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1. Delirium

Definition

DSM-5 Diagnostic Criteria (4 Key Features)

1. Disturbance in attention and awareness
2. Develops acutely, represents a change from baseline, fluctuates in severity during the day
3. Additional disturbances in cognition (memory, disorientation, language, visuospatial ability, perception)
4. Not better explained by another neurocognitive disorder; does not occur in the context of a coma

Subtypes by Psychomotor Activity

Risk Factors

Pathophysiology

• Cholinergic deficiency (most pronounced with anticholinergic drugs)
• Glutamatergic excess (hepatic encephalopathy, uremia, sepsis, alcohol withdrawal)
• GABAergic deficit
• Noradrenergic, serotonergic, and dopaminergic imbalance
• Neuroinflammation

Delirium vs. Dementia

Common Causes (AEIOU-TIPS mnemonic widely used)

• Metabolic: hypoglycemia (most common), hypoxia, hypo/hypernatremia, hypercapnia, hyperglycemia, uremia, hepatic failure
• Infection/Sepsis: any CNS or systemic infection
• Drugs: anticholinergics, benzodiazepines, opioids, steroids, poly-pharmacy
• Withdrawal: alcohol, sedative-hypnotics
• Structural CNS: stroke (usually with other deficits), trauma, CNS vasculitis
• Endocrine: thyroid storm, adrenal insufficiency
• Cardiac: hypoperfusion, post-cardiac surgery

Assessment Tools (ED Setting)

Management

• Treat the underlying cause
• Reorientation, familiar faces, minimize room changes
• Restore sleep-wake cycle (light during day, dark at night)
• Correct sensory deficits (glasses, hearing aids)
• Minimize anticholinergic and sedative medications
• Early mobilization

• Haloperidol 0.5-1 mg PO/IM - traditional first-line for hyperactive delirium
• Atypical antipsychotics (quetiapine, olanzapine) - similar efficacy
• Avoid benzodiazepines except in alcohol/sedative withdrawal delirium (worsens most other delirium)
• Dexmedetomidine in ICU setting
• Rosen's Emergency Medicine, p. 1478-1481 | Textbook of Family Medicine 9e, p. 47

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2. Types of Pain

1. Nociceptive Pain

• Transient pain in response to a noxious stimulus activating high-threshold afferents (nociceptors)
• Serves a protective function - warns of actual or potential tissue damage
• Stimulus-dependent: stops when stimulus removed
• Examples: acute injury, procedural pain
• Responds well to NSAIDs and opioids

2. Inflammatory Pain

• Spontaneous hypersensitivity to pain occurring in response to tissue damage and inflammation
• Two key phenomena: allodynia (pain from normally non-painful stimuli) and hyperalgesia (exaggerated pain response)
• Examples: postoperative pain, trauma, arthritis, rheumatic disease
• Responds well to NSAIDs/COX-2 inhibitors, steroids

3. Neuropathic Pain

• Spontaneous pain and hypersensitivity associated with damage to or lesions of the nervous system
• Can be peripheral (damage to peripheral nerves) or central (spinal cord/brain)
• Often described as burning, shooting, electric, stabbing
• Examples: peripheral neuropathy (diabetic), postherpetic neuralgia, phantom limb pain, CRPS
• Responds to anticonvulsants (gabapentin, pregabalin), TCAs, SNRIs; opioids less effective

4. Functional Pain

• Hypersensitivity to pain resulting from abnormal central processing of normal input (no identifiable tissue damage or nerve lesion)
• Central sensitization is the key mechanism
• Examples: fibromyalgia, irritable bowel syndrome (pathologic), functional abdominal pain
• Responds to centrally acting agents: SNRIs (duloxetine), TCAs, gabapentin, CBT

Clinical Relevance

"Primary analgesics are more efficacious in nociceptive and inflammatory pain, whereas adjuvant agents are more efficacious in neuropathic and functional pain." - Firestein & Kelley's Rheumatology

• Duration: Acute vs. chronic (>3 months)
• Etiology: Cancer pain, arthritis pain, cardiac pain
• Location: Headache, low back pain, visceral pain
• Mechanism: Somatic (well-localized) vs. visceral (poorly localized, referred) vs. neuropathic
• Firestein & Kelley's Textbook of Rheumatology, p. 1390 | Morgan & Mikhail's Clinical Anesthesiology 7e

