Intestinal obstruction (ileus) refers to the blockage of intestinal contents within the digestive tract. It is a common acute abdominal condition caused by various factors. Initially, the obstructed intestinal segment undergoes anatomical and functional changes, followed by fluid and electrolyte loss, impaired intestinal wall circulation, necrosis, and secondary infection. Ultimately, it can lead to toxemia, shock, and death. However, timely diagnosis and active treatment can often reverse the progression of the disease, leading to a cure.

bubble_chart Etiology

(1) Mechanical Intestinal Obstruction Common disease causes include:

1. Extraintestinal Causes

(1) Adhesions and adhesive band compression Adhesions can cause intestinal folding or torsion, leading to obstruction. Congenital adhesive bands are more common in children, while adhesions resulting from abdominal surgery or intra-abdominal inflammation are the most frequent causes of intestinal obstruction in adults. However, a few cases may occur without a history of abdominal surgery or inflammation.

(2) Incarcerated external or internal hernia.

(3) Intestinal volvulus, often caused by adhesions.

(4) Compression by extraluminal tumors or abdominal masses.

2. Intestinal Causes

(1) Congenital stenosis and atresia malformations.

(2) Stenosis due to inflammation, tumors, anastomotic surgery, or other factors, such as inflammatory bowel disease, intestinal tuberculosis, radiation injury, intestinal tumors (especially colorectal tumors), or intestinal anastomosis.

(3) Intussusception, which is less common in adults and mostly caused by polyps or other intestinal lesions.

3. Intraluminal Causes Intestinal obstruction caused by masses of roundworms, foreign bodies, or fecal impaction is now uncommon. Cases of gallstone ileus, where large gallstones enter the intestinal lumen through a cholecysto- or choledochoduodenal fistula, are occasionally reported.

1. Paralytic Paralytic ileus can complicate major abdominal surgery, peritonitis, abdominal trauma, retroperitoneal hemorrhage, certain medications, pneumonia, empyema, sepsis, hypokalemia, or other systemic metabolic disorders.

2. Spastic Temporary intestinal spasms can result from intestinal inflammation or neurological dysfunction.

(3) Vascular Intestinal Obstruction The main disease causes are mesenteric artery embolism or thrombosis and mesenteric vein thrombosis.

The frequency of intestinal obstruction caused by various disease factors varies depending on the era, region, ethnicity, and healthcare conditions. For example, 30 years ago, mechanical obstruction due to incarcerated hernia was the most common, but with advancements in medical care and the widespread adoption of prophylactic hernia repair, its incidence has significantly declined, while obstruction caused by adhesions has markedly increased.

bubble_chart Pathological Changes

Pathological Anatomy

After the occurrence of simple complete mechanical intestinal obstruction, the intestinal lumen above the obstruction site dilates. The intestinal wall becomes thin, and the mucous membrane is prone to erosion and ulceration. The serous membrane may be torn, and the entire intestinal wall may undergo necrosis and perforation due to impaired blood supply. The portion of the intestine below the obstruction is often empty and collapsed.

In paralytic intestinal obstruction, the intestine dilates and the intestinal wall becomes thin.

In the early stages of strangulated intestinal obstruction, due to obstructed venous return, small veins and capillaries may experience static blood, increased permeability, or even rupture, leading to the leakage of plasma or blood. At this stage, the intestine appears purple due to congestion and edema. Subsequently, stirred pulse blood flow obstruction and thrombosis occur, causing the intestinal wall to necrose due to ischemia. Bacteria and toxins within the intestine can pass through the injured intestinal wall and enter the abdominal cavity. The necrotic intestine turns purplish-black and may eventually rupture spontaneously.

The main pathophysiological changes in intestinal obstruction are distension, loss of body fluids and electrolytes, as well as infection and toxemia. The severity of these changes depends on the level of the obstruction, the duration of the obstruction, and whether there is impaired blood supply to the intestinal wall.

