Intestinal Obstruction Flashcards

1
Q

Acute intestinal obstruction can be divided into?

A

Mechanical (or dynamic) ileus, due to mechanical obstruction of the intestinal canal, is associated with abdomi-nal pain.
2. Paralytic (or adynamic) ileus, due to paralysis of the intestinal musculature, is characterized by the absence of pain.

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2
Q

Mechanical obstruction can bring divided Into

A

Acute
Chronic
Acute on chronic

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3
Q

What’s Acute Intestinal Obstruction

A

Acute intestinal obstruction is a condition where the normal flow of the intestinal contents is blocked. It can be classified based on the nature of the obstruction and the impact on the blood supply to the bowel.

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4
Q

What are the Types of mechanical acute intestinal Obstruction with examples

A
  1. Simple Obstruction
    • Nature: In this type, the bowel lumen is blocked, but there is no compromise to the blood supply of the bowel. The obstruction can occur due to various reasons, such as intra-abdominal adhesions, hernias, or uncommon causes like gallstones, bezoars, or even a mass of intestinal worms (ball of worms).
    • Treatment: Simple obstruction may respond to conservative management, which involves methods such as bowel rest, decompression, or fluid therapy.
  2. Strangulation Obstruction
    • Nature: In strangulation obstruction, not only is the bowel lumen occluded, but the blood supply to the affected segment is also compromised, leading to ischemia (lack of blood flow) and potentially bowel necrosis (tissue death).
    • Example: A strangulated inguinal hernia is a common example, where the bowel loop in the hernia sac is compressed, leading to a compromised blood supply. Additionally, this type of obstruction may also be seen in mesenteric thrombosis or embolism, where blood clots disrupt blood flow without a physical obstruction in the bowel lumen itself.
  3. Closed Loop Obstruction
    • Nature: In this scenario, the bowel loop is “closed off” at both ends, so that there is no way for the contents to move either proximally (upward) or distally (downward). This type of obstruction is often associated with an increased risk of blood supply impairment.
    • Example: It can occur in cases of colonic obstruction with a competent ileocecal valve, meaning the colon is blocked while the valve between the small and large intestines prevents the escape of contents.
    • Features in Combined Scenarios: In certain cases, multiple forms of obstruction may coexist. For instance, in a strangulated hernia, there may be:
      • Simple lumen occlusion due to the constriction.
      • Compromised blood flow, leading to strangulation.
      • Closed loop obstruction, where the segment is isolated within the hernia sac.
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5
Q

What’s the pathophysiology of simple intestinal obstruction

A
  1. Simple Obstruction
    • Below the Obstruction Site: Normal peristalsis (intestinal movement) continues for a while, and absorption proceeds until the contents are either absorbed or expelled, leading to collapse of the bowel below the obstruction.
    • Above the Obstruction Site: The bowel becomes distended as the contents accumulate. Initially, peristalsis is increased to try and overcome the blockage. However, if the obstruction remains unresolved, the distention worsens, which can eventually cause the loss of peristaltic activity and bowel function.
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6
Q

Whatre the possible Causes of Distension in intestinal obstruction.

A
  1. Gases Accumulation
  • The gases within the intestines primarily originate from swallowed air, comprising various components:
  • Nitrogen (70%)
  • Oxygen (10%)
  • Carbon dioxide (6-9%)
  • Hydrogen (1%)
  • Methane (1%)
  • Hydrogen sulfide (1-10%)
  • Additional gases are produced from the putrefaction and fermentation of intestinal contents by bacteria, and some gases diffuse from the blood into the intestines.
  1. Fluid Accumulation
  • The fluids consist of digestive juices, such as saliva, gastric juice, bile, pancreatic, and intestinal secretions. These fluids accumulate for two main reasons:
  • Loss of the absorbing surface below the obstruction, which prevents the reabsorption of fluids.
  • Disordered fluid and electrolyte transport within the obstructed segment. Over time, the absorption of water, sodium, and potassium significantly decreases and eventually stops (around 12 hours after obstruction onset), while the rate of secretion from the intestines increases.
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7
Q

List the Factors Influencing the Degree of Distension

A
  • Level of Obstruction:
  • In high intestinal obstructions, the fluid quickly reaches the stomach, leading to early vomiting that helps reduce some of the distension.
  • In low obstructions, the intestines have more room to accommodate the accumulating fluid, causing more significant distension and delaying the onset of vomiting.
  • Intraluminal Pressure Increase:
  • The normal pressure within the intestines is 2-4 mmHg, but with obstruction, it can rise to 10 mmHg in the small intestine and up to 25 mmHg in the colon.
  • This elevated pressure results from the increased peristaltic activity as the intestines attempt to overcome the obstruction and from the expanding volume of gas and fluids.
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8
Q

