Tetanus - Definition

The Organism

• Gram-positive, anaerobic, spore-forming bacillus
• Found naturally in soil and intestines of humans and animals
• Spores have a characteristic drumstick or tennis racket shape
• Enters the body through a wound, thriving in anaerobic (low-oxygen) conditions present in devitalized tissues

Mechanism (Pathobiology)

1. C. tetani spores germinate in low-oxygen wounds and produce tetanospasmin (tetanus neurotoxin)
2. The toxin is one of the most potent known microbial toxins - lethal at 2.5 ng/kg in humans
3. It binds peripheral nerve terminals and is transported intra-axonally (~75-250 mm/day) to spinal neurons
4. The light chain blocks release of neurotransmitters from inhibitory afferent motor neurons
5. Loss of inhibition --> sustained, uncontrolled muscle contraction and tetanic spasms
6. Toxin binding is irreversible - recovery depends on growth of new axon terminals

Key Clinical Features

• Incubation period: 3-21 days (mean 8 days); shorter = more severe disease
• Trismus (lockjaw) - initial complaint in ~75% of cases
• Risus sardonicus - spasm of facial muscles producing a characteristic grimace
• Opisthotonus - arching of the entire body due to paravertebral/extensor muscle spasm
• Reflex spasms triggered by even slight sensory stimuli (noise, touch)
• Laryngeal spasm leading to apnoea and potential respiratory arrest
• Autonomic involvement: labile BP, cardiac arrhythmias, diaphoresis, hyperthermia
• Patients typically remain lucid and afebrile unless complicated by secondary infection

Types

Definition

Etiology (Causes)

Pathophysiology

• Autodigestion of pancreatic parenchyma
• Local inflammatory response with release of cytokines
• Systemic inflammatory response (SIRS)
• In severe cases: distant organ injury (lungs, kidneys, cardiovascular system)

Classification (Atlanta Classification 2012)

By Type:

• Interstitial edematous pancreatitis - Most cases; diffuse inflammation + edema; usually resolves within the first week
• Necrotizing pancreatitis - ~5-10% of cases; involves pancreatic parenchyma ± surrounding tissue; necrosis may be sterile, liquefy, or become infected (infected = worse prognosis)

By Severity:

• Mild - No organ failure, no local or systemic complications
• Moderately severe - Transient organ failure (<48 hrs) and/or local complications
• Severe - Persistent organ failure (>48 hrs); mortality up to 30%

Clinical Features

• Persistent epigastric or left upper quadrant pain, often radiating to the back, chest, or flanks
• Pain may be relieved by sitting up or bending forward
• Nausea, vomiting, anorexia

• Fever, tachycardia (with inflammation)
• Hypotension and shock (severe cases)
• Jaundice (if obstructive cause)
• Cullen sign - bluish periumbilical discoloration (hemoperitoneum) - rare, poor prognosis
• Grey Turner sign - reddish-brown flank discoloration (retroperitoneal bleeding) - rare, poor prognosis
• Epigastric tenderness ± guarding
• Reduced/absent bowel sounds (ileus)

Diagnosis

1. Abdominal pain characteristic of AP
2. Serum lipase or amylase >3x the upper limit of normal
3. Characteristic findings on abdominal imaging

• Lipase - preferred; more sensitive and specific than amylase; remains elevated ~1-2 weeks
• Amylase - less specific; elevated in many other conditions; may be falsely normal in alcohol/hypertriglyceridemia-induced AP
• ALT/AST/bilirubin - evaluate for biliary cause (ALT >3x normal has ~95% PPV for biliary pancreatitis)
• Serum calcium, triglycerides, CBC, BMP

• CT/MRI - not routine; indicated for diagnostic uncertainty, ruling out other pathology, or assessing complications (best after 48-72 hrs of failed therapy; necrosis best seen at 3-7 days)
• Ultrasound - first-line to identify gallstones

