–Manteuffel sign- in case of volvulus of the sigmoid colon, no more than 0.5–1 liters of water can be administered using an enema.
15. Schlange's sign- upon examination, intestinal peristalsis is visible to the eye.
16. Symptom of “deafening silence”- due to intestinal necrosis and peritonitis, peristaltic sounds weaken and disappear.
17. Thévenard's sign- sharp pain when pressing on 2 transverse fingers below the navel along the midline, i.e., where the root of the mesentery passes. This symptom is especially characteristic of small intestinal volvulus.
18. Laugier's symptom- if the stomach is large, spherical and convex - an obstacle in the small intestines, if the stomach is large, flat, with widely stretched sides - an obstacle in the large intestines.
19. Bouveret's sign- if the cecum is swollen, then the place of obstruction is in the colon; if the cecum is in a collapsed state, then the obstruction is in the small intestines.
20. Delbe Triad(with volvulus of the small intestines) - rapidly increasing effusion in the abdominal cavity, bloating and non-fecaloid vomiting.

10918 0

Clinical picture

Leading symptoms acute intestinal obstruction - abdominal pain, bloating, vomiting, stool and gas retention. They have varying degrees of severity depending on the type of obstruction and its level, as well as on the duration of the disease.

Pain usually occur suddenly, regardless of food intake, at any time of the day, without any warning signs. They are characterized by their cramping nature, associated with periods of intestinal hyperperistalsis, without clear localization in any part of the abdominal cavity. With obstructive intestinal obstruction outside of a cramping attack, they usually disappear completely. Strangulation obstruction is characterized by constant sharp pain that periodically intensifies. As the disease progresses, acute pain usually subsides on days 2-3, when intestinal peristaltic activity stops, which is a poor prognostic sign. Paralytic intestinal obstruction occurs with constant dull arching pain in the abdomen.

Vomit at first it is of a reflex nature; with continued obstruction, the vomit is represented by stagnant gastric contents. In the later period, it becomes indomitable, the vomit takes on a fecal appearance and smell due to the rapid proliferation of Escherichia coli in the upper parts of the digestive tract. Fecal vomiting is an undoubted sign of mechanical intestinal obstruction, but for a confident diagnosis of this pathological condition one should not wait for this symptom, since it often indicates the “inevitability of death” (Mondor A.). The higher the level of obstruction, the more severe the vomiting. In the intervals between it, the patient experiences nausea, he is bothered by belching and hiccups. With low localization of the obstruction in the intestine, vomiting occurs later and at longer intervals.

Retention of stool and gas- a pathognomonic sign of intestinal obstruction. This is an early symptom of low obstruction. If its character is high, at the beginning of the disease, especially under the influence of therapeutic measures, there may be stools, sometimes multiple times due to bowel movements located below the obstacle. With intussusception, bloody discharge sometimes appears from the anus. This can cause a diagnostic error when acute intestinal obstruction is mistaken for dysentery.

Clinical manifestations of obstruction depend not only on its type and level of occlusion of the intestinal tube, but also on the phase (stage) of this pathological process.
It is customary to distinguish three stages acute intestinal obstruction:

• Initial- stage of local manifestations of acute disturbance of intestinal passage lasting 2-12 hours, depending on the form of obstruction. During this period, pain and local abdominal symptoms dominate.
• Intermediate- stage of imaginary well-being, characterized by the development of acute intestinal failure, water and electrolyte disorders and endotoxemia. Its duration is 12-36 hours. In this phase, the pain loses its cramping character, becomes constant and less intense. The abdomen is greatly distended, intestinal motility weakens, and a “splashing noise” is heard. Stool and gas retention is complete.
• Late- the stage of peritonitis and severe abdominal sepsis, often called the terminal stage, which is not far from the truth. It occurs 36 hours after the onset of the disease. This period is characterized by manifestations of a severe systemic inflammatory reaction, the occurrence of multiple organ dysfunction and failure, severe intoxication and dehydration, as well as progressive hemodynamic disorders. The abdomen is significantly distended, peristalsis cannot be heard, and peritoneal symptoms are characteristic.

