Clinical Assessment: Unconscious Female - Morphine Overdose + Hypoglycemia + Hyponatremia

Problem Summary

IMMEDIATE MANAGEMENT (First 5 minutes - simultaneous)

1. Airway, Breathing, Circulation (ABC)

• Position airway - jaw thrust, head tilt
• High-flow O2 via non-rebreather mask
• Attach pulse oximetry + continuous cardiac monitor
• IV access x2 (large bore)
• If respiratory rate <8/min or SpO2 <90% despite O2 - prepare for bag-mask ventilation or intubation

2. Correct Hypoglycemia FIRST (HGT 30 mg/dL)

• Give 50% Dextrose (D50W) 50 mL IV bolus (= 25 g glucose)
• Follow immediately with 10% dextrose infusion to maintain glucose
• Recheck HGT at 15 and 30 minutes
• If IV access fails: Glucagon 1 mg IM
• This must happen simultaneously with/before naloxone - hypoglycemia alone can cause unconsciousness and mimic opioid toxicity
• (Goldman-Cecil Medicine; Miller's Anesthesia 10e)

3. Naloxone for Opioid Reversal

Naloxone Dosing (Titrate to clinical response)

• IM: 0.4-2 mg
• Intranasal: 2 mg (as effective as IM/IV)

• Calculate "wake-up dose" (e.g., 0.8 mg), then infuse 2/3 of that per hour (= 0.5 mg/hr in this case) in normal saline
• Monitor for re-sedation (naloxone wears off before morphine does)
• (Tintinalli's Emergency Medicine; Roberts & Hedges' Clinical Procedures)

Investigations to Order

Urgent (bedside / stat):

• Serial HGT (every 15 min initially)
• ECG (Na 126 can cause arrhythmias)
• SpO2 / ABG (assess respiratory failure, CO2 retention)
• Urine dipstick

Blood tests (stat):

• Serum electrolytes (Na, K, Cl, bicarbonate) - confirm Na 126 and check K
• RFT (renal function - creatinine, BUN) - for cause of hyponatremia
• LFT (hepatic cause of altered sensorium)
• CBC (infection, bleeding)
• Serum osmolality + urine osmolality + urine Na (to classify hyponatremia: SIADH vs. hypovolemic vs. dilutional)
• Serum cortisol (adrenal insufficiency can cause both hyponatremia and hypoglycemia - important cause to rule out)
• Blood glucose (formal lab value)
• Urine/serum toxicology screen (confirm opioids; rule out poly-drug ingestion)
• Thyroid function (TSH) (hypothyroidism causes hyponatremia + hypoglycemia + CNS depression)
• Serum lactate (if shocked)
• Coagulation (if bleeding suspected)

Imaging (as needed):

• CT brain (if no response to glucose + naloxone - rule out structural cause of coma)
• CXR (aspiration pneumonia, pulmonary edema)

Management of Hyponatremia (Na 126 mEq/L)

• Target: raise Na by no more than 8-10 mEq/L per 24 hours to prevent osmotic demyelination syndrome (ODS/central pontine myelinolysis)
• If severely symptomatic (seizures, coma): 3% NaCl infusion - 150 mL bolus over 20 min; can repeat once; recheck Na hourly
• For less urgent: fluid restriction + treat underlying cause
• Identify and treat cause: SIADH, adrenal insufficiency, hypothyroidism, diuretics, polydipsia
• (Goldman-Cecil Medicine; Bradley & Daroff's Neurology)

Key Diagnostic Point

1. Opioid effect (morphine - miosis, CNS depression)
2. Severe hypoglycemia (HGT 30 mg/dL - can cause coma independently)
3. Symptomatic hyponatremia (Na 126 - CNS edema, encephalopathy)

CT Brain vs MRI Brain - When and What to Look For in This Patient

The Core Rule: Stabilise FIRST, Scan SECOND

• Has a protected airway (or is intubated)
• Has been given glucose (HGT 30 - treat before scan)
• Has received naloxone trial with reassessment
• Has blood pressure and SpO2 monitored