Severity Scoring

Complications

• Acute peripancreatic fluid collections (<4 weeks)
• Pancreatic pseudocyst (>4 weeks, encapsulated, fluid only)
• Acute necrotic collection
• Walled-off necrosis (WON) (>4 weeks)
• Bowel necrosis, splenic/portal vein thrombosis, GI bleeding, gastric outlet obstruction

• SIRS, ARDS, pleural effusion (up to 50%; more often left-sided)
• Cardiovascular collapse, acute kidney injury
• Coagulopathy/DIC
• Hyperglycemia, hypocalcemia

Management Principles

1. Fluid resuscitation - aggressive IV fluids (isotonic crystalloids preferred)
2. Analgesia - adequate pain control
3. Nutrition - early enteral feeding preferred over parenteral (nasogastric = nasojejunal in most cases)
4. ERCP - reserved for concurrent cholangitis or biliary obstruction (not routine)
5. Cholecystectomy - early (within 3 days) in mild biliary pancreatitis
6. Antibiotics - only for confirmed infected necrosis (not prophylactic)
7. ICU care - for organ failure and severe disease

Sonographic Images of Acute Pancreatitis

Fig. 25.7 - Ultrasound in Oedematous (Interstitial) Pancreatitis

Normal Pancreas for Comparison (US panels D & E)

Key Sonographic Features of Acute Pancreatitis

Important note: US may appear entirely normal in up to 20-30% of mild acute pancreatitis cases. US cannot reliably detect pancreatic necrosis. Contrast-enhanced CT remains the gold standard for staging severity and detecting necrosis (best performed 48-72 hrs after onset).

CT Imaging Patterns in Acute Pancreatitis

1. Timing of CT - Why It Matters

• Panel A (top): CT at 12 hours after onset - only minimal signs visible
• Panel B (bottom): Follow-up CT at Day 3 (due to clinical deterioration) - dramatically more severe inflammation is now apparent

Key teaching point: CT should NOT be done routinely in the first 24 hours. Necrosis takes 2-3 days to fully develop and may be underestimated early. Best performed at 48-72 hours in patients failing to improve.

2. Interstitial Oedematous Pancreatitis (Mild to Severe)

3. Pseudocyst (Late Complication, >4 Weeks)

• Two unilocular fluid collections (arrows) - one extending into the fissure of the ligamentum venosum, the other in the omental bursa
• Characteristic features: homogeneous low-attenuation fluid, well-defined enhancing fibrous wall, no solid debris

• 70% resolve spontaneously

4. Necrotising Pancreatitis - Key CT Patterns

• (A) Combined intrapancreatic + extrapancreatic necrosis (most common, 75-80%)
• (B & C) Extrapancreatic fat necrosis alone (arrows) - appears as mass-like hypodense areas (unlike simple stranding in oedema)
• (D) Intrapancreatic hypoenhancing necrosis alone (arrow) - minimal peripancreatic involvement
• (E) Necrosis in the swollen tail only

5. Walled-Off Necrosis (WON) - Evolution Over 4 Weeks

• Panel A: Early phase - Acute Necrotic Collection (ANC) involving pancreatic head and body (arrow) - heterogeneous, no wall
• Panel B: Follow-up at 4 weeks - evolution into a well-defined WON (arrow) containing fat-density debris inside. Note the thick wall that has now formed.

6. Infected WON - CT + Ultrasound Correlation

• Panel A (CT): Heterogeneous pancreatic parenchyma with hypoenhancing spotty necrosis + extrapancreatic ANC with fat necrosis chunks (arrow)
• Panel B (US): Collection with mixed fluid and solid material - cannot be mistaken for a simple pseudocyst (arrows)
• Panel C (follow-up CT at 6 weeks): Gas-fluid level (arrow) and gas bubbles (arrowheads) - pathognomonic of superinfection (infected necrosis). This carries ~80% of all mortality from acute pancreatitis.

Summary: CT Patterns at a Glance

CT Severity Index (CTSI): Scores 0-10 combining degree of pancreatic inflammation (0-4 pts), necrosis (0-4 pts), and extrapancreatic complications (2 pts). Scores 8-10 = severe disease with ~50% organ failure rate.