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Acquired intestinal obstruction. Bleeding from the digestive tract. Portal hypertension. Acquired obstruction of bowel.
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Acquired intestinal obstruction.Bleeding from the digestive tract.Portal hypertension.
Acquired obstruction of bowel • Refers to the common diseases of the abdominal cavity in children who require operative intervention: are taken a third place after surgery for acute appendicitis, congenital obstruction. For a long time was the most frequent cause of mortality in childhood. • The reason can be some congenital malformations, and the appearance of pathological factors that are explained in the classification.
Classification of Acquired obstruction of bowel • Depending on the level: high and low. • According to character of the process:acute, chronic,chronic-recurrent. • According to a particular mechanism of pathogenesis: mechanical, functional, strangulated, obstructive, obstructive-strangulated. • Mechanical: adhesive, intussusception (invagination of bowel), obstruction of the lumen of the intestine hair ball, biliary, fecal stones, helminth ravel, compression by external tumors, cysts, blood vessels and a Meckel`s diverticulum. • Dynamic obstruction: paralytic, spastic. • Intussusception (invagination of bowel):idiopathic on the basis of polyps, tumors, Meckel's diverticulum. Small intestine-small intestine, small intestine-large intestine (ileocecal), large intestine-large intestine intussusception. • Adhesive obstruction: early (paretic, delayed), late (after one month from the date of the surgery).
The most common type of the late obstruction of bowel (80%) is an adhesive intestinal obstruction. • Depending on the severity of obstruction of bowel may be a different symptomatic disease. Cramping abdominal pain, vomiting with intestinal contents, bile, not passing of bowel gas and feces, anxiety of the child, deterioration of general condition due to dehydration - the main anamnestic information. Examination of a patient shows that the patient changes position frequently, in some cases is knee-elbow position. There are tachycardia, dry tongue, decreased tissue turgor. At the beginning abdomen is moderately swollen, soft, involved in breathing, occasionally can be observed asymmetry of the abdomen. Intestine loops are visible on the front wall of abdomen, peristalsis is reinforced, can be audible "noise of a falling drop," "transfusion liquid", drum belly bowel noise (tympanitis) above the extended Intestine loops. In the rectal investigation is determined that rectum is inlarged and without fecal content.
later arise peritoneal symptoms: tension of the abdominal wall and other symptoms of irritation of the peritoneum. Very strong pain (even up to the development of collaptoid condition) is observed at strangulated ileus in which the abdomen is soft, painful at the place of a strangulation. • Diagnosis is clarified by roentgenography in an upright position (Kloyber`s cups), ultrasound (roentgenograms). • In acute and subacute, chronic recurrent types of obstruction initially is used conservative treatment for 8-12 hours [probe into the stomach, hypertonic solution into the vein (10% NaCl, 2 ml per life-year, 0.05% Neostigmine 0.1 ml per year of life , during 30-40 min. siphon enema], which allows to cure obstruction in 70-80% in patients. If this treatment is inefficient in children with strangulated ileus, they must be operated on urgently. A surgeon must eliminate the cause of ileus, necrotic part of bowel must be removed with the next creation of anastomosis of bowel if it`s possibly.
Intussusception • Intussusception is the implantation (intrusion) of a gut in to an its part which is lying below • The components of the intussusception: • deferent part of the intestine, • a head of the intussusceptum, • outer cylinder of the intussusceptum, • neck of the intussusceptum, • adducent part of the intestine. • A loop of bowel which was stacked in two cylinders (external and internal) is named an intussusceptum. • A loop of bowel with intussusceptum is named a vagina of it.
Classification. Small intestine-small intestine, small intestine-large intestine (ileocecal), large intestine-large intestine intussusception
Intussusception - a mixed form of intestinal obstruction: obstructed, strangulated. The intravascular hemolysis appears. Serum is enriched of hemoglobin. Increases the hydrostatic pressure. Blood plasma is filtered from the blood in the mucous membrane of intestine. The child has bloody stools appear dark cherry color. Blood is not coagulated. Age of children - 80% are children of first year of life, from 3 to 9 months. Reasons Functional: in boys with a large mass of the body; wrong feeding of children until one year old; especially in age of 3-9 months. Restriction (after 1 year) Meckel's diverticulum; Enlarging of lymphatic nodes; Tumors of the intestine.