(1) Intestinal Distension  In mechanical intestinal obstruction, the intestinal lumen above the obstruction distends due to the accumulation of fluid and gas. The initial response of the intestinal segment to the obstruction is increased peristalsis, and the intense peristalsis causes colicky pain. At this time, the upper esophageal sphincter reflexively relaxes, and the patient unconsciously swallows large amounts of air into the gastrointestinal tract during inhalation. Therefore, 70% of the gas in the intestinal lumen is swallowed air, most of which is nitrogen and is not easily absorbed by the gastrointestinal tract. The remaining 30% of the gas is produced by the neutralization of acids and bases in the intestine and bacterial fermentation, or by the diffusion of CO₂, H₂, CH₄, and other gases from the bloodstream into the intestinal lumen. Normally, adults secrete about 8L of saliva, gastric juice, bile, pancreatic juice, and intestinal juice daily, most of which is absorbed by the small intestine mucous membrane to maintain fluid balance. In intestinal obstruction, large amounts of fluid and gas accumulate proximal to the obstruction, causing intestinal distension. The distension inhibits the absorption of water by the intestinal wall mucous membrane and later stimulates increased secretion, leading to progressive accumulation of fluid in the intestinal lumen and worsening distension. In simple intestinal obstruction, the intraluminal pressure is generally low, initially often below 8cmH₂

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However, as the duration of the obstruction prolongs, the intraluminal pressure can even reach 18cmH₂O. In colonic obstruction, the average intraluminal pressure is often above 25cmH₂O, and in some cases, it can be as high as 52cmH₂O. The increase in intraluminal pressure can impair venous return in the intestinal wall, leading to congestion and edema of the intestinal wall and increased permeability. Continued elevation of intraluminal pressure can obstruct blood flow in the intestinal wall, transforming simple intestinal obstruction into strangulated intestinal obstruction. Severe intestinal distension can even elevate the diaphragm, affecting the patient's respiratory and circulatory functions.

(II) Loss of Body Fluids and Electrolytes Intestinal distension in intestinal obstruction can cause reflex vomiting. In high small intestine obstruction, vomiting is frequent, leading to the loss of large amounts of water and electrolytes. If the obstruction is located at the pylorus or the upper segment of the duodenum, excessive gastric acid is vomited, which can easily result in dehydration and hypochloremic hypokalemic alkalosis. If the obstruction is located at the lower segment of the duodenum or the upper segment of the jejunum, the loss of bicarbonate is severe. In low intestinal obstruction, vomiting is much less common than in high obstruction, but due to reduced absorption function of the intestinal mucosa and increased secretion, a large amount of fluid accumulates in the intestinal lumen above the obstruction, sometimes as much as 5–10 liters, containing significant amounts of sodium bicarbonate. Although these fluids are not expelled from the body, they are trapped in the intestinal lumen and cannot enter the bloodstream, effectively constituting a loss of body fluids. Additionally, excessive intestinal distension impairs venous return, leading to intestinal wall edema and plasma extravasation. In strangulated intestinal obstruction, the loss of blood and plasma is particularly severe. Consequently, patients often develop dehydration accompanied by oliguria, azotemia, and acidosis. If dehydration persists, further hemoconcentration can lead to hypotension and hypovolemic shock. Hypokalemia caused by potassium loss and lack of oral intake may induce intestinal paralysis, further exacerbating the progression of intestinal obstruction.

(3) Infection and Toxemia In normal individuals, intestinal peristalsis ensures the continuous forward movement and renewal of intestinal contents, keeping the small intestine sterile or nearly so, with only minimal bacterial presence. In cases of simple mechanical small intestine obstruction, even if bacteria and toxins are present in the intestine, they cannot pass through the normal intestinal mucosal barrier, thus posing little harm. However, if the obstruction progresses to strangulation, venous blood flow is initially obstructed, causing the affected intestinal wall to exude large amounts of blood and plasma, further reducing blood volume. Subsequently, the arterial blood flow is also obstructed, accelerating ischemic necrosis of the intestinal wall. The fluid within the strangulated intestinal segment contains a high concentration of bacteria (such as Clostridium, Streptococcus, and large intestine bacilli), blood, and necrotic tissue. The toxins produced by these bacteria, along with the breakdown products of blood and necrotic tissue, are highly toxic. When this fluid enters the peritoneal cavity through a damaged or perforated intestinal wall, it can cause severe peritoneal irritation and infection. Once absorbed by the peritoneum, it leads to septicemia. Severe peritonitis and toxemia are the primary causes of death in patients with intestinal obstruction.