Diagnostics

Anamnesis

Taking an anamnesis plays an important role in the successful diagnosis of acute intestinal obstruction. Previous operations on the abdominal organs, open and closed abdominal injuries, and inflammatory diseases often serve as a prerequisite for the occurrence of adhesive intestinal obstruction. Indications of periodic abdominal pain, bloating, rumbling, stool disorders, especially alternating constipation with diarrhea can help in making a diagnosis of tumor obstructive obstruction.

It is important to note the fact that the clinical picture of high intestinal obstruction is much more vivid, with the early appearance of symptoms of dehydration, severe disorders of the acid-base state and water-electrolyte metabolism.

The general condition of the patient can be moderate or severe, which depends on both the form and level of intestinal obstruction and the time that has passed from the onset of the disease. The temperature does not increase during the initial period of the disease. With strangulation obstruction, when collapse occurs, the temperature can drop to 35 °C. Subsequently, with the development of a systemic inflammatory reaction and peritonitis, hyperthermia occurs. The pulse at the onset of the disease does not change, the increase in the phenomena of endotoxemia and dehydration is manifested by tachycardia. Note the obvious discrepancy between the relatively low body temperature and rapid pulse (symptom of “toxic scissors”). The tongue is dry and covered with a dirty coating.

Clinical studies

Inspection

Examination of the abdomen of a patient with suspected intestinal obstruction it is necessary to begin with an examination of all possible locations of hernias to exclude their infringement as the cause of this dangerous syndrome. Particular attention is needed to femoral hernias in older women. Incarceration of a section of the intestine without a mesentery in a narrow hernial orifice is not accompanied by pronounced local pain, so patients do not always actively complain about the appearance of a small protrusion below the inguinal ligament, which precedes the onset of symptoms of obstruction.

Postoperative scars may indicate the adhesive nature of intestinal obstruction. The most consistent signs of obstruction include bloating. Its degree can be different, depending on the level of occlusion and the duration of the disease. With high obstruction, it can be insignificant and often asymmetrical: the lower the level of obstruction, the more pronounced this symptom is. Diffuse flatulence is characteristic of paralytic and obstructive colonic obstruction. As a rule, as the duration of the disease increases, so does the bloating.

Incorrect abdominal configuration and asymmetry more typical for strangulation intestinal obstruction. Sometimes, especially in emaciated patients, it is possible to see one or more distended intestinal loops through the abdominal wall, periodically peristalting. Visible peristalsis- an undoubted sign of mechanical intestinal obstruction. It usually occurs with slowly developing obstructive tumor obstruction, when the muscles of the adductor intestine have time to hypertrophy.

Local bloating with a swollen loop of intestine palpated in this area, over which high tympanitis is determined ( Valya's symptom), is an early symptom of mechanical intestinal obstruction. With volvulus of the sigmoid colon, the swelling is localized closer to the right hypochondrium, while in the left iliac region, that is, where it is usually palpated, a retraction of the abdomen is noted ( Schiemann's sign).

Palpation

Palpation of the abdomen during the interictal period (during the absence of cramping pain caused by hyperperistalsis) before the development of peritonitis is usually painless. There is no tension in the muscles of the anterior abdominal wall, as well as the Shchetkin-Blumberg symptom. In case of strangulation obstruction due to volvulus of the small intestine, it is positive Thévenard's sign- sharp pain when pressing on two transverse fingers below the navel in the midline, that is, where the root of its mesentery is usually projected. Sometimes upon palpation it is possible to identify the tumor, body of intussusception or inflammatory infiltrate that caused the obstruction.

With succussion (a slight shaking of the abdomen), you can hear a “splashing noise” - Sklyarov's symptom. Its identification is helped by auscultation of the abdomen using a phonendoscope while manually applying jerky movements of the anterior abdominal wall in the projection of the swollen loop of intestine. The detection of this symptom indicates the presence of an overstretched paretic loop of intestine, overflowing with liquid and gaseous contents. This symptom most likely indicates the mechanical nature of the obstruction.

Percussion

Percussion allows you to identify limited areas of zones of dullness, which corresponds to the location of intestinal loops filled with fluid, directly adjacent to the abdominal wall. These areas of dullness do not change their position when the patient turns, which is why they differ from dullness caused by effusion in the free abdominal cavity. Dullness is also detected over a tumor, inflammatory infiltrate or intestinal intussusception.

