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Lecture notes, cheat sheets
Pediatric surgery. Dynamic intestinal obstruction (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 15. Dynamic intestinal obstruction In emergency surgery of childhood, a special place is occupied by dynamic intestinal obstruction, which can occur after surgical interventions or accompany a number of surgical and other diseases. The cause of dynamic intestinal obstruction has not yet been elucidated. It is believed that the basis of dynamic obstruction is a violation of regional mesenteric circulation, a change in the excitability of the peripheral and central nervous apparatus that regulates the motor function of the intestine. The state of parabiosis of the neuromuscular structures of the intestine develops as a result of a violation of the blood circulation of its wall. Circulatory disorders can be the result of an inflammatory process (peritonitis), overstretching of the intestinal wall, dehydration and hypoxemia of various origins. As a result of inflammation and edema, functional and then organic damage to nerve devices develops, followed by a decrease in the susceptibility of the intestinal muscle elements to natural mediators of motor regulation. The excitability of the neuromuscular apparatus of the intestine also decreases with the pathology of electrolyte metabolism (potassium and sodium deficiency) and with changes in body temperature. Dynamic intestinal obstruction can be considered as an independent nosological unit in those cases when it occupies a leading place in the clinical picture of the disease and when it becomes necessary to exclude mechanical obstruction that requires urgent surgical intervention. Among all types of intestinal obstruction in children, dynamic obstruction is 8-11%. It is customary to distinguish between spastic and paralytic forms of dynamic intestinal obstruction. 1. Spastic intestinal obstruction Spastic intestinal obstruction is relatively rare. Usually the cause of its occurrence is helminthic invasion. clinical picture The clinical picture of spastic intestinal obstruction is characterized by the occurrence of short-term attacks of severe pain in the abdomen without a specific localization. In the vast majority of cases, the general condition of the child remains satisfactory. Body temperature is normal or subfebrile. Sometimes there is a single vomiting. Gases usually move away, there is no stool, but it may be normal. The abdomen is not swollen, symmetrical, sometimes sunken, on palpation - soft in all departments; in rare cases, it is possible to determine a spasmodic intestine. Auscultation clearly revealed peristaltic noises. There are no changes in hemodynamics. Blood and urine tests - no pathology. X-ray examination X-ray examination of the abdominal cavity has only differential diagnostic value. Differential diagnosis The differential diagnosis is carried out with mechanical obstruction and renal colic. In cases of acute and severe intestinal spasms, it is sometimes difficult to exclude mechanical obstruction. A carefully collected history (indication of existing ascariasis) and objective examination data (lack of visible peristalsis, local pain or tumor-like formations) allow us to think about intestinal spasm. Of certain importance is an x-ray examination of the abdominal cavity, which, with mechanical obstruction, helps to recognize the disease. Significant assistance in the diagnosis is provided by bilateral pararenal blockade or short-term epidural anesthesia. The persistent disappearance of pain after the blockade makes it possible to exclude mechanical intestinal obstruction, in which pain attacks do not go away, but often intensify. In doubtful cases, surgery should be considered as a last resort. Renal colic, in contrast to spastic obstruction, proceeds with excruciating attacks of pain, which are localized in the lumbar regions and are usually accompanied by typical irradiation. In addition, dysuric disorders and pathological urinalysis are characteristic of renal colic, and shadows of calculi can be detected on plain x-rays. Treatment Treatment of spastic obstruction usually consists of conservative measures. The child is prescribed antispastic agents, a cleansing enema, and a heating pad is placed on the stomach. In most cases, this is enough to relieve pain. In severe cases, a bilateral pararenal blockade according to A.V. Vishnevsky or prolonged (1-2 days) epidural anesthesia is performed several times. The cause of spastic obstruction (ascariasis, etc.) identified during the examination of the child is an indication for appropriate treatment (under the supervision of a surgeon). 2. Paralytic ileus Paralytic ileus, which is the most frequent and serious complication of the postoperative period, has the greatest practical significance in emergency surgery in children. In the presence of peritonitis (even after the elimination of the source of its origin), intestinal paresis in most cases acquires a leading role in a complex chain of developing systemic and local disorders. The increased intra-intestinal pressure resulting from paresis exacerbates circulatory disorders in the intestinal wall. Functional changes in intra-intestinal nerve endings are replaced by their organic damage. Loss of fluid, proteins, electrolytes in the intestinal lumen, a violation of the absorption process in it, leading to hypovolemia. corresponding disorders of central and peripheral hemodynamics. The permeability of the intestinal wall increases, and there is a risk of secondary infection of the abdominal cavity. Dehydration, bacteremia close the resulting vicious circle, which is the more difficult to break, the more time has passed since the onset of paresis. The failure of conservative treatment of postoperative intestinal paresis is mainly due to the following reasons: 1) insufficient assessment of systemic disorders that occur with paresis and their role in maintaining it; 2) the lack of sufficiently clear ideas about the nature of local pathophysiological disorders developing in the intestinal wall; 3) irrational treatment, ignoring the staging of systemic and local disorders in the clinical course of postoperative paresis. The