In addition to the three major pathophysiological changes mentioned above, strangulated intestinal obstruction is often accompanied by bleeding from the intestinal wall, peritoneal cavity, and intestinal lumen. The longer the strangulated intestinal loop, the greater the loss of blood, which also contributes to the mortality of patients with intestinal obstruction.

bubble_chart Clinical Manifestations

Intestinal obstruction varies in disease causes and manifestations, with significantly different prognoses. Therefore, a relatively clear classification of intestinal obstruction should be established.

(1) Based on the cause of obstruction, it can be divided into three categories:

1. Mechanical intestinal obstruction: The most common clinically, over 90% of acute intestinal obstructions are caused by mechanical factors that narrow or occlude the intestinal lumen, preventing the passage of intestinal contents. Examples include intestinal adhesions, intestinal inflammation or tumors, external mass compression, strangulated hernias, intussusception, intestinal volvulus, and ascaris blockage of the intestinal lumen.

2. Dynamic intestinal obstruction: Mainly due to disordered intestinal muscle activity, preventing the movement of intestinal contents, rather than mechanical factors inside or outside the intestinal lumen. The intestinal wall itself has no anatomical lesions. Dynamic intestinal obstruction can be further divided into:

(1) Paralytic ileus: Also known as adynamic ileus. Caused by factors such as infection, hypokalemia, myelitis, hypothyroidism, or abdominal surgery, which affect the balance of the intestinal autonomic nervous system, local nerve conduction, or the contraction of intestinal smooth muscle, leading to intestinal dilation and loss of peristalsis, preventing the propulsion of intestinal contents.

(2) Spastic intestinal obstruction: Relatively rare and transient, the obstruction is caused by spasmodic contraction of the intestinal muscles leading to narrowing of the lumen, occasionally seen in intestinal inflammation or neurological dysfunction.

3. Ischemic intestinal obstruction: The intestine has no mechanical blockage but loses motility due to circulatory disorders, seen in mesenteric vascular thrombosis or embolism.

(2) Based on intestinal blood supply, it can be divided into two categories:

1. Simple intestinal obstruction: Only involves blockage of the intestinal lumen without impairment of intestinal blood supply, known as simple intestinal obstruction. Commonly seen in obstructions caused by intraluminal blockages or external mass compression.

2. Strangulated intestinal obstruction: Involves blockage of the intestinal lumen with ischemia and necrosis due to strangulation of blood vessels, known as strangulated intestinal obstruction. Often caused by volvulus, intussusception, incarceration, or intestinal adhesions.

(3) Based on the location of obstruction, it can be divided into two categories:

1. Small intestine obstruction: Can be further divided into high small intestine obstruction, mainly occurring in the duodenum or jejunum, and low small intestine obstruction, mainly occurring in the distal ileum.

2. Colonic obstruction: Mostly occurs in the left colon, particularly the sigmoid colon or the junction between the sigmoid colon and rectum.

(4) Based on the degree of obstruction, it can be divided into complete obstruction and incomplete (or partial) obstruction.

(5) Based on the onset, it can be divided into acute intestinal obstruction and chronic intestinal obstruction.

The above classification terms serve to describe the nature and state of intestinal obstruction in clinical practice, and the various classifications are interrelated. For example, strangulated mechanical obstruction is necessarily acute and complete; chronic intestinal obstruction is mostly incomplete, and incomplete obstruction is mostly simple. It must be noted that the type of intestinal obstruction is not fixed and can change with the progression of the pathological process, such as transitioning from simple to strangulated, from incomplete to complete, or from chronic to acute.

Abdominal pain, vomiting, abdominal distension and fullness, constipation, and cessation of gas passage are typical symptoms of intestinal obstruction, but their severity varies among different types of obstructions.

