Rewrite the following exactly same without altering any words or numbering. Name : Abhishek Anand Group : 1350 1. Peptic Ulcer Disease — 10 Higher-Level MCQs 1. A patient with chronic NSAID use develops a gastric ulcer. Which mechanism most directly explains the ulcer formation? A. Increased gastrin secretion B. Increased gastric emptying C. Reduced prostaglandin-mediated mucosal protection D. Increased bicarbonate secretion Correct: C. Explanation: NSAIDs inhibit COX → ↓ prostaglandins → ↓ mucus/bicarbonate and mucosal blood flow. --- 2. A patient with recurrent ulcers and multiple distal duodenal ulcers has markedly elevated fasting gastrin. What is the most likely diagnosis? A. Menetrier disease B. Zollinger–Ellison syndrome C. Achalasia D. Crohn disease Correct: B. Explanation: Gastrinoma causes hypergastrinemia and excessive gastric acid secretion. --- 3. A patient with peptic ulcer disease suddenly develops severe generalized abdominal pain and free subdiaphragmatic air. What is the immediate priority? A. Oral PPI B. Endoscopy C. Resuscitation and urgent surgical consultation D. Colonoscopy Correct: C. Explanation: Perforation causes secondary peritonitis and requires rapid resuscitation + source control. --- 4. Which ulcer location is most strongly associated with massive upper GI hemorrhage? A. Lesser curvature B. Posterior duodenal wall C. Greater curvature D. Anterior duodenal wall Correct: B. Explanation: Posterior duodenal ulcers may erode the gastroduodenal artery. --- 5. Which finding most strongly suggests gastric outlet obstruction due to chronic peptic ulcer disease? A. Hematemesis B. Projectile vomiting of undigested food C. Melena alone D. Diarrhea Correct: B. Explanation: Pyloric/duodenal scarring causes obstruction → gastric retention and vomiting. --- 6. A patient has a gastric ulcer with weight loss and persistent vomiting. What is the most appropriate investigation? A. Abdominal X-ray only B. Colonoscopy C. Upper GI endoscopy with biopsy D. Serum amylase Correct: C. Explanation: Gastric ulcers require endoscopic assessment and biopsy to exclude malignancy. --- 7. Which finding best supports H. pylori eradication after treatment? A. Symptom improvement alone B. Repeat endoscopy in every patient C. Urea breath test after appropriate PPI withdrawal D. Serum antibody immediately after treatment Correct: C. Explanation: Urea breath test is useful for confirming eradication; antibodies may remain positive. --- 8. A patient with a perforated peptic ulcer has sudden severe epigastric pain followed by generalized rigidity. What explains the rigidity? A. Gastric spasm B. Chemical peritoneal irritation C. Intestinal hypermotility D. Pancreatic enzyme deficiency Correct: B. Explanation: Leakage of gastric/duodenal contents produces chemical peritonitis → reflex muscle guarding. --- 9. Which combination most strongly suggests Zollinger–Ellison syndrome? A. Single gastric ulcer + low gastrin B. Multiple/recurrent ulcers + high gastrin + high acid output C. Gastric ulcer + achlorhydria D. Duodenal ulcer + low acid secretion Correct: B. Explanation: Gastrinoma causes marked acid hypersecretion and recurrent/multiple ulcers. --- 10. A patient with a bleeding peptic ulcer becomes hypotensive despite endoscopic therapy. What is the next appropriate step? A. Continue oral PPI only B. Urgent angiographic embolization or surgery C. Colonoscopy D. Discharge after observation Correct: B. Explanation: Persistent/recurrent major bleeding requires definitive hemostasis by embolization or surgery. --- 2. Small Bowel Obstruction — Theoretical Questions Q1. Define small bowel obstruction and describe its major causes. Small bowel obstruction is a mechanical or functional interruption of intestinal passage. Common causes are postoperative adhesions, hernias, tumors and Crohn disease. Adhesions are the most common cause in patients with previous abdominal surgery. Closed-loop obstruction can rapidly cause ischemia and necrosis. Complete obstruction usually causes vomiting, distension, pain and obstipation. Early diagnosis is important to prevent strangulation