Acute Abdominal Emergencies — Part 4: Perforated Peptic Ulcer, Mesenteric Ischemia, Vascular Emergencies & Special Populations
Comprehensive guide to perforated peptic ulcer with Boey score, mesenteric ischemia types and management, ruptured AAA emergency management, ectopic pregnancy evaluation and treatment, and special populations including pediatric, elderly, immunocompromised, and pregnant patients.
9. Perforated Peptic Ulcer
9.1 Overview
Perforated peptic ulcer (PPU) remains a life-threatening surgical emergency, representing the second most common complication of peptic ulcer disease (after bleeding). Despite the widespread use of proton pump inhibitors and Helicobacter pylori eradication, PPU continues to affect approximately 2 to 10 per 100,000 population annually. Mortality ranges from 5% to 25%, increasing significantly with delayed presentation, advanced age, and comorbidities.1
Risk Factors:
- NSAID use (strongest modifiable risk factor; relative risk 3–5x)
- Helicobacter pylori infection
- Smoking
- Corticosteroid use (especially in combination with NSAIDs)
- Advanced age
- Prior peptic ulcer history
- Severe physiologic stress (ICU patients — stress ulceration)
- Crack cocaine use
9.2 Diagnosis
Clinical Presentation
The classic presentation is sudden-onset, severe epigastric pain that rapidly becomes generalized, progressing through three phases:
| Phase | Timing | Features |
|---|---|---|
| Chemical peritonitis | 0–2 hours | Sudden, severe, “knife-like” epigastric pain; chemical irritation from gastric acid/bile. Board-like rigidity; patient lies still. Shoulder pain (diaphragmatic irritation) |
| Intermediate | 2–12 hours | Pain may transiently improve (dilution of gastric contents by peritoneal fluid). The “treacherous period” — patient may appear to improve. Abdominal pain becomes diffuse |
| Bacterial peritonitis | >12 hours | Secondary bacterial contamination; fever, tachycardia, sepsis. Diffuse peritonitis; hemodynamic deterioration. If presentation occurs in this phase, mortality is significantly higher |
CT Abdomen/Pelvis
CT is the diagnostic study of choice with sensitivity >95% for detecting perforation.1
CT Findings:
| Finding | Description |
|---|---|
| Pneumoperitoneum | Free intraperitoneal air — most specific finding. May be small and localized near the perforation site or large and diffuse. Best detected on lung windows. Even small amounts of free air (detected on CT but not visible on plain films) are significant |
| Periduodenal/perigastric fluid | Fluid tracking along the duodenum or stomach near the site of perforation |
| Discontinuity of bowel wall | Direct visualization of the perforation site (not always identified) |
| Fat stranding | Inflammatory changes around the perforation |
| Free fluid | Intraperitoneal fluid, particularly in the Morrison pouch, paracolic gutters, and pelvis |
Upright Chest X-ray:
- Free air under the diaphragm (pneumoperitoneum) is visible in approximately 75–85% of PPU cases
- Left lateral decubitus film may detect smaller amounts of free air
- Normal plain films do NOT exclude perforation — CT is required when clinical suspicion is present
9.3 Risk Stratification — Boey Score
The Boey score is a simple, validated preoperative scoring system for predicting mortality after surgical repair of PPU.1 2
| Variable | Criteria | Points |
|---|---|---|
| Concurrent major medical illness | Significant comorbidities (ASA ≥3) | 1 |
| Preoperative shock | Systolic BP <90 mmHg on admission | 1 |
| Duration of perforation | >24 hours from symptom onset to surgery | 1 |
| Total | 3 |
Interpretation:
| Boey Score | Predicted Mortality |
|---|---|
| 0 | 1–2% |
| 1 | 10–15% |
| 2 | 30–45% |
| 3 | >50% |
9.4 Management
Preoperative Resuscitation
- IV fluid resuscitation with crystalloid (LR or NS)
- NPO, nasogastric tube to continuous suction (decompress stomach, reduce ongoing peritoneal contamination)
- IV proton pump inhibitor: Pantoprazole 80 mg IV bolus, then 8 mg/hour continuous infusion (or esomeprazole equivalent)
- Broad-spectrum antibiotics: Cover gram-negative and anaerobic organisms (piperacillin-tazobactam 4.5g IV, or ceftriaxone 2g IV + metronidazole 500mg IV)
- Foley catheter, arterial line, central venous access as indicated by hemodynamic status
