Nature of Pain in Acute Diseases of the Gastrointestinal Tract

1. Fundamental Mechanisms of Abdominal Pain

2. Types of Abdominal Pain

A. Visceral (Autonomic) Pain

• Transmitted via sympathetic afferent fibres (T1–L2 nerve roots)
• Deep, dull, poorly localised, often felt in the midline regardless of the side of the lesion
• Frequently accompanied by autonomic features: nausea, vomiting, sweating, restlessness
• Arises from hollow organ distension, smooth muscle spasm, or ischaemia
• Classic example: early appendicitis — crampy periumbilical pain before peritoneal involvement

B. Parietal (Somatic) Pain

• Arises when an inflamed organ comes into contact with the parietal peritoneum
• Transmitted via spinal somatic nerves — sharp, well-localised, and constant
• Localises to the segmental dermatome of the affected abdominal wall region
• Aggravated by movement, coughing, or deep breathing (peritonism)
• Classic example: acute appendicitis — pain migrates from periumbilical to right iliac fossa (McBurney's point) once the parietal peritoneum is involved

C. Referred Pain

• Felt at a site remote from the diseased organ, sharing the same nerve root supply
• Mechanism: convergence of visceral and somatic afferents on the same spinal cord segment
• Key examples:

3. Sensitisation and Progression of Pain

1. Peripheral sensitisation: Inflammatory mediators (prostaglandins, bradykinin, substance P) lower the threshold of nociceptor transducers, intensifying afferent signalling.
2. Recruitment of silent afferents: Afferents normally inactive at baseline become activated, broadening the pain field.
3. These acute mechanisms can also trigger central sensitisation, explaining referred hyperalgesia and allodynia around the affected area (e.g., cutaneous tenderness overlying an inflamed appendix or gallbladder).

4. Character of Pain by Condition

5. Clinical Significance of Pain Features

• Onset: Sudden ("thunderclap") onset suggests perforation or vascular catastrophe; gradual onset suggests inflammation.
• Character: Colicky (waxing/waning) pain implies hollow viscus obstruction (bowel, ureter, bile duct); constant pain implies inflammation or ischaemia.
• Murphy's sign: On deep inspiration, the descending inflamed gallbladder contacts the examining hand, worsening pain and causing the patient to arrest breathing — reflects parietal peritoneal involvement in acute cholecystitis (Bailey and Love's, p. 1074).
• Psoas sign: In retrocaecal appendicitis, the inflamed appendix irritates the psoas muscle; children adopt hip flexion to relieve psoas stretch.
• Rebound tenderness (Blumberg's sign): Release of hand pressure suddenly worsens pain — indicates parietal peritoneal irritation.
• Pain–signs disparity: Severe pain with minimal tenderness is the hallmark of mesenteric ischaemia and demands urgent investigation.

6. Neuroanatomical Basis of Pain Localisation

• Foregut derivatives (stomach to mid-duodenum, liver, biliary tree, spleen, pancreas): pain referred to the epigastrium
• Midgut derivatives (mid-duodenum to mid-transverse colon, including appendix): pain referred to the periumbilical region
• Hindgut derivatives (mid-transverse colon to rectum): pain referred to the hypogastrium/suprapubic region

Specific Symptoms of Pulmonary Embolism

Classification by Severity

Specific Symptoms

Respiratory Symptoms

• Dyspnea — the most common symptom; may be sudden in onset; present even at rest
• Pleuritic chest pain — sharp, stabbing, worsened by inspiration; occurs with peripheral emboli causing pulmonary infarction and pleural irritation
• Haemoptysis — blood-streaked sputum; signals pulmonary infarction (peripheral emboli)
• Cough — non-productive; less specific

Cardiovascular Symptoms

• Tachycardia (HR >100 bpm) — one of the most consistent signs; included in the Wells score (Bailey and Love's, 28th Ed., p. 345)
• Syncope / presyncope — hallmark of massive PE; reflects acute reduction in cardiac output and cerebral hypoperfusion
• Hypotension / cardiogenic shock — defines massive (high-risk) PE
• Cyanosis — in severe cases with massive occlusion