(1) Abdominal pain Most patients with intestinal obstruction experience abdominal pain. In cases of acute complete mechanical small intestine obstruction, abdominal pain manifests as paroxysmal colicky pain, caused by intense peristalsis of the intestinal tract above the obstruction site. The pain is often located in the mid-abdomen, with sudden onset that gradually intensifies to a peak, lasting several minutes before subsiding. The pain-free intervals may be completely painless, but the pain can recur after some time. The severity of colicky pain and the duration of pain-free intervals vary depending on the location of the obstruction and the urgency of the condition. Generally, in cases of duodenal or upper jejunal obstruction, vomiting can relieve pressure, resulting in milder colicky pain. In contrast, lower ileal obstruction may suppress peristalsis due to intestinal distension, leading to less severe colicky pain. However, acute jejunal obstruction often causes more intense colicky pain, typically occurring every 2–5 minutes. In incomplete intestinal obstruction, abdominal pain is milder and may subside after a bout of borborygmus or passing gas. Chronic intestinal obstruction also presents with milder pain and longer pain-free intervals. In acute mechanical colonic obstruction, abdominal pain is usually localized in the lower abdomen and is generally less severe than in small intestine obstruction. If the ileocecal valve functions normally in colonic obstruction, the colonic contents cannot reflux into the small intestine, leading to gradual dilation of the intestinal lumen and increased pressure. In such cases, in addition to paroxysmal colicky pain, persistent dull pain may occur, indicating the possibility of closed-loop intestinal obstruction. Persistent dull pain during pain-free intervals is also an early sign of strangulated intestinal obstruction. If intestinal wall ischemia or necrosis occurs, the pain becomes continuous and severe. In paralytic intestinal obstruction, since the intestinal muscles lose peristaltic ability, there is no colicky pain, but severe intestinal distension can cause persistent abdominal distending pain.

(2) Vomiting Almost all patients with intestinal obstruction experience vomiting. In the early stage, it is reflexive vomiting, often expelling gastric contents. In the late stage [third stage], it becomes reflux vomiting, which varies depending on the level of obstruction. The higher the obstruction, the more frequent and severe the vomiting. In low small intestine obstruction, vomiting is milder and less frequent. In colonic obstruction, there may be no vomiting initially due to the ileocecal valve preventing reflux. However, in the late stage [third stage], when the ileocecal valve becomes incompetent due to overdistension of the intestinal lumen, severe vomiting may occur, and the vomitus may contain fecal matter.

(3) Abdominal distension and fullness These are later symptoms, and their severity depends on the level of obstruction. In high small intestine obstruction, frequent vomiting often prevents significant abdominal distension and fullness. In low small intestine obstruction or advanced colonic obstruction, marked abdominal distension is common. In closed-loop obstruction, the distension of the affected segment is prominent and often asymmetrical. In paralytic ileus, the entire intestine is dilated, leading to significant abdominal distension and fullness.

(4) Constipation and cessation of flatus In complete intestinal obstruction, patients stop passing stool and flatus. However, in the first 2–3 days of high small intestine obstruction, if feces and gas remain in the intestinal lumen below the obstruction, defecation and flatus may still occur, which should not rule out complete obstruction. Similarly, in strangulated intestinal obstruction (e.g., volvulus, intussusception) or obstruction caused by intestinal cancer, bloody stools or pus-blood stools may still be passed.

(5) Systemic symptoms Patients with simple intestinal obstruction generally have no obvious systemic symptoms. However, those with frequent vomiting and severe abdominal distension inevitably experience dehydration. Hypokalemia may cause fatigue, drowsiness, lack of strength, and arrhythmias. Systemic symptoms are most pronounced in strangulated intestinal obstruction, with early collapse and rapid progression to shock. If intra-abdominal infection is present, abdominal pain persists and spreads to the entire abdomen, accompanied by fear of cold, fever, leukocytosis, and other signs of infection and toxemia.

The typical signs of intestinal obstruction are mainly observed in the abdomen.

1. Abdominal distension This is more common in the late stage [third stage] of low small intestine obstruction. Closed-loop obstruction often presents with asymmetrical local distension, while paralytic ileus shows marked generalized abdominal distension. Before abdominal palpation, it is best to perform auscultation for several minutes.

2. Hyperactive or absent borborygmi (or bowel sounds) In the early stage of mechanical intestinal obstruction, hyperactive borborygmi, such as a cluster of rushing water sounds, are often heard over the obstruction during episodes of colicky pain. When the intestinal lumen is significantly dilated, bowel sounds may become high-pitched and metallic. In paralytic ileus or mechanical obstruction complicated by peritonitis, bowel sounds are markedly reduced or completely absent.

