1.What is Meckel’s diverticulitis? How to treat?
Meckel’s diverticulum is a congenital malformation left behind by the partial non-closure of the yolk duct, mostly occurring in the end of the ileum 25-100cm from the ileocecal part on the opposite side of the mesentery. Simple Meckel’s diverticulum usually does not cause clinical symptoms, but once pathological changes occur, inflammation, ulceration, bleeding, perforation and intestinal obstruction can occur and have different clinical manifestations. The diagnosis of the disease is difficult and can usually be clearly diagnosed during barium examination or intraoperatively.
The diagnosis of Meckel’s diverticulum is based on the following.
(1) Lower abdominal pain, with the right lower abdomen as the heavy, accompanied by nausea or vomiting, with different degrees of fever; diverticular ulceration, there may be different degrees of intestinal bleeding.
(2) Pressure pain, rebound pain and muscle tension in the right lower abdomen near the midline; when septic perforation may appear as signs of acute diffuse peritonitis.
(3) Increased total white blood cell count and neutrophil count.
(4) X-ray barium examination of the gastrointestinal tract may show diverticula.
(5) Nuclear scan, which mostly shows diverticular shadow of ectopic gastric mucosa.
(6) When the diagnosis is acute appendicitis and no lesion is seen in the appendix at the time of surgery, the end 100 cm of the ileum should be routinely explored to avoid missing the Meckel diverticulum lesion.
Its treatment measures are mainly surgical.
(1) diverticulum base diameter less than 1.0cm, can be treated according to the appendectomy method.
(2) diverticulum base is wider, can not simply ligate, can be removed diverticulum, and then along the intestinal tube lateral suture, or remove diverticulum and part of the intestinal tube and intestinal end-to-end anastomosis.
2.What is short bowel syndrome?
Short bowel syndrome is a syndrome in which the remaining functional small bowel is too short due to extensive small bowel resection caused by various reasons, resulting in disorders of water and electrolyte metabolism and malabsorption of various nutrients. In adults, short bowel syndrome is caused by repeated resection of the small intestine due to recurrent diseases such as Crohn’s disease or recurrent intestinal obstruction or extra-intestinal fistula, and also due to vascular diseases such as infarction of mesenteric vessels, intestinal torsion, or traumatic vascular rupture or disruption, where a large number of small intestines are removed due to ischemic necrosis. Generally speaking, in adults, 100 cm of small intestine with ileocecal portion is preserved; or 150 cm of small intestine without ileocecal portion is preserved, and after natural compensation, most of the patients can maintain the nutrition required by the body through oral diet. It has also been reported in the literature that patients with a residual small intestine as short as 12-15 cm and with preserved ileocecal portion are able to maintain life with oral enteral nutrition. Although the compensatory capacity of the intestine is very strong, removal of 50% of the small intestine may not cause symptoms; however, removal of more than 75% of the small intestine usually results in severe diarrhea, malabsorption, water and electrolyte disorders, metabolic disorders and progressive malnutrition due to the reduction of absorption area. Before the introduction of parenteral nutrition, the main causes of death in patients with short bowel were the primary disease itself (such as extensive vascular lesions or tumors), malnutrition due to intestinal absorption dysfunction, and infection and liver and kidney impairment caused by parenteral nutrition and its complications. With the progress of parenteral nutrition technology and the in-depth understanding of the pathophysiological process and intestinal compensation mechanism of short bowel syndrome, the morbidity and mortality rate of the disease has been significantly reduced, and some patients have been able to survive for a long time.
3.What are the treatment means of short bowel syndrome?
The treatment of short bowel syndrome can be divided into two stages: early and late stage, and late stage includes compensated stage and compensated late stage. The early treatment usually lasts for 4 weeks, mainly to stabilize the patient’s internal environment and provide nutritional support, reduce the secretion of gastrointestinal tract and bile stimulation. The treatment focuses on the control of diarrhea with medications. Then, fluid and electrolyte supplementation to maintain acid-base balance, trace elements and vitamin supplementation, and parenteral nutrition are started. The main objective of this phase is to prevent the loss of large amounts of gastrointestinal fluids from causing an imbalance in homeostasis and the patient entering peripheral circulatory collapse. It can be considered that the application of parenteral nutrition via intravenous infusion changes the overall outcome of short bowel syndrome.
The later stage of treatment is to continue to maintain homeostasis, try to maintain the patient’s nutrition and promote intestinal function compensation, improve intestinal absorption and digestive function. After early treatment, the transition from intestinal decompensation to compensatory phase and late compensatory phase varies with the length of the residual intestinal segment and the body’s ability to compensate, ranging from a few months to 1 to 2 years. Generally, the duration of the compensatory period varies with the length of the residual intestinal segment and the body’s ability to compensate, ranging from a few months to 1 to 2 years. Since the 1970s, there have been significant advances in the late management of short bowel syndrome, which can be divided into four areas: nutritional support; intestinal rehabilitation; surgical treatment; and small bowel transplantation.