Other Symptoms

• Anxiety and sense of impending doom — common in large emboli due to sudden haemodynamic compromise
• Leg pain and swelling — from concurrent deep vein thrombosis (DVT), which is the source in ~70% of cases

Signs on Examination

Wells Score Clinical Features

Key Points

• No single symptom is pathognomonic — PE is notoriously non-specific in presentation
• The classic triad of dyspnea + chest pain + haemoptysis occurs in fewer than 20% of patients
• Massive PE presents with dyspnea, syncope, hypotension, and cyanosis
• Peripheral (small) PE tends to present with pleuritic chest pain and haemoptysis (infarction pattern)
• Central (large) PE tends to present with dyspnea, syncope, and haemodynamic collapse
• A high index of suspicion, combined with risk factor assessment and the Wells score, is the cornerstone of diagnosis

Myocardial Infarction — Detailed Review

Definition

Classification

By ECG Pattern

By Depth (Histological)

• Transmural MI — full thickness of myocardial wall; usually STEMI
• Subendocardial MI — inner layer only; usually NSTEMI

Universal Classification (Type 1–5)

Aetiology & Risk Factors

Primary Cause

Risk Factors

Pathophysiology

1. Atherosclerotic plaque develops in coronary arteries over years (lipid-rich core with fibrous cap)
2. Plaque rupture or erosion → exposure of subendothelial collagen and lipid core
3. Platelet adhesion and aggregation → thrombus formation
4. Coronary artery occlusion → cessation of oxygen delivery distal to the lesion
5. Ischaemia → within seconds: impaired contractility; within minutes: electrical instability
6. Irreversible necrosis begins after ~20–40 minutes of sustained ischaemia (subendocardium first, propagating outward — the "wavefront phenomenon")
7. Reperfusion injury can occur if flow is restored late

Zones of Injury (from centre outward):

• Zone of necrosis — dead tissue, no function
• Zone of injury — viable but injured myocytes (ST elevation on ECG)
• Zone of ischaemia — reversible ischaemia (T-wave changes on ECG)

Clinical Presentation

Symptoms

• Chest pain — the cardinal symptom
  • Crushing, squeezing, pressure-like ("elephant sitting on chest")
  • Central/retrosternal, may radiate to left arm, jaw, neck, back, epigastrium
  • Lasting >20 minutes (differentiates from stable angina)
  • Not relieved by nitrates
• Dyspnoea — from acute LV failure / pulmonary oedema
• Diaphoresis (profuse sweating) — autonomic activation
• Nausea and vomiting — especially in inferior MI (vagal stimulation)
• Palpitations — arrhythmias
• Syncope — from haemodynamic compromise or arrhythmia
• Sense of impending doom

Atypical Presentations (common in elderly, women, diabetics)

• Epigastric pain / "indigestion"
• Isolated jaw or arm pain
• Fatigue and weakness only
• Silent MI (no pain) — particularly in diabetics

Signs on Examination

Diagnosis

1. ECG

12-lead ECG showing anterolateral STEMI with convex ST elevation in V1–V6 and leads I, aVL, hyperacute T-waves in V2–V4, and reciprocal ST depression in inferior leads (II, III, aVF) — indicating proximal LAD occlusion.

2. Cardiac Biomarkers

3. Imaging

• Echocardiography: Regional wall motion abnormalities (RWMA); LV function; mechanical complications
• Coronary angiography: Definitive identification of culprit lesion; performed urgently in STEMI
• Chest X-ray: Pulmonary oedema, cardiomegaly; not diagnostic for MI

Management

Immediate (First 10 Minutes)

• MONA mnemonic:
  • Morphine (cautiously; may mask symptoms, use judiciously)
  • Oxygen (only if SpO₂ <90%)
  • Nitrates (sublingual GTN; avoid in RV infarction / hypotension / PDE5 inhibitor use)
  • Aspirin 300 mg loading dose (chewed)

Reperfusion Strategy (Management of ACS, p. 10)

Antiplatelet & Anticoagulation (Acute Phase)