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3. Lines for Fluid (Vascular Access)

Peripheral IV (PIV)

• First-line for most patients
• Sites: dorsal hand, forearm, antecubital fossa, external jugular
• For vasoactive medications: use large-gauge (18G or larger) at antecubital fossa or more proximally
• Ultrasound guidance can access brachial or proximal basilic veins in difficult access
• Note: standard 3-5 cm catheters in deep veins have high early failure/dislodgement rates

Central Venous Catheter (CVC) / Central Line

• Poor peripheral access
• Administration of vasopressors (safer - avoids extravasation injury)
• Measurement of CVP (though clinical utility debated)
• Simultaneous infusion of multiple incompatible drugs

• Single-lumen: simple fluid/drug delivery
• Triple-lumen: most common in ICU; allows CVP measurement + multiple infusions simultaneously

Intraosseous (IO) Access

• Used when peripheral and central access cannot be rapidly obtained
• Can deliver all fluids, drugs, blood products
• Sites: proximal tibia (most common), humeral head, distal femur, sternum
• "Easy and can provide a temporary method of administering fluid resuscitation and medications to adults and children"
• Temporary - convert to IV/CVC when feasible

Summary Hierarchy in Shock:

1. PIV x2 large bore (18G+) - attempt first
2. CVC (IJ, subclavian, femoral) - if PIV inadequate
3. IO - if above fail rapidly

• Rosen's Emergency Medicine, p. 62

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4. Olanzapine

Classification

• Second-generation (atypical) antipsychotic - thienobenzodiazepine class
• Mechanism: D2 antagonist + 5-HT2A antagonist + muscarinic, histaminergic, adrenergic antagonism

Licensed Indications

1. Schizophrenia - acute and maintenance; mildly sedating, useful in agitation
2. Bipolar mania/mixed states - monotherapy or adjunct to lithium/valproate
3. Bipolar I depression - combined with fluoxetine (Symbyax)
4. Acute agitation - IM formulation (schizophrenia or bipolar I mania)

Key Efficacy Points

• Superior to haloperidol on negative symptoms and depression rating
• In CATIE trial: lowest discontinuation rate among antipsychotics tested
• Effective for both psychotic and non-psychotic bipolar patients
• May be more effective than lithium in mania
• IM olanzapine: effective in acutely agitated patients; similar to IM haloperidol for positive symptoms, with more rapid onset

Dosing

• Oral: 5-20 mg/day (typical: 10 mg/day)
• IM (acute agitation): 10 mg IM; repeat doses possible

Adverse Effects

BLACK BOX WARNING

Metabolic Effects (most significant concern)

Other Adverse Effects

• Orthostatic hypotension (especially early in treatment)
• Sedation / somnolence (useful property in agitation, but side effect in outpatients)
• EPS (lower than FGAs, but still possible)
• Prolactin elevation (less than risperidone)
• Liver enzyme elevation (especially in pediatric patients)
• QTc prolongation (less than other antipsychotics)
• Excreted in breast milk (generally low concentration)

In Children/Adolescents

Monitoring

• Fasting glucose and lipid panel before and after starting
• Weight at baseline and regularly
• Liver enzymes (especially in children)

Olanzapine/Samidorphan Combination (Lybalvi)

• Available in some countries; minimizes metabolic side effects, particularly weight gain
• Maudsley Prescribing Guidelines 15e, p. 327 | Kaplan & Sadock's Psychiatry, p. 9265

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5. Vaseline Gauze (Petroleum Jelly / Petrolatum Gauze)

What It Is

Properties

• Non-adherent - petroleum jelly prevents gauze fibres sticking to the wound bed
• Maintains a moist wound environment to facilitate epidermal migration
• Allows gas exchange between wound and environment
• Sterile, non-toxic, non-allergenic, cost-effective

Ideal For

• Clean wounds with minimal exudate
• Low-risk contamination wounds
• Skin graft coverage
• Burns (as an alternative to topical agents; requires less frequent dressing changes than plain gauze)
• Post-surgical wounds, donor sites

Advantages vs. Disadvantages

Comparison with Other Dressings

• Bailey & Love's Surgery 28e, p. wound dressings | Rosen's Emergency Medicine, p. 837

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Menstruation Pain (Dysmenorrhea) - Treatment

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Definitions

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Pathophysiology of Primary Dysmenorrhea