Forming Stages of intussusceptum: hemafecia determination of intussusceptum in palpation. - Painful episodes lose sharpness; - The child is lethargic, does not play, and is sleepy; - Stomach is enlarged, but soft; - Vomiting contains greenness and bile. Stages of a desease:
Early symptoms can include nausea, vomiting (sometimes bile stained (green color), pulling legs to the chest area, and intermittent moderate to severe cramping abdominalpain. Pain is intermittent not because the intussusception temporarily resolves, but because the intussuscepted bowel segment transiently stops contracting. Later signs include rectal bleeding, often with "red currant jelly" stool (stool mixed with blood and mucus), and lethargy. Physical examination may reveal a "sausage-shaped" mass felt upon palpation of the abdomen. In children or those too young to communicate their symptoms verbally, they may cry, draw their knees up to their chest or experience dyspnea (difficult or painful breathing) with paroxysms of pain. Fever is not a symptom of intussusception. However, intussusception can cause a loop of bowel to become necrotic, secondary to ischemia due to compression to arterial blood supply. This leads to perforation and sepsis, which causes fever.
Bleeding in the child always causes great concern and anxiety as in a parent and in physician. This syndrome is observed in various diseases of the digestive tract, in different age groups. The intensity of the bleeding depends on the extent and amount of damage to blood vessels, coagulation status, adequacy of remedial measures. The manifestation of bleeding is determined by the level of bleeding vessels, the intensity of blood loss. Hemorrhagic disease of newborn due to insufficient production of clotting factors in the liver appears the first days after birth, less changed vomiting , unmodified blood or "coffee grounds", black, tarry stools, pallor, weakness of the child. Transfusion of plasma, blood, the introduction of Haemostatics allows you to quickly arrest the bleeding. In congenital pyloric stenosis, been vomiting with a touch of "coffee grounds". Refinement of the diagnosis of underlying disease and the implementation of treatment eliminates this symptom.
Diagnosis Intussusception is often suspected based on history and physical exam, including observation of Dance's sign. Per rectal examination is particularly helpful in children as part of the intussusceptum may be felt by the finger. A definite diagnosis often requires confirmation by diagnostic imaging modalities. Ultrasound is today considered the imaging modality of choice for diagnosis and exclusion of intussusception due to its high accuracy and lack of radiation. A target-like mass, usually around 3 cm in diameter, confirms the diagnosis. An x-ray of the abdomen may be indicated for evaluation of intestinal obstruction or the presence of free intraperitoneal gas; the latter finding would imply that bowel perforation has already occurred. In some institutions, air enema is used for diagnosis as the same procedure can be used for treatment.
Differential diagnosis Intussusception has three main differential diagnoses. These are acute gastroenteritis, Henoch–Schönlein purpura, and rectal prolapse. Abdominal pain, vomiting, and stool with mucus and blood are present in acute gastroenteritis, but diarrhea is the leading symptom. Rectal prolapse can be differentiated by projecting mucosa that can be felt in continuity with the perianal skin, whereas in intussusception the finger may pass indefinitely into the depth of sulcus. Henoch–Schönlein purpura presents the characteristic rash.
Treatment The condition is not usually immediately life-threatening. The intussusception can be treated with either a barium or water-soluble contrast enema or an air-contrast enema, which both confirms the diagnosis of intussusception, and in most cases successfully reduces it. The success rate is over 80%. However, approximately 5–10% of these recur within 24 hours If it cannot be reduced by an enema or if the intestine is damaged, then a surgical reduction is necessary. In a surgical reduction, the abdomen is opened and the part that has telescoped in is squeezed out (rather than pulled out) manually by the surgeon or if the surgeon is unable to successfully reduce it or the bowel is damaged, the affected section will be resected. More often, the intussusception can be reduced by laparoscopy, whereby the segments of intestine are pulled apart by forceps.