3. Visible peristalsis and peristaltic waves These are particularly noticeable in chronic intestinal obstruction and in patients with thin abdominal walls.

4. Abdominal tenderness Common in mechanical intestinal obstruction. Tenderness with muscle guarding and rebound tenderness is mainly seen in strangulated intestinal obstruction, especially when complicated by peritonitis.

5. Abdominal mass In obstruction caused by ascaris balls, gallstones, intussusception, or intestinal cancer, a corresponding mass may be palpable. In closed-loop obstruction, a tender, distended intestinal segment may sometimes be felt.

bubble_chart Diagnosis

Symptoms and signs: Typical intestinal obstruction is not difficult to diagnose, but cases lacking typical manifestations are more challenging. Abdominal X-ray fluoroscopy or radiography is highly helpful in confirming the clinical diagnosis and determining the location of the obstruction. In normal individuals, only small amounts of gas are visible in the stomach and colon on abdominal X-ray films. If gas and fluid levels are present in the {|###|}small intestine{|###|}, it indicates impaired passage of intestinal contents and suggests the presence of intestinal obstruction. Acute {|###|}small intestine{|###|} obstruction typically requires at least 6 hours for sufficient fluid and gas to accumulate in the intestines, forming distinct fluid levels. After 12 hours, the degree of intestinal dilation will definitely reach diagnostic levels. The time required for X-ray signs to appear in colonic obstruction is even longer. The gas-filled {|###|}small intestine{|###|}, particularly the jejunum, can be identified by the circular folds encircling the intestinal lumen and distinguished from the colon, which has haustral markings. Additionally, the typical {|###|}small intestine{|###|} pattern is mostly located in the central abdomen, while the colon appears at the periphery or in the pelvis. Depending on the patient's physical condition, upright or supine positions and anteroposterior or lateral views may be used for radiography, with serial films taken if necessary.

Once the diagnosis of intestinal obstruction is confirmed, further differentiation of the type of obstruction is necessary. Due to significant differences in treatment and prognosis—for example, mechanical intestinal obstruction often requires surgical intervention, while dynamic obstruction can be cured with conservative therapy—accurate classification is crucial. Strangulated intestinal obstruction should be treated surgically as early as possible, whereas simple mechanical obstruction may initially be managed conservatively. Key points for differentiation are as follows:

(1) Differentiating mechanical from dynamic intestinal obstruction: First, analyze the history for any mechanical obstructive factors. Dynamic intestinal obstruction includes the more common paralytic type and the rare spastic type. Mechanical obstruction is characterized by paroxysmal intestinal {|###|}colicky pain{|###|}, hyperactive {|###|}borborygmus{|###|}, and asymmetric {|###|}abdominal distension and fullness{|###|}. In contrast, paralytic obstruction features absence of {|###|}colicky pain{|###|}, disappearance of {|###|}borborygmus{|###|}, and uniform abdominal distension. Spastic obstruction may present with sudden onset and cessation of severe {|###|}abdominal pain{|###|}, irregular intervals, weakened but not absent {|###|}borborygmus{|###|}, and no {|###|}abdominal distension and fullness{|###|}. Abdominal X-ray films aid in differentiating the three: mechanical obstruction shows localized intestinal distension proximal to the obstruction; paralytic obstruction reveals generalized distension of the stomach, {|###|}small intestine{|###|}, and colon to a similar degree; and spastic obstruction shows no significant intestinal distension or dilation. Serial anteroposterior and lateral abdominal films taken every 5 minutes to observe {|###|}small intestine{|###|} motility can often distinguish mechanical from paralytic obstruction.

(2) Differentiating simple from strangulated intestinal obstruction

Strangulated intestinal obstruction can develop from simple mechanical obstruction, with 15–43% of simple cases progressing to strangulation due to inadequate treatment. The following signs should raise suspicion of strangulated obstruction:

1. Sudden onset of severe, unrelenting {|###|}abdominal pain{|###|}, or transition from paroxysmal {|###|}colicky pain{|###|} to persistent {|###|}abdominal pain{|###|}, with fixed localization. If the pain radiates to the back, it suggests mesenteric traction and further indicates strangulation.