Nutritional support: Nutritional support is the main and most basic treatment for short bowel syndrome, and other treatments are added on top of it. Enteral nutrition is better than parenteral nutrition in promoting intestinal mucosal compensation, and the intestinal mucosal atrophy is observed in complete parenteral nutrition support. Therefore, the timely administration of enteral nutrition is an indispensable measure for the management of short bowel syndrome. The administration of enteral nutrition can start from small amount of isotonic and easily absorbed enteral nutrition preparation, and then gradually increase with the patient’s adaptation and absorption,
Enteral nutrition usually starts with crystalline amino acid or short peptide preparation, isotonic concentration, at the rate of 20 mL per hour, continuously dripped through the nasal intestinal tube. The nasogastric drip is preferable to oral or nasogastric drip because it reduces gastric retention and stimulates gastric juice secretion. The continuous drip facilitates absorption and reduces the acceleration of intestinal peristalsis caused by the push-in method. As enteral nutrition is given for a longer period of time, patients who cannot tolerate the discomfort of long-term nasogastric tube placement may undergo PEG or PEJ (percutaneous endoscopic gastrostomy or percutaneous endoscopic jejunostomy). When the patient can tolerate enteral nutrition and the nutritional status is gradually improving, parenteral nutrition can be gradually reduced until all enteral nutrition is applied.
After enteral nutrition can be well adapted, according to the length of the residual intestinal segment and the compensation of the patient, daily oral nutrition will be added on the basis of enteral nutrition, with high sugar, high protein, low fat (40:40:20) and low residue diet, and attention will be paid to the addition of vitamins, trace elements and electrolyte supplementation. The transition from enteral nutrition to daily diet should also be gradual, with enteral nutrition preparations gradually reduced and daily diet gradually increased until the complete consumption of ordinary diet, but not in a hurry. Some patients’ digestive and absorption functions are not completely compensated, so they cannot stop using enteral nutrition preparations completely, but one of them should be the main one and the other one should be supplemented, depending on the patient’s small intestine compensation.
The time for intestinal compensation to tolerate enteral nutrition without parenteral nutrition is about 3-6 months, and it may take longer time. If the patient’s family has a good understanding of the process of intestinal compensation and can self-regulate, it will facilitate the compensation. On the contrary, it will slow down the compensation. Some patients can not self-control, in the process of compensation, can be due to improper diet, and the phenomenon of loss of compensation, digestion, absorption function is disturbed, intestinal peristalsis accelerated, the number of bowel movements increased, and even the phenomenon of water loss, the treatment has to start again. This repeatedly makes it difficult to complete the compensation of intestinal function. Of course, the residual small intestine is too short and there is no ileocecal part, so the intestinal compensation can only reach a certain degree, and some patients still need to rely on parenteral nutrition to maintain the needs of the body.
In order to promote intestinal function compensation and free more patients from parenteral nutrition, Byrne et al. proposed in 1995 to add growth hormone (recombinant human growth hormone), glutamine (glutamine) and dietary fiber to nutritional support. Experiments have shown that growth hormone can promote the growth of intestinal mucosal cells; glutamine is the main energy substance for intestinal mucosal cells and other fast-growing cells, which is called tissue specific nutrient; dietary fiber can produce short-chain fatty acids such as acetic acid, propionic acid and butyric acid after fermentation by intestinal bacteria, and butyric acid can not only provide energy for intestinal mucosal cells, but also promote the growth of intestinal mucosal cells. Therefore, this combination can promote the compensation of intestinal mucosal function. From 1995 to 2004, Nanjing General Hospital of Nanjing Military Region slightly improved on this basis, i.e., this treatment method was applied from the compensatory stage of short bowel syndrome, and during the whole treatment process, parenteral nutrition and enteral nutrition were carried out simultaneously, and parenteral nutrition was gradually removed, and satisfactory results were achieved.