and perforation. --- Q2. Describe the pathophysiology and complications of small bowel obstruction. Proximal to the obstruction, intestinal contents, fluid and gas accumulate. This causes bowel dilatation and increased intraluminal pressure. Venous congestion develops first, followed by arterial compromise and ischemia. Progressive ischemia can cause necrosis, perforation and peritonitis. Vomiting and third-spacing produce dehydration and electrolyte abnormalities. Severe cases may progress to sepsis, shock and multiorgan failure. --- Q3. Describe the management of small bowel obstruction. Initial management includes NPO, IV fluids, electrolyte correction and nasogastric decompression. Analgesia and antiemetics are given, with close clinical monitoring. CT abdomen with contrast helps identify the level, cause and signs of ischemia. Stable partial adhesive obstruction may initially be managed conservatively. Strangulation, ischemia, perforation, peritonitis or failed conservative treatment requires surgery. Surgical treatment involves adhesiolysis, hernia repair or resection of nonviable bowel as required. --- 3. Clinical Case — Peritonitis Clinical Case Presentation 1. Patient Identification Patient: 24-year-old male Occupation: Student Sex: Male Presentation: Emergency department 2. Chief Complaints Severe abdominal pain — 24 hours Vomiting — 12 hours Fever — 12 hours Abdominal distension — 8 hours 3. History of Present Illness Pain initially started around the umbilicus and migrated to the right lower quadrant. Pain subsequently became generalized and severe. Associated fever, anorexia, nausea and vomiting. Patient reports increasing abdominal rigidity and difficulty walking because of pain. No previous similar episode. 4. Past Medical & Surgical History No significant medical illness. No previous abdominal surgery. No history of peptic ulcer disease. 5. Personal History No smoking or alcohol abuse. Normal bowel and urinary habits before the current illness. No recent abdominal trauma. 6. Family History No significant family history of gastrointestinal disease. 7. General Examination Conscious but toxic-looking. Temperature: 39°C Pulse: 118/min BP: 100/65 mmHg Respiratory rate: 24/min Mild dehydration present. 8. Abdominal Examination Abdomen distended. Diffuse severe tenderness. Marked guarding and rigidity. Rebound tenderness present. Bowel sounds markedly reduced. McBurney point tenderness positive. 9. Systemic Examination Cardiovascular: tachycardia. Respiratory: tachypnea; basal air entry preserved. CNS: conscious and oriented. No other major abnormality. 10. Laboratory Investigations WBC: 18,500/µL Neutrophils: 90% CRP: markedly elevated. Hemoglobin: 13.2 g/dL Serum lactate: 3.2 mmol/L Electrolytes: mild dehydration-related abnormalities. Renal function: mildly impaired due to dehydration. 11. Imaging Investigations Ultrasound: Enlarged, non-compressible appendix. Periappendiceal fluid. CT abdomen: Inflamed appendix with appendicolith. Appendiceal wall discontinuity. Periappendiceal collection and free intraperitoneal fluid. Findings consistent with perforation and generalized peritonitis. 12. Differential Diagnosis Perforated acute appendicitis Perforated peptic ulcer Acute cholecystitis with perforation Perforated diverticulitis Intestinal perforation Mesenteric ischemia 13. Clinical Scoring — Alvarado Score Finding Score Migration of pain 1 Anorexia 1 Nausea/vomiting 1 RLQ tenderness 2 Rebound tenderness 1 Fever 1 Leukocytosis 2 Neutrophilia 1 Total 10/10 Interpretation: Very high probability of acute appendicitis. 14. Provisional Diagnosis Perforated acute appendicitis with generalized peritonitis. 15. Final Diagnosis Perforated gangrenous acute appendicitis causing secondary generalized bacterial peritonitis with early sepsis. 16. Treatment / Management Immediate NPO. Two large-bore IV lines. Rapid IV crystalloid resuscitation. IV broad-spectrum antibiotics covering Gram-negative and anaerobic organisms. Analgesia and antiemetics. Urinary catheter and strict fluid balance. Monitor BP, urine output, lactate and vital signs. Urgent surgical source control. 