2. Abdominal tenderness, rebound tenderness, and rigidity, with less prominent {|###|}abdominal distension and fullness{|###|} or hyperactive {|###|}borborygmus{|###|}.

3. Blood in {|###|}vomiting{|###|} material, gastrointestinal decompression drainage, or peritoneal aspirate, possibly accompanied by {|###|}hematochezia{|###|}.

4. Rapid systemic deterioration, marked toxemia, and potential shock.

5. X-ray films may show dilated, fluid-filled intestinal segments proximal to the obstruction, resembling a tumor or displaying a "C" shape (the "{|###|}coffee bean{|###|} sign"), often with {|###|}ascites{|###|} between dilated loops.

(3) Differentiating {|###|}small intestine{|###|} from colonic obstruction: High {|###|}small intestine{|###|} obstruction presents with frequent {|###|}vomiting{|###|} and mild {|###|}abdominal distension and fullness{|###|}, whereas low {|###|}small intestine{|###|} obstruction shows the opposite. Colonic obstruction clinically resembles low {|###|}small intestine{|###|} obstruction but can be distinguished by abdominal X-rays. In {|###|}small intestine{|###|} obstruction, gas-filled loops are widespread with multiple fluid levels, while the colon remains unremarkable. In colonic obstruction, dilated colon and haustra are visible peripherally, with minimal gas in the {|###|}small intestine{|###|}.

(4) Differentiating complete intestinal obstruction from incomplete intestinal obstruction Complete intestinal obstruction is mostly acute in onset with obvious symptoms, while incomplete intestinal obstruction is often chronic with mild symptoms and tends to be intermittent in nature. Plain X-ray films show significant gas-filled distension of intestinal loops in complete obstruction, but not in incomplete obstruction.

(5) Differential diagnosis of intestinal obstruction causes. Determining the cause of the disease can be approached through analysis of factors such as age, medical history, physical examination, and X-ray findings. For example, a history of previous abdominal surgery, trauma, or infection should raise suspicion of intestinal adhesions or adhesive band obstruction. If the patient has subcutaneous nodules in the lungs, consider the possibility of intestinal tuberculosis or peritoneal tuberculosis causing intestinal obstruction. In patients with rheumatic valvular heart disease accompanied by atrial fibrillation, atherosclerosis, or occlusive arteritis, mesenteric artery embolism should be considered. Portal hypertension and portal vein inflammation can lead to portal vein thrombosis. These arterial and venous blood flow obstructions are common causes of vascular intestinal obstruction. In children, intestinal blockage caused by roundworms is occasionally seen; primary intussusception is more common in infants under 3 years old. In young and middle-aged patients, common causes include intestinal adhesions, incarcerated external hernias, and intestinal volvulus. In elderly patients, common causes are colorectal cancer, sigmoid volvulus, and fecal impaction, with 90% of colon obstruction cases being cancerous. Adult intussusception is rare and mostly secondary to Meckel's diverticulitis, intestinal tumors, or neoplasms. During abdominal examination, special attention should be paid to surgical scars and concealed external hernias.

Paralytic ileus is relatively common in both medical and surgical clinical practice. Major abdominal surgeries and intra-abdominal infections are frequent causes. Other conditions such as systemic sepsis, severe pneumonia, drug poisoning, hypokalemia, retroperitoneal hemorrhage, intestinal bleeding, and ureteral colic can also lead to paralytic ileus. Careful analysis of medical history and comprehensive examination are crucial for diagnosis.

bubble_chart Treatment Measures

The treatment of intestinal obstruction depends on the cause, nature, location, severity, and the patient's overall condition. However, regardless of the treatment method, it is essential to correct the water, electrolyte, and acid-base imbalances caused by the obstruction, perform gastrointestinal decompression to improve blood circulation in the intestinal segments above the obstruction, and control infection.