Surgical treatment: Before parenteral nutrition was applied to short bowel syndrome, there were and still are authors who designed surgical methods to prolong the passage time of chyme in the residual intestinal segment or to increase the absorption area or length of the residual small intestine. Therefore, several surgical procedures have been tried, such as artificial construction of sphincter or valve, interposition of retroperitoneal segment, interposition of colon, construction of intestinal loops and longitudinal incision of small intestinal loops to lengthen the intestinal segment, etc., but all have failed to achieve satisfactory results. Interposition of retroperitoneal segments is an easy procedure and has been tried more often. However, this method is obviously not in line with the physiology, is artificially caused by chronic intestinal obstruction, a little longer, the upper intestinal segment dilated, intestinal wall thickening, and chronic inflammation, celiac storage time is too long easily induced bacterial multiplication, celiac corruption, fermentation, thus producing toxins, resulting in a series of symptoms, such as abdominal pain, abdominal distension, nausea, vomiting, hypothermia, etc., and there is obvious malnutrition, and even bone decalcification The patient had to be operated again to remove the interposed retroperitoneal segment, but the patient’s organism had already suffered damage, which was difficult to reverse. Nanjing General Hospital of Nanjing Military Region reported 6 patients with short bowel syndrome who underwent interposition of retroperitoneal segments and had to be operated again to remove the retroperitoneal segments due to serious complications. Unfortunately, two cases died due to the poor condition of the organism and no condition for reoperation. Therefore, until an effective surgical procedure is available, short bowel syndrome should not be treated by surgical procedures such as prolonging the passage time of celiac disease.
Small intestine transplantation: Small intestine transplantation should be a reasonable way to treat short bowel syndrome, but because of its:
①High rejection rate;
②Multiple and heavy infections;
The summary report of the 9th International Small Bowel Transplantation Conference in May 2005 stated that 1,210 small bowel transplants (1,292 cases) were registered worldwide from 1985 to 2005. There are only 20 countries, including China, and 65 hospitals in the world that can perform intestinal transplantation. The survival rates of small bowel transplantation at 1, 3 and 5 years are 70%, 60% and 45%, respectively, but the 1-year survival rate is 90% for patients who can tolerate it with nutritional support. The conference concluded that “when patients cannot tolerate nutritional support, intestinal transplantation is the current ideal treatment for the end stage of short bowel syndrome, but the first choice of treatment for intestinal failure is still nutritional support”. However, the technology of organ transplantation and immunotherapy continues to evolve, as does small bowel transplantation, and as it continues to develop, it will be the ideal treatment for those patients with short bowel syndrome who are not well compensated.
4. What is small bowel transplantation all about? What is the current status of its development?
Commonly speaking, small bowel transplantation is the surgical transplantation of a viable allogeneic small bowel into the abdominal cavity of a patient with short bowel or no bowel. In fact, Detterling tried small bowel transplantation as early as 1964, but it failed due to rejection and other problems, and subsequent attempts have not been successful. Because the small intestine and its mesentery contain a large amount of lymphoid tissue, it is the organ with the highest incidence of rejection and the heaviest rejection rate among many organs transplanted. In addition, it is difficult to recover intestinal function after transplantation, and bacterial translocation and infection in the intestinal cavity are more obvious than in other organs, so the early results of small intestine transplantation were disappointing, and it is the earliest, the latest and the most difficult of all organ transplants.
Another reason is that total gastrointestinal nutrition was once considered to replace the gastrointestinal tract and keep patients alive for a long time, so it was called “artificial gastrointestinal”, and there were doubts about the need to study small intestine transplantation, resulting in the research of small intestine transplantation being shelved for some time. After a period of clinical practice, it was found that total parenteral nutrition has obvious shortcomings, especially the long-term application of total parenteral nutrition will produce liver damage, which is also the reason why some patients need to perform combined liver and intestinal transplantation. In 1987, Starzl et al. successfully performed the first multi-organ transplant containing small intestine in a 3-year-old child with intestinal failure who survived for 6 months after surgery, the first case of functional long-term survival of a human small intestine transplant. Later, Grant et al. reported the first successful combined liver and small bowel transplantation in which the patient survived 58 months, and in 1988 Deltz et al. performed a living segmental small bowel transplantation that survived 61 months with nutritional support, the first successful small bowel transplantation alone in the world. Although the application of cyclocilin A has improved the experimental results of small bowel transplantation, the prevention and control of rejection is still not completely solved, unlike kidney, heart, liver and pancreas transplants, where the total number of transplants has reached hundreds of thousands and mature experience and complete management routines are available, clinical small bowel transplantation is still in the trial stage.
The modern concept of clinical small bowel transplantation is no longer limited to the traditional small bowel transplantation alone, but includes three types.