Auscultation

Auscultation of the abdomen, in the figurative expression of our surgical teachers, is necessary in order to “hear the noise of the beginning and the silence of the end” (Mondor A.). In the initial period of intestinal obstruction, loud, resonant peristalsis is heard, which is accompanied by the appearance or intensification of abdominal pain. Sometimes you can hear the “noise of a falling drop” ( Spasokukotsky-Wilms symptom) after the sounds of fluid transfusion in distended intestinal loops. Peristalsis can be induced or enhanced by tapping the abdominal wall or palpating it. As obstruction develops and paresis increases, bowel sounds become short, rare and of higher pitch. In the late period, all sound phenomena gradually disappear and are replaced by “dead (grave) silence” - undoubtedly an ominous sign of intestinal obstruction. During this period, with a sharp bloating of the abdomen, you can listen not to peristalsis, but to breathing sounds and heart sounds, which are not normally conducted through the abdomen.

Digital rectal examination

The examination of a patient with acute intestinal obstruction must be supplemented digital rectal examination. In this case, it is possible to identify a “fecal blockage”, a tumor of the rectum, the head of the intussusception and traces of blood. A valuable diagnostic sign of low colonic obstruction, determined during rectal examination, is atony of the anal sphincter and balloon-like swelling of the empty ampulla of the rectum ( Obukhov Hospital symptom, described by I.I. Grekov). This type of obstruction is also characterized by Tsege-Manteuffel sign, which consists in the small capacity of the distal intestine when performing a siphon enema. In this case, no more than 500-700 ml of water can be introduced into the rectum.

A.I. Kirienko, A.A. Matyushenko

SYMPTOMS

1. Kivul's symptom - upon percussion, you can hear a tympanic sound with a metallic tint over a distended intestinal loop.

Kivulya's symptom is characteristic of acute intestinal obstruction.

2. Wilms symptom of a falling drop (M. Wilms) is the sound of a falling drop of liquid, determined by auscultation against the background of peristalsis noises with intestinal obstruction.

3. “splashing noise” described by I.P. Sklyarov (1923). This symptom is detected with a slight lateral concussion of the abdominal wall; it can be localized or detected throughout the abdomen. The appearance of this phenomenon indicates the presence of an overstretched paretic loop filled with liquid and gas. Mathieu described the appearance of a splashing noise during rapid percussion of the supra-umbilical region. Some authors consider the appearance of a splashing noise to be a sign of advanced ileus and, if it is detected, consider emergency surgery indicated.

4. Rovsing's symptom: sign of acute appendicitis; with palpation in the left iliac region and simultaneous pressure on the descending colon, gas pressure is transferred to the ileocecal region, which is accompanied by pain.
The cause of Rovsing's symptom: redistribution of intra-abdominal pressure and irritation of the interoreceptors of the inflamed appendix occurs
5. Sitkovsky’s symptom: sign of appendicitis; When the patient is positioned on the left side, pain appears in the ileocecal region.

Cause of Sitkovsky's symptom: irritation of interoreceptors as a result of stretching of the mesentery of the inflamed appendix
6. Barthomier-Michelson's sign: sign of acute appendicitis; pain on palpation of the cecum, increasing when lying on the left side.

The cause of the Filatov, Bartemier - Michelson symptom: tension of the mesentery of the appendix

7. Description of Razdolsky’s symptom - pain on percussion in the right iliac region.
Cause of Razdolsky's symptom: irritation of the receptors of the inflamed appendix

8. Cullen's symptom - limited cyanosis of the skin around the navel; observed in acute pancreatitis, as well as in the accumulation of blood in the abdominal cavity (more often with ectopic pregnancy).

9. Gray Turner's symptom - the appearance of subcutaneous bruises on the sides. This symptom appears 6-24 months after retroperitoneal hemorrhage in acute pancreatitis.

10. Dalrymple's sign is a widening of the palpebral fissure, which is manifested by the appearance of a white strip of sclera between the upper eyelid and the iris of the eye, caused by increased tone of the muscle that lifts the eyelid.

Dalrymple's sign is characteristic of diffuse toxic goiter.

11. Mayo-Robson symptom (pain at the point of the pancreas) Pain is detected in the area of ​​the left costovertebral angle (with inflammation of the pancreas).

12. Voskresensky’s symptom: a sign of acute appendicitis; when quickly running the palm along the anterior abdominal wall (over the shirt) from the right costal edge downwards, the patient experiences pain.

