NLE Endocrine & Metabolic Nursing — Pituitary, Thyroid & Parathyroid DisordersStudy Notes

The posterior pituitary releases ADH (vasopressin), which acts on the kidneys' collecting ducts to promote water reabsorption, concentrating the urine and maintaining serum osmolality. ADH disorders present as mirror-image pathologies: excessive water retention versus excessive water loss. ### 1.1 Syndrome of Inappropriate Antidiuretic Hormone (SIADH) — Excess ADH **Pathophysiology:** Excessive ADH release causes the kidneys to reabsorb more water than normal, diluting the blood and resulting in hyponatremia (low serum sodium). This occurs without the typical fluid retention and edema seen in other conditions because the excess water distributes throughout the intracellular and extracellular compartments. **Common Causes:** - Malignancies: small-cell lung cancer (most common), pancreatic cancer, bladder cancer - Central nervous system disorders: head injury, subarachnoid hemorrhage, meningitis, encephalitis, seizures - Respiratory conditions: pneumonia, tuberculosis, positive-pressure ventilation - Medications: antidepressants (SSRIs), antipsychotics, carbamazepine, cyclophosphamide, vincristine, oxytocin - Post-operative state following major surgery or trauma - Idiopathic (unknown cause) **Clinical Manifestations:** - **Neurological (most critical):** headache, confusion, lethargy, personality changes, disorientation, irritability - **Severe/progressive:** seizures, coma, death (from cerebral edema and increased intracranial pressure) - **Fluid/electrolyte signs:** absence of edema despite fluid retention (distinguishes SIADH from other causes of hyponatremia), weight gain without visible swelling, nausea and vomiting - **Urinary:** decreased urine output, concentrated/dark urine **Laboratory Findings:** - **Serum sodium <130 mEq/L** (severe if <120 mEq/L) - **Serum osmolality <280 mOsm/kg** (diluted blood) - **Urine osmolality >100 mOsm/kg** (inappropriately concentrated despite dilute serum) - **Urine sodium >40 mEq/L** - **Normal renal, adrenal, and thyroid function** (rules out other causes) **NANDA Nursing Diagnoses (Maslow-Prioritized):** 1. **Risk for seizures/Risk for injury** (Physiologic safety—Level 2) related to severe hyponatremia and cerebral edema 2. **Fluid volume excess** (Physiologic—Level 1) related to inappropriate ADH release 3. **Acute confusion** (Cognitive/psychological—Level 3) related to hyponatremia and altered osmolality 4. **Deficient knowledge** (Education—Level 4) regarding fluid restriction and medication adherence **Clinical Management:** **Acute/Severe (sodium <120 mEq/L with symptoms):** - **Hypertonic saline (3% NaCl) intravenously**, initiated slowly; goal is to raise sodium by **8–10 mEq/L in 24 hours** or **10–12 mEq/L if symptomatic**—rapid correction risks osmotic demyelination syndrome (permanent neurological damage) - **Continuous cardiac and neurological monitoring** - **Maintain IV access**; some settings require ICU-level care **Chronic/Mild-Moderate (sodium >125 mEq/L):** - **Strict FLUID RESTRICTION** (cornerstone of therapy): typically 500–1000 mL/24 hours or 800 mL/day - **Normal saline (0.9% NaCl) may paradoxically worsen hyponatremia** because it is hypotonic relative to urine osmolality; use carefully and only if sodium is severely low - **Demeclocycline** (600–900 mg/day in divided doses): tetracycline antibiotic that blocks ADH action in the kidney; takes 1–2 weeks for full effect - **Vaptans (vasopressin-receptor antagonists),** e.g., tolvaptan: newer agents that block V2 receptors, promoting aquaresis (urinary water loss); used cautiously in specialized settings **Nursing Interventions:** - **Restrict ALL fluid intake** (oral and IV), including foods that are liquids (gelatin, soup, ice cream); post the restriction at the bedside and educate the patient/family about the rationale (can be difficult when the patient is thirsty) - **Daily weight:** same scale, same time (morning before breakfast), light clothing; expected weight loss of 0.5–1 kg/day with fluid restriction - **Strict intake and output:** measure all fluid intake and output; even small volumes count (e.g., 30 mL of juice, 50 mL of IV medication) - **Serum sodium checks:** serial labs as ordered (often every 4–6 hours initially until stable, then daily) - **Neurological assessments:** hourly or per protocol—level of consciousness, orientation, presence/absence of headache, seizure activity; use a standardized scale (e.g., Glasgow Coma Scale if altered consciousness) - **Seizure precautions:** padded side rails, call bell within reach, oxygen and suction at bedside, emergency medications (lorazepam, diazepam) readily available - **Mouth care:** because fluid restriction increases thirst, frequent oral care (mouth rinse without swallowing, ice chips if permitted, lip balm) helps comfort - **Patient/family education:** explain the fluid restriction, rationale, expected duration, and signs of over-correction (water intoxication: drowsiness, weight gain, return of hyponatremia if DDAVP-like substances are given) - **Monitor for complications:** correction that is too rapid → osmotic demyelination syndrome (confusion, ataxia, seizures, coma) occurring 24–72 hours after sodium correction; if sodium rises >12 mEq/L in 24 hours, slow the rate of correction --- ### 1.2 Diabetes Insipidus (DI) — Deficient ADH **Pathophysiology:** Insufficient ADH (central/neurogenic DI) or renal resistance to ADH (nephrogenic DI) prevents adequate water reabsorption. The kidney loses massive amounts of dilute urine, leading to severe water loss, volume depletion, and hypernatremia (high serum sodium). The term "diabetes" refers to polyuria and polydipsia (not blood sugar). **Types:** - **Central (neurogenic) DI:** destruction or dysfunction of the hypothalamic-posterior pituitary axis; causes include pituitary/hypothalamic tumors, head trauma, post-neurosurgery, infection (meningitis), infiltrative diseases (sarcoidosis, tuberculosis), or idiopathic - **Nephrogenic DI:** kidneys are unresponsive to ADH; causes include chronic kidney disease, hypercalcemia, hypokalemia, lithium therapy, amphotericin B, or genetic mutations **Clinical Manifestations:** - **Polyuria:** up to 3–20 L/day (compared to normal 1.5 L/day); sudden onset - **Polydipsia:** intense, unquenchable thirst; patient drinks constantly, often preferring cold/ice water - **Nocturia:** multiple awakenings at night to void - **Dehydration signs:** dry mucous membranes, decreased skin turgor, weakness, fatigue - **If uncorrected/fluids restricted:** confusion, irritability, seizures, hypernatremia-induced altered mental status **Laboratory Findings:** - **Serum sodium >145 mEq/L** (high) - **Serum osmolality >295 mOsm/kg** - **Urine osmolality <200 mOsm/kg** (dilute; inappropriate for high serum osmolality) - **Urine specific gravity <1.005** (very dilute) **Diagnostic Test: Water Deprivation Test** For suspected DI, restrict water and monitor urine output/osmolality and serum sodium: - **Central DI:** urine osmolality increases and polyuria decreases when desmopressin (synthetic ADH) is given - **Nephrogenic DI:** urine osmolality remains low despite desmopressin; no response **NANDA Nursing Diagnoses (Maslow-Prioritized):** 1. **Deficient fluid volume** (Physiologic—Level 1) related to ADH deficiency/renal unresponsiveness 2. **Risk for hypernatremia** (Physiologic—Level 1) related to excessive water loss 3. **Interrupted sleep pattern** (Physiologic—Level 1) related to nocturia 4. **Deficient knowledge** (Education—Level 4) regarding lifelong desmopressin therapy and fluid replacement **Clinical Management:** **For Central DI:** - **Desmopressin (DDAVP, synthetic ADH):** replacement therapy - **Routes:** intranasal (spray, metered-dose inhaler, or intranasal tube), oral (tablets), subcutaneous/IM, or IV - **Intranasal dosing:** typically 5–20 mcg once or twice daily; spray or inhaler form allows self-titration - **Oral dosing:** 0.1–0.2 mg three times daily; titrate to response - **Onset:** intranasal 15–30 minutes, oral 1–2 hours; duration 8–24 hours - **Adjust dose based on thirst, polyuria reduction, and serum sodium** (goal: normal, 135–145 mEq/L) **For Nephrogenic DI:** - Desmopressin is ineffective (kidneys do not respond); instead use: - **Thiazide diuretics** (hydrochlorothiazide): paradoxically reduces urine output in nephrogenic DI by mild volume depletion (increases proximal tubule reabsorption) - **NSAIDs** (indomethacin): reduce prostaglandin-mediated ADH antagonism - **Adequate hydration and low-sodium diet** to minimize stimulus for polyuria **For All DI:** - **Free access to water** (never restrict fluid in a conscious patient with DI—they will become severely dehydrated and hypernatremic) - **Replace fluid output:** calculate as intake = urine output + insensible losses (approximately 500 mL/day) - **Maintain IV access** if unable to drink (e.g., post-operative, comatose state) **Nursing Interventions:** - **Accurate intake and output:** measure ALL urine (even overnight), note time and volume; calculate 24-hour output - **Daily weight:** assess for dehydration (loss) or over-treatment (gain) - **Serum sodium:** monitor before and after desmopressin initiation, and whenever dose adjusted - **Desmopressin administration:** - **Intranasal:** teach patient to blow nose gently first, insert spray/device, inhale gently; avoid excessive sniffing; rotate nares to prevent irritation - **Oral tablets:** take with or without food; water/fluids taken at meal times - **Document effectiveness:** time dosed, urine output reduction, patient response - **Patient education (critical for outpatient success):** - Lifelong therapy; never stop abruptly - Carry medication at all times (especially during travel) - Signs of over-treatment: headache, drowsiness, nausea, confusion, weight gain, increased thirst = water retention/hyponatremia → reduce dose - Signs of under-treatment: excessive thirst, polyuria, weakness = inadequate replacement → increase dose - Drink to thirst; maintain access to fluids - If nausea or polyuria worsens, or headache develops, notify health care provider - Medical alert identification helpful - **Sleep support:** nocturia often improves as desmopressin dose is optimized; ensure bathroom safety at night (e.g., night light, bedside commode) - **Skin integrity:** frequent urination increases perineal moisture; teach perineal hygiene, use protective pads if needed --- **Memory Aid for Posterior Pituitary Disorders:** **SIADH = "Soaked" (water intoxicated):** - Excess ADH → water retained, sodium diluted (LOWSodium) - Concentrated urine, dilute blood - Management: RESTRICT fluids, correct sodium slowly **DI = "Dry" (water depleted):** - Deficient ADH → water lost, sodium concentrated (HIGHsodium) - Dilute urine, concentrated blood - Management: REPLACE fluids + desmopressin (central DI)

The thyroid gland produces thyroid hormones T3 (triiodothyronine) and T4 (thyroxine), which increase cellular metabolic rate, heat production, oxygen consumption, and sensitivity to catecholamines. Thyroid-stimulating hormone (TSH) from the anterior pituitary drives hormone synthesis and release. Thyroid disorders result in excess (hyperthyroidism) or deficiency (hypothyroidism) of thyroid hormone, with two life-threatening crises: thyroid storm (dangerous excess) and myxedema coma (dangerous deficiency). ### 2.1 Thyroid Function Assessment **Key Laboratory Tests:** - **TSH (thyroid-stimulating hormone):** most sensitive screening test; moves *opposite* to hormone level in primary thyroid disease (low TSH = hyperthyroid gland; high TSH = hypothyroid gland) - **Free T4 and Free T3:** actual circulating hormone levels; not bound to proteins - **Total T4 and T3:** includes protein-bound hormone; less useful clinically - **Thyroid antibodies:** TPO (thyroid peroxidase) and anti-thyroglobulin in autoimmune thyroid disease - **Radioactive iodine uptake (RAIU):** functional scan; high uptake in Graves' disease (gland is hyperactive), low uptake in thyroiditis or factitious thyroid hormone use **Interpretation in Primary Thyroid Disease:** | Condition | TSH | Free T4 | Free T3 | |---|---|---|---| | Hyperthyroidism | **LOW** | **HIGH** | **HIGH** | | Hypothyroidism | **HIGH** | **LOW** | **LOW** | | Normal | Normal | Normal | Normal | **Goiter Assessment:** Any visible or palpable enlargement of the thyroid gland; can occur in hyper- or hypothyroid states. Assess for: - Size and consistency of gland - Dysphagia (difficulty swallowing) or dyspnea (difficulty breathing) suggesting tracheal compression - Stridor or hoarseness (nerve compression) - Venous engorgement or bruit on auscultation (hyperthyroid goiter may be vascular) --- ### 2.2 HYPERTHYROIDISM: Thyroid Hormone Excess **Pathophysiology:** Excessive thyroid hormone accelerates metabolism, increasing heat production, oxygen consumption, and sympathomimetic effects. Graves' disease (autoimmune) is the most common cause worldwide (90% of hyperthyroidism cases). **Causes:** - **Graves' disease** (autoimmune): thyroid-stimulating immunoglobulin (TSI) antibodies bind TSH receptors, stimulating hormone synthesis and gland growth; associated with exophthalmos (eye protrusion) and pretibial myxedema (non-pitting edema of the shins) - **Toxic multinodular goiter** (Plummer's disease): autonomously functioning nodules, usually in older patients - **Toxic adenoma:** single hyperactive nodule - **Thyroiditis (subacute, silent):** viral or autoimmune inflammation causing release of preformed hormone (transient phase) - **Iodine excess (Jod-Basedow effect):** iodine-containing drugs (amiodarone, contrast agents) in susceptible patients - **Factitious hyperthyroidism:** intentional ingestion of thyroid hormone - **Pituitary adenoma:** rare, causes elevated TSH + high T4 (secondary hyperthyroidism) **Clinical Manifestations ("Everything sped up"):** - **Metabolic:** weight loss despite increased appetite, heat intolerance, diaphoresis (excessive sweating), increased BMR - **Cardiovascular:** tachycardia (>90 bpm at rest), palpitations, arrhythmias (atrial fibrillation), hypertension, widened pulse pressure - **Neuropsychiatric:** nervousness, anxiety, irritability, emotional lability, insomnia, tremor (fine), hyperreflexia, personality changes (aggression, emotional instability) - **Gastrointestinal:** increased appetite but net weight loss, diarrhea (increased GI motility), nausea - **Integumentary:** warm, moist skin; fine hair; alopecia (hair loss) - **Ocular (Graves' disease only):** exophthalmos (bulging eyes, due to orbital tissue inflammation/edema), lid retraction (upper lid higher than normal), lid lag (eyelid lags behind eye when looking downward), periorbital edema, conjunctival injection - **Musculoskeletal:** muscle weakness, fatigue (despite hyperactivity), osteoporosis (chronic excess hormone) - **Reproductive:** irregular menses, decreased libido, gynecomastia (men), reduced fertility **Laboratory Findings:** - **LOW TSH** (<0.5 mIU/L) - **HIGH Free T4 and/or Free T3** - **RAIU scan:** high uptake (Graves'), low uptake (thyroiditis or factitious) - **TSI (thyroid-stimulating immunoglobulin):** positive in Graves' disease **NANDA Nursing Diagnoses (Maslow-Prioritized):** 1. **Ineffective thermoregulation** (Physiologic—Level 1) related to increased metabolic rate and heat production 2. **Decreased cardiac output/Risk for arrhythmia** (Physiologic—Level 1) related to sympathomimetic excess (tachycardia, palpitations) 3. **Imbalanced nutrition: less than body requirements** (Physiologic—Level 1) related to hypermetabolism and weight loss 4. **Anxiety** (Psychological—Level 3) related to hypermetabolic state and catecholamine sensitivity 5. **Disturbed sleep pattern** (Physiologic—Level 1) related to hyperactivity and nervous tension 6. **Risk for injury to eyes** (Physiologic safety—Level 2) related to exophthalmos and lid changes (Graves') 7. **Deficient knowledge** (Education—Level 4) regarding antithyroid drugs, beta-blockers, and management strategies **Clinical Management:** **First-Line Pharmacology:** **1. Antithyroid Drugs (inhibit hormone synthesis, NOT hormone release):** - **Methimazole (Tapazole):** - Dose: 10–40 mg/day in divided doses (or higher initially) - Onset: slow, 2–4 weeks for clinical effect (must block synthesis first); effect peaks at 4–8 weeks - Preferred in non-pregnant patients - Side effects: rash, arthralgia, hepatitis (rare), **agranulocytosis** (1 in 500) - Monitoring: baseline and periodic WBC, liver function tests - **Propylthiouracil (PTU):** - Dose: 100–300 mg/day in divided doses (or higher initially) - Onset: slow, similar to methimazole - **Preferred in first trimester pregnancy** (crosses placenta less than methimazole; methimazole causes rare fetal abnormalities—methimazole embryopathy) - Side effects: rash, arthralgia, **hepatotoxicity** (more common than with methimazole), **agranulocytosis** - Monitoring: baseline and periodic WBC, liver function tests (LFTs, especially AST/ALT) - **Patient Teaching for Antithyroid Drugs:** - **Report immediately: sore throat, fever, unusual bleeding/bruising, severe rash, right upper quadrant (RUQ) pain, clay-colored stools, jaundice → signs of agranulocytosis or hepatitis** - Effect is slow; expect 2–4 weeks for clinical improvement - Take regularly; do not stop abruptly (may precipitate thyroid storm) - Minor rash (not itchy) is common and often resolves without stopping drug - Monitor for hypothyroidism (opposite problem) as dose reduced; may need levothyroxine added **2. Beta-Blockers (symptom relief, NOT thyroid hormone reduction):** - **Propranolol 10–40 mg three to four times daily (or 40–160 mg long-acting daily):** - Blocks adrenergic effects: tachycardia, tremor, palpitations, anxiety - Onset: fast, within hours—patient feels relief while waiting for antithyroid effect - **Additional advantage:** propranolol also reduces peripheral conversion of T4 → T3 (more active form) - Contraindications: asthma, COPD, bradycardia, heart block, heart failure - Side effects: fatigue, sexual dysfunction, depression, hypoglycemia in diabetics - Monitor: heart rate (target 60–80 bpm), blood pressure, symptoms improvement - **Other beta-blockers:** atenolol, metoprolol, or others per clinical need; not as effective as propranolol for peripheral T4→T3 conversion **3. Iodine Preparations (used only PRE-OPERATIVELY to reduce gland vascularity):** - **Lugol's solution (5% iodine + 10% potassium iodide) or SSKI (saturated solution of potassium iodide):** - **MUST be given AFTER antithyroid drugs (methimazole or PTU) are initiated** (3–7 days) to prevent iodine from serving as substrate for hormone synthesis - Effect: rapid (1–3 days); reduces gland vascularity, decreases hormone release, decreases hormone synthesis (Wolff-Chaikoff effect) - Dose: 5–7 drops of Lugol's or SSKI three times daily, **diluted in water or juice** (for taste and to prevent tooth staining) - **Given THROUGH A STRAW** (to minimize teeth staining) - Onset of effect: 24–48 hours; duration: 1–2 weeks - Side effects: iodism (metallic taste, sore mouth/throat, swollen salivary glands, increased salivation, GI upset) - Duration: only weeks; not for long-term use - **Do NOT use long-term** (leads to iodine escape and worsening hyperthyroidism) **4. Radioactive Iodine (I-131) Ablation:** - Mechanism: iodine concentrates in the thyroid; radioactive iodine destroys thyroid follicles, reducing gland mass and hormone production - Indications: Graves' disease (especially relapse after antithyroid drugs), toxic nodules, toxic multinodular goiter - Advantages: simple single dose, curative - Disadvantages: **most patients eventually become hypothyroid** (months to years) and require lifelong levothyroxine replacement; transient worsening of hyperthyroidism possible 1–2 weeks post-treatment (if thyroid hormones released from destroyed cells); contraindicated in pregnancy and lactation - Dose: calculated based on gland size and uptake - **Nursing Considerations:** - Pre-treatment: antithyroid drugs often given to control symptoms beforehand - Post-treatment radiation precautions (minimal exposure in most settings; saliva and urine contain radioactivity for days): avoid prolonged close contact with pregnant women and small children for 3–7 days; sleep separately if possible; use separate utensils/bathroom; dispose of waste per protocol - Post-treatment monitoring: TSH and free T4 at 6–8 weeks, then periodically to detect hypothyroidism - Patient education: lifelong levothyroxine likely needed; follow-up labs essential; report symptoms of hypothyroidism (fatigue, cold intolerance, weight gain) **5. Thyroidectomy (Surgical Ablation):** - Indications: large goiter with airway/swallowing symptoms, pregnancy (if antithyroid drugs fail or intolerant), patient preference, thyroid cancer - Pre-operative: - Antithyroid drugs to achieve euthyroid state (normal hormone levels) and reduce symptoms - Iodine solution (Lugol's or SSKI) 7–10 days pre-op to reduce gland vascularity (given AFTER antithyroid drugs) - Beta-blockers continued until surgery - Educate on post-operative care expectations - Post-operative nursing priorities (CRITICAL for safety): 1. **Airway management is top priority (Maslow Level 1—physiologic safety):** - Keep patient in semi-Fowler's position (30–45 degrees); support head/neck with pillows (prevents tension on incision) - **Keep tracheostomy set, oxygen, and suction at the bedside** (ready for emergency airway access if swelling obstructs) - Assess for stridor, dyspnea, or drooling (signs of airway obstruction) - Monitor voice quality hourly initially: hoarseness, voice changes, vocal cord dysfunction - NPO until fully alert and swallow reflex present 2. **Hemorrhage prevention and detection:** - **Check dressing and behind the neck frequently** (bleeding may drain posteriorly, not just on the anterior dressing) - Check for blood pooling under the patient (roll onto side, look under neck) - Monitor vital signs for shock (tachycardia, hypotension, decreased urine output) - If hemorrhage suspected: notify surgeon immediately, keep patient flat, prepare for emergency intubation 3. **Hypocalcemia/tetany (from parathyroid injury or removal):** - Monitor for signs: **tingling around mouth or fingers, muscle cramps, carpal spasm, positive Chvostek's sign** (facial twitching when tapping the cheek below the eye) **and Trousseau's sign** (carpopedal spasm when blood pressure cuff inflated above systolic BP for 3 minutes) - Check serum calcium and ionized calcium - Have **calcium gluconate (10%) or calcium chloride ready** for IV administration if tetany develops - If hypocalcemia severe/symptomatic: IV calcium as ordered; may need ongoing calcium + vitamin D supplementation 4. **Pain management:** - Mild to moderate neck pain is expected; assess and provide analgesia - Avoid excessive neck movement/tension 5. **Infection prevention:** - Sterile dressing changes - Monitor for signs: fever, redness, warmth, drainage at incision 6. **Thyroid crisis (thyroid storm) prevention:** - Ensure antithyroid preparation was adequate pre-operatively - Continue beta-blockers post-op - Avoid stress/agitation; provide calm, quiet environment - Monitor for signs of thyroid storm (see section 2.3) 7. **Early mobilization:** - Encourage patient to turn, cough, deep-breathe - Assist with ambulation once stable **Environmental/Supportive Management:** - **Cool environment:** air-conditioned room, light clothing, minimal bedding - **High-calorie, nutritious diet:** 3000–4000 kcal/day to offset hypermetabolism; frequent small meals; adequate fluids - **Activity management:** allow rest periods; provide calm, structured environment; reduce stimuli (noise, visitors, stress) - **Eye care (Graves' disease with exophthalmos):** - Artificial tears (lubricating drops) to keep cornea moist - Eye ointment at night - Sunglasses to reduce photophobia - Eye taping or protective eye patch at night to prevent corneal abrasion (if unable to close lid fully) - Elevate head of bed to reduce orbital edema - Cold compress to eyes to reduce inflammation - Notify provider if pain, visual changes, or redness develop (risk of corneal ulceration or optic nerve compression) - Educate patient that eye changes improve slowly with hormone normalization (weeks to months) --- ### 2.3 THYROID STORM (Thyrotoxic Crisis, Thyroid Crisis) — LIFE-THREATENING EMERGENCY **Pathophysiology:** A life-threatening exacerbation of hyperthyroidism resulting from sudden massive release of thyroid hormone into the circulation. This overwhelms the body's adaptive capacity, causing extreme sympathomimetic effects, altered thermoregulation, cardiovascular collapse, and altered mental status. Mortality is 10–20% if untreated. **Precipitating Factors:** - Untreated or poorly controlled hyperthyroidism - Abrupt discontinuation of antithyroid drugs - Infection (pneumonia, UTI, streptococcal infection, tuberculosis, appendicitis) - Surgery or anesthesia (especially without pre-operative preparation) - Trauma or severe stress (emotional, physical) - Iodine administration without prior antithyroid drug coverage - Thyroiditis (release of stored hormone) - Excessive thyroid hormone intake (factitious) **Clinical Manifestations (SEVERE):** - **Fever:** HIGH, sustained fever 38.5–40.5°C or higher (up to 41–42°C); **does NOT respond to antipyretics** (aspirin is contraindicated—see below); cooling measures do not lower temperature as in typical fever - **Cardiovascular:** severe tachycardia (120–200+ bpm), arrhythmias (especially atrial fibrillation with rapid ventricular response), hypotension, shock - **CNS:** extreme agitation, restlessness, delirium, confusion, disorientation, emotional lability (may be combative), tremor, headache, weakness - **GI:** severe nausea, vomiting, diarrhea, abdominal pain - **Integumentary:** profuse diaphoresis, warm flushed skin - **Respiratory:** tachypnea, dyspnea, pulmonary edema (if heart failure) - **Progression:** altered consciousness → coma → death (if untreated) **Differentiation from Septic Shock:** Both present with fever, tachycardia, altered mental status; however, thyroid storm has: - Normal or only mildly elevated WBC (sepsis has markedly elevated WBC) - Absence of typical infection signs (except precipitating infection if present) - Positive history of hyperthyroidism or signs of exophthalmos/goiter **NANDA Nursing Diagnoses (Maslow-Prioritized—EMERGENCY):** 1. **Hyperthermia** (Physiologic—Level 1) related to uncontrolled metabolic rate and catecholamine excess 2. **Decreased cardiac output/Risk for shock** (Physiologic—Level 1) related to severe tachycardia and arrhythmias 3. **Acute confusion** (Cognitive/psychological—Level 3) related to thyroid hormone excess and hyperthermia 4. **Risk for injury** (Safety—Level 2) related to agitation, confusion, and altered mental status 5. **Imbalanced fluid volume: deficient** (Physiologic—Level 1) related to excessive diaphoresis and GI losses **Clinical Management (IMMEDIATE/EMERGENT—ICU-LEVEL CARE):** **1. Reduce