Surgical Aspect of Typhoid Enteritis

Typhoid enteritis is the intestinal manifestation of typhoid septicemia, an infection by the Salmonella organism. Typhoid fever, or enteric fever, is a potentially fatal multisystemic infection primarily caused by Salmonella enterica serotype typhi. Typhoid fever is a leading cause of acute abdomen, especially in developing countries.

The Salmonella bacteria enter the body through the distal ileum, adhering to the epithelium over Peyer's patches. The bacteria induce macrophages to attract more macrophages. Typhoid thrives in conditions of poor sanitation, crowding, and social chaos. The bacteria can survive a stomach pH as low as 1.5.

Antacids, histamine-2 receptor antagonists, proton pump inhibitors, gastrectomy, and achlorhydria decrease stomach acidity and facilitate S. typhi infection.

Typhoid fever is spread through:

• Oral transmission of food or beverages handled by an asymptomatic carrier who sheds the bacteria in their stool or urine
• Hand-to-mouth transmission after using a contaminated toilet
• Oral transmission via sewage-contaminated water or shellfish

The incubation period for Salmonella typhi is 10-14 days.

Typhoid fever is more common in developing countries. It thrives in conditions of poor sanitation, crowding, and social chaos.

In the pre-antibiotic era, there were 35,994 cases of typhoid in the United States reported in 1920. By 2006, there were only 314 cases in the United States. Improved sanitation and antibiotic treatment have decreased the incidence of typhoid fever in developed nations like the United States.

Globally, 80% of typhoid cases originate from Bangladesh, China, India, Indonesia, Laos, Nepal, Pakistan, or Vietnam. Typhoid fever infects about 21.6 million people per year, killing an estimated 200,000.

Intestinal perforation is one of the two most common complications of typhoid fever. Between 1884-1909, before antibiotics were available, the mortality rate associated with intestinal perforation from typhoid fever was 66%-90%.

In sub-Saharan Africa, mortality rates associated with intestinal perforation range from 10% to 30%. Almost 50% of surgical acute abdomens in one rural Nigerian hospital were attributed to typhoid perforation, and 72% of those typhoid perforation cases occurred in children. A study in Malawi found that intestinal perforations were associated with a high mortality rate.

The number of typhoid intestinal perforation cases is likely underestimated because many areas where typhoid occurs lack the capacity for microbiology and pathology testing. Data on the burden of typhoid intestinal perforation in sub-Saharan Africa is limited, but it is likely substantial in certain settings.

The occurrence of typhoid intestinal perforation may be a better indicator of underlying typhoid burden than blood culture results, especially in areas with limited culture testing capability.

Salmonella typhi and Salmonella paratyphi are the causes of typhoid/enteric fever. The bacteria enter the body through the distal ileum, adhering to the epithelium of Peyer's patches. Peyer's patches are clusters of lymphoid tissue that serve as a relay point for macrophages traveling from the gut to the lymphatic system.

S. typhi induces host macrophages to attract more macrophages, creating aggregates called typhoid nodules. Typhoid nodules are commonly found in the intestines, mesenteric lymph nodes, spleen, liver, and bone marrow, and may also be found in the kidneys, testes, and parotid glands.

The bacteria use their fimbriae, which bind to the cystic fibrosis transmembrane conductance receptor (CFTR), to enter intestinal epithelial cells. The Vi capsular antigen of S. typhi masks its pathogen-associated molecular patterns (PAMPs), preventing a neutrophil-based inflammatory response. In contrast, S. paratyphi, the most common paratyphi serovar, does not have the Vi capsular antigen, which may explain the greater infectivity of typhi isolates.

S. typhi infection leads to four classic pathologic stages in the intestines:

1. Hyperplastic changes
2. Intestinal mucosa necrosis
3. Sloughing of the mucosa
4. Development of ulcers

The ulcers can perforate into the peritoneal cavity.