restriction of intestinal motor function that occurred after the operation should probably be considered as a biologically justified, reflex protective reaction that develops in response to bacterial, mechanical or chemical irritation of the peritoneum and nerve endings of the abdominal organs. The chain of this reflex can be closed not only in the higher ones. but also in the spinal regions of the central nervous system. The latter, obviously, is responsible for the occurrence of intestinal paresis in pneumonia, trauma and inflammatory processes of the urinary tract. In accordance with modern pathophysiological views, it is believed that, regardless of the causes that caused intestinal paresis, two interrelated circumstances contribute mainly to maintaining it: the degree of disturbances in the peripheral nervous apparatus and the severity of microcirculation disorders in the intestinal wall. clinical picture Stage I occurs immediately after surgery. At this stage of paresis, there are no organic changes in the intramural plexuses; microcirculatory changes in the intestinal wall are transient (spasm of arterioles and metaarterioles with arteriovenous shunting in the intestinal vessels). The general condition of patients, indicators of hemodynamics and external respiration, shifts in water and electrolyte balance are due to the trauma and duration of surgery and are not threatening in case of replenished blood loss. The abdomen is moderately, evenly swollen; during auscultation, peristaltic noises, uneven in strength, are clearly heard throughout; vomiting is frequent (with light stomach contents) or rare (with a small admixture of duodenal contents). It is possible that this stage of paralytic ileus is preceded by a spastic stage, but it cannot be detected clinically in a postoperative patient. II stage. With it, along with functional, there are also organic changes in the peripheral nerve devices, due to more pronounced microcirculation disorders. The general condition of the patients is severe. Children are restless, there is shortness of breath, tachycardia; blood pressure is kept at normal levels or increased. The study of water and electrolyte balance reveals: hyponatremia, hypochloremia, in some cases hypokalemia; BCC is reduced to 25% in comparison with the initial data, mainly due to plasma volume. The abdomen is significantly swollen, with auscultation it is occasionally possible to listen to sluggish single peristaltic noises; vomiting of duodenal contents is often repeated. III stage. In this stage of paresis, morphological changes in the nervous apparatus of the intestinal wall and abdominal autonomic nerve plexuses predominate; microcirculatory changes are characterized by paretic expansion of precapillaries and pathological deposition of blood in the capacitive veins. The general condition of the patients is very serious. Children are rarely excited, more often inhibited. Severe tachycardia and tachypnea, a decrease in systolic blood pressure to 90 mm Hg are noted. Art. and lower, oliguria up to anuria, Biochemical studies reveal: a decrease in BCC ranging from 25 to 40% compared with baseline data, hyponatremia, hypochloremia, hypokalemia, a shift in CBS towards metabolic acidosis (in children under the age of one year, quite often metabolic alkalosis). The abdomen is sharply, evenly swollen, sometimes rises above the costal arches; during auscultation, it is not possible to listen to peristalsis throughout its entire length - "dumb stomach". With percussion, dullness in sloping places is most often determined; the latter is more due to the accumulation of fluid in the lumen of the stretched loops ("heavy intestine") rather than its presence in the free abdominal cavity. This stage of paresis is characterized by vomiting with an admixture of stagnant intestinal contents. Stages II and III of intestinal paresis are most often a manifestation of peritonitis, which continues to develop, despite the prompt elimination of the source of its occurrence. Therefore, the treatment of advanced intestinal paresis is almost identical to the treatment of peritonitis. The clinical picture of paralytic ileus that develops in children with severe toxicosis of any etiology usually corresponds to a condition characteristic of the stage Differential diagnosis The differential diagnosis is carried out with early postoperative adhesive obstruction. Mechanical obstruction differs from the paralytic acuteness of its first manifestations (cramping abdominal pain, vomiting, gas and stool retention, increased intestinal peristalsis). It is much more difficult to diagnose early postoperative adhesive obstruction 8 hours or more after its onset, when there is no or almost no symptom of visible peristalsis. L. M. Roshal in such cases recommends the use of contrast irrigography. The presence of a collapsed colon indicates mechanical obstruction; its normal or enlarged diameter makes it possible to suspect intestinal paresis. In complex cases, for differential diagnosis, a set of measures aimed at restoring the motor-evacuation function of the intestine should be carried out; after repeated epidural blockades (2-3 with an interval of 2-2,5 hours), inject the child intravenously with the age dose of prozerin. With dynamic obstruction, the patient's condition improves, vomiting stops, gas discharge is restored, and sometimes stools pass. With mechanical obstruction, after the measures taken, abdominal pain and bloating increase, vomiting becomes more frequent, and gas and stool do not pass. Treatment Treatment of paralytic ileus consists of the correction of systemic disorders of homeostasis and the fight against local manifestations of paresis. In the elimination of systemic disorders, the leading role belongs to rational infusion therapy. Measures for the treatment of local manifestations of paresis can be conditionally divided into three groups. 1. Activities aimed at passive evacuation of stagnant contents: constant probing of the stomach; operational methods of decompression of the intestine by probing it through the gastrostomy, through the enterostomy, through the cecostomy, retrograde insertion of the probe through the rectum. 