(1) Correcting dehydration, electrolyte loss, and acid-base imbalance: The degree of dehydration and electrolyte loss is related to the severity and type of the condition. It should be estimated based on clinical experience and blood test results. Generally, adults with mild symptoms require about 1,500 ml of fluid replacement, while those with significant vomiting need 3,000 ml. In cases of peripheral circulatory collapse and hypotension, more than 4,000 ml of fluid may be required. If the condition does not improve promptly, additional fluid replacement is needed to account for losses from gastrointestinal decompression, urinary excretion, and daily maintenance requirements. Potassium supplementation is necessary when urinary output is normal. Low intestinal obstruction often leads to acidosis due to loss of alkaline intestinal fluid, whereas high intestinal obstruction tends to cause alkalosis due to loss of gastric fluid and potassium. Both conditions require appropriate correction. In advanced stages of strangulated or mechanical intestinal obstruction, loss of plasma and whole blood may occur, leading to hemoconcentration or hypovolemia. Thus, whole blood, plasma, or albumin should be administered to effectively correct circulatory disturbances.

When formulating or modifying the treatment plan, adjustments must be made based on the patient's vomiting status, signs of dehydration, hourly urine output and specific gravity, blood sodium, potassium, chloride, CO2 combining power, serum creatinine, hematocrit, and central venous pressure measurements. Due to acidosis, hemoconcentration, and potassium efflux from cells, blood potassium levels may not accurately reflect cellular potassium deficiency. Electrocardiogram monitoring should be performed as a supplementary measure. The goal of fluid and electrolyte replacement and acid-base balance correction is to maintain the body's internal stability, preserve its disease resistance, and help the patient endure the crisis until the obstruction is resolved, enabling them to undergo surgical treatment under favorable conditions.

(2) Gastric decompression: Gastrointestinal tube decompression can remove swallowed gas and stagnant fluid, relieve intestinal distension, prevent aspiration pneumonia, reduce vomiting, and improve circulatory and respiratory distress caused by abdominal distension and fullness. To some extent, it also improves static blood, edema, and blood circulation in the intestinal segments above the obstruction. In a few mild cases of simple intestinal obstruction, effective decompression may restore intestinal patency. Gastrointestinal decompression can reduce surgical difficulties and enhance surgical safety.

There are generally two types of decompression tubes: a shorter one (Levin tube) can be placed in the stomach or duodenum, which is convenient to operate and effective for decompression in high small intestine obstruction; another longer tube (Miller-Abbott tube) is suitable for decompression in lower small intestine obstruction and paralytic ileus, but its placement is time-consuming and requires fluoroscopy to confirm the tube's position. In cases of colonic obstruction with intestinal distension, tube decompression is often ineffective, and surgical decompression is usually necessary.

(3) Controlling infection and toxemia: Prolonged intestinal obstruction or strangulation often leads to infection of the intestinal wall and peritoneum by various bacteria (e.g., Escherichia coli, Clostridium, Streptococcus, etc.). Aggressive intravenous broad-spectrum antibiotic therapy targeting Gram-negative bacilli is crucial. Animal experiments and clinical practice have confirmed that antibiotics can significantly reduce the mortality rate of intestinal obstruction.

(4) Relieving obstruction and restoring intestinal function: For general simple mechanical intestinal obstruction, especially early incomplete obstruction caused by factors such as ascarids, fecal impaction, or inflammatory adhesions, non-surgical treatment may be sufficient. Early intussusception or volvulus-induced obstruction can also be managed non-surgically under close observation. Dynamic intestinal obstruction does not require surgery unless accompanied by surgical complications.

In addition to the aforementioned treatments, non-surgical measures may include the following:

1.Chinese medicinals   Composite Major Purgative Decoction: Magnolia Bark 15g, Stir-fried Radish Seed 30g, Immature Orange Fruit 9～15g (to be decocted later), Mirabilite 9～15g (to be taken after dissolving). Suitable for general intestinal obstruction with significant bloating. Gansui Root for relieving intestinal obstruction: Gansui Root powder 1g (to be taken after dissolving), Peach Kernel 9g, Red Peony Root 15g, Raw Achyranthes Root 9g, Magnolia Bark 15g, Raw Rhubarb Rhizome 15～24g (to be decocted later), Aucklandia Root 9g. Suitable for severe intestinal obstruction with excessive fluid accumulation. The above Chinese medicinals can be decocted into 200ml and taken orally in divided doses or administered through a gastrointestinal decompression tube.

2. Oils: Paraffin oil, raw soybean oil, or vegetable oil (200–300 ml) can be administered orally in divided doses or injected through a gastrointestinal decompression tube. Suitable for patients with severe conditions and weaker constitutions.