13. Shchetkin-Blumberg sign: after gentle pressure on the anterior abdominal wall, the fingers are sharply torn off. With inflammation of the peritoneum, pain occurs, which is greater when the examining hand is lifted from the abdominal wall than when pressing on it.

14. Kehr’s symptom (1): a sign of cholecystitis; pain when inhaling during palpation of the right hypochondrium.

15. Kalka's symptom - pain on percussion in the projection of the gallbladder

16. Murphy's symptom: sign o. cholecystitis; the patient is in a supine position; the left hand is positioned so that the thumb fits below the costal arch, approximately at the location of the gallbladder. The remaining fingers of the hand are along the edge of the costal arch. If you ask the patient to take a deep breath, he will be interrupted before reaching the top, due to acute pain in the abdomen under the thumb.

17. Ortner's symptom: sign o. cholecystitis; the patient is in a supine position. When you tap the edge of your palm on the edge of the costal arch on the right, pain is detected.

18. Symptom of Mussi-Georgievsky (phrenicus symptom): sign of o. cholecystitis; pain when pressing with a finger above the collarbone between the front legs of m. SCM.

19. Lagophthalmos (from the Greek lagoos - hare, ophthalmos - eye), hare eye - incomplete closure of the eyelids due to muscle weakness (usually a sign of damage to the facial nerve), in which an attempt to cover the eye is accompanied by a physiological upward rotation of the eyeball, the space of the palpebral fissure is occupied only the protein membrane (Bell's symptom). Lagophthalmos creates conditions for drying out of the cornea and conjunctiva and the development of inflammatory and dystrophic processes in them.

The cause of damage to the facial nerve, leading to the development of lagophthalmos, is usually neuropathy, neuritis, as well as traumatic damage to this nerve, in particular during surgery for neuroma VIII

cranial nerve. The inability to close the eyelids is sometimes observed in seriously ill people, especially young children.

The presence of paralytic lagophthalmos or the inability to close the eyes for another reason requires measures aimed at preventing possible damage to the eye, primarily its cornea (artificial tears, antiseptic drops and ointments on the conjunctiva of the eyes). If necessary, which is especially likely in case of damage to the facial nerve, accompanied by dry eye (xerophthalmia), temporary stitching of the eyelids - blepharorrhaphy - may be advisable.

20. Val’s symptom: a sign of intestinal obstruction; local flatulence or protrusion of the proximal intestine. Wahl (1833-1890) - German surgeon.

21. Graefe's symptom, or eyelid delay, is one of the main signs of thyrotoxicosis. It is expressed in the inability of the upper eyelid to droop when lowering the eyes. To identify this symptom, you need to bring your finger, pencil or other object to a level above the patient’s eyes, and then lower it down, watching the movement of his eyes. This symptom appears when, as the eyeball moves downwards, a white stripe of sclera appears between the edge of the eyelid and the edge of the cornea, when one eyelid drops more slowly than the other, or when both eyelids drop slowly and tremble (see Definition of Graefe's symptom and bilateral ptosis). Eyelid retardation occurs due to chronic contraction of the Müller muscle in the upper eyelid.

22. Kerte’s symptom – the appearance of pain and resistance in the area where the body of the pancreas is located (in the epigastrium 6-7 centimeters above the navel).

Kerte's symptom is characteristic of acute pancreatitis.

23. Obraztsov’s symptom (psoas symptom): a sign of chronic appendicitis; increased pain during palpation in the ileocecal region with the right leg raised.

^ PRACTICAL SKILLS

1. 
   Compatibility test for blood groups of the ABO system (on a plane)

The sample is performed on a plate with a wetted surface.

1. The tablet is marked, for which the full name is indicated. and recipient's blood group, full name. and the donor’s blood type and blood container number.

2. Carefully pipet the serum from the test tube with the recipient’s blood and apply 1 large drop (100 µl) to the plate.

3. From a segment of the tube of a plastic bag with a transfusion medium, which is prepared for transfusion specifically to this patient, take a small drop (10 μl) of donor red blood cells and apply next to the recipient's serum (serum to red blood cell ratio 10:1).