17. Surgical Management Emergency exploratory laparoscopy/laparotomy depending on clinical stability and surgical expertise. Appendectomy with removal of perforated appendix. Peritoneal lavage/source control. Drain placement if clinically indicated. Drainage of any localized abscess. Peritoneal fluid obtained for culture when appropriate. 18. Postoperative Management Continue IV antibiotics according to severity and source control. IV fluids and electrolyte correction. Analgesia and antiemetics. Early mobilization and gradual return to oral diet. Monitor wound, drain output, temperature, WBC and renal function. Monitor for postoperative sepsis or intra-abdominal collection. 19. Complications Sepsis/septic shock Intra-abdominal abscess Wound infection Paralytic ileus Adhesive intestinal obstruction Anastomotic/bowel injury if bowel resection is required Multiorgan dysfunction in severe infection 20. Prognosis Good with early antibiotic therapy and adequate surgical source control. Prognosis worsens with delayed treatment, established sepsis, extensive contamination or organ dysfunction.
Peptic ulcer disease small bowel obstruction peritonitis clinical education overview
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Peptic Ulcer Disease — 10 Higher-Level MCQs
-
A patient with chronic NSAID use develops a gastric ulcer. Which mechanism most directly explains the ulcer formation?
- A patient with recurrent ulcers and multiple distal duodenal ulcers has markedly elevated fasting gastrin. What is the most likely diagnosis?
- A patient with peptic ulcer disease suddenly develops severe generalized abdominal pain and free subdiaphragmatic air. What is the immediate priority?
- Which ulcer location is most strongly associated with massive upper GI hemorrhage?
- Which finding most strongly suggests gastric outlet obstruction due to chronic peptic ulcer disease?
- A patient has a gastric ulcer with weight loss and persistent vomiting. What is the most appropriate investigation?
- Which finding best supports H. pylori eradication after treatment?
- A patient with a perforated peptic ulcer has sudden severe epigastric pain followed by generalized rigidity. What explains the rigidity?
- Which combination most strongly suggests Zollinger–Ellison syndrome?
- A patient with a bleeding peptic ulcer becomes hypotensive despite endoscopic therapy. What is the next appropriate step?
- Small Bowel Obstruction — Theoretical Questions
- Clinical Case — Peritonitis
- Patient Identification
- Chief Complaints
- History of Present Illness
- Past Medical & Surgical History
- Personal History
- Family History
- General Examination
- Abdominal Examination
- Systemic Examination
- Laboratory Investigations
- Imaging Investigations
- Differential Diagnosis
- Clinical Scoring — Alvarado Score
- Provisional Diagnosis
- Final Diagnosis
- Treatment / Management
- Surgical Management
- Postoperative Management
- Complications
- Prognosis
Rewrite the following article exactly same without altering any words or numbering. Name : Abhishek Anand Group : 1350 A . Peptic Ulcer Disease — 10 MCQs 1. A patient with chronic NSAID use develops a gastric ulcer. Which mechanism most directly explains the ulcer formation? A. Increased gastrin secretion B. Increased gastric emptying C. Reduced prostaglandin-mediated mucosal protection D. Increased bicarbonate secretion Correct: C. Explanation: NSAIDs inhibit COX → ↓ prostaglandins → ↓ mucus/bicarbonate and mucosal blood flow. --- 2. A patient with recurrent ulcers and multiple distal duodenal ulcers has markedly elevated fasting gastrin. What is the most likely diagnosis? A. Menetrier disease B. Zollinger–Ellison syndrome C. Achalasia D. Crohn disease Correct: B. Explanation: Gastrinoma causes hypergastrinemia and excessive gastric acid secretion. --- 3. A patient with peptic ulcer disease suddenly develops severe generalized abdominal pain and free subdiaphragmatic air. What is the immediate priority? A. Oral PPI B. Endoscopy C. Resuscitation and urgent surgical consultation D. Colonoscopy Correct: C. Explanation: Perforation causes secondary peritonitis and requires rapid resuscitation + source control. --- 4. Which ulcer location is most strongly associated with massive upper GI hemorrhage? A. Lesser curvature B. Posterior duodenal wall C. Greater curvature D. Anterior duodenal wall Correct: B. Explanation: Posterior duodenal ulcers may erode the gastroduodenal artery. --- 5. Which finding most strongly suggests gastric outlet obstruction due to chronic peptic ulcer disease? A. Hematemesis B. Projectile vomiting of undigested food C. Melena alone D. Diarrhea Correct: B. Explanation: Pyloric/duodenal scarring causes obstruction → gastric retention and vomiting. --- 6. A patient has a gastric ulcer with weight loss and persistent vomiting. What is the most appropriate investigation? A. Abdominal X-ray only B. Colonoscopy C. Upper GI endoscopy with biopsy D. Serum amylase Correct: C. Explanation: Gastric ulcers require endoscopic assessment and biopsy to exclude malignancy. --- 7. Which finding best supports H. pylori eradication after treatment? A. Symptom improvement alone B. Repeat endoscopy in every patient C. Urea breath test after appropriate PPI withdrawal D. Serum antibody immediately after treatment Correct: C. Explanation: Urea breath test is useful for confirming eradication; antibodies may remain positive. --- 8. A patient with a perforated peptic ulcer has sudden severe epigastric pain followed by generalized rigidity. What explains the rigidity? A. Gastric spasm B. Chemical peritoneal irritation C. Intestinal hypermotility D. Pancreatic enzyme deficiency Correct: B. Explanation: Leakage of gastric/duodenal contents produces chemical peritonitis → reflex muscle guarding. --- 9. Which combination most strongly suggests Zollinger–Ellison syndrome? A. Single gastric ulcer + low gastrin B. Multiple/recurrent ulcers + high gastrin + high acid output C. Gastric ulcer + achlorhydria D. Duodenal ulcer + low acid secretion Correct: B. Explanation: Gastrinoma causes marked acid hypersecretion and recurrent/multiple ulcers. --- 10. A patient with a bleeding peptic ulcer becomes hypotensive despite endoscopic therapy. What is the next appropriate step? A. Continue oral PPI only B. Urgent angiographic embolization or surgery C. Colonoscopy D. Discharge after observation Correct: B. Explanation: Persistent/recurrent major bleeding requires definitive hemostasis by embolization or surgery. --- B. Small Bowel Obstruction — (Theoretical Questions) Q1. Define small bowel obstruction and describe its major causes. Small bowel obstruction is a mechanical or functional interruption of intestinal passage. Common causes are postoperative adhesions, hernias, tumors and Crohn disease. Adhesions are the most common cause in patients with previous abdominal surgery. Closed-loop obstruction can rapidly cause ischemia and necrosis. Complete obstruction usually causes vomiting, distension, pain and obstipation. Early diagnosis is important to prevent strangulation and perforation. --- Q2. Describe the pathophysiology and complications of small bowel obstruction. Proximal to the obstruction, intestinal contents, fluid and gas accumulate. This causes bowel dilatation and increased intraluminal pressure. Venous congestion develops first, followed by arterial compromise and ischemia. Progressive ischemia can cause necrosis, perforation and peritonitis. Vomiting and third-spacing produce dehydration and electrolyte abnormalities. Severe cases may progress to sepsis, shock and multiorgan failure. --- Q3. Describe the management of small bowel obstruction. Initial management includes NPO, IV fluids, electrolyte correction and nasogastric decompression. Analgesia and antiemetics are given, with close clinical monitoring. CT abdomen with contrast helps identify the level, cause and signs of ischemia. Stable partial adhesive obstruction may initially be managed conservatively. Strangulation, ischemia, perforation, peritonitis or failed conservative treatment requires surgery. Surgical treatment involves adhesiolysis, hernia repair or resection of nonviable bowel as