- Blood products as needed for resuscitation
Surgical Repair
| Approach | Technique | Indication |
|---|---|---|
| Omental patch repair (Graham patch) | Closure of the perforation with an omental (tongue) flap sutured over the defect. Does NOT require formal ulcer excision for duodenal perforations | Standard of care for most PPU. Laparoscopic approach is preferred when expertise is available (faster recovery, less pain, shorter hospital stay). Open approach for hemodynamically unstable patients or when laparoscopic repair is not feasible |
| Primary closure with omental reinforcement | Simple suture closure of the perforation + omental patch | Small perforations (<1 cm) without significant tissue loss |
| Ulcer excision | Excision of the ulcer followed by primary closure | Required for gastric perforations to exclude malignancy (all gastric ulcer tissue should be sent for histopathology). Not required for duodenal perforations |
| Definitive ulcer surgery | Truncal vagotomy with pyloroplasty, or highly selective vagotomy | Rarely performed in the acute setting in the modern era. May be considered for chronic, refractory duodenal ulcer disease in the rare patient failing maximum medical therapy |
| Damage control | Temporary closure, omental packing, planned re-exploration | Severely ill, hemodynamically unstable patients with lethal triad (hypothermia, acidosis, coagulopathy) |
Non-Operative Management (Conservative/Taylor Method)
Non-operative management may be considered in highly selected patients in whom:1
- Symptoms have been present for >24 hours AND the patient is clinically stable
- CT demonstrates a sealed or contained perforation (no free leak on water-soluble contrast study)
- No signs of sepsis or generalized peritonitis
- Patient can be closely monitored with serial examinations
Conservative management protocol:
- NPO, NGT suction, IV PPI, IV antibiotics
- Serial clinical examinations every 4–6 hours
- Repeat imaging if any clinical deterioration
- If no improvement within 12–24 hours, proceed to surgery
Failure rate: 10–30%; non-operative management should only be considered when surgical backup is immediately available.
Postoperative Care
- Continue IV PPI therapy (transition to oral PPI when tolerating diet)
- Test for H. pylori and treat if positive (triple or quadruple therapy)
- Discontinue NSAIDs permanently if possible; if NSAIDs are essential, use the lowest effective dose with PPI co-therapy and consider switching to a COX-2 selective inhibitor
- Follow-up endoscopy at 6–8 weeks for gastric ulcers to confirm healing and exclude malignancy
10. Acute Mesenteric Ischemia
10.1 Overview
Acute mesenteric ischemia (AMI) is a life-threatening vascular emergency with mortality rates of 50% to 80%, primarily because of delayed diagnosis. AMI results from sudden reduction in blood flow to the intestines, leading to bowel ischemia, infarction, and necrosis. The classic teaching — “pain out of proportion to physical examination” — remains one of the most important clinical clues, particularly in the early stages.3 4
10.2 Types of Acute Mesenteric Ischemia
| Type | Frequency | Etiology | Key Features |
|---|---|---|---|
| Arterial embolism (SMA embolism) | 40–50% | Embolus to the superior mesenteric artery (SMA), usually originating from the heart (atrial fibrillation, recent MI, valvular disease, endocarditis) | Sudden onset, severe abdominal pain. Often occurs 15–30 cm distal to the SMA origin (past the first jejunal branches), potentially sparing the proximal jejunum. History of atrial fibrillation or recent cardiac event. Rapid bowel necrosis if untreated |
| Arterial thrombosis (SMA thrombosis) | 20–30% | Thrombotic occlusion of a chronically diseased (atherosclerotic) SMA at its origin | May have antecedent history of chronic mesenteric ischemia (“intestinal angina”): postprandial pain, food fear, weight loss. More extensive bowel involvement (from jejunum to mid-transverse colon). Collateral circulation may provide some protection initially |
| Mesenteric venous thrombosis (MVT) | 5–15% | Thrombosis of the superior mesenteric vein (SMV) or portal vein | More indolent onset (days to weeks). Risk factors: hypercoagulable states, portal hypertension, cirrhosis, malignancy, pancreatitis, recent abdominal surgery, OCP use. Younger patients. Better prognosis than arterial forms if diagnosed early |