Core Temperature (WITHOUT aspirin):** - **DO NOT USE ASPIRIN** (salicylates inhibit plasma protein binding of thyroid hormones, increasing free hormone levels—makes crisis worse) - **Acetaminophen** may be used but is not effective for thyroid storm fever (fever is not immune-mediated) - **Cooling measures:** - Cool environment (air conditioning, open clothing) - Cool (not ice-cold, which causes vasoconstriction and shivering) IV fluids - Ice packs to groin, axillae (large vessels) - Cool water baths or cooling blankets - Goal: reduce core temperature to <39°C; reduce metabolic rate **2. Block Thyroid Hormone Synthesis and Release:** - **Antithyroid drug (PTU preferred over methimazole in acute crisis):** - PTU 600–1000 mg/day in divided doses (can give IV in some settings) - Blocks synthesis; also has minor effect blocking peripheral T4→T3 conversion - Onset: 15–30 minutes (faster than methimazole) - **Given FIRST, before iodine** (if iodine given first, it will serve as substrate for hormone synthesis, worsening the crisis) - **Iodine solution (Lugol's or SSKI):** - Given 30 minutes to 1 hour AFTER antithyroid drug - Rapidly decreases hormone release from gland and reduces synthesis - Dose: 2 grams of iodine/day (usually given as 5–7 drops Lugol's or SSKI three to four times daily) - Effect: begins within hours; peaks at 24 hours - Duration: days to weeks; not for long-term use **3. Block Sympathomimetic (Catecholamine) Effects:** - **Propranolol 40–80 mg IV every 4–6 hours, or 20–40 mg PO every 4 hours:** - Rapidly relieves tachycardia, arrhythmias, tremor, agitation - Also reduces T4→T3 conversion peripherally (synergistic with antithyroid drugs) - Monitor: heart rate (goal 60–80 bpm), blood pressure, signs of bradycardia/hypotension **4. Suppress Inflammatory/Immune Response (Corticosteroids):** - **Dexamethasone or hydrocortisone 100 mg IV every 6–8 hours (or higher doses in shock):** - Reduces inflammatory cascade, blocks peripheral T4→T3 conversion, stabilizes catecholamine receptors - Given for 24–48 hours, then tapered **5. Maintain Hemodynamic Stability:** - **IV fluids:** normal saline or dextrose (hypermetabolism depletes glucose) - Calculate fluid needs based on insensible losses (massive sweating) + urinary output - Monitor urine output (goal >0.5 mL/kg/hr) - Avoid fluid overload (risk of pulmonary edema) - **Cardiac monitoring:** continuous, watch for arrhythmias - **Vasopressors** if hypotensive (dopamine, norepinephrine) after fluid resuscitation - **Blood transfusion** if hemoglobin drops significantly (from hypermetabolism) **6. Treat/Prevent Complications:** - **Pulmonary edema:** elevate head of bed, oxygen, diuretics as needed - **Hypoglycemia:** frequent glucose monitoring; dextrose in IV fluids or dextrose tablets - **Electrolyte abnormalities:** monitor K+, Mg2+, Ca2+; replace as needed - **Seizures/altered mental status:** seizure precautions, sedation (e.g., lorazepam) as needed for agitation **7. Identify and Treat Precipitating Factor:** - Blood cultures, urinalysis, chest X-ray, abdominal exam - Antibiotics if infection suspected - Emergency surgery if needed **8. Supportive Care:** - **ICU monitoring:** hourly vital signs, continuous cardiac monitoring, frequent labs (TSH, free T4, electrolytes, glucose, CBC) - **Airway management:** intubation and mechanical ventilation if altered consciousness/respiratory failure - **Infection prevention:** sterile technique, antibiotics as indicated - **Nutrition:** high-calorie diet or TPN if prolonged illness - **Psychological support:** family presence (if patient stable), reassurance **Nursing Actions During Thyroid Storm:** 1. **Assess and stabilize:** ABC (airway, breathing, circulation), vital signs, continuous monitoring 2. **Report to provider immediately:** activate emergency protocol, notify critical care team 3. **Prepare medications:** have propranolol, antithyroid drugs, iodine, corticosteroids, IV fluids, cooling equipment ready 4. **Administer medications per order:** PTU first, then iodine, then propranolol, corticosteroids 5. **Manage temperature:** cool environment, cool fluids, cooling blanket; monitor core temperature frequently 6. **Monitor vitals and labs:** continuous cardiorespiratory monitoring; frequent labs as ordered 7. **Maintain IV access:** large-bore IV for medications/fluids 8. **Comfort measures:** turn frequently, mouth care, catheterize if incontinent (reduces skin breakdown from diaphoresis) 9. **Communication:** inform family of critical status, provide updates 10. **Document:** all interventions, response to treatment, vital signs, medication administration **Prognosis:** With aggressive treatment, most patients recover without permanent sequelae; mortality is significantly lower with early recognition and ICU-level care. --- ### 2.4 HYPOTHYROIDISM: Thyroid Hormone Deficiency **Pathophysiology:** Insufficient thyroid hormone slows metabolism, energy production, heat generation, and cardiovascular function. Hashimoto's thyroiditis (autoimmune) is the most common cause in iodine-sufficient regions. **Causes:** - **Autoimmune (Hashimoto's thyroiditis):** most common in developed countries; antibodies to TPO and thyroglobulin attack thyroid tissue; slow progressive destruction - **Iodine deficiency:** most common cause worldwide; especially in mountainous regions and developing countries (WHO target: eliminate iodine deficiency via salt iodization) - **Post-thyroidectomy or radioactive iodine:** intentional ablation; expected - **Post-thyroiditis:** viral or autoimmune; may be permanent or transient - **Medications:** antithyroid drugs (if over-treated), lithium (interferes with iodine utilization and hormone synthesis), amiodarone (iodine-rich), interferon-alpha, TNF-alpha inhibitors - **Pituitary/hypothalamic dysfunction (secondary/central hypothyroidism):** TSH deficiency from pituitary tumor, pituitary surgery, radiation, infiltrative disease - **Congenital:** dysgenesis, dyshormonogenesis (enzyme defects), iodine deficiency in utero → cretinism if untreated **Clinical Manifestations ("Everything slowed down"):** - **Metabolic:** weight gain (despite normal/decreased appetite), fatigue, lethargy, cold intolerance (prefers warm environments), decreased BMR - **Cardiovascular:** bradycardia (<60 bpm), decreased cardiac contractility, decreased stroke volume, diastolic hypertension (if advanced), myocardial ischemia risk - **CNS:** decreased mental acuity, poor concentration, memory impairment, depression, dulled affect, delayed speech, hair loss, skin changes - **GI:** constipation (decreased GI motility), abdominal bloating, weight gain - **Integumentary:** dry, coarse, cool skin; dry brittle hair; alopecia; **non-pitting periorbital and facial edema (myxedema)** — due to mucopolysaccharide accumulation - **Reproductive:** menorrhagia (heavy menses, irregular), infertility, impotence - **Musculoskeletal:** muscle aches, stiffness, slow movements, proximal weakness - **Ocular:** puffy eyes (myxedema) - **Ears/nose:** hoarseness, husky voice (edema of vocal cords), delayed reflexes (slow relaxation phase) **Laboratory Findings (Primary Hypothyroidism):** - **HIGH TSH** (>4.0 mIU/L, often markedly elevated in severe disease) - **LOW Free T4** (<normal) - **Normal or LOW Free T3** (body tries to conserve by increasing reverse T3) **Secondary Hypothyroidism (Pituitary):** - **LOW or Normal TSH** (suppressed from lack of stimulation) - **LOW Free T4** - Requires different investigation (pituitary imaging, ACTH stimulation test) **NANDA Nursing Diagnoses (Maslow-Prioritized):** 1. **Fatigue** (Physiologic—Level 1) related to decreased metabolic rate and reduced oxygen delivery 2. **Hypothermia/intolerance to cold** (Physiologic—Level 1) related to reduced heat production 3. **Constipation** (Physiologic—Level 1) related to decreased GI motility 4. **Imbalanced nutrition: more than body requirements** (Physiologic—Level 1) related to decreased metabolism and fatigue-related inactivity 5. **Ineffective tissue perfusion** (Physiologic—Level 1) related to bradycardia and decreased cardiac output 6. **Depression** (Psychological—Level 3) related to metabolic effects on mood 7. **Deficient knowledge** (Education—Level 4) regarding levothyroxine therapy and lifelong management **Clinical Management:** **Pharmacology: Levothyroxine (Synthetic T4 — Synthroid, others)** **Dosing and Administration:** - **Initial dose:** 25–50 mcg/day (lower in elderly/cardiac patients; higher doses increase myocardial oxygen demand and arrhythmia risk) - **Titration:** increase by 25–50 mcg every 4–6 weeks based on TSH response (goal TSH 0.5–2.5 mIU/L in most; higher in post-thyroidectomy cancer surveillance) - **Usual maintenance:** 75–150 mcg/day (varies widely based on age, weight, absorption, and comorbidities) - **Maximum effect:** 4–6 weeks after each dose change (hormone has long half-life) **CRITICAL Administration Rules:** 1. **Take on an EMPTY STOMACH, 30–60 minutes BEFORE breakfast** (empty stomach increases absorption; food, especially