What are the Consequences of Distension

A
  1. Venous Compression and Congestion
  • When the increased intraluminal pressure surpasses the venous pressure, it compresses the veins, leading to venous congestion and edema (fluid buildup) of the intestinal wall.
  • This pressure further causes the leakage of fluid from the blood plasma into the intestinal lumen and peritoneal cavity, worsening the distension.
  1. Ischemia and Mucosal Damage
  • The elevated pressure compromises the blood supply, especially to the bowel’s mucosa, leading to necrosis (tissue death) in patches of the mucosal layer.
  1. Distension and Fluid Secretion Cycle
  • The process becomes a vicious cycle where distension promotes further fluid secretion, which then exacerbates the distension. As the intestines stretch, they also become more permeable, allowing more fluid to accumulate.
  1. Loss of Bowel Tone
  • After several days, the distended bowel becomes atonic, meaning it loses its normal tone and peristaltic activity, further complicating the condition.
  1. Impact on Respiration
  • Severe abdominal distension interferes with breathing, potentially leading to respiratory failure or acidosis (an abnormal increase in the acidity of body fluids).

In summary, distension in acute intestinal obstruction arises from the buildup of gases and digestive fluids due to the inability to move contents past the obstruction. The resulting high intraluminal pressures can lead to compromised blood flow, mucosal damage, and severe systemic consequences such as respiratory failure, necessitating prompt medical intervention to relieve the obstruction and manage fluid balance.

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9
Q

As a year 4 medical student on block posting ( surgical block posting) about to write an exam, I want you to come up with at least 7 possible long essay question. ( Note if needed you can split the question to 1,1a, 1b and so on)

A
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10
Q

Dehydration and Electrolyte Imbalance in Intestinal Obstruction

Intestinal obstruction can lead to significant disturbances in fluid and electrolyte balance due to various mechanisms. Let’s delve into how these imbalances occur and their effects:

What are the Causes of Dehydration and Electrolyte Imbalance

A
  1. Vomiting: When there is an obstruction, the body’s natural response is to vomit. This results in the loss of fluids and electrolytes, particularly sodium, potassium, and chloride, which are normally present in the gastrointestinal secretions.
  2. Accumulation of Gastrointestinal Secretions: The gastrointestinal (GI) tract secretes about 7-10 liters of fluid daily, which includes digestive juices and other secretions. In cases of intestinal obstruction, the secretions increase and accumulate within the bowel lumen, unable to be reabsorbed.
  3. Fluid Sequestration in the Bowel Wall and Peritoneal Cavity: When the gut is obstructed, there is an accumulation of fluid not just inside the lumen but also within the bowel wall and potentially leaking into the peritoneal cavity (the space surrounding the abdominal organs). This loss of fluid into these areas is referred to as third-space loss, where the fluid is effectively trapped and unavailable to the circulatory system.
  4. Diminished Oral Intake and Decreased Absorption: Due to nausea, vomiting, and the inability of the obstructed bowel to properly absorb fluids and nutrients, oral intake is often reduced, exacerbating dehydration.
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11
Q

Mechanism of Electrolyte Disturbance

The fluid that accumulates in the obstructed gut has a higher concentration of sodium and potassium than normal. Because of the obstruction, the body cannot effectively reabsorb these electrolytes, leading to a loss of:

  • Extracellular fluid (ECF): This includes the fluids present in blood and tissues. When fluids are lost to the gut or peritoneal cavity, it reduces the volume of circulating blood, resulting in hypovolemia (decreased blood volume). This can manifest as dehydration or even shock.
  • Sodium (hyponatremia), potassium (hypokalemia), and chloride (hypochloremia) deficiencies: As these electrolytes are lost, the body’s balance is disrupted, which can affect normal cellular and organ functions.
  • Hypovolemia may also contribute to renal (kidney) failure, as decreased blood flow to the kidneys can impair their ability to filter waste and regulate electrolyte levels.

Why Electrolytes May Initially Appear Normal

In the early stages, serum electrolytes (those measured in the blood) might still appear within the normal range despite significant fluid losses. This happens because the fluid being lost is isotonic to plasma, meaning it has a similar concentration of electrolytes as the blood. Thus, the concentration in the bloodstream may not immediately reflect the losses occurring in the gut.

A
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12
Q

What are the Impacts of Obstruction Level on Fluid and Electrolyte Imbalance

A
  • High Obstruction (proximal):
    • Faster onset of fluid and electrolyte imbalance: In obstructions occurring higher up in the GI tract, such as in the small intestine, the absorptive surface area is significantly reduced. This means that there is less opportunity to reabsorb fluids and electrolytes. Additionally, vomiting occurs earlier and is more severe, leading to quicker dehydration and imbalances.
    • Metabolic Alkalosis: The fluid lost through vomiting is rich in stomach acid (HCl). When significant amounts of acidic fluid are lost, the body may develop alkalosis (a condition where the blood becomes too alkaline). The kidneys may exacerbate this by reabsorbing bicarbonate in place of chloride, further raising blood pH.
  • Low Obstruction (distal):
    • Slower onset of fluid and electrolyte imbalance: In lower obstructions, such as in the colon, there is a larger surface area available for fluid reabsorption, which delays the onset of significant dehydration and electrolyte disturbances. Vomiting tends to occur later, which further slows the development of these imbalances.
    • Metabolic Acidosis: Here, the fluid sequestered in the bowel is more alkaline because it originates from lower in the GI tract, where the secretions are less acidic. If this alkaline fluid remains trapped in the gut, the body can develop acidosis (a condition where the blood becomes too acidic).
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13
Q