| Non-occlusive mesenteric ischemia (NOMI) | 15–25% | Low-flow state causing mesenteric vasospasm without vessel occlusion | Critically ill patients: cardiogenic shock, sepsis, post-cardiac surgery, hemodialysis, vasopressor use (especially high-dose norepinephrine or vasopressin). Often in ICU patients. Diagnosis of exclusion — CTA shows patent vessels with diffuse mesenteric vasoconstriction. High mortality (~70%) |
10.3 Diagnosis
Clinical Presentation
| Finding | Description |
|---|---|
| “Pain out of proportion” | Severe abdominal pain with a relatively benign abdominal exam in early stages — the hallmark of AMI. As ischemia progresses, peritoneal signs develop |
| Rapid symptom onset | Sudden onset in arterial embolism; may be more gradual in venous thrombosis |
| GI symptoms | Nausea, vomiting, diarrhea (often bloody/melanotic — hematochezia is a late finding indicating mucosal sloughing) |
| Peritoneal signs | Indicate transmural ischemia/infarction — a LATE finding suggesting non-viable bowel |
| Hemodynamic deterioration | Tachycardia, hypotension, sepsis — late findings |
Laboratory Findings
| Test | Finding | Significance |
|---|---|---|
| Lactate | Elevated (>2 mmol/L) | Sensitivity ~86% but specificity limited (~44%). Normal lactate does NOT exclude early mesenteric ischemia. Markedly elevated lactate (>4 mmol/L) with clinical suspicion for AMI strongly suggests bowel ischemia |
| WBC | Leukocytosis (often >15,000/mcL) | Nonspecific but commonly present |
| Metabolic acidosis | Elevated anion gap, decreased bicarbonate | Indicates tissue ischemia/necrosis |
| D-dimer | Elevated | High sensitivity (~96%) but very low specificity. A normal D-dimer has significant negative predictive value for AMI |
| LDH, CPK | Elevated | Markers of tissue necrosis — late findings |
| Amylase | May be elevated | Nonspecific; may confuse with pancreatitis |
Critical point: There is NO reliable serum biomarker that can definitively diagnose or exclude mesenteric ischemia. The diagnosis is fundamentally a clinical and imaging diagnosis. Do not wait for laboratory confirmation to pursue imaging if clinical suspicion is present.
CT Angiography (CTA)
CTA of the abdomen and pelvis (with arterial and portal venous phase) is the imaging study of choice for suspected AMI.3 4
| Parameter | Value |
|---|---|
| Sensitivity | 93–100% |
| Specificity | 94–100% |
CTA Findings:
| Finding | Significance |
|---|---|
| Arterial occlusion (filling defect in SMA) | SMA embolism or thrombosis — location and extent of occlusion guide management |
| Venous thrombosis (filling defect in SMV/portal vein) | Mesenteric venous thrombosis — seen on portal venous phase |
| Bowel wall thickening | Edema from venous congestion or ischemia |
| Absent bowel wall enhancement | Non-enhancing bowel wall on IV contrast = ischemic/non-viable bowel |
| Bowel wall thinning (“paper-thin” wall) | Arterial ischemia — thinned, non-enhancing wall indicates infarction |
| Pneumatosis intestinalis | Gas within the bowel wall — indicates bowel wall necrosis |
| Portal venous gas / mesenteric venous gas | Gas in the portal venous system — ominous sign of advanced ischemia/necrosis |
| Mesenteric fat stranding / free fluid | Inflammatory response to ischemic bowel |
| “Target sign” | Alternating layers of enhancement and edema in the bowel wall — subacute ischemia |
| Diffuse mesenteric vasoconstriction | Patent but narrowed mesenteric vessels — suggests NOMI |
10.4 Management
Immediate Resuscitation
- Aggressive IV fluid resuscitation — patients are often profoundly hypovolemic due to third-spacing
- Broad-spectrum antibiotics — prophylaxis against bacterial translocation from ischemic bowel (piperacillin-tazobactam or carbapenem)
- Systemic anticoagulation with heparin — initiated as soon as AMI is suspected (unless actively hemorrhaging), unfractionated heparin bolus 80 U/kg then 18 U/kg/hour
- Nasogastric tube decompression
- Correct metabolic acidosis, electrolyte abnormalities