(1) Small bowel transplantation alone, for patients with intestinal failure who have still good liver function;
(2) combined hepatic and small bowel transplantation for intestinal failure combined with total parenteral nutrition-related liver dysfunction;
(3) combined abdominal (including small intestine) multi-organ transplantation for patients with extensive gastrointestinal lesions caused by absorption, motility and vascular lesions combined with liver failure. According to the survey, small intestine transplantation alone accounts for about 42%, combined liver and small intestine transplantation accounts for about 44%, and combined abdominal (including small intestine) multi-organ transplantation accounts for about 14%. With the advancement of technology, especially in the development of new immunosuppressive agents, the effectiveness of small bowel transplantation has progressed by leaps and bounds in recent years. After the application of some new immunosuppressive agents such as anti-CD52 monoclonal antibody (Campath), the 1-year survival rate of transplanted small intestine in some transplant centers or hospitals is over 90%, and the 3-year survival rate is about 70%, which has reached or is close to the level of more mature liver and kidney transplantation, and the number of patients receiving small intestine transplantation has also increased significantly. Therefore, in recent years, the evaluation of small bowel transplantation in the international medical community has been greatly improved, and the recommended scope of patients has been expanded from patients with short bowel syndrome combined with liver dysfunction to all patients with short bowel syndrome. The Institute of General Surgery, Nanjing General Hospital, Nanjing Military Region, is one of the first units to start the research of small bowel transplantation in China. In the past two years, several small bowel transplantation cases have achieved good results, and many small bowel transplantation patients are now surviving well and have resumed eating ordinary diet by mouth, and their quality of life is close to that of normal people.
Compared with total parenteral nutrition, small intestine transplantation is more in line with normal human physiology, and the quality of life of patients can be greatly improved, which is the main advantage of small intestine transplantation, except for the above mentioned liver function damage caused by total parenteral nutrition. However, small intestine transplantation also has obvious disadvantages, namely, the success rate is still not at the ideal level, the cost is still large, lifelong immunosuppressive drugs are required, and the donor source is tight. After all, small bowel transplantation is still a highly sophisticated and risky treatment, so patients with short bowel syndrome and their families should consult with a specialist to understand the pros and cons before making a decision to help you make your decision.
5.What is an intestinal fistula?
An enterocutaneous fistula is an abnormal perforation in the intestinal wall that allows the contents of the intestine to leak out of the body or into other cavities in the abdominal cavity, called an enterocutaneous fistula. The causes of enterocutaneous fistula include: traumatic: such as surgical accidental injury to the intestinal canal or poor healing of the intestinal anastomosis, abdominal firearm injuries or stab wounds causing damage to the intestinal canal. Non-traumatic: such as intestinal infection, abdominal infection, perforation due to ischemia and necrosis of the intestinal wall, advanced malignant tumors of the intestine, etc. Intestinal fistulas are divided into tubular fistulas and labyrinthine fistulas according to the morphology of the fistula; high fistulas are jejunal fistulas and duodenal fistulas within 100 cm of the beginning of the jejunum; fistulas below this are called low fistulas. High-flow fistulas are those in which the amount of intestinal fluid flowing out of the fistula exceeds 500 ml per day, and those less than this amount are called low-flow fistulas. The local manifestations of fistulas vary, with fistulas in the intestinal wall discharging fluid, gas and food, depending on the size and location of the fistula. Duodenal fistulas often discharge large amounts of fluid containing bile, high fistulas discharge yellow egg-like fluid, low fistulas discharge “fecal-like” fluid, and the skin around the fistula is eroded, flushed, bleeding and infected. Systemic symptoms of enterocutaneous fistula are often seen in patients with high-flow enterocutaneous fistula, with dehydration and acidosis, hypokalemia, emaciation, cachexia, etc., and may be accompanied by severe systemic infection. The systemic symptoms of low-flow enterocutaneous fistula are sometimes not obvious.
6. How is an enterocutaneous fistula diagnosed and treated?
The diagnosis of most intestinal fistulas is not difficult, but the following tests are often needed to clarify the diagnosis and to understand the course of the fistula.
① oral dye examination, commonly used bone charcoal powder, methylene blue, etc., if it appears in the fistula, it can confirm the existence of the fistula, and depending on the time of its appearance, it can determine the height of the fistula location;
(ii) fistulography and barium gastrointestinal meal. In addition to these tests for enterocutaneous fistulas there are also tests to understand and evaluate the general condition such as blood and urine routine, liver and kidney function and electrolytes.
The treatment of extra-intestinal fistulas is a difficult problem in gastrointestinal surgery and requires different plans depending on the situation. Generally speaking, there are several aspects.
(1) Early and adequate drainage and control of abdominal infection.
In patients with signs of peritonitis after gastrointestinal surgery and abdominal trauma, dissection is feasible when fistula is suspected to occur, and when gastrointestinal fistula is confirmed, the abdominal cavity should be thoroughly flushed, drainage tubes should be placed for adequate drainage, and multiple drains or double cannulae placed for continuous negative pressure suction if necessary. Based on the results of bacterial culture, choose antibiotics to control the infection.
(2) Maintenance of nutrition.