Pathogenesis of Ileus in Typhoid Enteritis

Ileus, a disruption of the normal propulsive activity of the intestines, can occur as a complication of typhoid enteritis. The following factors contribute to this condition:

• Severe Enteritis: Typhoid fever, caused by Salmonella Typhi, primarily affects the lower ileum, particularly the Peyer's patches. The bacteria invade and multiply within these patches, leading to inflammation and swelling. In severe cases, this inflammation can disrupt the normal muscular contractions of the intestines, resulting in ileus.
• Sepsis: Typhoid fever can progress to sepsis, a life-threatening condition characterized by a dysregulated immune response to infection. Sepsis can cause widespread inflammation and damage to organs, including the intestines. This can disrupt intestinal motility and contribute to ileus.
• Electrolyte Imbalance: Electrolyte disturbances, such as hypokalemia (low potassium levels), are common in typhoid fever due to factors like poor oral intake, vomiting, and diarrhea. Electrolytes play a crucial role in nerve and muscle function, and imbalances can disrupt the coordinated muscle contractions required for normal intestinal peristalsis, leading to ileus.

Gaseous distention is a possible accompanying feature of ileus in typhoid enteritis. This distention likely results from the impaired intestinal motility, leading to the accumulation of gas within the bowel.

How Salmonella Typhi Escapes Gastric Acidity

• Large Inoculum: Ingestion of a substantial number of Salmonella Typhi organisms increases the likelihood of some surviving the acidic environment of the stomach.
• Volume of Food and Water: Consuming Salmonella Typhi with a considerable amount of food or water, or as part of a large meal (bolus), can dilute the gastric acid and provide a buffer, enhancing bacterial survival.
• Reduced Gastric Acidity: Individuals with hypochlorhydria (low stomach acid) or achlorhydria (absence of stomach acid), potentially due to conditions like partial or total gastrectomy or the use of anti-ulcer medications, are more susceptible to Salmonella Typhi infection as the bacteria can more easily bypass the stomach's acidic barrier.

The bacteria target the Peyer's patches in the ileum, using specialized fimbriae to attach to the epithelium. The bacteria then multiply within macrophages, eventually leading to their destruction, and enter the bloodstream.

Symptoms of ileal perforation, which usually arise in the second week of illness (can be seen in the first week in Africa), often include:

• Abdominal pain
• Signs of peritonitis
• Fever
• Abdominal distension
• Jaundice
• Rebound tenderness
• Shortness of breath
• Anorexia
• Diarrhea
• Constipation
• Vomiting
• Blood in the stool
• Headache

There is no single symptom that definitively indicates perforation. The patient is often toxic, critically ill, dehydrated, and febrile.

It is important to note that because microbiology and pathology resources are often limited in areas where typhoid is prevalent, many cases of ileal perforation may not be reported as being caused by typhoid.

Vitals

• Tachycardia: Obliteration of the Faget sign of relative bradycardia
• Tachypnea: From peritonitis, metabolic demands, anemia
• Blood Pressure: Hypotension is a common finding

Abdomen

No single sign clinches perforation. Common features include:

• Distension from a combination of fluid or fecaloid collection from the free perforation and gas

Features of Peritonitis

• Reduced movement
• Umbilical tap sign: Positive (overly sensitive)
• Generalized tenderness
• Percussion tenderness
• Percussion note varies depending on the volume of fluid
• Hepatic dullness absent in 60-80% (very useful)
• Bowel sounds absent
• Rectal: Full and tender recto-vesical pouch

Presentations of Typhoid Ileal Perforation vs Perforated Appendix

Typhoid Ileal Perforation: Fever often precedes abdominal pain. Prominent systemic symptoms like sore throat, rose spots, and potential nosebleeds may occur before abdominal pain. Free peritoneal gas is common due to free perforation.

Perforated Appendix: Abdominal pain typically precedes fever. Systemic symptoms are generally limited until perforation occurs. Free peritoneal gas is uncommon.