4. The drops are mixed with a glass rod.

5. Observe the reaction for 5 minutes, constantly shaking the tablet. After this time, add 1-2 drops (50-100 µl) of sodium chloride solution, 0.9%.

the reaction in the drop can be positive or negative.

a) a positive result (+) is expressed in the agglutination of red blood cells; agglutinates are visible to the naked eye in the form of small or large red aggregates. The blood is incompatible and cannot be transfused! (see Figure 1).

Figure 1. Recipient and donor blood are incompatible

b) with a negative result (-), the drop remains homogeneously colored red, and no agglutinates are detected in it. The donor's blood is compatible with the recipient's blood (see Figure 2).

Figure 2. Donor's blood is compatible with recipient's blood

3.2. Tests for individual compatibility according to the Rhesus system

3.2.1. Compatibility test using 33% polyglucin solution

Procedure for conducting the study:

1. For the study, take a test tube (centrifuge or any other, with a capacity of at least 10 ml). The test tube is marked, for which the full name is indicated. and the blood group of the recipient, and the full name of the donor, the number of the container with blood.

2. From the test tube with the recipient’s blood being tested, carefully take the serum with a pipette and add 2 drops (100 μl) to the bottom of the test tube.

3. From a segment of the tube of a plastic bag with a transfusion medium, which is prepared for transfusion to this particular patient, take one drop (50 μl) of donor red blood cells, add it to the same test tube, add 1 drop (50 μl) of a 33% polyglucin solution.

4. The contents of the test tube are mixed by shaking and then slowly rotated along the axis, tilting almost to a horizontal position so that the contents spread along its walls. This procedure is performed within five minutes.

5. After five minutes, add 3-5 ml of saline to the test tube. solution. The contents of the test tubes are mixed by inverting the test tubes 2-3 times (without shaking!)

Interpretation of reaction results:

the result is taken into account by viewing the test tubes with the naked eye or through a magnifying glass.

If agglutination is observed in the test tube in the form of a suspension of small or large red lumps against the background of cleared or completely discolored liquid, it means that the donor’s blood is not compatible with the recipient’s blood. You can't overfill!

If the test tube contains a uniformly colored, slightly opalescent liquid without signs of red blood cell agglutination, this means that the donor’s blood is compatible with the recipient’s blood with respect to Rhesus system antigens and other clinically significant systems (see Figure 3).

Figure 3. Results of compatibility testing using the Rhesus system (using a 33% polyglucin solution and a 10% gelatin solution)

3.2.2. Compatibility test using 10% gelatin solution

The gelatin solution must be carefully reviewed before use. If cloudiness or appearance of flakes occurs, as well as loss of gelling properties at t+4 0 C...+8 0 C, gelatin is unsuitable.

Procedure for conducting the study:

1. For research, take a test tube (capacity of at least 10 ml). The test tube is marked, for which the full name, blood group of the recipient and donor, and the number of the container with blood are indicated.

2. From a segment of a tube of a plastic bag with a transfusion medium, which is prepared for transfusion to this particular patient, take one drop (50 μl) of donor red blood cells, add it to a test tube, add 2 drops (100 μl) of a 10% gelatin solution heated in a water bath until liquefaction at a temperature of +46 0 C...+48 0 C. Carefully take serum from a test tube with the recipient’s blood with a pipette and add 2 drops (100 μl) to the bottom of the test tube.

3. The contents of the test tube are shaken to mix and placed in a water bath (t+46 0 C...+48 0 C) for 15 minutes or in a thermostat (t+46 0 C...+48 0 C) for 45 minutes.

4. After the end of incubation, the test tube is removed, 5-8 ml of saline is added. solution, the contents of the test tube are mixed by inverting once or twice and the result of the study is assessed.

Interpretation of reaction results.

the result is taken into account by viewing the test tubes with the naked eye or through a magnifying glass, and then viewing them by microscopy. To do this, a drop of the contents of the test tube is placed on a glass slide and viewed under low magnification.

If agglutination is observed in the test tube in the form of a suspension of small or large red lumps against the background of cleared or completely discolored liquid, this means that the donor’s blood is incompatible with the recipient’s blood and should not be transfused to him.

If the test tube contains a uniformly colored, slightly opalescent liquid without signs of red blood cell agglutination, this means that the donor’s blood is compatible with the recipient’s blood with respect to the Rhesus system antigens and other clinically significant systems (see Figure 3).
3.3. Compatibility test in gel test

When performing a gel test, compatibility tests are carried out immediately according to the ABO system (in a Neutral microtube) and a compatibility test according to the Rhesus system (in a Coombs microtube).