1. During the luteal phase, progesterone stimulates prostaglandin production in the endometrium
2. After progesterone withdrawal at the end of the cycle, the endometrium sloughs and releases PGF2α in large amounts
3. PGF2α stimulates myometrial contractions → decreased uterine blood flow → ischemia ("uterine angina")
4. This ischemia produces the cramping pain

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Clinical Features of Primary Dysmenorrhea

• Onset: within 6-12 months of menarche (almost always within 2 years)
• Pain: sharp, spasmodic, lower abdomen/suprapubic
• Timing: begins within hours of menstrual flow onset, peaks on day of heaviest flow, resolves within 2-3 days
• Associated symptoms: nausea, vomiting, diarrhea, headache, fatigue
• Normal pelvic examination and ultrasound

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Treatment of Primary Dysmenorrhea

Step 1 - First-Line: NSAIDs (Prostaglandin Synthase Inhibitors)

• Start 1-3 days before expected menses onset (or at the very first sign of pain/minimal bleeding - if cycles are irregular)
• Take continuously every 6-8 hours (not on-demand) - this prevents reformation of prostaglandin byproducts
• Continue for the first 2-3 days of menstrual flow
• Allow a 4-6 month trial before concluding failure

If a drug from one NSAID class is not effective, try a drug from a different NSAID class before declaring NSAID failure.

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Step 2 - Second-Line: Hormonal Contraceptives

• NSAIDs fail or are contraindicated
• Patient also desires contraception (can be used as first-line in this context)

• Inhibit ovulation
• Decrease endometrial proliferation
• Create an endocrine milieu similar to the early proliferative phase - when prostaglandin levels are naturally lowest

• Combined OCP (estrogen + progestin) - cyclic or continuous/extended cycle (continuous is equally efficacious and reduces total number of periods)
• Progestin-only pills
• Transdermal patch
• Vaginal ring (NuvaRing)
• Injectable progestin (Depo-Provera)
• Levonorgestrel-releasing IUD (Mirena) - reduces endometrial proliferation and prostaglandin production

Combination therapy (NSAIDs + hormonal contraception) may be more effective than either alone.

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Step 3 - If Steps 1+2 Fail (2-3 months)

• Weak opioids (codeine, hydrocodone) for 2-3 days/month - short-term bridge while investigating for secondary causes
• Before adding narcotics, assess and address psychological factors contributing to pain

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Non-Pharmacological Options

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Surgical Options (Rarely Used)

• Laparoscopic uterine nerve ablation (LUNA)
• Presacral neurectomy - interrupts pain signal pathways
• Hysterectomy - last resort

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Secondary Dysmenorrhea

Key Differences from Primary

Common Causes

1. Endometriosis (most common cause of secondary dysmenorrhea)
   • Endometrial glands/stroma outside the uterus (ovaries, cul-de-sac, peritoneum)
   • Associated features: dyspareunia, dyschezia (painful defecation), subfertility, cyclic pelvic pain starting up to 2 weeks before menses
   • Definitive diagnosis: laparoscopy
2. Adenomyosis - endometrial tissue within the myometrium; uterus often enlarged and tender
3. Copper (non-hormonal) IUD - increases local prostaglandin production
4. Subacute endometritis / PID
5. Ovarian cysts
6. Cervical stenosis
7. Congenital pelvic malformations

Treatment Principle

• For endometriosis: OCPs, progestins (Depo-Sub Q Provera 104), GnRH agonists (leuprolide), danazol; laparoscopic excision/ablation
• For copper IUD: switch to LNG-IUD or remove
• For PID/endometritis: antibiotics

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Summary Treatment Algorithm

Dysmenorrhea
     │
     ├── Primary (normal exam + US)
     │        │
     │        ├── 1st line: NSAIDs (start 1-3 days before, q6-8h)
     │        ├── 2nd line: Hormonal contraceptives (or combine with NSAIDs)
     │        ├── Adjuncts: Heat, TENS, acupuncture
     │        └── Refractory: Short opioids / surgical nerve ablation
     │
     └── Secondary (pelvic pathology present)
              └── Treat the underlying cause
                  (endometriosis → OCP/GnRH agonist/surgery
                   copper IUD → switch to LNG-IUD
                   PID → antibiotics)

• Berek & Novak's Gynecology, p. 573-576 | Swanson's Family Medicine Review, p. 406 | Harrison's Principles of Internal Medicine 22e