In patients with high-flow fistulas who cannot resume gastrointestinal feeding, total extragastric nutrition therapy can be performed by deep venous cannulation. Some high-flow fistulas can be treated by inserting a nasal feeding tube into the distal intestine of the fistula or by performing a jejunostomy or trans-fistula cannula and sending the tube to the distal side of the fistula for tube feeding or giving an elemental diet until it is possible to eat through the mouth.
(3) Local management of the fistula.
(1) For tubular fistulas, after 2 to 4 weeks of adequate drainage, the abdominal infection is controlled and the amount of gastrointestinal contents discharged gradually decreases, the drainage tube can be gradually removed until the fistula heals spontaneously.
If the fistula is large and the fistula is short, a silicone film can be used to block the fistula, which often restores the patient’s diet and improves the patient’s nutritional status for early surgery.
(3) When the skin around the fistula is eroded, zinc oxide ointment can be applied to protect the skin to prevent the gastrointestinal contents from eroding the skin.
(4) Surgical treatment.
①Indications: fistula still does not heal for a long time after the above treatment or the fistula has been epithelialized. Labyrinthine fistula. Small intestinal fistula treated as described above, fistula discharge >5000ml/day. Obstruction of the intestine distal to the fistula.
② Timing of surgery: abdominal infection is limited or controlled. Good systemic nutritional status. General fistula for more than 3 months. However, for small intestinal fistulas with a large amount of drainage, surgery can be performed as soon as possible after the inflammation is controlled and the nutritional status is improved.
(③) Surgical procedure: Currently, the most commonly used surgical procedures are: intestinal resection anastomosis. It is suitable for patients with early small intestinal fistula and light abdominal infection. Open fistula surgery. The fistula is left open and the small intestine near and distal to the fistula is anastomosed to restore the continuity of the intestine. It is suitable for small bowel and colonic fistulas. Repair of intestinal pulp muscle piece with vascular tip: suitable for repairing fistulas that are difficult to resect, such as duodenal fistulas.
(5) Prevention and control of complications.
Strict monitoring of cardiac and pulmonary function and monitoring of blood electrolytes. Treatment of infectious shock, gastrointestinal hemorrhage, respiratory failure and other complications should be prompt.
The treatment of enterocutaneous fistulas varies greatly depending on the condition, from those that may heal spontaneously to those that require a period of nutritional support followed by definitive surgery, to those that can be performed early and definitively. Because most enterocutaneous fistulas are complex and treatment options vary from person to person, it is difficult for patients and their families to have the expertise to choose a treatment option, so it is important to follow the professional advice of medical professionals.
Some aspects of treatment that patients and their families need to know include.
(1) Enterocutaneous fistulas, especially complex and severe ones, still have a high mortality rate. It has been reported that the mortality rate of fistulas was as high as 50% to 60% before the 1970s and is still 15% to 20%.
The treatment time for episiotomy is generally calculated in months, usually more than 3 months, and in some cases up to several years, so patients and their families should be fully prepared for this. In addition, because of the long treatment time and the complexity of the treatment, the treatment is usually very expensive.
The patient’s family should be more concerned, considerate and understand the patient, help the patient to establish a correct understanding of the disease, and encourage him to establish confidence in the treatment.
④ Patients with parenteral fistula often have more tubes inserted in their bodies during treatment, such as double cannulae for flushing at the fistula, drainage tubes after surgery, stoma tubes for giving nutrition, etc. Family members should understand the purpose and precautions for clearing various tubes from medical staff when caring for them, keep them open, fix them properly, record their drainage flow and properties regularly, and contact medical staff in time if there is any situation.
⑤Family members should learn to infuse enteral nutrition fluid and intestinal fluids that need to be returned to the patient from the nasal intestinal tube or other tubes.
(6) Learn to protect the skin around the fistula, encourage the patient who is bedridden for a long time to move in bed, help him/her to turn over, keep the skin of the whole body clean and prevent bed sores.
7.What is acute peritonitis? What are the common causes?
Acute peritonitis is an acute inflammatory lesion of the peritoneum caused by infection, chemical substances (such as gastric fluid, intestinal fluid, bile, pancreatic fluid, etc.) or injury. Bacterial infection is the most frequent cause.
There are many causes of acute peritonitis, the main ones being the following.
(a) Acute perforation and rupture of intra-abdominal organs: mostly occurs in organs with existing lesions. Perforation of cavernous organs often occurs suddenly due to the progression of ulcerative or gangrenous lesions, such as acute appendicitis, peptic ulcer, acute cholecystitis, typhoid ulcer, gastric or colon cancer, ulcerative colitis, ulcerative intestinal tuberculosis, amoebic enteropathy, diverticulitis, and other perforations that lead to acute peritonitis. Rupture of parenchymal organs, such as liver and spleen, can also occur due to abscesses or cancer.