- Optimize cardiac output — avoid/minimize vasopressors if possible (worsen mesenteric vasoconstriction); if vasopressors are needed, dobutamine or milrinone may be preferred over norepinephrine for the inotropic component
Type-Specific Management
| Type | Primary Treatment | Additional Considerations |
|---|---|---|
| SMA embolism | Surgical embolectomy (open SMA embolectomy via laparotomy) is the traditional standard. Endovascular therapy (aspiration thrombectomy, catheter-directed thrombolysis) is increasingly used for proximal SMA emboli when bowel viability is not in question and peritoneal signs are absent. After revascularization: assess bowel viability; resect non-viable bowel; “second-look” laparotomy at 24–48 hours | If peritoneal signs or CT evidence of bowel necrosis: proceed directly to laparotomy for embolectomy + bowel resection. Endovascular approach may be combined with surgical exploration |
| SMA thrombosis | Surgical revascularization: open thrombectomy with antegrade or retrograde SMA bypass graft. Endovascular: SMA stenting with or without thrombectomy/thrombolysis. Hybrid approach: endovascular revascularization followed by surgical assessment of bowel viability | More extensive bowel involvement expected; often requires resection + revascularization. Long-term antithrombotic therapy |
| Mesenteric venous thrombosis | Systemic anticoagulation (heparin, transition to warfarin or DOAC) is the primary treatment if no signs of bowel infarction. Surgery (laparotomy/laparoscopy) for peritoneal signs or CT evidence of bowel necrosis (resect non-viable bowel). Catheter-directed thrombolysis for extensive SMV thrombosis without peritoneal signs | Evaluate for underlying hypercoagulable state (thrombophilia workup). Long-term anticoagulation (minimum 6 months; indefinite if unprovoked or underlying thrombophilia). CT venography to monitor thrombus resolution |
| NOMI | Optimize cardiac output — treat underlying cause (cardiogenic shock, sepsis). Discontinue/minimize vasopressors. Intra-arterial papaverine (30–60 mg/hour via SMA catheter) for mesenteric vasospasm. Surgery only for peritoneal signs or bowel necrosis | Prevention is key: avoid excessive vasopressors, optimize cardiac output, maintain adequate MAP. Consider mesenteric angiography with papaverine infusion early |
Damage Control Surgery
In hemodynamically unstable patients or those with extensive bowel necrosis, a damage control approach may be used:3
- Resect clearly non-viable bowel
- Leave bowel ends in discontinuity (stapled or tied)
- Temporary abdominal closure (vacuum-assisted closure)
- ICU resuscitation for 24–48 hours
- Planned second-look laparotomy at 24–48 hours to reassess bowel viability, perform additional resection if needed, and restore continuity (anastomosis or ostomy)
The second-look laparotomy is a critical component of AMI management — it should be planned at the time of the index operation and should NOT be omitted based on clinical improvement alone, as delayed necrosis progression is common.
11. Ruptured Abdominal Aortic Aneurysm
11.1 Overview
Ruptured abdominal aortic aneurysm (rAAA) is a catastrophic vascular emergency with an overall mortality of 65% to 85% (including prehospital deaths). For patients who reach the hospital alive, operative mortality ranges from 30% to 50%. Rapid diagnosis and immediate surgical intervention are the only life-saving measures.5
11.2 Clinical Presentation — Classic Triad
| Feature | Description | Sensitivity |
|---|---|---|
| Abdominal or back pain | Sudden onset, severe, tearing. May radiate to the back, flank, or groin. May present as syncope | Present in ~75–90% |
| Hypotension | Hypovolemic shock; may be transient if retroperitoneal containment temporarily tamponades the rupture | Present in ~50–70% at presentation |
| Pulsatile abdominal mass | Palpable pulsatile mass in the epigastrium/periumbilical region; may be difficult to detect in obese patients | Present in ~25–50% |
The complete triad is present in only 25–50% of cases. A high index of suspicion is essential.
Misdiagnosis pitfalls: rAAA is commonly misdiagnosed as renal colic, diverticulitis, musculoskeletal back pain, or GI hemorrhage. Any patient >50 years with sudden abdominal or back pain and hemodynamic instability should be assumed to have a rAAA until proven otherwise.