required. --- C. Clinical Case — Peritonitis Clinical Case Presentation 1. Patient Identification Patient: 24-year-old male Occupation: Student Sex: Male Presentation: Emergency department 2. Chief Complaints Severe abdominal pain — 24 hours Vomiting — 12 hours Fever — 12 hours Abdominal distension — 8 hours 3. History of Present Illness Pain initially started around the umbilicus and migrated to the right lower quadrant. Pain subsequently became generalized and severe. Associated fever, anorexia, nausea and vomiting. Patient reports increasing abdominal rigidity and difficulty walking because of pain. No previous similar episode. 4. Past Medical & Surgical History No significant medical illness. No previous abdominal surgery. No history of peptic ulcer disease. 5. Personal History No smoking or alcohol abuse. Normal bowel and urinary habits before the current illness. No recent abdominal trauma. 6. Family History No significant family history of gastrointestinal disease. 7. General Examination Conscious but toxic-looking. Temperature: 39°C Pulse: 118/min BP: 100/65 mmHg Respiratory rate: 24/min Mild dehydration present. 8. Abdominal Examination Abdomen distended. Diffuse severe tenderness. Marked guarding and rigidity. Rebound tenderness present. Bowel sounds markedly reduced. McBurney point tenderness positive. 9. Systemic Examination Cardiovascular: tachycardia. Respiratory: tachypnea; basal air entry preserved. CNS: conscious and oriented. No other major abnormality. 10. Laboratory Investigations WBC: 18,500/µL Neutrophils: 90% CRP: markedly elevated. Hemoglobin: 13.2 g/dL Serum lactate: 3.2 mmol/L Electrolytes: mild dehydration-related abnormalities. Renal function: mildly impaired due to dehydration. 11. Imaging Investigations Ultrasound: Enlarged, non-compressible appendix. Periappendiceal fluid. CT abdomen: Inflamed appendix with appendicolith. Appendiceal wall discontinuity. Periappendiceal collection and free intraperitoneal fluid. Findings consistent with perforation and generalized peritonitis. 12. Differential Diagnosis Perforated acute appendicitis Perforated peptic ulcer Acute cholecystitis with perforation Perforated diverticulitis Intestinal perforation Mesenteric ischemia 13. Clinical Scoring — Alvarado Score Finding Score Migration of pain 1 Anorexia 1 Nausea/vomiting 1 RLQ tenderness 2 Rebound tenderness 1 Fever 1 Leukocytosis 2 Neutrophilia 1 Total 10/10 Interpretation: Very high probability of acute appendicitis. 14. Provisional Diagnosis Perforated acute appendicitis with generalized peritonitis. 15. Final Diagnosis Perforated gangrenous acute appendicitis causing secondary generalized bacterial peritonitis with early sepsis. 16. Treatment / Management Immediate NPO. Two large-bore IV lines. Rapid IV crystalloid resuscitation. IV broad-spectrum antibiotics covering Gram-negative and anaerobic organisms. Analgesia and antiemetics. Urinary catheter and strict fluid balance. Monitor BP, urine output, lactate and vital signs. Urgent surgical source control. 17. Surgical Management Emergency exploratory laparoscopy/laparotomy depending on clinical stability and surgical expertise. Appendectomy with removal of perforated appendix. Peritoneal lavage/source control. Drain placement if clinically indicated. Drainage of any localized abscess. Peritoneal fluid obtained for culture when appropriate. 18. Postoperative Management Continue IV antibiotics according to severity and source control. IV fluids and electrolyte correction. Analgesia and antiemetics. Early mobilization and gradual return to oral diet. Monitor wound, drain output, temperature, WBC and renal function. Monitor for postoperative sepsis or intra-abdominal collection. 19. Complications Sepsis/septic shock Intra-abdominal abscess Wound infection Paralytic ileus Adhesive intestinal obstruction Anastomotic/bowel injury if bowel resection is required Multiorgan dysfunction in severe infection 20. Prognosis Good with early antibiotic therapy and adequate surgical source control. Prognosis worsens with delayed treatment, established sepsis, extensive contamination or organ dysfunction.