high-fiber and high-fat, decreases absorption) 2. **Same time EVERY DAY** (consistency important; once daily is standard) 3. **No calcium, iron, magnesium, aluminum, or antacids for 4 hours before or after** (bind levothyroxine, reducing absorption) 4. **Separate from other medications** by at least 4 hours (especially calcium supplements, iron supplements, multivitamins, proton pump inhibitors, H2 blockers) 5. **Take with water only**; sip slowly and wait before eating/other medications **Monitoring:** - **TSH and Free T4:** baseline, then 4–6 weeks after each dose change, then annually once stable - **Clinical response:** energy level, temperature tolerance, weight, bradycardia resolution, depression improvement (takes weeks to months) - **Signs of over-replacement (Maslow Level 1):** palpitations, tremor, heat intolerance, anxiety, tachycardia, atrial fibrillation → reduce dose - **Signs of under-replacement:** continued fatigue, cold intolerance, weight gain, constipation, depression → increase dose **Special Populations:** **Elderly Patients:** - Higher risk of myocardial ischemia/angina from excess thyroid hormone - Start with lower dose (12.5–25 mcg/day) - Increase slowly; monitor for chest pain, palpitations, arrhythmias - Target TSH may be higher (1–3 mIU/L) to avoid over-treatment **Cardiac Disease Patients:** - Similar caution as elderly; risk of triggering angina or arrhythmias - Baseline ECG and cardiac assessment before starting - Start low; increase gradually - May need beta-blocker co-therapy to prevent tachycardia/arrhythmias during initial therapy **Pregnancy and Postpartum:** - Hypothyroidism untreated in pregnancy increases miscarriage, preterm delivery, intellectual disability in fetus - TSH goal in pregnancy: 0.5–3.0 mIU/L (lower than non-pregnant due to physiologic increase in thyroid hormone needs) - Levothyroxine requirements often increase 25–30% in pregnancy (due to increased thyroid-binding globulin) - Monitor TSH every 6–8 weeks in pregnancy and adjust dose accordingly - Continue levothyroxine during breastfeeding (minimal transfer to breast milk; safe) **Important Drug Interactions:** - **Calcium, iron, magnesium, aluminum:** reduce levothyroxine absorption (separate by 4 hours) - **Proton pump inhibitors/H2 blockers:** reduce absorption (separate timing) - **Estrogen (oral contraceptives, HRT):** increase thyroid-binding globulin, may increase levothyroxine need - **Anticonvulsants (phenytoin, carbamazepine):** accelerate levothyroxine metabolism (may need higher doses) - **Warfarin/anticoagulants:** hyperthyroidism from over-replacement increases anticoagulant effect (monitor INR closely) **Patient Education—CRITICAL for Compliance:** 1. **Lifelong therapy:** hypothyroidism from Hashimoto's is permanent; must take levothyroxine for life 2. **Never stop abruptly:** stopping can precipitate myxedema coma (if severely hypothyroid) or return of hypothyroid symptoms 3. **Correct administration:** empty stomach, 30–60 min before breakfast, same time daily, no other medications/foods for 4 hours 4. **Expect slow improvement:** energy, mood, and weight may take 4–6 weeks to improve significantly 5. **Regular monitoring:** TSH/free T4 labs needed; do not assume dose is correct without lab confirmation 6. **Report signs of over-replacement:** palpitations, tremor, chest pain, heat intolerance, anxiety → may need dose reduction 7. **Report signs of under-replacement:** persistent fatigue, cold intolerance, weight gain, depression → may need dose increase 8. **Medication interactions:** inform all providers (doctors, dentists, pharmacists) that taking levothyroxine; ask about interactions with new medications 9. **Iodine sufficiency:** adequate dietary iodine (seafood, iodized salt) helps; do not restrict iodine unnecessarily 10. **Fertility/pregnancy:** notify provider if planning pregnancy (may need dose adjustment); safe during pregnancy and breastfeeding --- ### 2.5 MYXEDEMA COMA (Myxedemic Crisis) — LIFE-THREATENING EMERGENCY **Pathophysiology:** Severe, decompensated hypothyroidism resulting in profound depression of all metabolic and physiologic functions. This is a medical emergency with mortality 25–60% even with treatment. **Precipitating Factors:** - Untreated or inadequately treated hypothyroidism - **Abrupt discontinuation of levothyroxine** (most common preventable cause) - Cold exposure - Infection (pneumonia, UTI, sepsis) - CNS depressants (sedatives, opioids, anesthetics) - Trauma, surgery, or severe illness - Myocardial infarction or stroke - Medications (beta-blockers, lithium, amiodarone) **Clinical Manifestations (SEVERE "slow-down"):** - **Hypothermia:** core temperature often <35°C (95°F), not responsive to rewarming in early stage; slow, progressive drop - **CNS:** altered mental status progressing from confusion → lethargy → coma; slow speech/thinking; psychosis possible - **Cardiovascular:** severe bradycardia (30–40 bpm), hypotension, shock; decreased cardiac output; risk of arrhythmias; myocardial ischemia - **Respiratory:** hypoventilation, respiratory depression, decreased responsiveness to CO₂; hypercapnia (elevated CO₂) and hypoxia - **GI:** severe constipation, ileus, abdominal distension, nausea, vomiting - **Integumentary:** myxedema (non-pitting edema of face, hands), pale cool skin, dry skin/hair - **Metabolic:** **hypoglycemia** (decreased glucose production and utilization), **hyponatremia** (water intoxication from ADH excess + decreased renal water excretion) - **Fluid/electrolyte:** **fluid retention without edema**, weight gain (myxedema), hypovolemia in advanced stage - **Laboratory:** severe hyperlipidemia (cholesterol, triglycerides), elevated CPK, elevated myoglobin (from muscle injury) **Diagnostic Findings:** - **Very HIGH TSH** (if primary hypothyroidism) or LOW TSH (if secondary) - **Very LOW Free T4** - **Elevated LDH, CPK, myoglobin** (from muscle damage) - **Hyponatremia** (often <130 mEq/L) - **Hypoglycemia** - **Respiratory acidosis** (from hypoventilation: elevated CO₂, low pH) - **Imaging:** chest X-ray may show cardiomegaly, pericardial effusion; brain imaging if altered mental status (rule out stroke) **Differentiation from Other Emergencies:** | Feature | Myxedema Coma | Sepsis | Hypothermia (Environmental) | |---|---|---|---| | History | Hypothyroidism/non-compliance | Infection | Exposure | | TSH | Very high | Normal | Normal | | Free T4 | Very low | Normal | Normal | | Fever | Usually absent | Present | Absent | | Infections signs | Absent (unless precipitating) | Present | Absent | **NANDA Nursing Diagnoses (Maslow-Prioritized—EMERGENCY):** 1. **Hypothermia** (Physiologic—Level 1) related to profound metabolic depression 2. **Ineffective breathing pattern/Hypoventilation** (Physiologic—Level 1) related to CNS depression and weakened respiratory muscles 3. **Decreased cardiac output/Shock** (Physiologic—Level 1) related to severe bradycardia and myocardial depression 4. **Acute confusion/Coma** (Cognitive—Level 3) related to severe hypothyroidism and metabolic abnormalities 5. **Risk for aspiration** (Safety—Level 2) related to altered consciousness 6. **Imbalanced fluid volume: Excess** (Physiologic—Level 1) related to ADH excess and decreased GFR **Clinical Management (IMMEDIATE/EMERGENT—ICU-LEVEL CARE):** **1. Manage Temperature (CRITICAL—Passive Rewarming ONLY initially):** - **DO NOT actively rewarm** (active external rewarming—heating blankets, warm baths—causes peripheral vasodilation, which drops core temperature further due to peripheral cold blood returning to core; "afterdrop"). This is called **"afterdrop" phenomenon** - **Passive rewarming only:** blankets, warm environment, remove wet clothing - **Slow, gradual warming:** core temperature should rise 0.5–1°C/hour - Core temperature monitoring: esophageal, bladder, or pulmonary artery catheter (rectal unreliable due to slow peripheral rewarming) - Do NOT assume patient is dead until "warm and dead" (resuscitate even if very cold; prolonged cardiac arrest may be reversible with rewarming) **2. Restore Thyroid Hormone (CRITICAL—IV route):** - **IV levothyroxine (T4):** - Initial loading dose: 200–500 mcg IV over 15–30 minutes (faster than oral; bypasses GI absorption issues) - Maintenance: 50–100 mcg IV daily until patient can take oral - Effect: slow, but begins hours; free T4 rises but clinical improvement takes days - Alternative: some clinicians give **IV liothyronine (T3)** 5–20 mcg every 4–12 hours (faster acting, but risk of arrhythmias) instead of or with T4; currently used less commonly - **Combination therapy:** some experts recommend both IV T4 (for steady-state hormone) and IV T3 (for rapid effect); more evidence needed **3. Maintain Airway and Ventilation:** - **Assess baseline respiratory status:** respiratory rate, oxygen saturation, arterial blood gas (ABG) - **Supplemental oxygen:** maintain SpO₂ >90%; monitor for hypoventilation (CO₂ retention) - **Intubation and mechanical ventilation** if altered consciousness/respiratory depression/hypercapnia (CO₂ >50 mmHg) - **Caution with sedatives:** myxedema coma is CNS depression; sedatives worsen respiratory depression; use minimum necessary - Avoid masks/heavy coverings on face (monitor for adequate ventilation) **4. Maintain Hemodynamic Stability:** - **Continuous cardiac monitoring:** watch for bradycardia, arrhythmias, conduction blocks - **IV access:** establish before shock develops - **Fluid management:** cautious; patients are often fluid-overloaded despite hypovolemia (paradoxical); - Avoid hypotonic fluids (increase hyponatremia) - Use **normal saline** for volume support - Fluid restriction if severe hyponatremia (<120 mEq/L) - **Vasopressors:** if systolic BP <90 mmHg despite fluids, use dopamine or norepinephrine cautiously (risk of arrhythmias with rewarming) - **Avoid diuretics** unless pulmonary edema present (fluid status complex) **5. Correct Metabolic Abnormalities:** - **Hypoglycemia:** dextrose IV (50 mL of D50W); monitor glucose closely, repeat as needed - **Hyponatremia:** if symptomatic/severe (<120 mEq/L), cautious hypertonic saline (3%) slowly (risk of osmotic demyelination); correct no faster than 8–10 mEq/L/24 hours - **Electrolytes:** check K+, Mg2+, Ca2+; correct deficiencies - **ABG/acid-base:** monitor for respiratory acidosis (CO₂ retention); may improve with rewarming and thyroid hormone **6. Treat/Prevent Complications:** - **Infection:** infection often precipitates myxedema coma; obtain cultures (blood, urine, sputum); start broad-spectrum antibiotics if infection suspected (empiric coverage until culture results) - **Pericardial effusion:** may develop; monitor with echocardiography if clinical signs (muffled heart sounds, elevated JVD) - **Seizures:** rare but possible from severe hyponatremia or hypoglycemia; seizure precautions, benzodiazepines if occur - **Aspiration:** elevate head of bed if possible; hold NPO; consider nasogastric tube if ileus - **Rhabdomyolysis/myoglobinuria:** monitor CPK, myoglobin, urinary myoglobin; hydrate aggressively to prevent acute kidney injury **7. Supportive Care:** - **ICU monitoring:** hourly vital signs, continuous cardiac monitoring - **Labs:** baseline TSH, free T4, free T3; repeat every 24 hours; glucose, electrolytes (Na+, K+, Mg2+, Ca2+), lipids, CPK, urinalysis, ECG - **Airway/ventilation:** prepare for intubation; avoid excessive sedation - **Nutrition:** TPN or feeding tube if prolonged (metab needs high due to rewarming); avoid oral until conscious - **Skin integrity:** turn every 2 hours, avoid pressure areas (myxedematous skin is fragile) - **Catheterization:** if incontinent; maintain strict asepsis (infection risk) - **Medications:** hold most sedatives; minimal anesthesia if surgery needed (sensitivity to CNS depressants) **8. Identify and Treat Precipitating Factor:** - Review medication compliance (missed levothyroxine doses?) - Culture if infection suspected; imaging if trauma/stroke - Adjust/restart levothyroxine as soon as diagnosis confirmed **Nursing Actions During Myxedema Coma:** 1. **Activate emergency protocol:** ICU admission, continuous monitoring 2. **Assess airway/breathing/circulation:** prepare for intubation if needed 3. **Obtain IV access:** large-bore for medications/fluids 4. **Baseline labs:** TSH, free T4, glucose, electrolytes, ABG, ECG; repeat frequently 5. **Administer IV levothyroxine** as ordered; document dose/time 6. **Passive rewarming:** blankets, warm environment; monitor core temp; NO active rewarming 7. **Correct hypoglycemia:** dextrose IV as needed; monitor glucose 8. **Fluid management:** normal saline carefully; monitor I&O 9. **Monitor vitals hourly:** heart rate (assess for arrhythmias), BP, respirations, temperature, O₂ saturation 10. **Neurological checks:** hourly; assess consciousness, orientation, responses 11. **Maintain NPO** pending conscious state 12. **Infection precautions:** aseptic technique, antibiotic administration if needed 13. **Family communication:** explain critical status, expected slow improvement, prognosis 14. **Documentation:** all interventions, vital signs, lab results, medication administration, response to treatment **Prognosis and Recovery:** - Recovery is **slow** (days to weeks) even with aggressive treatment; thyroid hormone effect is gradual - **Mental status** may improve before physical status - Most survivors eventually achieve hypothyroid state requiring lifelong levothyroxine - Mortality remains significant (25–60%); higher in older patients, those with severe precipitating illness --- **THYROID DISEASE SUMMARY TABLE:** | Feature | Hyperthyroidism | Hypothyroidism | |---|---|---| | **Hormone Levels** | ↑T3/T4, ↓TSH | ↓T3/T4, ↑TSH (primary) | | **Metabolism** | Sped up | Slowed | | **Weight** | Loss (despite appetite) | Gain | | **Temperature** | Heat intolerant | Cold intolerant | | **Heart Rate** | Tachycardia | Bradycardia | | **GI** | Diarrhea, appetite | Constipation | | **Skin** | Warm, moist | Cool, dry, myxedema | | **CNS** | Nervousness, tremor | Lethargy, depression | | **Management** | Antithyroid, beta-blockers, iodine, I-131, surgery | Levothyroxine (lifelong) | | **Crisis** | Thyroid storm (fever, tachycardia, delirium) | Myxedema coma (hypothermia, bradycardia, coma) | | **Crisis Treatment** | Cooling (NOT aspirin), PTU, iodine, propranolol, steroids | IV levothyroxine, passive rewarming, supportive care |

The parathyroid glands (four glands embedded in the thyroid) secrete parathyroid hormone (PTH), which is the **primary regulator of serum calcium**. PTH's main actions are to: 1. **RAISE serum calcium:** stimulates osteoclast activity (bone breakdown, releasing calcium and phosphate), increases GI absorption of calcium (via activation of vitamin D), and increases renal tubular reabsorption of calcium 2. **LOWER serum phosphate:** increases renal excretion of phosphate (PTH inhibits phosphate reabsorption in the proximal tubule) **Key Concept:** **Calcium and phosphate move in OPPOSITE directions.** When PTH is high, calcium rises and phosphate falls. The parathyroids sense serum ionized (free) calcium and adjust PTH secretion: **low calcium → PTH secretion increases; high calcium → PTH secretion suppressed.** **Normal Serum Calcium Range:** 8.5–10.5 mg/dL (total) or 4.5–5.5 mg/dL (ionized); ~50% of total calcium is protein-bound (especially to albumin), so corrected calcium should account for albumin level. **Formula for Corrected Serum Calcium:** **Corrected Ca2+ = Measured Total Ca2+ + 0.8 × (4.0 − Serum Albumin g/dL)** Example: If total calcium is 7.5 mg/dL and albumin is 2.5 g/dL: Corrected Ca2+ = 7.5 + 0.8 × (4.0 − 2.5) = 7.5 + 1.2 = 8.7 mg/dL (normal; patient is NOT hypocalcemic despite low total calcium) ### 3.1 HYPERPARATHYROIDISM — Too Much PTH → High Calcium **Pathophysiology:** Excessive PTH leads to hypercalcemia (elevated serum calcium) and hypophosphatemia (low phosphate). Chronic hypercalcemia causes bone demineralization (osteoporosis), kidney stones (from high urinary calcium), and altered neuromuscular/mental function. **Causes:** - **Primary hyperparathyroidism (most common):** parathyroid adenoma (80%), hyperplasia (15%), carcinoma (<5%); autonomous hormone secretion not suppressed by high calcium - **Secondary hyperparathyroidism:** appropriate PTH increase in response to sustained hypocalcemia (e.g., chronic kidney disease, vitamin D deficiency, malabsorption); PTH is appropriately elevated - **Tertiary hyperparathyroidism:** continued PTH elevation after correction of stimulus (e.g., post-kidney transplant); glands have "reset" to higher set-point **Clinical Manifestations:** Often remembered as **"Bones, Stones, Groans, and Psychiatric Moans":** - **Skeletal ("Bones"):** bone pain, pathologic fractures, osteoporosis (chronic hypercalcemia causes bone resorption > bone formation) - **Renal ("Stones"):** kidney stones (hypercalciuria—high urine calcium; calcium oxalate or calcium phosphate stones), nephrolithiasis, nephrocalcinosis - **GI ("Groans"):** abdominal/GI upset, constipation, nausea, vomiting, peptic ulcer disease (calcium stimulates gastrin and gastric acid) - **Neuropsychiatric ("Psychiatric Moans"):** depression, anxiety, irritability, memory problems, personality changes, confusion, lethargy - **Neuromuscular:** muscle weakness, fatigue - **Metabolic:** polyuria and polydipsia (hypercalcemia impairs ADH response in kidney—nephrogenic DI–like state) - **Integumentary:** hypertension (calcium affects vascular smooth muscle), band keratopathy (calcium deposits in cornea—rare, advanced disease) **Severity-Related Manifestations:** - **Mild hypercalcemia (10.5–12 mg/dL):** often asymptomatic or mild symptoms - **Moderate (12–14 mg/dL):** GI, neuromuscular, and psychiatric symptoms common - **Severe (>14 mg/dL) or acute:** hypercalcemic crisis (see complications) **Laboratory Findings:** - **HIGH serum calcium** (>10.5 mg/dL; total and ionized) - **LOW serum phosphate** (<2.5 mg/dL) - **HIGH PTH** (in primary; suppressed in secondary/tertiary) - **HIGH urinary calcium** (hypercalciuria) - **Normal