Procedure for conducting the study:

1. Before the study, check the diagnostic cards. Do not use cards if there are suspended bubbles in the gel, the microtube does not contain a supernatant, or there is a decrease in the volume of the gel or its cracking.

2. Microtubes are signed (last name of the recipient and number of the donor sample).

3. From a segment of a tube of a plastic bag with a transfusion medium, which is prepared for transfusion to this particular patient, 10 μl of donor red blood cells are taken with an automatic pipette and placed in a centrifuge tube.

4. Add 1 ml of dilution solution.

5. Open the required number of microtubes (one Coombs and Neutral microtube each).

6. Using an automatic pipette, add 50 μl of diluted donor red blood cells into Coombs and Neutral microtubes.

7. Add 25 μl of recipient serum to both microtubes.

8. Incubate at t+37 0 C for 15 minutes.

9. After incubation, the card is centrifuged in a centrifuge for gel cards (time and speed are set automatically).

Interpretation of the results:

if a sediment of red blood cells is located at the bottom of the microtube, then the sample is considered compatible (see Figure 4 No. 1). If agglutinates linger on the surface of the gel or in its thickness, then the sample is incompatible (see Figure 4 No. 2-6).

№1 №2 №3 №4 №5 №6

Figure 4. Results of testing samples for individual compatibility according to the Rhesus system using the gel method

3.4. Biological sample

To conduct a biological test, blood and its components prepared for transfusion are used.

Biological sample carried out regardless of the volume of the blood transfusion medium and the speed of its administration. If it is necessary to transfuse several doses of blood and its components, a biological test is carried out before the start of the transfusion of each new dose.

Technique:

transfuse 10 ml of blood transfusion medium once at a rate of 2-3 ml (40-60 drops) per minute, then stop the transfusion and observe the recipient for 3 minutes, monitoring his pulse, respiratory rate, blood pressure, general condition, skin color, measure body temperature. This procedure is repeated twice more. The appearance during this period of even one of the clinical symptoms such as chills, lower back pain, a feeling of heat and tightness in the chest, headache, nausea or vomiting requires immediate cessation of the transfusion and refusal to transfuse this transfusion medium. The blood sample is sent to a specialized blood service laboratory for individual selection of red blood cells.

The urgency of transfusion of blood components does not exempt from performing a biological test. During this procedure, it is possible to continue transfusion of saline solutions.

When transfusing blood and its components under anesthesia, the reaction or incipient complications are judged by an unmotivated increase in bleeding in the surgical wound, a decrease in blood pressure and an increase in heart rate, a change in the color of urine during bladder catheterization, as well as by the results of a test to detect early hemolysis. In such cases, the transfusion of this blood transfusion medium is stopped, the surgeon and the anesthesiologist-resuscitator, together with the transfusiologist, are obliged to find out the cause of the hemodynamic disturbances. If nothing other than transfusion could cause them, then this blood transfusion medium is not transfused; the issue of further transfusion therapy is decided by them depending on clinical and laboratory data.

A biological test, as well as a test for individual compatibility, is also required in cases where red blood cell mass or suspension, individually selected in the laboratory or phenotyped, is transfused.

After the end of the transfusion, the donor container with a small amount of the remaining blood transfusion medium used for individual compatibility tests must be preserved for 48 hours at a temperature of +2 0 C...+8 0 C.

After the transfusion, the recipient remains in bed for two hours and is observed by the attending physician or the doctor on duty. His body temperature and blood pressure are measured hourly, recording these indicators in the patient’s medical record. The presence and hourly volume of urine output and the color of urine are monitored. The appearance of red coloration of urine while maintaining transparency indicates acute hemolysis. The next day after the transfusion, a clinical blood and urine test must be performed.

When performing an outpatient blood transfusion, the recipient after the end of the transfusion must be under the supervision of a physician for at least three hours. Only in the absence of any reactions, the presence of stable blood pressure and pulse, and normal urination can the patient be released from the hospital.