What are the Clinical Consequences of simple intestinal obstruction

A

The ultimate danger in intestinal obstruction is not merely the mechanical blockage itself but rather the severe loss of water and electrolytes, which can lead to:

  • Hypovolemic shock: A life-threatening condition where low blood volume results in insufficient blood flow to the organs.
  • Electrolyte imbalances: Such as hyponatremia, hypokalemia, and hypochloremia, which can lead to muscle weakness, heart rhythm disturbances, and other serious conditions.
  • Renal failure: Due to the decreased blood flow to the kidneys and the effects of prolonged hypovolemia.

Death from simple intestinal obstruction often results from dehydration and electrolyte imbalance, emphasizing the importance of timely recognition and management of these issues in obstructive conditions.

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14
Q

What’s strangulated intestinal obstruction

A

Strangulation Obstruction

Strangulation obstruction refers to a type of intestinal obstruction where, in addition to the blockage of the bowel lumen, there is also a compromise of the blood supply to the affected section of the gut. This can lead to severe and life-threatening consequences due to the combined effects of mechanical blockage and impaired blood circulation.

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15
Q

What’s the Pathophysiology of Strangulation Obstruction?

A
  1. Venous Engorgement:
    • When an external force, such as a band or twisted loop, compresses the intestines, it may exceed the venous pressure (pressure in the veins draining the intestines). This results in venous congestion, where blood cannot effectively leave the bowel wall, causing swelling and engorgement.
    • The bowel wall becomes cyanosed (bluish-purple in color) due to reduced oxygen levels and accumulation of deoxygenated blood.
  2. Hypovolemia and Shock:
    • If the strangulated segment of bowel is large, it can trap a significant amount of blood, effectively removing it from the circulating blood volume. This sequestration of blood contributes to hypovolemia (low blood volume), potentially leading to shock and even death if untreated.
  3. Fluid Leakage and Infection:
    • As venous pressure increases, it leads to fluid leakage from the blood vessels into the bowel wall and lumen. This fluid can carry bacteria, particularly Escherichia coli (E. coli), and their toxins (both endotoxins and exotoxins), deeper into the bowel tissues.
    • The infection can spread to the peritoneal cavity (space around the abdominal organs) and enter the bloodstream, leading to peritonitis, septicemia, or endotoxic shock.
    • If the obstruction is suddenly relieved, there is a risk of severe endotoxic shock due to the rapid absorption of toxins from the compromised bowel.
  4. Bleeding and Capillary Rupture:
    • Increased venous pressure also causes rupture of small blood vessels (capillaries) within the bowel wall. This leads to bleeding into the lumen (inside the bowel), the bowel wall itself, and the peritoneal cavity.
    • The presence of blood-stained fluid (pink hemorrhagic fluid) may be noted in a strangulated hernia sac or the peritoneal cavity, and patients may pass melena stools (black, tarry stools) indicating bleeding in the gastrointestinal tract.
  5. Arterial Obstruction and Bowel Infarction:
    • The occlusion may be severe enough to compress the arteries supplying blood to the bowel or cause the arteries to go into spasm as a reflex response to venous congestion. This leads to reduced arterial blood flow, resulting in ischemia (lack of blood supply) and infarction (tissue death) of the bowel wall.
    • Additionally, the stasis of blood in the congested veins promotes the formation of blood clots (thrombosis) in the bowel wall and mesenteric veins, accelerating necrosis (tissue death).
    • The oxygen-deprived environment (hypoxia or anoxia) in the affected area favors the growth of anaerobic bacteria, such as Clostridia and Bacteroides, which can worsen the infection.
  6. Bowel Perforation and Peritonitis:
    • As the affected bowel becomes increasingly distended and its wall weakened by the accumulation of blood, there is a risk of perforation (rupture), leading to the escape of bowel contents into the peritoneal cavity. This causes secondary peritonitis, a life-threatening inflammation of the peritoneum.
    • The bowel initially appears congested and bright red, but as gangrene (localized tissue death due to loss of blood supply) develops, usually within 6 hours, it becomes black, green, or grey due to the breakdown of blood within the tissues. The site of strangulation may show a furrowed, grey appearance, and perforation may occur.
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16
Q

Clinical Consequences of strangulation Obstruction

A
  • Early Shock:
    • Patients with strangulation obstruction may rapidly develop shock due to both hypovolemia and endotoxemia (toxins in the blood), which can lead to a life-threatening condition if not managed promptly.
  • Severe Endotoxic Shock upon Release:
    • When the obstruction is relieved, there is a risk of severe endotoxic shock because the sudden release of the strangulated loop allows bacteria and their toxins to flood the systemic circulation, overwhelming the body’s defense mechanisms.