3. For paralytic ileus without surgical complications, treatments such as neostigmine injections or hot compresses with mirabilite on the abdomen may be used.

4. Acupuncture at points such as Zusanli (ST36), Zhongwan (CV12), Tianshu (ST25), Neiguan (PC6), Hegu (LI4), and Neiting (ST44) can serve as adjunctive therapy.

The vast majority of mechanical intestinal obstructions require surgical intervention, while ischemic and strangulated intestinal obstructions necessitate prompt surgical management.

The main objectives of surgical procedures include: ① Releasing adhesions or incarcerated hernias, reducing twisted or intussuscepted intestines, etc., to eliminate the local causes of obstruction; ② Resecting necrotic or tumorous intestinal segments, draining abscesses, etc., to address localized lesions; ③ Enterostomy can relieve intestinal distension and facilitate segmental resection, while intestinal anastomosis can bypass diseased segments to restore intestinal patency.

bubble_chart Prognosis

The mortality rate of simple intestinal obstruction is approximately 3%, while that of strangulated intestinal obstruction can reach 10-20%. The key to improving prognosis lies in early diagnosis and timely intervention.

bubble_chart Prevention

Intestinal obstruction has many disease causes. In terms of prevention, children with ascariasis should receive active deworming treatment, hernias should be repaired promptly, and abdominal surgery should be performed gently. There are reports that placing sodium carboxymethyl cellulose in the abdominal cavity postoperatively and taking vitamin E orally can reduce the occurrence of intestinal adhesions.

bubble_chart Differentiation

Chronic intestinal pseudo-obstruction

Chronic intestinal pseudo-obstruction is a syndrome characterized by symptoms and signs of intestinal obstruction without evidence of mechanical blockage. Paralytic ileus, as mentioned earlier, is an acute form of intestinal pseudo-obstruction. Here, we focus on chronic intestinal pseudo-obstruction.

It is generally believed that this syndrome results from degeneration of the intestinal wall nerves, as pathological examinations in some cases reveal lesions in the ganglion cells of the enteric plexus. However, others attribute it to intestinal smooth muscle pathology, as some cases exhibit familial visceral myopathy, such as degeneration and fibrosis of the small intestine and bladder smooth muscles. Since 30% of patients have a family history, this suggests a genetic component to the syndrome.

Symptoms often begin in childhood or adolescence, with a minority appearing between the ages of 30 and 40. The course of the disease typically involves recurrent acute episodes alternating with remission. During episodes, symptoms resemble those of mechanical obstruction, including varying degrees of nausea, vomiting, intestinal colicky pain, abdominal pain, diarrhea or steatorrhea, and abdominal tenderness. During the stage of remission, symptoms may be absent or mild, such as abdominal distension and fullness.

Intestinal pseudo-obstruction can affect the entire digestive tract or an isolated organ, such as the esophagus, stomach, small intestine, or colon. Symptoms are most pronounced when the small intestine is obstructed. If only the duodenum is involved, it may present as megaduodenum, often with severe vomiting and weight loss, easily misdiagnosed as superior mesenteric artery syndrome. If only the colon is affected, the main manifestations are chronic constipation and recurrent fecal impaction. Some cases may also involve bladder emptying disorders.

X-ray examinations may reveal significant dilation and delayed motility in the affected esophagus, stomach, small intestine, and colon.

Intestinal pseudo-obstruction can be secondary to connective tissue diseases (such as scleroderma, dermatomyositis, systemic lupus erythematosus), amyloidosis, primary myopathies (myotonic dystrophy, progressive muscular dystrophy), endocrine disorders (myxedema, diabetes, pheochromocytoma), neurological diseases (Parkinson's disease, familial dysautonomia), and drug factors (such as phenothiazines, tricyclic antidepressants, anti-Parkinsonian drugs) or surgical factors (such as jejunoileal bypass). Primary intestinal pseudo-obstruction should only be considered after excluding these potential secondary causes.

Treatment primarily involves symptomatic and supportive care. Surgical intervention should be avoided unless the condition is localized to a small segment of the digestive tract.

The main cause of death in this syndrome is complications such as aspiration pneumonia.