Prognosis Intussusception may become a medical emergency if not treated early, as it will eventually cause death if not reduced. In developing countries where medical hospitals are not easily accessible, especially when the occurrence of intussusception is complicated with other problems, death becomes almost inevitable. When intussusception or any other severe medical problem is suspected, the person must be taken to a hospital immediatelyThe outlook for intussusception is excellent when treated quickly, but when untreated it can lead to death within 2–5 days. Fast treatment is a necessity, because the longer the intestine segment is prolapsed the longer it goes without bloodflow, and the less effective a non-surgical reduction will be. Prolonged intussusception also increases the likelihood of bowel ischemia and necrosis, requiring surgical resection.
Doubling the various divisions of the intestinal tube is accompanied by a noticeable or not admixture of blood in the stool, anemia and often detectable in the I-II year of life. Depending on the level of doubling the blood in the stool has a different color (from almost black to bright). Diagnosis of doubling is very difficult, but very important an examination is laparoscopy. Meckel's diverticulum is complicated by bleeding, most often manifested by the end of the first - the second year of life by the sudden release of blood from the anus of color "rotten cherries" moderate anxiety, decreased Hb, erythrocyte count. Moderate pain in the right half of the abdomen, the characteristic color of blood, ultrasound can clarify the diagnosis and to direct (after haemostatic activities) on a surgery - removal of diverticulum. Bleeding from the lower bowel from the colon polyps, ulcerative colitis are characterized by constant bowel bleeding, the development of anemia. The diagnosis confirmed by endoscopy. Individual polyps must be removed In total damage of bowel treatment usually is very expensive, difficult and it doesn`t have an exact positive result.
Portal hypertension In medicine, portal hypertension is hypertension (high blood pressure) in the portal vein and its tributaries. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 10 mmHg or greater. Causes Causes can be divided into prehepatic, intrahepatic, and posthepatic. Intrahepatic causes include liver cirrhosis, and hepatic fibrosis (e.g. due to Wilson's disease, hemochromatosis, or congenital fibrosis). Prehepatic causes include portal vein thrombosis or congenital atresia. Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.
Signs and symptoms • Consequences of portal hypertension are caused by blood being forced down alternate channels by the increased resistance to flow through the systemic venous system rather than the portal system. They include: • Ascites (free fluid in the peritoneal cavity). • Hepatic encephalopathy. • Increased risk of spontaneous bacterial peritonitis. • Increased risk of hepatorenal syndrome. • Splenomegaly (enlargement of the spleen) with consequent sequestrationtherein ofred blood cells, white blood cells, and platelets, together leading to mild pancytopenia. • Portacaval anastomoses: Esophageal varices, gastric varices, anorectal varices (not to be confused with hemorrhoids), and caput medusae. Esophageal and gastric varices pose an ongoing risk of life-threatening hemorrhage, with hematemesis or melena.
Diagram of the portal system. BB - Vienna portae, СВ - splenic Vienna, ВБВ - superior mesenteric Vienna, ЛЖВ - the left gastric Vienna, НБВ - inferior mesenteric Vienna.
The scheme of portal blood flow in the extrahepatic portal hypertension.ВБВ - superior mesenteric Vienna, ЛЖВ- the left gastric Vienna, НБВ - inferior mesenteric Vienna.
Surgery of devaskulyarisation of stomach and esophagus, splenectomy (by Sugiura).
X-ray contrast examination of mesenteric vessels in a child with extrahepatic portal hypertension.
Diagnostics HVPG (hepatic venous pressure gradient) measurement has been accepted as thegoldstandardfor assessing the severity of portal hypertension, and replaced the old one - contrast angiography. Portal hypertension is defined as HVPG greater than 5mm Hg. Treatment Prophylaxis of variceal bleeding Both pharmacological (B-blocker like Propranolol and isosorbide mononitrate) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is superior to either of them at reducing rate of rebleeding. Disadvantages of TIPS include high cost and increased risk of hepatic encephalopathy, and it does not improve the mortality rate. Management of active variceal bleeding After resuscitation, the management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide or terlipressin), endoscopic banding ligation, balloon tamponade and TIPS. Management of ascites This should be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, renal failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, transjugula intrahepati portosystemic shunt (TIPS) and peritoneovenous shunt. Control of hepatic encephalopathy This includes reduction of dietary protein, followed by lactulose and use of oral antibiotics.