Strangulation obstruction is a serious condition that involves not only the mechanical blockage of the intestine but also a compromise of blood supply to the affected bowel segment. This can rapidly lead to shock, infection, bowel infarction, perforation, and death. Early recognition and surgical intervention are crucial to prevent these potentially fatal outcomes.

17
Q

What’s closed loop obstruction

A

Closed Loop Obstruction

A closed loop obstruction occurs when both the afferent (incoming) and efferent (outgoing) segments of the bowel are obstructed, leading to a closed segment where the trapped contents cannot escape. This situation is commonly seen in colonic obstructions when a competent ileocaecal valve (valve between the small intestine and colon) prevents the passage of gas and liquid stool back into the small intestine.

18
Q

What’s the Pathophysiology of closed loop obstruction

A
  1. Gas and Fluid Accumulation:
    • With the ileocaecal valve remaining closed, gases and liquid stool accumulate within the obstructed segment, especially in the caecum (the first part of the large intestine). The rich bacterial flora in the colon contributes significantly to the production of gases.
    • The increasing accumulation of gases and fluids leads to rapid distension of the bowel, which raises intraluminal pressure.
  2. Impairment of Blood Circulation:
    • As the intraluminal pressure rises due to distension, it begins to compress blood vessels, impairing circulation to the bowel wall.
    • The caecum is the most vulnerable area because it experiences the greatest degree of distension. Reduced blood flow eventually leads to necrosis (tissue death).
  3. Bowel Perforation and Peritonitis:
    • Necrosis weakens the bowel wall, increasing the risk of perforation. When the bowel wall ruptures, faecal contents and bacteria escape into the peritoneal cavity, leading to fulminating peritonitis. This is a rapidly progressing, life-threatening inflammation of the peritoneum.
19
Q

What are the possible Causes of Death in Acute Intestinal Obstruction

A

Death in cases of acute intestinal obstruction can occur due to several mechanisms:

  1. Shock:
    • Hypovolemic Shock:
      • Results from the loss of extracellular fluid (ECF) due to vomiting, sequestration in the bowel, or fluid shifts into the peritoneal cavity.
      • Sequestration of blood within the engorged bowel may also reduce the circulating blood volume.
    • Endotoxic Shock:
      • Occurs when bacterial toxins (endotoxins) enter the bloodstream due to mucosal damage or bowel perforation, leading to septicemia and a systemic inflammatory response.
  2. Dehydration:
    • Fluid loss through vomiting, sequestration in the bowel, and decreased intake leads to dehydration, which exacerbates shock and other complications.
  3. Electrolyte and Metabolic Imbalance:
    • Hypokalemia (low potassium):
      • Results from vomiting and decreased intestinal absorption. It can cause muscle weakness, arrhythmias, and renal complications.
    • Hyponatremia (low sodium):
      • Occurs due to vomiting, fluid shifts, and intestinal losses. This imbalance can cause confusion, seizures, and coma.
    • Acid-Base Imbalance:
      • Metabolic alkalosis is common in high obstruction due to loss of acidic gastric secretions.
      • Metabolic acidosis can develop in low obstruction or when there is severe bowel necrosis due to accumulation of lactic acid from tissue hypoxia.
  4. Peritonitis:
    • The escape of bowel contents into the peritoneal cavity leads to infection and inflammation of the peritoneum. Peritonitis can rapidly cause septic shock and multiple organ failure.
  5. Septicemia:
    • Occurs when bacteria and their toxins spread from the bowel or peritoneum into the bloodstream, leading to a systemic infection and potentially severe sepsis.
  6. Renal Failure:
    • Pre-renal failure results from dehydration and hypovolemia, where the kidneys do not receive enough blood to function properly.
    • Acute tubular necrosis (ATN) can occur due to prolonged shock, causing damage to the renal tubules from inadequate blood supply.
  7. Respiratory Failure:
    • Severe abdominal distension may impair diaphragm movement, leading to respiratory distress and respiratory acidosis due to impaired ventilation.
  8. Multiple Organ Failure:
    • This occurs as a final, severe complication when the shock, infection, and metabolic imbalances affect multiple organs, including the heart, kidneys, liver, and lungs, leading to their failure.

Summary

Closed loop obstruction poses a higher risk than other types of bowel obstruction because of its rapid progression to severe complications like necrosis, perforation, and peritonitis. Early recognition and prompt surgical intervention are crucial to prevent life-threatening outcomes such as shock, septicemia, and multi-organ failure.