1. 
   Determining indications for blood transfusion

Acute blood loss is the most common damage to the body along the entire path of evolution, and although for some time it can lead to significant disruption of life, medical intervention is not always necessary. Determining acute massive blood loss requiring transfusion intervention is associated with a large number of necessary reservations, since it is these reservations, these particulars that give the doctor the right to carry out or not to carry out a very dangerous operation of transfusion of blood components. Acute blood loss is considered to be massive, requiring transfusion assistance, if within 1-2 hours the approximately estimated blood loss was at least 30% of it original volume.

Blood transfusion is a serious intervention for the patient, and the indications for it must be justified. If it is possible to provide effective treatment to a patient without blood transfusion or there is no confidence that it will benefit the patient, it is better to refuse blood transfusion. Indications for blood transfusion are determined by the purpose it pursues: replacement of the missing volume of blood or its individual components; increased activity of the blood coagulation system during bleeding. Absolute indications for blood transfusion are acute blood loss, shock, bleeding, severe anemia, severe traumatic operations, including those with artificial circulation. Indications for transfusion of blood and its components are anemia of various origins, blood diseases, purulent-inflammatory diseases, severe intoxications.

Determination of contraindications to blood transfusion

Contraindications to blood transfusion include:

1) decompensation of cardiac activity due to heart defects, myocarditis, myocardiosclerosis; 2) septic endocarditis;

3) stage 3 hypertension; 4) cerebrovascular accident; 5) thromboembolic disease, 6) pulmonary edema; 7) acute glomerulonephritis; 8) severe liver failure; 9) general amyloidosis; 10) allergic condition; 11) bronchial asthma.

1. 
   Determination of indications

Definition of contraindications

^ Preparing the patient To blood transfusion. The patient has

admitted to the surgical hospital, the blood type and Rh factor are determined.

Studies are being carried out on cardiovascular, respiratory, urinary

systems in order to identify contraindications to blood transfusion. 1-2 days before

transfusions perform a general blood test before blood transfusion to the patient

must empty the bladder and bowels. Blood transfusion is best done

in the morning on an empty stomach or after a light breakfast.

Choice of transfusion environment, method of transfusion. Transfusion of whole

blood for the treatment of anemia, leukopenia, thrombocytopenia, coagulation disorders

system, when there is a deficiency of individual blood components, is not justified, since

how others are used to replenish individual factors, the need for

which the patient does not need to administer. The therapeutic effect of whole blood in such cases

lower, and blood consumption is significantly greater than with the introduction of concentrated

blood components, for example red or leukocyte mass, plasma,

albumin, etc. So, with hemophilia, the patient only needs to be administered factor VIII.

To cover the body's needs for it with whole blood, it is necessary

administer several liters of blood, whereas this need can only be met

several milliliters of antihemophilic globulin. With plaster and

afibrinogenemia, it is necessary to transfuse up to 10 liters of whole blood to replenish

fibrinogen deficiency. Using the blood product fibrinogen, it is enough to inject

its 10-12 g. Whole blood transfusion can cause sensitization of the patient,

formation of antibodies to blood cells (leukocytes, platelets) or plasma proteins,

which is fraught with the danger of severe complications during repeated blood transfusions or

pregnancy. Whole blood is transfused in case of acute blood loss with sudden

decrease in blood volume, during exchange transfusions, during artificial circulation in

time of open heart surgery.

When choosing a transfusion medium, you should use the component in which

the patient also needs blood substitutes.

The main method of blood transfusion is intravenous drip using

puncture of the saphenous veins. With massive and long-term complex transfusion

therapy, blood along with other media is injected into the subclavian or external

jugular vein. In extreme situations, blood is administered intra-arterially.

Grade validity canned blood and its components for

transfusion. Before transfusion, determine the suitability of blood for

transfusions: take into account the integrity of the packaging, expiration date, violation of the regime

blood storage (possible freezing, overheating). Most appropriate

transfuse blood with a shelf life of no more than 5-7 days, since with prolongation

during storage, biochemical and morphological changes occur in the blood,

which reduce its positive properties. On macroscopic assessment, blood

must have three layers. At the bottom there is a red layer of red blood cells, it is covered

a thin gray layer of leukocytes and slightly transparent on top

yellowish plasma. Signs of unsuitable blood are: red or

pink coloration of plasma (hemolysis), appearance of flakes in plasma, turbidity,

the presence of a film on the surface of the plasma (signs of blood infection), the presence

clots (blood clotting). For urgent transfusion of unsettled blood