General Emergency Treatment

• They come with contracted intravascular volume Increased metabolic demands Oxygen debt and acidosis Strive for adequate BP and urine of 30-50mls per hour
• PASS NASOGASTRIC TUBE
• Relieves the distress of vomiting
• Prevents aspiration
• Rests the bowel - less secretion and more absorption
• Prevents respiratory embarrassment
• Eases the discomfort of distension
• ANTIBIOTICS

For higher dose note that

1. CEFTRIAZONE - (TIME DEPENDENT)
2. METRONIDAZOLE (DOSE DEPENDENT)
3. COMBINING WITH CIPROFLOXACIN MAY BE NECESSARY - FOUND TO BE SYNERGISTIC
• Analgesics - be generous with it even when unsure of diagnosis
• Will not mask signs
• May help clinical signs and diagnosis
• Patient more comfortable
• Patient more cooperative
• Signs better localized
• Aids respiration

INTRAOPERATIVE FINDINGS

LOCATION OF PERFORATION

• Antimesenteric location
• Terminal ileum
• Proximal ileum and cecum
• Colonic solely

OTHER FINDINGS

• Fecaloid or bilious collection
• Bread and butter adhesions
• Friable bowel loops
• Edematous bowel

COPIOUS LAVAGE VERY IMPORTANT

• Identify point of leakage
• Control spillage
• Suck out collection
• Run the bowel
• Tackle the perforation
• Very copious lavage
• Freshen and close in layers (omental patch)
• Wedge or sleeve resection
• Segmental resection (multiple, friable bowel)
• Limited hemicolectomy (too close to the ICJ)
• Loop ileostomy or colostomy
• Closure (plus bypass or proximal ileostomy)

Intestinal Hemorrhage

Commonly appears during the second-third week of illness. A sudden drop in temperature, rise in pulse, and signs of shock followed by dark or fresh blood in the stool.

Treatment:

Always try to avoid operating.

• Full blood count (platelet count)
• Bedside clotting and bleeding time
• PT/PTTK
• Transfuse to 30%
• Use of procoagulants (dicynone 250mg q 6-8hr)

Close monitoring. Watch out for DIC (on few occasions this may occur with higher mortality).

Paralytic Ileus

1. Ensure no perforation:
   • Tympanic percussion
   • Sound absent
   • No overt features of peritonitis
   • Check for hepatic dullness
   • X-ray for pneumoperitoneum and gas distribution
2. Start general management:
   • Suck and drip
   • Correct electrolyte imbalance
   • Treat sepsis
   • Monitor girth
3. Consider active treatment:
   • Prokinetic
   • Antiflatulent
   • Parasympathomimetic
   • Alvimopan

Common complications include:

• Burst abdomen
• Option a - Closure with tension stitches
• Option b - No evisceration, poor risk
• Treat malnutrition and sepsis
• Allow to fix (bread and butter adhesions)
• Allow to granulate and epithelialize (hernia). Treat incisional hernia later.
• Enterocutaneous fistula
• Treat fluid and electrolyte imbalance
• Correct anemia
• Treat sepsis
• Correct malnutrition
• Feed well orally
• Most will close
• Surgical site infection
• Lay the wound open
• Dress regularly
• Secondary closure

Natural History

Early signs and symptoms (first 1-3 weeks):

• Fever (high grade continuous, step ladder rise)
• Chills and rigors (uncommon)
• Rose spots
• Frontal throbbing headache
• Body aches
• Dry cough

Later signs and symptoms (enteritis, after a week):

• Abdominal pains (mild)
• Constipation or diarrhea (constipation more common)
• Vomiting (not common)

Surgical Complications

• Perforation
• Generalized pain
• Distension
• Bleeding
• Hematochezia

Neurological Complications

• Cerebral abscess
• Meningitis
• Typhoid spine

Ear Complications

• Mastoiditis
• Otitis

Heart Complications

• Pericardial effusion
• Pancarditis

Lung Complications

• Pleural effusion
• Empyema thoracis
• Lung abscess

Gallbladder Complications

• Cholelithiasis
• Cholecystitis

Kidney Complications

• Renal stone
• Pyelonephritis
• Cystitis
• Acute urinary retention

Musculoskeletal Complications

• Osteomyelitis
• Deep muscular abscess

Other Complications

• Zenker's muscle rupture