20
Q

What are the Clinical Features of Mechanical Intestinal Obstruction

In mechanical bowel obstruction, it is essential to differentiate between simple obstruction (without compromised blood supply) and strangulating obstruction (with compromised blood supply). Here are the key clinical features to look out for:

A
  1. Pain:
    • Pain is often the first symptom. It is typically severe, cramping, rhythmically intermittent, and colicky.
    • In small bowel obstruction, pain tends to be central in the abdomen, whereas in large bowel obstruction, it is located in the hypogastric region (lower abdomen).
    • Each pain episode (spasm) intensifies rapidly, lasts for a few seconds, and then subsides slowly, allowing relief in between spasms.
    • In cases of strangulation, there is persistent pain between the episodes of colicky pain, indicating ongoing ischemia and potential tissue damage.
  2. Vomiting:
    • Early and profuse vomiting is common in high obstructions (near the stomach or upper small intestine).
    • In low obstructions (lower small intestine or colon), vomiting may be late or absent.
    • The nature of the vomit changes with time: it is initially colourless or greenish due to bile, then turns light brown, and eventually becomes dark brown and foul-smelling (faeculent) due to bacterial decomposition of intestinal contents and blood.
  3. Absolute Constipation:
    • There is a failure to pass both stool and gas (flatus), known as absolute constipation. This is a significant sign of complete obstruction.
    • Occasionally, the patient may pass one or two stools as the bowel below the obstruction empties.
    • In Richter’s hernia (where only part of the bowel circumference is involved), faeces and flatus may still be passed because the obstruction is not complete.
  4. Distension:
    • Distension varies inversely with vomiting. In high obstructions, where vomiting occurs early and copiously, distension is minimal.
    • In low obstructions (colon), distension is often marked due to the buildup of intestinal contents.
    • Central abdominal distension occurs in small bowel obstructions, while flank distension is more typical in colonic obstructions.
    • In cases like sigmoid volvulus, the distension can be very severe, filling the entire abdomen.
  5. Visible Peristalsis:
    • Peristalsis (rhythmic contractions of the intestine) may be visible on the abdomen in cases of obstruction.
    • Auscultation reveals increased, high-pitched bowel sounds, indicating hyperactive intestinal activity trying to overcome the blockage.
  6. Examination of Hernial Orifices and Rectum:
    • It is crucial to examine hernial orifices and the rectum, as these may be the sites of obstruction.
    • In obese patients, a femoral hernia may escape notice unless specifically searched for.
  7. Abdominal Scars:
    • The presence of abdominal scars suggests a history of previous surgery, indicating that post-operative adhesions could be the cause of the obstruction.
  8. Signs of Strangulation:
    • Rebound tenderness, guarding, and localized tenderness suggest the presence of strangulation due to inflammation or ischemia.
    • A palpable mass may also indicate a strangulated hernia or an obstructed segment of bowel.
  9. General Signs of Dehydration and Shock:
    • Look for symptoms such as sunken eyes, dry tongue, dry skin, a rapid pulse, low blood pressure, and mental confusion.
    • These signs indicate dehydration, shock, and electrolyte imbalance due to fluid loss and reduced circulating blood volume.
  10. Urine Output:
    - Scanty and highly concentrated urine is seen as a result of hypovolemia.
21
Q

What are the nvestigations you will like to do for Intestinal Obstruction

A
  1. Enema:
    • A simple enema may have a poor result if the bowel distal to the obstruction is not empty. If successful, the result will be temporary.
    • If the result is good, it can be repeated after half an hour. A poor outcome on repeat suggests obstruction.
  2. Plain X-ray of the Abdomen:
    • When the diagnosis is uncertain, a plain X-ray of the abdomen, both supine and erect, is helpful.
    • In the erect film, dilated loops of bowel with fluid-air levels can be observed.
      • If the obstruction is ileal (small bowel), the dilated loops appear mainly in the center of the abdomen.
      • If it is colonic, the loops appear more laterally (in the flanks).
    • In the supine position, the characteristic features of different bowel segments are evident:
      • The jejunum and proximal ileum may show a ladder pattern due to circular folds (valvulae conniventes).
      • Colonic obstruction is indicated by haustration (pouch-like indentations).
      • The terminal ileum, however, appears normal (“unremarkable”), lacking distinctive features.
  3. Laboratory Tests:
    • Urea levels may be elevated due to dehydration and reduced kidney perfusion.
    • Initially, serum electrolyte levels may not change significantly, as the fluid lost is isotonic.
    • In the later stages, potassium, sodium, and chloride levels may be depressed, despite ongoing dehydration.
    • Metabolic alkalosis may occur in high obstruction, whereas acidosis is more likely in low obstruction.
    • Raised hematocrit indicates hemoconcentration due to dehydration.

Summary

Early differentiation between simple and strangulating obstructions is critical to prevent severe complications such as shock, peritonitis, and multiple organ failure. Clinical features like pain characteristics, vomiting, absolute constipation, and distension can help localize the obstruction and determine its severity. Additionally, abdominal imaging and laboratory tests are essential for confirmation and guiding appropriate management.