to elevated 1,25-vitamin D** (PTH-stimulated; inappropriately normal when calcium high) - **High alkaline phosphatase** (from bone turnover) **NANDA Nursing Diagnoses (Maslow-Prioritized):** 1. **Risk for injury** (Safety—Level 2) related to bone demineralization and pathologic fractures 2. **Acute pain** (Physiologic—Level 1) related to bone resorption and potential kidney stones 3. **Risk for fluid volume deficit** (Physiologic—Level 1) related to polyuria/nephrogenic DI 4. **Imbalanced nutrition: less than body requirements** (Physiologic—Level 1) related to GI upset and constipation 5. **Constipation** (Physiologic—Level 1) related to hypercalcemia effects on bowel motility 6. **Anxiety/Depression** (Psychological—Level 3) related to neuropsychiatric effects of hypercalcemia 7. **Deficient knowledge** (Education—Level 4) regarding dietary calcium restriction, hydration, and follow-up **Clinical Management:** **Medical Management (for symptomatic or acute hypercalcemia):** **1. Hydration (cornerstone):** - **IV normal saline (0.9% NaCl):** 200–500 mL/hour, to total 3–6 L/day depending on severity and fluid status - Goal: increase urinary calcium excretion (saline increases GFR and reduces proximal tubule calcium reabsorption) - **Monitor fluid status:** daily weight, I&O, vital signs, JVD, lung sounds (risk of fluid overload in cardiac/renal disease) - Discontinue when calcium normalizes **2. Loop Diuretics (after hydration initiated):** - **Furosemide (Lasix) 40–80 mg IV every 4–6 hours:** - Blocks calcium reabsorption in loop of Henle (opposite of thiazides, which increase reabsorption) - Used in conjunction with saline (saline alone is first-line; diuretics second) - Monitor: K+, Mg2+, Na+ (diuretics cause losses); may need electrolyte replacement - Monitor urine output and fluid status - Currently less commonly used than previously; saline + bisphosphonates preferred **3. Bisphosphonates (for moderate to severe):** - **Pamidronate (Aredia) 30–90 mg IV over 2–4 hours (may repeat)** OR **zoledronic acid (Zometa) 4 mg IV over 15 minutes:** - Inhibit osteoclast activity (bone resorption) - Effect: takes 2–4 days; duration 2–3 weeks - Side effects: transient hypocalcemia (initially), renal dysfunction, osteonecrosis of jaw (rare, chronic use) - Monitor: calcium, phosphate, renal function, adequate hydration **4. Calcitonin (for rapid but temporary effect):** - **Calcitonin (from salmon) 4 IU/kg IV or IM every 6–12 hours:** - Directly inhibits osteoclasts; lowers calcium rapidly (within hours) - Duration: only 48–72 hours (tachyphylaxis—loss of effect with continued use) - Used for acute symptomatic hypercalcemia pending other treatments (bisphosphonates, surgery) - Side effects: flushing, nausea; antibodies may develop (salmon calcitonin is immunogenic) **5. Phosphate Binders (if hyperphosphatemia concurrent, rare in hyperparathyroidism):** - Generally not needed; hyperparathyroidism causes LOW phosphate **6. Vitamin D and Vitamin A Antagonists (specialized):** - **Corticosteroids** (prednisone) in granulomatous diseases (sarcoidosis, tuberculosis, histoplasmosis) where 1,25-vitamin D is elevated from granuloma conversion; not standard for primary hyperparathyroidism **7. Parathyroidectomy (definitive cure for primary hyperparathyroidism):** - **Surgical indications:** - Symptomatic hypercalcemia (bone disease, nephrolithiasis, neuromuscular symptoms) - Asymptomatic hypercalcemia with criteria: age <50, serum calcium >1.0 mg/dL above normal, 24-hour urinary calcium >400 mg, eGFR <60 mL/min, or bone T-score <−2.5 (osteoporosis) - All primary hyperparathyroidism in pregnancy (risk of fetal loss) - **Pre-operative preparation:** - Calcium, magnesium, and phosphate normalization - Hydration - Imaging to localize parathyroid adenoma (sestamibi scan, ultrasound, CT) - Anesthesia considerations (electrolyte abnormalities) - **Post-operative care** (see section 3.1 complications and nursing care) **Nursing Interventions for Hyperparathyroidism:** - **Hydration:** encourage oral fluids (target 3–4 L/day if asymptomatic); monitor I&O; assess skin turgor, mucous membranes - **Mobility:** encourage activity/weight-bearing exercise to slow bone loss; safety precautions for pathologic fractures (assist with ambulation, remove trip hazards, non-slip footwear) - **Diet:** - **Limit dietary calcium** (some patients): avoid milk, cheese, yogurt if instructed (especially if post-parathyroidectomy—risk of hypocalcemia) - **Adequate hydration:** fluids with meals - **Avoid high sodium** (increases urinary calcium losses) - **Fiber:** manage constipation from hypercalcemia - **Monitor for kidney stone formation:** assess for flank pain, hematuria; strain urine if indicated - **Patient education:** - Importance of hydration (3–4 L/day) - Signs of kidney stones (flank pain, hematuria, nausea) → report immediately - Signs of hypercalcemia (confusion, lethargy, muscle weakness) → report - Avoid vitamin D supplements (excess worsens hypercalcemia) - Avoid thiazide diuretics (increase calcium reabsorption) - Adequate exercise (bones need weight-bearing for strength) - Medication adherence if on bisphosphonates - If parathyroidectomy planned: pre-op and post-op expectations - **Pain management:** analgesics as needed for bone pain --- ### 3.2 HYPOPARATHYROIDISM — Too Little PTH → Low Calcium **Pathophysiology:** Insufficient PTH leads to hypocalcemia (low serum calcium) and hyperphosphatemia (high phosphate). The kidneys cannot reabsorb calcium or activate vitamin D, and bone resorption decreases. Severe hypocalcemia causes neuromuscular hyperexcitability (tetany, seizures) and potentially fatal cardiac arrhythmias. **Causes:** - **Post-thyroid/parathyroid surgery:** most common; accidental removal or devascularization of parathyroid glands during thyroidectomy or parathyroidectomy - **Autoimmune:** rare; antibodies destroy parathyroid tissue - **Genetic/congenital:** DiGeorge syndrome (22q11 deletion; absent/hypoplastic parathyroids + other abnormalities), hypoparathyroidism with developmental delay - **Infiltrative diseases:** sarcoidosis, tuberculosis, amyloidosis (parathyroid replacement) - **Radiation:** head/neck radiation therapy for cancer - **Idiopathic:** unknown cause **Clinical Manifestations (Hyperexcitability):** All relate to **increased neuromuscular excitability** from low ionized calcium: - **Acute/Severe:** - **Tetany:** involuntary muscle contractions, especially hands/feet; **carpopedal spasm** (wrist/hand flexion) - **Paresthesias:** numbness/tingling, especially around the mouth (perioral) and fingers - **Muscle cramps and spasms:** legs, back, face - **Laryngospasm:** life-threatening; upper airway obstruction from vocal cord spasm - **Seizures:** from severe hypocalcemia - **Cardiac arrhythmias:** from QT prolongation and altered repolarization - **Respiratory distress:** from respiratory muscle tetany or laryngospasm - **Chronic (mild–moderate):** - **Chvostek's sign:** facial twitch elicited by tapping the cheek just below the zygomatic bone (anterior to the ear); **positive sign** is twitching of the nose/upper lip/facial muscles → indicates latent tetany - **Trousseau's sign:** carpopedal spasm induced by inflating a blood pressure cuff above systolic BP for 3 minutes → indicates latent tetany - **Neuropsychiatric:** memory problems, depression, anxiety, irritability, personality changes, frank psychosis (rare) - **Integumentary:** alopecia (hair loss), brittle nails, dry skin, subcutaneous ossifications (bone in soft tissue—unique to hypoparathyroidism) - **Ocular:** cataracts (from chronic hypocalcemia) - **Dental:** delayed tooth eruption, enamel dysplasia (if hypoparathyroidism in childhood) **Laboratory Findings:** - **LOW serum calcium** (<8.5 mg/dL, especially ionized calcium) - **HIGH serum phosphate** (>2.5 mg/dL) - **LOW PTH** (or inappropriately normal when calcium is low) — this is the key finding that confirms hypoparathyroidism - **LOW 1,25-vitamin D** (PTH normally activates this) - **Normal kidney function** (rules out secondary causes) **Diagnostic Confirmation:** In suspected hypoparathyroidism after parathyroid surgery: - Serum calcium and phosphate: immediately post-op and 4–6 hours post-op (parathyroid hormone's effect takes hours to manifest) - If calcium drops and PTH is low/normal → parathyroid dysfunction confirmed **NANDA Nursing Diagnoses (Maslow-Prioritized—EMERGENCY if severe):** 1. **Risk for injury/Risk for seizures** (Safety—Level 2) related to tetany and neuromuscular hyperexcitability 2. **Ineffective airway clearance/Risk for laryngospasm** (Physiologic—Level 1) related to respiratory muscle tetany or vocal cord spasm 3. **Acute pain** (Physiologic—Level 1) related to muscle spasms and cramps 4. **Anxiety** (Psychological—Level 3) related to neurological symptoms and risk of seizures/tetany 5. **Deficient knowledge** (Education—Level 4) regarding calcium supplementation, vitamin D, signs of recurrence **Clinical Management:** **Acute Treatment (symptomatic hypocalcemia with