- A patient with chronic NSAID use develops a gastric ulcer. Which mechanism most directly explains the ulcer formation?
- A patient with recurrent ulcers and multiple distal duodenal ulcers has markedly elevated fasting gastrin. What is the most likely diagnosis?
- A patient with peptic ulcer disease suddenly develops severe generalized abdominal pain and free subdiaphragmatic air. What is the immediate priority?
- Which ulcer location is most strongly associated with massive upper GI hemorrhage?
- Which finding most strongly suggests gastric outlet obstruction due to chronic peptic ulcer disease?
- A patient has a gastric ulcer with weight loss and persistent vomiting. What is the most appropriate investigation?
- Which finding best supports H. pylori eradication after treatment?
- A patient with a perforated peptic ulcer has sudden severe epigastric pain followed by generalized rigidity. What explains the rigidity?
- Which combination most strongly suggests Zollinger–Ellison syndrome?
- A patient with a bleeding peptic ulcer becomes hypotensive despite endoscopic therapy. What is the next appropriate step?
- Patient Identification
- Chief Complaints
- History of Present Illness
- Past Medical & Surgical History
- Personal History
- Family History
- General Examination
- Abdominal Examination
- Systemic Examination
- Laboratory Investigations
- Imaging Investigations
- Differential Diagnosis
- Clinical Scoring — Alvarado Score
- Provisional Diagnosis
- Final Diagnosis
- Treatment / Management
- Surgical Management
- Postoperative Management
- Complications
- Prognosis
Make a clinical case presentation on peritonitis
WSES guidelines 2024 intra-abdominal infections peritonitis source control antibiotics
peritonitis AND source control
Clinical Case Presentation: Secondary Generalized Peritonitis
1. Patient Identification
Occupation: Student
Sex: Male
Place of presentation: Emergency Department
2. Chief Complaints
- Severe abdominal pain for 24 hours
- Vomiting for 12 hours
- Fever for 12 hours
- Abdominal distension for 8 hours
3. History of Present Illness
4. Past Medical and Surgical History
- No history of diabetes mellitus, hypertension, tuberculosis, or chronic liver disease.
- No previous abdominal surgery.
- No known history of peptic ulcer disease.
- No known drug allergies.
5. Personal History
- No history of smoking or alcohol abuse.
- No recent abdominal trauma.
- Bowel and bladder habits were normal before onset of the present illness.
- Appetite has been reduced since the onset of pain.
6. Family History
7. General Examination
- Patient is conscious, oriented, and toxic-looking.
- Temperature: 39°C
- Pulse: 118/min, thready
- Blood pressure: 100/65 mmHg
- Respiratory rate: 24/min
- Oxygen saturation: 97% on room air
- Mild dehydration present.
- No pallor, icterus, cyanosis, clubbing, lymphadenopathy, or pedal edema.
8. Abdominal Examination
- Abdomen is moderately distended.
- Umbilicus is central.
- No visible scars, sinuses, dilated veins, or obvious hernia.
- Abdominal movements are markedly reduced with respiration.
- Diffuse severe abdominal tenderness is present.
- Maximum tenderness is present in the right iliac fossa.
- Marked guarding and board-like rigidity are present.
- Rebound tenderness is positive.
- McBurney point tenderness is positive.
- Diffuse abdominal tenderness is elicited on percussion.