22
Q

What are the differential diagnosis in intestinal obstruction, why you think so and how you can differentiate them

A

Differential Diagnosis of Intestinal Obstruction

When evaluating a patient with symptoms suggesting intestinal obstruction, it is crucial to differentiate between true mechanical obstruction and other conditions that mimic similar clinical features. Here are some important differential diagnoses:

  1. Paralytic Ileus Following Inflammatory Processes:
    • Paralytic ileus occurs when the intestinal muscles are paralyzed, leading to an inability to move contents through the bowel. It often arises after an inflammatory process or abdominal surgery.
    • Causes include conditions such as:
      • Acute appendicitis: Inflammation of the appendix.
      • Cholecystitis: Inflammation of the gallbladder.
      • Salpingitis: Inflammation of the fallopian tubes.
      • Perforated peptic ulcer: A hole in the wall of the stomach or duodenum due to an ulcer.
      • Generalized peritonitis: Widespread inflammation of the peritoneum.
    • Clinical features:
      • Presents with constant abdominal pain rather than the colicky pain typical of mechanical obstruction.
      • There is often tenderness, rebound tenderness, guarding, or rigidity of the abdomen.
      • Pyrexia (fever) is common, indicating an inflammatory or infectious process.
      • Bowel sounds are absent because the intestines are not actively moving.
  2. Acute Pancreatitis:
    • Inflammation of the pancreas, which may present similarly to intestinal obstruction.
    • Key features:
      • The patient may appear collapsed or in severe distress.
      • There is typically tenderness and guarding in the upper abdomen.
      • The Cullen’s sign (bruising around the umbilicus) or Grey Turner’s sign (bruising along the flanks) may be present due to retroperitoneal hemorrhage.
      • An upper abdominal mass may be felt, corresponding to the inflamed pancreas.
  3. Typhoid Perforation:
    • Complication of typhoid fever, a systemic infection caused by Salmonella typhi.
    • Clinical clues:
      • A history of fever, headache, and diarrhea preceding the onset of abdominal symptoms.
      • Generalized abdominal tenderness, guarding, or rigidity, indicating widespread peritoneal irritation due to perforation.
      • Often seen in regions where typhoid is endemic.
  4. Severe Constipation:
    • Severe constipation with impacted feces can mimic bowel obstruction.
    • Signs:
      • Impacted fecal masses may be felt on rectal examination.
      • Symptoms typically improve with enema, unlike true mechanical obstruction where enemas have little to no effect.

These differential diagnoses are essential to consider because the management of each condition varies significantly. Proper identification ensures appropriate treatment and prevents complications associated with delayed diagnosis.

23
Q

How do you manage intestinal obstruction
General M
Conservative M
Operative M

A

Treatment of Intestinal Obstruction

The management of intestinal obstruction aims to urgently relieve the blockage while simultaneously stabilizing the patient’s general condition. Initial steps include correcting fluid and electrolyte imbalances and starting antimicrobial therapy to prevent infection.

General Measures

  1. Correction of Fluid, Electrolyte, and Metabolic Imbalances
    • Intravenous fluid replacement is crucial to correct dehydration and restore electrolyte balance. Commonly used fluids include Ringer’s lactate, dextrose/saline solution, or dextrose water.
    • Potassium chloride is administered only after urine output is confirmed to be over 30 ml/h, indicating that the kidneys are functioning.
    • In cases of severe strangulation, where there may be significant blood loss or sequestration in the bowel, blood transfusion may be required after initial resuscitation with crystalloid fluids.
    • Continuous monitoring is essential:
      • Pulse and blood pressure are checked every 15 minutes.
      • Urine output is monitored hourly.
      • Central venous pressure (CVP) monitoring helps assess fluid status.
      • A fluid balance chart is maintained to track all inputs and outputs.
      • Serum electrolytes and blood urea levels are checked twice daily to detect ongoing imbalances.
  2. Nasogastric Decompression
    • Nasogastric tube insertion is performed to aspirate gastric contents, helping reduce bowel distension by removing air and intestinal fluids that may have refluxed into the stomach.
    • This decompression reduces the secretion of water and electrolytes into the intestines, thereby alleviating further distension.
    • It also prevents aspiration of gastric contents into the respiratory tract during induction of anesthesia, which could cause respiratory complications.
    • Respiratory distress caused by abdominal distension is minimized.
  3. Sedation
    • Pain management is important in treating intestinal obstruction. Medications such as morphine (10-15 mg) or pethidine (100 mg) are used to relieve pain and discomfort.
    • Care must be taken not to mask symptoms of worsening obstruction or strangulation.
  4. Antibiotics
    • Broad-spectrum antibiotics are administered to control or prevent bacterial infection. Common choices include:
      • Ciprofloxacin or cefuroxime/ceftazidime combined with metronidazole to cover a broad range of potential pathogens.
      • Ceftriaxone may also be used as an alternative.