11.3 Diagnosis
| Hemodynamic Status | Recommended Approach |
|---|---|
| Hemodynamically unstable (SBP <90 mmHg or signs of shock) | Bedside POCUS to identify AAA (>3 cm). If AAA confirmed in an unstable patient, proceed directly to the operating room. Do NOT delay for CT. If POCUS is unavailable or inconclusive, proceed to OR based on clinical judgment |
| Hemodynamically stable | CT angiography (CTA) of the abdomen and pelvis — delineates aneurysm morphology, identifies rupture (retroperitoneal hematoma, active contrast extravasation), and provides anatomic information for EVAR planning |
POCUS for AAA:
- Sensitivity 95–100% for identifying AAA (>3 cm)
- Cannot reliably distinguish ruptured from unruptured AAA
- A visualized AAA in a patient with the classic clinical picture is sufficient to proceed to OR
11.4 Management
Immediate Resuscitation
| Principle | Details |
|---|---|
| Permissive hypotension | Target SBP 70–90 mmHg (MAP 50–60 mmHg) until aortic control is achieved. Avoid aggressive fluid resuscitation, which can dislodge clot, increase blood loss, and worsen coagulopathy. Sufficient blood pressure to maintain consciousness is the clinical target |
| Massive transfusion protocol (MTP) | Activate MTP immediately. Target 1:1:1 ratio of pRBCs:FFP:platelets. Early use of tranexamic acid (TXA) 1g IV (extrapolated from trauma data). Type O negative blood if crossmatch is not available |
| Minimize crystalloid | Limit crystalloid to avoid hemodilution and worsening of the lethal triad (hypothermia, acidosis, coagulopathy) |
| Vasopressors | Avoid if possible; vasopressors increase afterload and may worsen aortic bleeding. Use only as a bridge to the OR in extremis |
| Do NOT delay for workup | Unstable patients go directly to the OR. Central lines, arterial lines, and Foley catheter are placed in the OR |
Surgical Repair
| Approach | Details | Selection Criteria |
|---|---|---|
| EVAR (Endovascular Aneurysm Repair) | Percutaneous or femoral cutdown placement of an endovascular stent-graft to exclude the aneurysm. Requires suitable aortic anatomy (adequate proximal neck length ≥10–15 mm, appropriate iliac access). Performed in a hybrid OR or angiography suite | Preferred when anatomically feasible and expertise/equipment available. Associated with lower 30-day mortality compared to open repair in most studies (21–25% vs 35–48%). Faster procedure, less physiologic insult. Not all patients are anatomically suitable |
| Open surgical repair | Midline laparotomy, proximal aortic cross-clamp (infrarenal or suprarenal as needed), aneurysm opened, inlay synthetic graft (tube or bifurcated) | Required when EVAR is not feasible (hostile anatomy, no EVAR availability). Standard approach at centers without EVAR capability |
Postoperative Complications
- Abdominal compartment syndrome — monitor bladder pressures; decompressive laparotomy if intra-abdominal pressure >20 mmHg with organ dysfunction
- Renal failure — suprarenal clamping, hypotension, contrast exposure
- Colonic ischemia — check for bloody diarrhea, monitor lactate; sigmoidoscopy if concern
- Spinal cord ischemia — lower extremity weakness/paralysis (rare with infrarenal AAA repair)
- EVAR-specific: Endoleak (type I, II, III), graft migration, limb thrombosis
12. Ectopic Pregnancy
12.1 Overview
Ectopic pregnancy occurs in approximately 1% to 2% of all pregnancies and is the leading cause of maternal mortality in the first trimester. The most common location is the fallopian tube (ampulla ~70%, isthmus ~12%, fimbria ~11%). Ruptured ectopic pregnancy is a life-threatening surgical emergency.6
12.2 Diagnosis
Clinical Presentation
- Classic triad: Amenorrhea (missed period), vaginal bleeding, and lower abdominal/pelvic pain — present in only about 50% of cases
- Pain may be unilateral or bilateral; may present as shoulder pain (hemoperitoneum causing diaphragmatic irritation)
- Ruptured ectopic: Sudden severe pelvic/abdominal pain, signs of hemorrhagic shock (tachycardia, hypotension, pallor), peritoneal signs, cervical motion tenderness
Diagnostic Evaluation
| Test | Key Details |
|---|---|
| Serum beta-hCG (quantitative) | Mandatory in ALL reproductive-age women with abdominal/pelvic pain. The discriminatory zone is the beta-hCG level above which an intrauterine pregnancy (IUP) should be visible on ultrasound. Transvaginal US discriminatory zone: beta-hCG >1,500–3,000 mIU/mL (institution-dependent; many use 3,000 mIU/mL as the threshold for TVUS). If beta-hCG is above the discriminatory zone and no IUP is seen on TVUS, ectopic pregnancy must be strongly considered |
