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general functions of the endocrine system
Growth and development stimulation during childhood and adolescence
Coordination of male and female reproductive systems
Maintenance of optimal internal environment (homeostasis)
Emergency responses to adaptive and corrective demands
pituitary gland key fx
”Master Gland” or Hypophysis
Size of pea located in the Sella turcica under hypothalamus at base of brain above the sphenoid bone.
Consist of two parts: Anterior & Posterior
what are the two parts of the pituitary gland
Anterior Pituitary - Controls growth, appetite, metabolism, temperature, sexual development
Posterior Pituitary - Releases vasopressin (ADH) to help the body hold water and keep fluids balanced; it is essential for maintaining normal BP and hydration
what is hypopituitarism
Deficiency of one or more hormones from the pituitary gland -> it can disrupt normal regulation if it is too low
common causes of hypopituitarism
Pituitary tumor (most common) - compress and damage surrounding tissue
Tumor or damage to the hypothalamus
Head trauma, brain surgery, or radiation
Severe shock or hypotension → ↓ blood flow → ↓ hormones
Malnutrition or rapid fat loss
Infection (HIV/AIDS)
Idiopathic (unknown cause)
what are the most life-threatening hormone losses with hypopituitarism
↓ ACTH (adrenocortical tropic hormone) → ↓ adrenal hormones → risk for shock
↓ TSH (thyroid stimulating hormone) → ↓ thyroid hormones → slowed metabolism, ↓ vital signs, lethargy
nursing focus for hypopituitarism
Recognize early signs of adrenal or thyroid failure
Monitor vital signs, mental status, and stress response
Provide education and emotional support
assessment findings of hypopituitarism
Hormone Deficiencies → Target Organ Changes
Gonadotropin (LH (luteinizing hormone) & FSH (follicle stimulating hormone)) Deficiency
Men: ↓ facial/body hair, ↓ libido, impotence
Women: amenorrhea, ↓ libido, painful intercourse, infertility
Both: Dry skin, breast atrophy, ↓ axillary & pubic hair
Neurologic Symptoms (Tumor Effects)
Vision changes (especially peripheral)
Headache, double vision, limited eye movement
diagnotic findings for hypopituitarism
Measure pituitary hormones or their target gland effects
Osmolality (concentration) tests for blood/urine - high concentration = high osmolality
Imaging (CT/MRI) - tumors, pressure against pituitary gland
Angiogram: rules out aneurysm or vascular cause
lifelong management of hypopituitarism
Requires lifelong hormone replacement therapy (HRT) to maintain normal body function
Continue HRT during hospital admissions
Patients may be seen in any care setting (acute, outpatient, community)
Must NOT be interrupted
goal of tx for hypopituitarism
Replace deficient hormones to restore normal cellular function, prevent life-threatening complications
what is hyperpituitiarism
Over secretion of one or more pituitary hormones
causes of hyperpituitiarism
Pituitary tumors (most common cause) - adenoma (benign pituitary tumor)
Tissue hyperplasia – overgrowth of pituitary cells
Hypothalamic overstimulation → excessive releasing hormones → pituitary overproduction
what might you see as pituitary tumors grow with hyperpituitiarms
Headache
Vision changes (esp. peripheral vision loss)
↑ Intracranial pressure (ICP) → nausea, vomiting, altered LOC
assessment findings of hyperpituitiarism - excess growth hormone
Acromegaly - rare condition acquired as an adult after growth plates have closed
Occurs slowly
Bones can’t lengthen, but the width can increase - Enlarged bone features → enlarged hands, feet, facial features, jaw
Tongue enlarged (soft tissue growth), Deep voice (hypertrophy of vocal cords)
Vision changes, Headache - from adenoma pressing
Hyperglycemia (insulin hormone is inactive)
assessment findings of hyperpituitiarism - excess ACTH
Overstimulates adrenal glands -> Cushing Syndrome
assessment findings of hyperpituitiarism - excess prolactin
Sexual dysfunction (infertility, production of breast milk in both men/women)
nonsurgical management of hyperpituitiarism
Dopamine agonists: Inhibits release of GH and PRL
Somatostatin analogs- inhibits growth hormone (somatotropin) production
Targeted Radiation Therapy – Gamma Knife (targets specific area that is causing hypersecretion by radiation -> used when medications do not work and surgery isn’t an option)
surgical management of hyperpituitiarism
Hypophysectomy
Most common treatment for hyperpituitarism
Removes the tumor and/or pituitary gland to reduce hormone overproduction
There are different techniques to remove the tumor depending on the size and location of it