2. Activities aimed at enhancing intestinal motility due to the direct activation of its neuromuscular apparatus: 1) strengthening the tone of parasympathetic innervation with the help of cholinesterase inhibitors (prozerin), M-cholinomimetics (aceclidin); 2) activation of the smooth muscles of the intestine (pituitrin); 3) strengthening of local reflexes: enemas, intestinal electrical stimulation; 4) the impact on the intestinal osmoreceptors by intravenous administration of a hypertonic solution of sodium chloride sorbitol, sormantol. 3. Measures aimed at improving regional blood flow, interrupting the flow of pathological impulses from the inflammatory focus and creating "functional rest" of the intestine: 1) repeated one-time perirenal blockades; prolonged pararenal blockade; 2) repeated introduction into the abdominal cavity of a 0,25% solution of novocaine; 3) intramuscular and intravenous administration of gangliolytics; 4) prolonged epidural blockade; 5) hyperbaric oxygenation. In the treatment of late-stage paresis, continuous transnasal intubation of the stomach is an indispensable condition as long as the stagnant nature of the contents persists. It is necessary to take into account the volume of losses every 6 hours and adequately replenish it during parenteral nutrition. Fractional feeding with liquid food with a gradual expansion of the diet (taking into account the underlying disease and the nature of the surgical intervention) begins only after the elimination of congestion in the stomach. The use of group II measures in children with stage III paresis only aggravates it and may eventually force the surgeon to perform an extremely risky and unjustified relaparotomy. To restore impaired bowel function, regional vegetative blockades (perinephric, epidural) are of paramount importance. The antiparetic effect of epidural blockade is most pronounced with its prophylactic use. In this regard, prolonged epidural anesthesia is absolutely indicated in all children operated on for peritonitis, intestinal obstruction and other severe diseases of the abdominal organs. When using prolonged epidural anesthesia in children operated on for peritonitis, the effects of intestinal paresis of stage II-III stop in the vast majority of cases no later than 2 - the beginning of 3 days. Prolonged epidural blockade leads to the restoration of the motor-evacuation function of the intestine in the first days after surgery and thus largely prevents the increase in intoxication. The beneficial effect of epidural blockade in the treatment of postoperative paresis is due to the following factors: 1) long-term regional sympathetic blockade; 2) anesthesia and reduction of intra-abdominal pressure by reducing muscle tension; 3) a distinct effect of enhancing intestinal motility and early recovery of its motor-evacuation function. It is difficult to overestimate the importance of any of these factors. However, the first one is the most important. Only in the case when regional sympathetic blockade is achieved during epidural anesthesia, one can count on the maximum effect in the treatment of late stages of paresis and peritonitis. Moreover, by analogy with the known effect of perinephric blockade according to A.V. Vishnevsky, epidural anesthesia actively affects the inflammatory process in the abdominal organs by eliminating vasospasm and improving microcirculation in the intestinal wall and peritoneum. The maximum blockade of sympathetic innervation to the greatest extent contributes to the activation of parasympathetic activity, leading to an increase in intestinal motility. To achieve regional sympathetic blockade during epidural anesthesia (if it is used to treat late stages of paresis), it is necessary that the injected anesthetic block the roots of the IV-XI thoracic spinal segments - the site of formation of the celiac nerves. As you know, the large, small and smallest celiac nerves make up the sympathetic portion of the celiac plexus - the main autonomic center for regulating trophism and motor function of the intestine. Systematic X-ray monitoring and analysis of treatment results revealed a clear regular dependence of the antiparetic effect on the level of the end of the catheter inserted into the epidural space. The most optimal is the location of the inner end of the catheter, introduced into the epidural space, at the level of IV-V thoracic vertebrae. In children under the age of 3 years, this is achievable with puncture and catheterization in the lower thoracic region; due to the small size of the peridural space, the injected anesthetic will also cover the upper thoracic segments. In older children, it is necessary to catheterize the epidural space at the level of the VI-VIII thoracic vertebrae. Currently, in all cases, X-ray control of the location of the catheter inserted into the epidural space is performed. In order to contrast the catheter during radiography, it is necessary to introduce any water-soluble contrast agent (urotrast, diode, verografin) into its lumen at the rate of 0,1-0,15 ml of the solution for every 20 cm of the catheter length; preference should be given to radiopaque catheters. The location of the catheter shadow medial to the base of the transverse processes on the direct image and in front of the base of the spinous processes on the lateral one suggests that the catheter is in the projection of the bony spinal canal. The absence of symptoms of a spinal block after the introduction of a "dose of action" of trimecaine indicates the location of the catheter in the epidural space. With x-ray confirmation of the location of the catheter in the epidural space at the appropriate level (IV-VI thoracic vertebrae), the complete absence of signs of resolution of intestinal paresis after successive 6-8 epidural blockades allows us to assume with a high degree of probability the occurrence of a situation requiring repeated surgical intervention (mechanical obstruction). Equally, this provision applies to cases of resumption of intestinal paresis after its temporary resolution in the early stages. Authors: Drozdov A.A., Drozdova M.V. << Back: Adhesive intestinal obstruction (Early adhesive intestinal obstruction. Late adhesive intestinal obstruction)
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