| Transvaginal ultrasound (TVUS) | Imaging study of choice. Findings: (1) No IUP with beta-hCG above discriminatory zone — ectopic until proven otherwise; (2) Adnexal mass or extrauterine gestational sac; (3) “Tubal ring” or “bagel sign”; (4) Free fluid in the pelvis or Morrison pouch (hemoperitoneum) |
| beta-hCG trending | In a normal IUP, beta-hCG should rise by approximately 49–66% every 48 hours (previously taught as “doubling”). A rise of less than 35% over 48 hours is highly suspicious for ectopic or non-viable pregnancy. A declining beta-hCG suggests non-viable pregnancy (ectopic or miscarriage) |
| Progesterone | Serum progesterone <5 ng/mL is highly suggestive of non-viable pregnancy (ectopic or miscarriage). Progesterone >20 ng/mL strongly suggests viable IUP. Intermediate values (5–20 ng/mL) are indeterminate |
12.3 Management
Ruptured Ectopic Pregnancy — Emergent Surgical Management
Ruptured ectopic pregnancy with hemodynamic instability is a surgical emergency requiring immediate intervention:6
- Emergent salpingectomy (removal of the affected fallopian tube with the ectopic pregnancy) via laparoscopy (preferred if hemodynamically stable enough) or laparotomy (if hemodynamically unstable)
- Massive transfusion protocol may be needed
- Do NOT delay surgery for imaging — clinical diagnosis (positive beta-hCG + hemodynamic instability + peritoneal signs) is sufficient to proceed to OR
- Cell saver/autotransfusion of recovered hemoperitoneum may be utilized
Stable, Unruptured Ectopic — Methotrexate
Methotrexate (MTX) is the standard medical treatment for hemodynamically stable, unruptured ectopic pregnancy in appropriately selected patients.6
Criteria for Methotrexate Eligibility (ALL must be met):
| Criterion | Detail |
|---|---|
| Hemodynamically stable | No signs of rupture or active bleeding |
| beta-hCG | Ideally <5,000 mIU/mL (higher levels associated with higher failure rate; some centers use <10,000 as cutoff) |
| No fetal cardiac activity on TVUS | Presence of cardiac activity is a relative contraindication (lower success rate) |
| Ectopic size | <3.5–4 cm on imaging |
| Patient reliability | Able to comply with follow-up (serial beta-hCG monitoring) |
| No contraindications to MTX | No hepatic/renal disease, no immunodeficiency, no active pulmonary disease, no peptic ulcer, no breastfeeding, normal CBC |
Methotrexate Protocol (Single-Dose Regimen):
- Methotrexate 50 mg/m^2 IM (single dose)
- Check beta-hCG on day 4 and day 7
- If beta-hCG declines by ≥15% between day 4 and day 7: continue weekly monitoring until beta-hCG reaches non-pregnant level (<5 mIU/mL)
- If decline is <15%: administer a second dose of MTX 50 mg/m^2 IM
- If beta-hCG rises or does not decline adequately after second dose: consider surgical management
- Success rate: 82–94% for single-dose protocol when selection criteria are met
Expectant Management
May be considered in highly selected, reliable patients with:
- beta-hCG <200 mIU/mL and declining
- No symptoms of rupture
- Small ectopic (<2 cm) without cardiac activity
- Close follow-up possible
- Success rate approximately 50–70% in this highly selected population
13. Special Populations
13.1 Pediatric Abdominal Emergencies
Intussusception
Intussusception is the most common cause of bowel obstruction in children aged 3 months to 6 years (peak incidence 5–10 months). It results from telescoping of one segment of bowel into an adjacent segment (most commonly ileocolic).7
| Feature | Details |
|---|---|
| Classic triad | Intermittent, colicky abdominal pain; “currant jelly” stool (blood and mucus); palpable sausage-shaped mass (RUQ). Complete triad present in only ~20–40% of cases |
| Presentation | Episodes of severe, inconsolable crying (drawing up knees) alternating with periods of quiet lethargy. Vomiting. Bloody stool is a late finding. Lethargy may be the predominant symptom in young infants |
| Diagnosis | Ultrasound: “Target sign” or “doughnut sign” on transverse view; “pseudokidney” sign on longitudinal view. Sensitivity >98%, specificity >98%. X-ray may show soft tissue mass, absent cecal gas, or signs of obstruction but is unreliable for diagnosis |