Conservative Management

  1. Simple Obstruction of the Small Intestine Due to Adhesions
    • Postoperative adhesions are a common cause of small bowel obstruction. In these cases, conservative management is preferred as surgery may lead to the formation of new adhesions.
    • Surgical intervention (laparotomy) is indicated if there is no resolution, as evidenced by:
      • Increased abdominal distension or persistent aspiration of gastric contents.
      • Worsening abdominal pain and tenderness, indicating possible ischemia or strangulation.
      • Tachycardia (increased pulse rate), which may signal worsening sepsis or hypovolemia.
  2. Acute-on-Chronic Obstruction of the Left Colon
    • This condition often responds to repeated enemas, which help relieve the blockage by softening and removing fecal material from the colon.
    • If there is no improvement with conservative measures, surgical intervention may be required.

Operative Treatment of Intestinal Obstruction

Surgical intervention for intestinal obstruction is often required urgently, especially when there is a risk of strangulation. The goal is to perform the operation as soon as the patient’s condition is stabilized and can withstand surgery. The choice of surgical approach depends on the cause and location of the obstruction.

  1. Timing of Surgery
    • In acute obstruction, where there is a significant risk of strangulation, urgent surgical intervention is necessary to avoid complications like bowel ischemia and necrosis.
    • Surgery is performed as soon as the patient’s condition allows, prioritizing the stabilization of fluid and electrolyte imbalances.
  2. Surgical Approach
    • The specific procedure depends on the cause and location of the obstruction:
      • Herniotomy may be performed if the obstruction is due to a strangulated hernia.
      • A laparotomy is performed if the obstruction is suspected to be due to intra-abdominal causes.
    • Laparotomy Procedure:
      • The abdomen is opened, typically through a median incision centered at the umbilicus.
      • The caecum is examined first:
        • If it is distended, this suggests that the site of the obstruction is in the colon.
        • If it is not distended, the site is likely in the small intestine.
      • The distal collapsed segment is traced upwards to the dilated portion of the bowel, indicating the location of the obstruction at the junction of the collapsed and dilated segments.
  3. Operative Measures
    • Depending on the underlying cause, the following procedures may be performed:
      • Adhesiolysis: Surgical removal of adhesions causing the obstruction.
      • If the bowel is gangrenous or non-viable, it is resected (surgically removed) and the bowel continuity is restored through end-to-end anastomosis.
    • Criteria for Non-Viable Bowel:
      • The bowel appears flabby, dull, and lustreless, with a dark purple, black, or grey color.
      • Peristalsis is absent, even after stimulation.
      • There is a lack of arterial pulsation in the mesentery, and venous thrombosis may be present.
      • The bowel does not change color after administration of oxygen or local application of a warm saline pack.
  4. Post-Operative Management
    • After surgery, intravenous fluid therapy is continued to maintain hydration and electrolyte balance.
    • Nasogastric aspiration may be maintained until bowel sounds reappear or flatus is passed, indicating the return of bowel function.

Summary
Initial management of intestinal obstruction focuses on stabilizing the patient with fluid resuscitation, nasogastric decompression, and antibiotic therapy. Conservative treatment may be effective for certain types of obstruction, such as those caused by adhesions or colonic impaction, but surgical intervention is necessary if the condition does not improve or if signs of strangulation or ischemia are present.

24
Q

What are the Causes of Acute Mechanical Intestinal Obstruction

A

Intestinal obstructions can be categorized based on the location of the cause:

  1. Intraluminal Causes (Inside the Lumen)
    • Ascaris infection (Ascaris lumbricoides): A type of intestinal roundworm that can cause blockage.
    • Foreign bodies: Items ingested that obstruct the passage through the intestines.
    • Pedunculated tumors: Tumors with a stalk that can obstruct the lumen.
    • Impacted feces: Severe constipation causing hardened stool that blocks the intestine.
  2. Intramural Causes (Within the Wall)
    • Atresia: A congenital absence or closure of a normal body opening or tubular structure.
    • Anorectal anomalies: Congenital malformations affecting the rectum and anus.
    • Intussusception: A condition where a part of the intestine folds into an adjacent section.
    • Aganglionic megacolon (Hirschsprung’s disease): Absence of nerve cells in the intestinal wall, leading to a lack of bowel motility.
    • Internal constrictions due to:
      • Tumors: Growths within the intestinal wall.
      • Inflammatory lesions: Conditions such as diverticulitis, Crohn’s disease, or ileo-caecal tuberculosis.
      • Strictures at previous strangulation sites, causing narrowed sections (known as intestinal obstruction of Garre’s).
  3. Extramural Causes (Outside the Wall)
    • Strangulated hernia: The bowel is trapped in a hernia sac, leading to obstruction.
    • External constriction from adhesions or bands: Scar tissue or fibrous bands can wrap around the bowel.
    • Volvulus: Twisting of a bowel loop around itself and its mesentery, causing obstruction.
  4. Mesenteric Vascular Occlusion
    • This occurs when blood flow to a segment of the intestine is blocked, leading to ischemia and bowel necrosis.

