What are the possible diagnosis and differential diagnoses for a patient presenting with severe vomiting, abdominal pain, and loss of consciousness?

Possible Diagnosis and Differential Diagnoses

Primary Diagnosis: Acute Mesenteric Ischemia with Bowel Necrosis

The most likely diagnosis is acute mesenteric ischemia (AMI) progressing to bowel necrosis and septic shock, given the 48-hour course of severe projectile vomiting, escalating epigastric pain, rapid progression to cardiovascular collapse with bradycardia, and refractory asystole despite maximal resuscitation. 1, 2

Key Diagnostic Features Supporting AMI

• Severe abdominal pain out of proportion to physical findings is the hallmark of acute mesenteric ischemia and should be considered until proven otherwise 2
• The 48-hour progression from epigastric pain and projectile vomiting to cardiovascular collapse fits the typical timeline of arterial occlusion evolving to transmural bowel necrosis 1
• Pre-transfer bradycardia preceding complete cardiovascular collapse suggests profound metabolic derangement from bowel necrosis, likely severe lactic acidosis and hyperkalemia 1, 3
• Refractory asystole despite 14 doses of epinephrine indicates irreversible metabolic catastrophe, consistent with massive bowel infarction and overwhelming septic shock 1

Pathophysiologic Mechanism

• Acute mesenteric arterial embolism or thrombosis causes sudden-onset severe abdominal pain with vomiting 1
• Without prompt diagnosis and intervention, ischemia progresses to transmural necrosis within 6-12 hours 1
• Elevated lactate >2 mmol/L indicates irreversible intestinal ischemia (hazard ratio 4.1) and is associated with metabolic acidosis in 88% of AMI patients 1
• Severe metabolic acidosis, hyperkalemia from cell death, and septic shock from bacterial translocation across necrotic bowel lead to cardiovascular collapse 1, 3

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Critical Differential Diagnoses

1. Severe Electrolyte Emergency (Hypokalemia or Hyperkalemia)

Severe electrolyte disturbances can cause cardiac arrest and must be considered given the projectile vomiting and rapid progression to asystole. 4, 5

• Profound hypokalemia from prolonged vomiting (>10 episodes over 48 hours) can cause muscle weakness, numbness, bradycardia, and cardiac arrest 4, 5
• Hypokalemia-induced cardiac arrhythmias progress from bradycardia to asystole, especially when potassium <2.5 mEq/L 5, 3
• The neuromuscular signs (weakness, numbness) are consistent with severe hypokalemia 4
• However, the severe epigastric pain and projectile vomiting pattern suggests a primary abdominal catastrophe rather than simple gastroenteritis 2

2. Perforated Viscus with Septic Shock

Gastric or duodenal perforation from peptic ulcer disease could cause epigastric pain, vomiting, and rapid progression to septic shock. 1

• Perforated peptic ulcer presents with sudden severe epigastric pain, vomiting, and signs of peritonitis 1
• Progression to septic shock occurs when peritoneal contamination leads to overwhelming sepsis 1
• Mortality in septic shock from intra-abdominal infection is 67.8%, explaining the refractory arrest 1
• The lack of documented peritoneal signs (no physical exam details provided) makes this less likely than AMI, where pain precedes peritonitis 1, 2

3. Acute Bowel Obstruction with Strangulation

Small bowel obstruction with strangulation can cause projectile vomiting, severe pain, and progression to shock from bowel necrosis. 2, 6

• Bilious or feculent projectile vomiting indicates mechanical obstruction and requires immediate intervention 2
• Strangulated obstruction leads to bowel ischemia, necrosis, and septic shock within 24-48 hours 2
• However, the absence of prior abdominal surgery (which has 85% sensitivity for adhesive obstruction) makes this less likely 2
• The epigastric location of pain is more consistent with proximal vascular occlusion than distal mechanical obstruction 1, 2

4. Acute Pancreatitis with Complications

Severe acute pancreatitis can cause epigastric pain, vomiting, and progression to shock, though the clinical course is atypical. 1, 6

• Epigastric pain and vomiting are cardinal features of acute pancreatitis 6
• Severe pancreatitis can cause hypovolemic and septic shock 6
• However, elevated amylase occurs in only 50% of AMI patients and can lead to misdiagnosis as pancreatitis, delaying critical interventions 1
• The rapid 48-hour progression to death is more consistent with mesenteric ischemia than uncomplicated pancreatitis 1

5. Septic Shock from Intra-Abdominal Infection

Overwhelming intra-abdominal sepsis from any source can cause the observed clinical deterioration. 1

• Septic shock mortality is 67.8% in intra-abdominal infections, explaining the refractory cardiac arrest 1
• Progression from sepsis to septic shock occurs when mean arterial pressure cannot be maintained despite vasopressors and lactate >2 mmol/L 1
• The 48-hour timeline with escalating symptoms fits the progression from localized infection to overwhelming sepsis 1
• However, the absence of fever and the specific pattern of epigastric pain with projectile vomiting point more toward a vascular catastrophe 1, 2

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Environmental and Demographic Risk Factors

Water Source Contamination

• Water from refilling stations in crowded urban Manila raises concern for infectious gastroenteritis, but the severity and rapid progression suggest a more catastrophic process 1
• Infectious causes (bacterial, parasitic) typically cause diarrhea in addition to vomiting, which was not reported 7

Age and Activity Level

• 16-year-old athletic male has low baseline risk for atherosclerotic mesenteric thrombosis 1
• However, acute mesenteric arterial embolism can occur in young patients with undiagnosed cardiac sources (endocarditis, arrhythmia, structural heart disease) 1
• Thrombophilia or hypercoagulable states should be considered in young patients with arterial thrombosis 1

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Critical Diagnostic Gaps

The absence of laboratory and imaging data represents a catastrophic failure in diagnostic evaluation that likely contributed to the fatal outcome. 1, 2

• CT angiography should be performed without delay in any patient with suspicion for AMI, as every 6 hours of delay doubles mortality 1
• Lactate, D-dimer, and leukocyte count would have supported the diagnosis, with lactate >2 mmol/L indicating irreversible ischemia 1
• Serum electrolytes would have identified life-threatening hypokalemia or hyperkalemia from vomiting or cell death 4, 5, 3
• The patient's presentation to a clinic before transfer represents a critical missed opportunity for early diagnosis and intervention 1

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Most Likely Clinical Sequence

Based on the available evidence, the most probable sequence is:

1. Acute mesenteric arterial embolism or thrombosis causing sudden severe epigastric pain 1
2. Projectile vomiting from bowel distension and ileus proximal to ischemic segment 2
3. Progressive bowel ischemia over 48 hours evolving to transmural necrosis 1
4. Severe lactic acidosis, hyperkalemia, and septic shock from necrotic bowel and bacterial translocation 1, 3
5. Bradycardia from severe metabolic acidosis and hyperkalemia 3
6. Refractory asystole from irreversible metabolic catastrophe and overwhelming septic shock 1

The failure to obtain CT angiography and measure lactate during the initial 48 hours represents a missed opportunity for potentially life-saving intervention, as early diagnosis and surgical revascularization are the only treatments that reduce the 30-70% mortality of AMI. 1