| Treatment | Air enema (preferred) or hydrostatic (saline) enema under fluoroscopic or US guidance for reduction. Success rate: 80–95%. Contraindications: peritonitis, perforation, hemodynamic instability, shock. Surgical reduction/resection for: failed enema reduction (after up to 3 attempts at some centers), signs of perforation/peritonitis, recurrence after multiple enema reductions, pathologic lead point suspected (consider in children >2 years) |
| Recurrence | 5–10% after successful enema reduction |
Hypertrophic Pyloric Stenosis
| Feature | Details |
|---|---|
| Epidemiology | Typically presents at 2–8 weeks of age; more common in males (4:1); firstborn children. Incidence approximately 2–5 per 1,000 live births |
| Presentation | Non-bilious, projectile vomiting after feeds (classically “hungry vomiter” — feeds eagerly after vomiting). Progressive dehydration. Weight loss or failure to thrive. Hypochloremic, hypokalemic metabolic alkalosis (from loss of gastric acid/HCl). Palpable “olive” in the epigastrium/RUQ (hypertrophied pylorus) in 60–80% of cases |
| Diagnosis | Ultrasound: Pyloric muscle thickness >3 mm (single wall); pyloric channel length >15–17 mm. Sensitivity and specificity >95% |
| Management | (1) Correct dehydration and electrolyte abnormalities FIRST (fluid resuscitation with NS, then D5 1/2NS with KCl 20 mEq/L once urine output established; target chloride >100, bicarbonate <30, potassium >3.5 before surgery). (2) Ramstedt pyloromyotomy (laparoscopic or open) — division of the hypertrophied pyloric muscle fibers down to the submucosa. Curative |
Meckel Diverticulum
| Feature | Details |
|---|---|
| Rule of 2s | Present in 2% of the population; 2 feet (60 cm) from the ileocecal valve; 2 inches (5 cm) long; 2 types of ectopic mucosa (gastric and pancreatic); symptomatic by age 2 (though only ~4% become symptomatic in a lifetime) |
| Presentations | (1) Painless lower GI bleeding (most common in children — ectopic gastric mucosa causes ulceration of adjacent ileum); (2) Diverticulitis (mimics appendicitis but in the LLQ or periumbilical region); (3) Small bowel obstruction (intussusception with Meckel as lead point, or volvulus around a vitellointestinal band); (4) Perforation |
| Diagnosis | Meckel scan (Technetium-99m pertechnetate scintigraphy): detects ectopic gastric mucosa. Sensitivity ~85% in children, lower in adults. CT may show a blind-ending outpouching from the ileum. Often diagnosed intraoperatively |
| Management | Symptomatic Meckel: surgical resection (diverticulectomy or segmental small bowel resection with primary anastomosis). Incidentally discovered Meckel: resection is debated; generally recommended if the diverticulum appears abnormal (thickened wall, palpable ectopic tissue, associated band) |
13.2 Elderly Patients
Elderly patients (>65 years) present unique challenges in the evaluation of acute abdominal pain:8
| Challenge | Clinical Implication |
|---|---|
| Atypical presentations | Blunted pain perception, diminished fever response, less pronounced peritoneal signs, minimal leukocytosis. Fever may be absent in up to 30% of elderly patients with intra-abdominal sepsis |
| Higher surgical acuity | Mortality for virtually all acute abdominal conditions is 2–10x higher in elderly patients compared to younger adults |
| Delayed presentation | Average time from symptom onset to ED presentation is longer; higher rate of complicated appendicitis, perforated diverticulitis, and advanced bowel obstruction at presentation |
| Polypharmacy | Beta-blockers mask tachycardia; anticoagulants increase bleeding risk; NSAIDs predispose to perforation; corticosteroids suppress inflammatory response and mask peritoneal signs |
| Vascular disease | Higher prevalence of mesenteric ischemia, AAA; atherosclerotic disease affects visceral arteries |
| Malignancy | LBO from colorectal cancer is far more common in the elderly; always exclude malignancy as cause of obstruction |
| Frailty assessment | Frailty index, nutritional status, functional independence, and goals of care discussion should inform surgical decision-making |
Recommendation: In elderly patients with abdominal pain, maintain a low threshold for CT imaging, early surgical consultation, and aggressive workup even when symptoms and signs appear mild.