(ii) Spread of acute infection of intra-abdominal organs: for example, acute appendicitis, cholecystitis, pancreatitis, diverticulitis, rising infection of the female genital tract (e.g., puerperal fever, tubal inflammation), etc., can spread to the peritoneum causing acute inflammation.
(iii) Acute intestinal obstruction: after strangulated intestinal obstruction caused by intestinal entrapment, intestinal torsion, incarcerated hernia, mesenteric vascular embolism or thrombosis, etc., bacteria in the intestine can invade the peritoneal cavity through the intestinal wall and produce peritonitis due to damage to the intestinal wall and loss of the normal barrier effect.
(D) abdominal surgical conditions: sharps, bullets through the abdominal wall, can penetrate the cavity organs, or the introduction of external bacteria into the abdominal cavity, abdominal bruises sometimes can also rupture the viscera, producing acute peritonitis. During abdominal surgery, bacteria can be brought to the abdominal cavity due to lax sterilization; also due to surgical carelessness, so that the local infection spreads, or the sutures of the stomach, intestines, bile, pancreas overflow, sometimes due to abdominal puncture and release of fluid or for peritoneal dialysis when ignoring the aseptic operation, can cause the consequences of acute peritonitis.
(E) Blood-borne disseminated infection: can cause primary acute peritonitis.
The most common bacteria in peritoneal infections are Escherichia coli, Enterococcus, Pseudomonas aeruginosa, Aspergillus, Pneumocystis aeruginosa, and other anaerobic bacteria. In most cases there is a mixed type of infection.
8, What are the manifestations of acute peritonitis? How to diagnose?
The main clinical manifestations of acute peritonitis are abdominal pain, abdominal tenderness and abdominal muscle tension, often accompanied by nausea, vomiting, abdominal distention, fever, hypotension, rapid pulse, shortness of breath, leukocytosis and other toxic phenomena. Because acute peritonitis is mostly a complication of a disease in the abdominal cavity, there are often symptoms of the original disease before and after the onset of the disease.
(A) Symptoms.
(1) Acute abdominal pain: abdominal pain is the main and most common symptom, mostly sudden, persistent and rapidly expanding, the nature of which depends on the type of peritonitis (chemical or bacterial), the extent of inflammation and the patient’s response. In acute perforation of the stomach, duodenum, gallbladder and other organs causing diffuse peritonitis, irritation of the peritoneum by digestive juices produces sudden and intense all-abdominal pain and even so-called peritoneal shock. In a few cases, before the occurrence of bacterial secondary infection, the illusion of improvement of abdominal pain and peritoneal irritation signs may occur because of the large amount of fluid exuded from the peritoneum, diluting the irritant; when the secondary bacterial infection occurs, the abdominal pain increases again. Peritonitis caused by bacterial infection is usually preceded by local pain from the primary lesion (e.g. appendicitis, cholecystitis, etc.), and the abdominal pain is slow to start when perforated, with distension or dull pain, unlike the acute perforation of the stomach or gallbladder, and the pain gradually increases and spreads from the area of the lesion to the whole abdomen. The degree of abdominal pain varies from person to person, with some patients complaining of abnormally severe and persistent pain and others reporting only dull pain or discomfort, while frail or elderly patients, such as those with severe typhoid fever, may not feel pain during acute perforation.
(2) Nausea and vomiting: These are common symptoms that appear very early. At the beginning, due to peritoneal irritation, nausea and vomiting are reflexive and intermittent, and the vomit is gastric contents, sometimes with bile; later, due to paralytic intestinal obstruction, vomiting becomes continuous without nausea, and the vomit is brownish-yellow intestinal contents, which may have bad odor.
(3) Other symptoms: in the acute perforation of the cavity organs produce peritonitis, due to peritoneal shock or toxemia, the phenomenon of deficiency is common, when the body temperature is more than normal or close to normal; when the deficiency improves and peritonitis continues to develop, the body temperature begins to gradually increase. If the primary disease is acute infection (e.g., acute appendicitis and acute cholecystitis), the temperature is often higher than the original when acute peritonitis occurs. In cases of acute diffuse peritonitis, the effective circulating blood volume and total blood potassium are significantly reduced due to the large amount of fluid exuded from the peritoneum, the high degree of peritoneal and intestinal wall congestion and edema, the accumulation of large amounts of fluid in the paralyzed intestinal lumen, and vomiting water loss. In addition, due to reduced renal blood flow, increased toxemia, impaired cardiac, renal and peripheral vascular function, patients often have hypotension and shock manifestations, a fine pulse or inability to palpate, and also thirst, oliguria or anuria, abdominal distention, and no anal venting. Sometimes there is frequent eructation, the cause of which may be that the inflammation has reached the diaphragm.
(ii) Physical signs.