- Liver dullness may be reduced if free intraperitoneal air is present.
- Bowel sounds are markedly reduced or absent.
9. Systemic Examination
10. Laboratory Investigations
| Investigation | Result |
|---|---|
| Hemoglobin | 13.2 g/dL |
| Total leukocyte count | 18,500/µL |
| Neutrophils | 90% |
| C-reactive protein | Markedly elevated |
| Serum lactate | 3.2 mmol/L |
| Serum creatinine | Mildly elevated |
| Serum electrolytes | Mild dehydration-related abnormalities |
| Blood culture | Sent before antibiotics, if this does not delay treatment |
| Urinalysis | No significant abnormality |
11. Imaging Investigations
- Enlarged, non-compressible appendix.
- Periappendiceal fluid collection.
- Free intraperitoneal fluid.
- Dilated inflamed appendix with appendicolith.
- Appendiceal wall discontinuity.
- Periappendiceal collection.
- Free intraperitoneal fluid and inflammatory changes in the peritoneum.
- Findings suggestive of perforated acute appendicitis with generalized peritonitis.
12. Differential Diagnosis
- Perforated acute appendicitis with generalized peritonitis
- Perforated peptic ulcer
- Perforated diverticulitis
- Perforated hollow viscus due to typhoid ileal perforation
- Acute cholecystitis with perforation
- Acute pancreatitis with peritonitis
- Mesenteric ischemia with bowel perforation
13. Clinical Scoring: Alvarado Score
| Finding | Score |
|---|---|
| Migration of pain | 1 |
| Anorexia | 1 |
| Nausea/vomiting | 1 |
| Right lower quadrant tenderness | 2 |
| Rebound tenderness | 1 |
| Fever | 1 |
| Leukocytosis | 2 |
| Neutrophilia | 1 |
| Total | 10/10 |
14. Provisional Diagnosis
15. Final Diagnosis
16. Initial Management
- Keep the patient nil per oral.
- Establish two large-bore intravenous lines.
- Begin rapid intravenous crystalloid resuscitation.
- Monitor pulse, blood pressure, respiratory rate, temperature, oxygen saturation, urine output, and serum lactate.
- Insert a urinary catheter for strict input-output monitoring.
- Insert a nasogastric tube if there is persistent vomiting, ileus, or significant abdominal distension.
- Administer analgesics and antiemetics.
- Start empiric intravenous broad-spectrum antibiotics with Gram-negative and anaerobic coverage, according to local antimicrobial policy.
- Obtain blood and peritoneal cultures when possible, without delaying treatment.
- Arrange urgent surgical consultation and source control.
17. Surgical Management
- Emergency exploratory laparoscopy or laparotomy, depending on hemodynamic stability, extent of contamination, and available surgical expertise.
- Identification of the perforated appendix.
- Appendectomy.
- Removal of contaminated fluid, pus, and fibrinous material.
- Thorough peritoneal lavage.
- Drainage of any localized abscess or collection, if present.
- Placement of a drain only when clinically indicated.
- Send peritoneal fluid for culture and sensitivity when appropriate.
18. Postoperative Management
- Continue intravenous antibiotics based on clinical severity, source control, and culture results.
- Continue intravenous fluids and correct electrolyte abnormalities.
- Maintain analgesia and antiemetic therapy.
- Monitor temperature, pulse, blood pressure, urine output, total leukocyte count, CRP, lactate, renal function, wound condition, and drain output.
- Encourage early mobilization and deep-breathing exercises.
- Gradually resume oral intake after return of bowel function and clinical improvement.
- Monitor for residual intra-abdominal collection, wound infection, ileus, or sepsis.
19. Possible Complications
- Septic shock
- Intra-abdominal abscess
- Wound infection
- Paralytic ileus
- Adhesive intestinal obstruction
- Fecal fistula
- Acute kidney injury
- Respiratory complications
- Multiorgan dysfunction syndrome
- Death in severe untreated infection