• Dual antiplatelet therapy (DAPT): Aspirin + P2Y₁₂ inhibitor (ticagrelor, prasugrel, or clopidogrel)
• Anticoagulation: Unfractionated heparin (UFH) or low molecular weight heparin (LMWH) or fondaparinux

Secondary Prevention (Long-term)

Complications

Early (Hours–Days)

Late (Days–Weeks)

Prognosis

• In-hospital mortality for STEMI with PPCI: ~5%
• 30-day mortality (untreated STEMI): ~30%
• Key determinants: time to reperfusion, infarct size, LV ejection fraction, age, comorbidities
• TIMI and GRACE scores are used for risk stratification in ACS

Summary Algorithm

Chest pain / suspected ACS
         ↓
     ECG within 10 min
         ↓
   ┌─────────────────────┐
   │ ST elevation or LBBB│ → STEMI → Primary PCI (≤90 min) or Fibrinolysis
   └─────────────────────┘
         ↓ (no ST elevation)
   Serial troponins (0h, 1–3h)
         ↓
   ┌───────────┐     ┌──────────┐
   │ Troponin ↑│     │Troponin N│
   └───────────┘     └──────────┘
       NSTEMI         Unstable angina
         ↓                  ↓
   Risk stratify (GRACE score)
         ↓
   Angiography ± PCI (timing by risk)

Atypical Presentations of Myocardial Infarction

Who Presents Atypically?

Atypical Symptom Patterns

1. Epigastric / GI Presentation

• Pain in upper abdomen mimicking peptic ulcer, gastritis, or indigestion
• Nausea, vomiting, belching
• Most common in inferior MI (diaphragmatic surface irritation + vagal stimulation)
• Frequently misdiagnosed and sent home with antacids

2. Jaw / Dental Pain

• Isolated jaw ache or toothache without chest pain
• Referred pain via shared cervical and trigeminal pathways
• Patients often see a dentist before a cardiologist

3. Arm / Shoulder Pain Only

• Left arm heaviness, aching, or numbness without chest involvement
• Can occur in isolation, especially in women

4. Back Pain

• Interscapular or mid-back pain
• May mimic musculoskeletal pain or aortic dissection
• Common in posterior MI

5. Neck / Throat Tightness

• Sensation of throat constriction or choking
• Mistaken for anxiety, GERD, or oesophageal spasm

6. Dyspnoea Alone (Anginal Equivalent)

• Sudden breathlessness without chest pain
• Reflects acute LV dysfunction / flash pulmonary oedema
• Common in elderly women and diabetics

7. Fatigue / Weakness

• Profound, unexplained fatigue — especially in women
• May precede MI by days to weeks (prodromal symptom)
• Often dismissed as viral illness or stress

8. Syncope / Collapse

• Loss of consciousness due to arrhythmia or haemodynamic compromise
• No preceding chest pain
• Common in massive MI or MI complicated by VT/VF

9. Silent MI (Completely Asymptomatic)

• Patient has no symptoms at all; MI discovered incidentally on ECG (Q-waves) or imaging
• Accounts for up to 20–30% of all MIs
• Strongly associated with diabetes mellitus (autonomic neuropathy)

Late Gadolinium Enhancement (LGE) Cardiac MRI showing silent MI in three patients. White arrows indicate hyperintense (bright) areas of myocardial scarring — subendocardial and transmural — in the inferolateral, septal, and inferior segments, all clinically unrecognized at the time of injury.

10. Acute Confusion / Delirium

• Seen in the very elderly
• MI reduces cardiac output → cerebral hypoperfusion → confusion
• No chest pain reported

Comparison: Classic vs. Atypical MI

Clinical Importance

• Atypical MI carries higher mortality than classic MI — primarily due to delayed diagnosis and treatment
• A high index of suspicion must be maintained in at-risk groups
• ECG + high-sensitivity troponin should be obtained in any patient with unexplained dyspnoea, syncope, epigastric pain, or fatigue — especially if risk factors are present
• The phrase "rule out MI" exists precisely because atypical presentations are common and dangerous

In women presenting with acute MI, the most common symptom is not chest pain — it is fatigue, followed by dyspnoea and jaw/arm discomfort. Chest pain occurs in only ~57% of women vs. ~70% of men.