tetany/seizures/laryngospasm):** **1. IV Calcium (IMMEDIATE):** - **Calcium gluconate 10% solution:** - **10 mL (91 mg elemental calcium) IV over 5–10 minutes** for symptomatic hypocalcemia - Can repeat every 4–6 hours as needed - **MUST be given via central line if possible** (calcium gluconate is less irritating than calcium chloride to peripheral veins) - If peripheral IV used, **dilute in D5W and infuse slowly** to minimize vein irritation - **CONTRAINDICATION:** do NOT push rapidly (risk of ventricular fibrillation) - **Cardiac monitoring** during infusion (monitor for QT prolongation, arrhythmias) - Effect: rapid, within minutes; calcium levels rise immediately (but may decrease again as IV calcium distributes; ongoing oral/vitamin D treatment needed) - **Alternative: Calcium chloride** (more ionizable but more irritating): - 500–1000 mg IV slowly (if calcium gluconate unavailable) - **ONLY through central line** (very irritating peripherally; can cause tissue necrosis) **2. Manage Acute Complications:** - **Seizures:** benzodiazepines (lorazepam 2–4 mg IV) if seizures occur (in addition to calcium) - **Laryngospasm:** oxygen, airway positioning (jaw thrust); be prepared for intubation; calcium IV should relieve spasm - **Respiratory tetany:** provide oxygen; reassure patient; calcium should resolve **3. Cardiac Monitoring:** - Continuous monitoring during IV calcium infusion - Watch for peaked T waves, prolonged QT interval, arrhythmias - Have defibrillator ready **Chronic Management (maintenance):** **1. Oral Calcium Supplementation:** - **Calcium carbonate or calcium citrate:** 1–2 grams of elemental calcium TID with meals (start conservatively, titrate based on serum calcium response) - **Calcium carbonate** (40% elemental calcium): requires acidic environment (take with meals); cheaper - **Calcium citrate** (21% elemental calcium): better absorbed in low-acid states (achlorhydria, PPI use); take with or without meals - Monitor: serum calcium target 7.5–8.5 mg/dL (not normal, to avoid suppression of PTH-mediated compensation and excessive hypercalciuria) - Adjust dose to keep ionized calcium in low-normal range **2. Active Vitamin D (1,25-dihydroxyvitamin D or calcitriol):** - **Calcitriol (Rocaltrol) 0.25–0.5 mcg TID** (or divided dosing): - Active form of vitamin D; promotes GI calcium and phosphate absorption - Onset: within hours; full effect in 3–7 days - Monitor: serum calcium (risk of hypercalcemia from vitamin D excess); urinary calcium (avoid hypercalciuria) - Adjust dose based on serum calcium and 24-hour urinary calcium - **OR ergocalciferol (Vitamin D2):** 50,000 IU weekly, but less ideal (inactive metabolite; requires liver/kidney conversion) **3. Phosphate Binders (if hyperphosphatemia causes symptoms):** - Not usually necessary; calcium + vitamin D lower phosphate by decreasing GI absorption - If needed: **calcium-based phosphate binder** (calcium acetate, calcium carbonate) serves dual purpose (calcium supplement + phosphate binder) **4. Dietary Management:** - **High-calcium diet:** milk products, fortified foods, greens (though high oxalate content may impair absorption) - **Low-phosphate diet:** avoid processed foods, phosphate additives, excessive red meat - **Adequate vitamin D:** sunlight exposure, fatty fish, fortified milk (in addition to calcitriol) **5. Parathyroid Transplantation (rarely considered):** - Experimental in specialized centers; not standard care **Post-Parathyroidectomy Nursing Protocol (for hyperparathyroidism surgery, but patient may develop temporary/permanent hypoparathyroidism):** **Immediate Post-operative (first 4–6 hours):** 1. **Baseline serum calcium and ionized calcium:** taken immediately post-op and 4–6 hours post-op 2. **Assess for HYPOCALCEMIA signs:** perioral paresthesias, finger tingling, muscle twitching, cramping 3. **Perform Chvostek's and Trousseau's signs hourly** or per protocol 4. **Keep calcium gluconate IV READY at bedside** (have 10% solution drawn up, ready to push if tetany develops) 5. **Maintain IV access:** large-bore for rapid medication administration if needed 6. **Neurological checks:** level of consciousness, seizure risk, emotional changes 7. **Cardiac monitoring** if symptomatic 8. **Airway assessment:** observe for stridor, hoarseness (laryngeal nerve damage), or laryngospasm 9. **If calcium drops significantly or symptoms develop:** - Administer IV calcium gluconate 10 mL over 5–10 minutes - Repeat every 4–6 hours as needed - Notify surgeon **Ongoing Management:** - Serum calcium monitoring: daily × 3 days, then every 3–4 days until stable - **If hypoparathyroidism is transient:** calcium/vitamin D supplementation for days to weeks until parathyroid function recovers (edema resolves, vascular supply restored) - **If hypoparathyroidism is permanent:** lifelong calcium + vitamin D therapy **Nursing Interventions for Hypoparathyroidism:** **Acute Phase (symptomatic):** - **Safety first:** keep bed rails padded and raised (seizure precautions), remove hazards, non-slip footwear - **Quiet environment:** minimize stimulation (can trigger tetany) - **IV calcium administration:** have ready, push slowly if tetany/seizures occur; monitor during infusion - **Reassurance:** explain symptoms are from low calcium and will improve with treatment; tetany, while frightening, is not immediately life-threatening - **Monitor vital signs and cardiac rhythm:** continuous monitoring if symptomatic - **Assess neurological status:** hourly checks for worsening symptoms, seizure activity **Chronic Phase (maintenance):** - **Oral calcium administration:** TID with meals or as prescribed; ensure compliance - **Vitamin D supplementation:** calcitriol as prescribed; teach correct dosing (often 2–3 times daily) - **Monitoring labs:** serum calcium and phosphate every 3–6 months (once stable, then annually); 24-hour urinary calcium if hypercalciuria develops - **Patient education—CRITICAL:** - **Lifelong therapy:** calcium and vitamin D are permanent replacements for PTH; must not stop - **Symptoms to report:** return of paresthesias, muscle cramps, tetany, confusion → may indicate under-treatment; weight gain, polyuria, nausea → may indicate over-treatment (hypercalcemia) - **Foods high in calcium:** milk, cheese, yogurt, fortified foods, leafy greens (oxalates may impair absorption) - **Vitamin D sources:** sunlight (15–30 min daily), fatty fish (salmon, mackerel), fortified milk - **Avoid phosphate-rich foods:** processed foods, cured meats, cola beverages (high phosphate additives) - **Regular follow-up:** labs and provider visits essential to adjust dosages as needed - **Medic-Alert identification:** helpful if unconscious; indicates need for IV calcium --- ### 3.3 HYPERCALCEMIC CRISIS (Hypercalcemia of Malignancy, Severe Acute Hypercalcemia) **Pathophysiology:** Severe, acute elevation of serum calcium (usually >14 mg/dL, often >18 mg/dL) from PTH-related protein (PTHrP) secretion by tumors (lung, kidney, ovary) or osteolytic metastases (myeloma, lymphoma) or extramedullary 1,25-vitamin D production (granulomatous lymphomas). The body's compensatory mechanisms (renal excretion) are overwhelmed, leading to life-threatening multi-organ dysfunction. **Clinical Manifestations:** - **Early:** polyuria, polydipsia, nausea, vomiting, constipation, abdominal pain - **Progressive:** confusion, lethargy, irritability, depression - **Advanced:** altered consciousness, coma - **Cardiovascular:** hypertension, arrhythmias (from QT prolongation), shock (hypovolemia from polyuria) - **Renal:** azotemia (acute kidney injury), oliguric renal failure - **Metabolic:** dehydration (profound) **Emergency Management:** - **Aggressive IV hydration:** 200–500 mL/hour normal saline to restore intravascular volume and promote renal calcium excretion - **Loop diuretics:** furosemide after hydration (increases urinary calcium losses) - **Bisphosphonates:** pamidronate or zoledronic acid (blocks osteoclast activity, lowers calcium over 2–4 days) - **Calcitonin:** for rapid but temporary effect (48–72 hours) - **Treat underlying malignancy:** chemotherapy, radiation, or surgery if possible - **Dialysis:** if renal failure or life-threatening arrhythmias unresponsive to medical management --- **PARATHYROID DISEASE SUMMARY TABLE:** | Feature | Hyperparathyroidism | Hypoparathyroidism | |---|---|---| | **Hormone** | ↑ PTH | ↓ PTH | | **Serum Calcium** | HIGH (>10.5 mg/dL) | LOW (<8.5 mg/dL) | | **Serum Phosphate** | LOW (<2.5 mg/dL) | HIGH (>2.5 mg/dL) | | **Manifestations** | Bones, stones, groans, moans; weakness; nephrolithiasis | Tetany, paresthesias, Chvostek's, Trousseau's; laryngospasm; seizures | | **Causes** | Adenoma, hyperplasia, carcinoma | Post-parathyroid surgery, autoimmune, DiGeorge, infiltration | | **Management** | Hydration, bisphosphonates, calcitonin, parathyroidectomy | IV calcium (emergency), oral calcium + vitamin D (chronic) | | **Nursing Priority** | Hydration, mobility, kidney stone prevention | Seizure/laryngospasm precautions; calcium gluconate ready |