Patients with peritonitis tend to have painful expressions. Coughing, breathing, and turning the body can increase abdominal pain. Patients are forced to adopt a supine position with both lower limbs flexed and breathing superficially and frequently. In the late stage of toxemia, due to hyperthermia, absence of diet, water loss, acidosis and other conditions, the central nervous system and all vital organs are in a state of inhibition, when the patient presents with mental depression, generalized syncope, pallor, dry skin, sunken eyes and cheeks, sharp nose, and cold sweat from the forehead.
Abdominal examination reveals the classic triad of peritonitis – abdominal pressure, abdominal wall muscle spasm and rebound pain. In limited peritonitis, the triad is confined to one part of the abdomen, whereas in diffuse peritonitis, it spreads throughout the abdomen and may be seen with shallow abdominal breathing, loss of abdominal wall reflexes, and decreased or absent bowel sounds. Pressure pain and rebound pain are almost always present, while the degree of muscle spasm of the abdominal wall varies with the patient’s general condition. Generally, in acute perforation of peptic ulcer, the abdominal wall muscles are plank-like and tonic, whereas in extremely debilitating cases such as perforated enteric fever or advanced toxemia, the signs of abdominal muscle spasm or tonicity can be very mild or absent. Mobile turbid sounds may be detected in the presence of large amounts of intra-abdominal exudate. When gas is released from the abdominal cavity due to gastrointestinal perforation, the hepatic turbid zone shrinks or disappears in about 55-60% of cases. When the inflammation is confined, a confined abscess or inflammatory mass is formed and is near the abdominal wall, a mass with indistinct margins may be palpable. Masses or abscesses in the pelvis can sometimes be visualized by rectal palpation.
Acute peritonitis can be classified in a variety of different ways as follows.
(1) According to the extent of inflammation it can be classified as diffuse peritonitis and limited peritonitis.
(2) Secondary peritonitis and primary peritonitis can be classified according to the origin of the lesion. The vast majority of peritonitis is secondary to peritonitis, either secondary to pre-existing disease and injury of intra-abdominal organs or secondary to trauma and foreign contamination. Primary peritonitis is rare in which there are no intra-abdominal lesions and the germs infect the peritoneum from extra-abdominal foci via hematogenous or lymphatic dissemination, mostly in cases of immunocompromised cirrhosis, nephrotic syndrome, and infants and children.
(3) The disease is classified as aseptic peritonitis or infectious peritonitis according to the nature of the disease at its initial onset. Aseptic peritonitis is commonly caused by leakage of gastric, intestinal and pancreatic fluids into the peritoneal cavity due to acute perforation of the stomach and duodenum, acute pancreatitis, etc., which irritates the peritoneum. However, if the lesion persists, it will also develop secondary bacterial infection after 2 to 3 days and is no different from infectious peritonitis.
The diagnosis of acute peritonitis is generally not difficult based on symptoms and signs.
Peritoneal puncture and aspiration of peritoneal fluid is extremely important for the diagnosis of peritonitis.
For secondary peritonitis, the site of the primary lesion should be identified to consider further treatment. However, this is sometimes not easy when signs of peritonitis are evident. Generally, an X-ray showing free gas under the diaphragm suggests gastrointestinal perforation. If the symptoms do not improve after gastrointestinal decompression and initial treatment, the possibility of gallbladder perforation should be considered. Female patients should consider tubal and ovarian inflammation, and elderly patients should consider the possibility of colon cancer or diverticulum perforation.
Pleurisy and pneumonia can cause fever and epigastric pain, and acute myocardial infarction can also have severe epigastric pain. Acute pancreatitis, perinephric abscess, and even herpes zoster can also cause fever and abdominal pain. However, it is not difficult to differentiate based on history, signs and corresponding examination.
The symptoms and signs of primary peritonitis are similar to those of secondary peritonitis, and the laboratory findings are mostly the same. However, only non-surgical treatment is available, which is very different from secondary peritonitis. Therefore, attention should be paid to differentiation. The main points of differentiation between primary peritonitis and secondary peritonitis are as follows.
(1) Primary peritonitis is mainly seen in patients with cirrhotic ascites, nephrotic syndrome and other immunocompromised patients and infants, especially girls under 10 years of age. Secondary peritonitis, on the other hand, is mostly without such limitations.
(2) Primary peritonitis in patients with cirrhotic ascites has a slow onset, and the “peritonitis triad” of abdominal signs is often less pronounced. Primary peritonitis occurring in infants and young children has a more rapid onset and the “peritonitis triad” is often less pronounced than secondary peritonitis.
(3) The absence of primary infectious lesions in the abdominal cavity is the key to differentiate primary peritonitis from secondary peritonitis, and X-rays that reveal free gas under the diaphragm are evidence of secondary peritonitis.