Operative treatment of intestinal obstruction requires a prompt and tailored approach based on the cause and location of the blockage. The surgical procedure often involves laparotomy, followed by specific measures to resolve the obstruction, such as adhesiolysis or resection of a non-viable bowel segment. Understanding the various causes of obstruction aids in deciding the most appropriate surgical approach. Post-operatively, close monitoring and supportive care are essential to ensure recovery.

25
Q

What are the Factors Affecting Prognosis in Acute Intestinal Obstruction

A

The prognosis for acute intestinal obstruction depends on various factors that influence the outcome, including the timeliness of treatment, the type of obstruction, and the patient’s overall health. These factors can affect the chances of recovery, the likelihood of complications, and the mortality rate. Below is a detailed explanation of each factor:

  1. Interval Between Onset and Time of Treatment
    • Early and prompt treatment significantly improves outcomes in acute intestinal obstruction, even if strangulation is present. The quick resolution of the obstruction helps avoid serious complications.
    • Delays in treatment—either due to the patient waiting to seek medical attention or healthcare providers delaying intervention—are associated with higher mortality rates. This is because delays can lead to worsening fluid and electrolyte imbalances, as well as the development of complications such as peritonitis (inflammation of the abdominal lining) and septicemia (blood infection).
  2. Nature of the Obstruction
    • Strangulated obstructions have a poor prognosis because they can lead to early shock due to trapped blood, followed by endotoxic shock, septicemia, peritonitis, or bowel gangrene. These complications can quickly result in a rapid deterioration of the patient’s condition and potentially lead to death.
    • Closed-loop obstructions, particularly in the large intestine, also carry a high risk due to circulatory impairment, which can cause bowel perforation and peritonitis from bacterial and fecal contamination.
    • In contrast, simple occlusions without strangulation may last several days. If the obstruction is lower in the intestine, significant water and electrolyte loss may occur later, giving more time for intervention.
  3. Level of Obstruction
    • High-level obstructions (near the stomach or upper small intestine) have a worse prognosis because they cause an early and severe loss of fluids and electrolytes, due to the limited absorptive surface and frequent vomiting. This can rapidly lead to dehydration and electrolyte imbalances.
    • Low-level obstructions (near the large intestine or rectum) allow for slower fluid loss, providing a relatively better prognosis as there is more time to correct imbalances before severe complications arise.
  4. Adequacy of Pre-Operative Correction of Fluid and Electrolyte Imbalances
    • Patients whose fluid and electrolyte imbalances are properly corrected before surgery tend to have a better prognosis, as their bodies are better equipped to handle the stress of surgery.
    • Insufficient correction of fluid and electrolyte deficits, along with poor renal function before the operation, worsens outcomes due to the increased risk of perioperative complications such as cardiovascular instability and renal failure.
  5. Non-Viability of the Bowel
    • If the bowel is non-viable (dead or severely damaged), it may need to be resected (removed). This significantly increases the mortality risk because of the potential for post-operative complications, such as anastomotic leakage (leakage at the surgical connection of the bowel) and peritonitis.
    • Patients who have undergone bowel resection often have a poorer general condition before surgery, contributing to a higher risk of adverse outcomes.
  6. Cause of the Obstruction
    • Some causes of obstruction inherently carry a higher mortality rate due to their severity:
      • Mesenteric embolism or thrombosis (blockage of the blood supply to the intestines) has a high mortality rate of around 80%, as it leads to extensive bowel ischemia and necrosis.
      • Volvulus of the sigmoid colon (twisting of the bowel) has a mortality rate of approximately 30%, due to risks of bowel strangulation and ischemia.
      • On the other hand, strangulated external hernias have a low mortality rate (less than 4%), especially if treated promptly, because they can be effectively managed through surgical intervention.
  7. Pre-Existing Diseases
    • The presence of underlying health conditions such as diabetes, respiratory diseases, cardiovascular conditions, or renal impairments negatively affects prognosis. These conditions can make it harder for the body to recover from the stress of intestinal obstruction and surgery.
    • Chronic illnesses often worsen outcomes because they impair the body’s ability to heal and maintain physiological stability during and after the obstruction.
  8. Age of the Patient
    • Younger, healthy adults are more likely to tolerate the effects of intestinal obstruction and recover from surgery.
    • In contrast, elderly patients and young children are at a higher risk due to their reduced physiological reserves and weaker immune responses, making them less able to cope with the associated dehydration, electrolyte disturbances, and surgical stress.

Summary
The prognosis in acute intestinal obstruction is influenced by factors such as the timeliness of treatment, the type and location of the obstruction, and the patient’s overall health status. Early intervention, effective correction of fluid and electrolyte imbalances, and addressing non-viable bowel segments are crucial steps in improving outcomes. Understanding these factors helps guide clinical decision-making to optimize the management and treatment of patients with acute intestinal obstruction.