1. IV dextrose (glucose correction)
2. Naloxone 0.4-2 mg IV with repeat doses
3. Supportive airway management

CT Brain (Non-Contrast) - Do FIRST

When to do it in this patient:

• No response to naloxone up to 10 mg total + glucose correction
• Focal neurological signs appear (asymmetric pupils, hemiplegia, extensor posturing)
• Suspected head injury (fall at time of collapse)
• History unclear - need to rule out structural cause of coma
• New onset seizure
• Evidence of raised ICP (hypertension + bradycardia + irregular breathing = Cushing's triad)

Why CT first (not MRI):

• Faster (minutes vs. 20-40 min for MRI)
• Available at almost all emergency departments
• Does not require patient cooperation or stillness for long periods
• Better for detecting acute bleeds, skull fractures, mass effect
• Safer for unstable patients

What CT Brain will show in this patient's context:

MRI Brain - Do AFTER CT or When CT is Normal but Patient Doesn't Improve

When to do MRI in this patient:

The most important MRI scenario in THIS patient - Osmotic Demyelination Syndrome (ODS):

• Timing: Symptoms appear 2-7 days after sodium correction
• Clinical: Initially improves, then deteriorates again with: dysarthria, dysphagia, spastic quadriparesis, locked-in syndrome, coma
• MRI findings:
  • T2/FLAIR hyperintensity in the central pons (trident or bat-wing pattern)
  • May also involve thalami, basal ganglia, corpus callosum
  • DWI (diffusion-weighted imaging) shows restricted diffusion early
• CT is often normal in early ODS - this is exactly why MRI is needed

MRI Sequences - What to Request

Practical Decision Flow for This Patient

Glucose + Naloxone given
        |
        ↓
    Patient wakes up?
   /              \
 YES               NO
  |                 |
Elective CT      URGENT CT Brain (non-contrast)
brain if          (rule out bleed, mass, herniation)
clinically              |
indicated         CT Normal?
                 /        \
              YES           NO → Act on finding
               |             (neurosurgery, etc.)
        MRI Brain
        (if still not
        responding or
        Na overcorrected)

Key Points Summary

Dysplasia vs Metaplasia

Head-to-Head Comparison Table

Metaplasia - Detailed

Classic Examples:

Squamous Metaplasia (Bronchus) - Diagram and Histology:

Dysplasia - Detailed

Morphological Features of Dysplasia:

Spectrum of Dysplasia (cervix as model):

Normal epithelium
      ↓ (persistent HPV / irritant)
Mild dysplasia (CIN I) - lower 1/3 involved
      ↓
Moderate dysplasia (CIN II) - lower 2/3 involved
      ↓
Severe dysplasia (CIN III) - full thickness involved
      ↓
Carcinoma in Situ (CIS) - full thickness, NO basement membrane breach
      ↓
Invasive Carcinoma - basement membrane BREACHED

The Relationship Between the Two

Chronic Injury / Irritant
        ↓
   METAPLASIA  ──────────────────→  Metaplastic epithelium (survives better)
        ↓ (if stimulus persists)
   DYSPLASIA  ────────────────────→  Premalignant change (mutations accumulate)
        ↓
  Carcinoma in Situ
        ↓
  Invasive Carcinoma

• Bronchial squamous metaplasia (smoker) → can develop squamous cell carcinoma
• Barrett's oesophagus (intestinal metaplasia) → can develop dysplasia → adenocarcinoma
• Gastric intestinal metaplasia → risk factor for gastric adenocarcinoma

One-Line Memory Hooks

• Metaplasia = "Wrong cell, right behaviour" - adaptive, orderly, reversible
• Dysplasia = "Right place, wrong behaviour" - disordered, abnormal, premalignant
• Carcinoma in situ = dysplasia so severe it fills the full epithelial thickness - but hasn't crossed the basement membrane yet