(4) Laparotomy to obtain ascites or peritoneal exudate for bacterial smear and culture examination. Primary peritonitis is a single bacterial infection, while secondary peritonitis is almost always a mixed bacterial infection.
9, what are the treatment measures for acute peritonitis? How effective is the treatment?
The basic principle in the treatment of acute peritonitis is to control and clear the existing infection, not to spread and expand it, and to correct the pathophysiological disorders caused by peritonitis.
In general, where the diagnosis of acute peritonitis is clear and the location of the primary lesion has been identified or presumed, surgery should be performed as soon as possible if the patient’s condition permits, such as suturing the gastrointestinal perforation, removing the appendix, gallbladder and other lesions, and cleaning or draining the abdominal cavity of purulent exudate.
In cases diagnosed as primary peritonitis, or diffuse peritonitis with a duration of more than 1 to 2 days and a tendency for the inflammation to be limited, or in those who are elderly and have severe toxic symptoms, medical supportive therapy may be administered first and the evolution of the disease should be closely monitored.
The supportive medical treatment can of course be considered as a preparation for surgery, as surgery is still needed if necessary. Supportive medical treatment includes.
(1) bed rest: a semi-recumbent position with a forward tilt of 30° to 45° is recommended to facilitate the flow of inflammatory exudate to the pelvis and easy drainage. If the shock is severe, the patient should be placed in a flat position.
(2) Fasting and gastrointestinal decompression.
(3) Correct the imbalance of fluid, electrolyte and acid-base balance. Adequate fluids should be given to ensure that the daily urine volume is about 1500ml. In addition, the amount of potassium chloride or sodium salt to be given should be calculated according to the results of blood electrolyte measurement, and the use of sodium bicarbonate should be considered according to the blood carbon dioxide binding rate or the pH of blood.
(4) If available, it is best to give intravenous nutrient infusion, or a small amount of plasma or whole blood transfusion to improve the patient’s general condition and enhance immunity.
(5) Antibacterial therapy is the most important medical treatment for acute peritonitis. In general, secondary peritonitis is mostly a mixed infection of aerobic and anaerobic bacteria, so it is appropriate to use broad-spectrum antibiotics or use several antibiotics in combination. If you can get the pathogenic bacteria, according to the results of drug sensitivity test selection of antimicrobial better.
(6) For severe pain or irritability, if the diagnosis is clear, pethidine and phenobarbital can be used as appropriate. If there is shock, anti-shock treatment should be actively carried out, etc.
Due to advances in diagnosis and treatment, the prognosis of acute peritonitis has improved compared to the past. However, the morbidity and mortality rate is still around 5-10%. Primary peritonitis occurring on the basis of cirrhotic ascites is even as high as 40%. The prognosis is poor in those with delayed diagnosis and late treatment, in children, the elderly and those with heart, lung and kidney disease and diabetes.
10.What is tuberculous peritonitis?
Tuberculous peritonitis is mainly caused by the direct spread of intestinal tuberculosis, mesenteric lymph node tuberculosis, tuberculosis of fallopian tubes, etc., while a few are caused by hematogenous tuberculosis. It can occur at any age, but is most common between 20 and 30, with more women than men.
Due to the different reactivity and immune status of the organism, the number, virulence, type and mode of infection of the invading tuberculosis bacilli, and the different treatment measures, the pathological changes of the peritoneum can be manifested as exudate, adhesion and cheese. The adherent type is the most common, the exudative type is the second most common, and the caseous type is the least common. Clinically, the three types often coexist with each other and are called mixed types.
(1) Exudative type: The peritoneum is congested and edematous, and the surface is covered with fibrin exudate, and many small yellow-white or gray-white nodules can be seen, or fused with each other. There is accumulation of plasma fibrin exudate in the abdominal cavity, and the ascites is yellow and sometimes slightly bloody.
(2) Adherent type: marked thickening of the peritoneum and massive fibrous tissue hyperplasia. The intestinal loops are closely adherent to each other or to other apparatus, and the intestinal curvature may be compressed by the fascia and obstruction may occur. The intestinal mesentery is thickened and shortened, and the greater omentum is also thickened and stiffened in the form of masses, and in severe cases the abdominal cavity is completely occluded.
(3) Cheese type: Cheese like necrosis is the main lesion. The intestinal flexure, greater omentum, mesentery or intra-abdominal organs are adherent to each other and separated into many small atria, and there is cloudy or purulent fluid in the cavity of the small atria, while the mesenteric lymph nodes with caseous necrosis are involved, forming a tuberculous abscess. Sometimes the hilum may penetrate into the intestinal flexure, vagina or abdominal wall and form a fistula.