13.3 Immunocompromised Patients
Immunocompromised patients (HIV/AIDS, organ transplant recipients, patients on chronic immunosuppressive therapy, active chemotherapy, neutropenic patients) require special consideration:8
| Consideration | Details |
|---|---|
| Broadened differential | Opportunistic infections: CMV colitis, Clostridium difficile, typhlitis (neutropenic enterocolitis — particularly cecal inflammation in neutropenic patients), mycobacterial infections, fungal infections |
| Blunted inflammatory response | Diminished WBC (may be neutropenic), minimal peritoneal signs, absence of fever despite significant infection. CRP may be more reliable than WBC in immunosuppressed patients |
| Typhlitis (neutropenic enterocolitis) | Inflammation of the cecum in profoundly neutropenic patients (ANC <500). CT: cecal wall thickening, pericolonic stranding, pneumatosis. Management: bowel rest, broad-spectrum antibiotics (including antifungals), supportive care. Surgery reserved for perforation, uncontrolled hemorrhage, or clinical deterioration. Mortality 30–50% |
| Lower threshold for imaging | CT should be obtained early and liberally. Repeat imaging with low threshold if clinical status changes |
| Transplant-specific | Post-transplant lymphoproliferative disorder (PTLD) can present as bowel obstruction or perforation. Rejection can affect transplanted organs (e.g., transplant enteropathy in small bowel transplant) |
13.4 Pregnant Patients
Evaluation of abdominal pain in pregnancy requires balancing the maternal and fetal risks of both the underlying condition and the diagnostic/therapeutic interventions:9
| Principle | Details |
|---|---|
| Always exclude obstetric causes first | Placental abruption, preterm labor, uterine rupture, HELLP syndrome, preeclampsia — obstetric consultation is essential |
| Physiologic changes of pregnancy | Leukocytosis (WBC up to 15,000–16,000 is normal; up to 29,000 in labor); mild alkaline phosphatase elevation (placental origin); displaced abdominal organs (appendix migrates cephalad); increased GFR lowers the “normal” creatinine range; physiologic hydronephrosis (right > left) |
| Imaging approach | Ultrasound first for all suspected pathology. MRI without gadolinium as second-line. CT when US and MRI are inconclusive or unavailable AND the clinical situation is urgent — the risk of missed surgical pathology outweighs the small radiation risk. Gadolinium contrast is contraindicated in pregnancy (crosses placenta). Iodinated IV contrast can be used when CT is necessary (minimal fetal thyroid risk with a single exposure) |
| Surgical considerations | (1) Laparoscopy is safe in all trimesters (pneumoperitoneum pressures 10–15 mmHg; left lateral tilt after 20 weeks to avoid aortocaval compression). (2) Delayed surgery carries greater risk to the fetus than the surgery itself (perforation risk in delayed appendicitis). (3) Fetal monitoring: continuous external fetal monitoring before and after surgery (after viability, approximately 24 weeks). Tocolytics only if preterm contractions develop. (4) Obstetric consultation for all pregnant patients undergoing surgery |
| Common surgical conditions in pregnancy | Appendicitis (1/1,000–2,000 pregnancies — most common non-obstetric surgical emergency); cholecystitis (1/1,600–10,000 pregnancies — second most common); bowel obstruction (1/10,000–66,000); ovarian torsion |
14. Summary — Emergency Decision Framework
The following rapid-reference table summarizes the key decision points for the most time-sensitive acute abdominal emergencies:
| Condition | Key Diagnostic Step | Emergent Intervention Trigger | Time-Critical Action |
|---|---|---|---|
| Ruptured AAA | Bedside POCUS (unstable) or CTA (stable) | Hemodynamic instability + known/suspected AAA | Immediate OR: EVAR or open repair |
| Mesenteric ischemia | CTA abdomen/pelvis | Peritoneal signs, elevated lactate, CT signs of bowel necrosis | Anticoagulation + emergent revascularization/laparotomy |
| Perforated viscus | CT abdomen/pelvis | Pneumoperitoneum + peritonitis | Emergent laparotomy or laparoscopy |
| Ruptured ectopic pregnancy | Positive beta-hCG + POCUS (free fluid) | Hemodynamic instability + positive beta-hCG | Emergent salpingectomy |
| Strangulated SBO | CT abdomen/pelvis | Peritoneal signs, absent bowel wall enhancement, closed-loop | Emergent laparotomy |
| Gangrenous cholecystitis | CT or US | Grade III cholecystitis with sepsis, emphysematous changes | IV antibiotics + urgent cholecystectomy or cholecystostomy |
| Severe cholangitis | Labs (LFTs, cultures) + US/MRCP | Grade III cholangitis with organ failure | Emergent ERCP or PTBD |
| Sigmoid volvulus with ischemia | CT abdomen/pelvis | Signs of gangrene, peritonitis | Emergent laparotomy (no endoscopic decompression) |
| Perforated diverticulitis (Hinchey III/IV) | CT abdomen/pelvis | Generalized peritonitis, free air, free fecal material | Emergent laparotomy: Hartmann or PRA |
References
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