how is hypophysectomy completed
Usually performed by minimally invasive endoscopic nasal approach or transsphenoidal (through sphenoid sinus)
A bone or fat graft is used to seal the surgical opening and prevent CSF leakage
Transsphenoidal approach – nasal pack and mustache dressing may be used
neuro and surgical monitoring post hyppphysectomy
Monitor neuro status q hour(vision, LOC, strength)
Watch for complications (DI (low secretion of ADH), CSF leak, Infection (meningitis: nuchal rigidity (stiff neck), h/a, fever), ↑ ICP)
Keep HOB elevated - for increased ICP
Report postnasal drip or increased swallowing - leaking CSF
Check nasal drainage for glucose or halo sign
Persistent severe headache may indicate CSF in sinuses
CSF leaks typically heal on their own with bedrest and fluid hydration
activity precautions post hypophysectomy
Do NOT cough, sneeze, blow nose, or bend forward
Avoid straining during bowel movements → increases ICP
Use stool softeners, fluids, and high-fiber diet
To pick up objects, bend at the knees, not the waist
respiratory and oral care post hypophysectomy
Encourage deep breathing hourly (no coughing)
Rinse mouth frequently; apply lubricant to lips
No toothbrushing for ~2 weeks to protect surgical incision; use mouth rinse & flossing
Decreased sense of smell may last 3-4 months
hormone replacement post hypophysectomy
If pituitary gland removed → lifelong hormone replacement
Thyroid hormones, glucocorticoids, gonadal hormones (support sexual function and reproduction)
Vasopressin may be needed for fluid balance and prevention of dehydration
Teach self-management - Do not skip doses, f/u w/ HCP
Report any return of hyperpituitarism symptoms immediately
function of antidiuretic hormone (ADH)
Helps kidneys balance water in body; when it is released, it travels to the kidneys to signal to hold onto fluid -> stops kidneys from excreting urine -> does this when BP is low; it lowers the body’s osmolality -> increases blood volume -> increases BP. If this doesn’t correct it in a timely manner, your brain stimulates your thirst receptors
problems of ADH
Diabetes Insipidus (DI) - hormone deficiency
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) - hormone excess
patio of diabetes insipid (DI)
Decreased Antidiuretic hormone (ADH) →
Decreased water reabsorption in renal tubules →
Decreased intravascular fluid volume →
Increased serum osmolality (excessive concentrated blood; hypernatremia) and Excessive dilute urine output
causes of DI
Hypothalamus gland doesn’t make enough ADH
Pituitary gland that doesn’t release enough ADH into the blood.
Damage to the hypothalamus or pituitary gland r/t trauma, tumor or during surgery or radiation (neurogenic DI)
Decreased renal response to ADH (nephrogenic DI) - d/t CKD, AKI, specific medications (lithium)
reveiwing hx for DI
Brain surgery, trauma, medication use, inadequate fluid intake; regardless of cause, s/s always the same
assessment findings of DI
Dry Inside
Diurese - Polyuria (Excessive dilute urination) - >2L/day
Dilute urine with low specific gravity (<1.005) with ↓ osmolality
Drinking a lot - Polydipsia (Excessive thirst)
Dehydrated - Fluid volume deficit
Decreased BP - Due to fluid loss
High and dry serum labs - High osmolality (highly concentrated blood) & Hypernatremia
DI interventions
Desmopressin (DDAVP) - ONLY if it is neurogenic cause
Prevention or management of dehydration and electrolyte imbalance
Encourage the client to drink fluids equal to the amount of urinary output
Measure & record intake and output, and urine specific gravity
Monitor vital signs & record: monitor fluid volume deficit and poor tissue perfusion
Measure and record weight daily - At least 2.2 lbs in a day
Desmopressin key fx
Synthetic vasopressin (synthetic ADH) - Makes body hold onto water
Route: intranasal, po, (IV route 10x stronger)
Dose depends on how well they respond to medication
pt teaching for permanent DI
Should not be deprived of fluid over 4 hours
Lifelong drug replacement is necessary
Call 911 for S/S water toxicity (can cause hyponatremia): persistent H/A, acute confusion, N/V
Polyuria and polydipsia are signals for the need for another drug dose
Measure & record daily weights to estimate dehydration
Side effects of nasal sprays - can erode nasal cavity
Teaching how to self-inject the drug if discharge using parenteral dose
Chronic DI: wear a medical alert bracelet or necklace at all times
patho of syndrome of inappropriate antidiuretic hormone (SIADH)
Increased Antidiuretic hormone (ADH) despite normal or ↑ plasma volume →
Increased water reabsorption in renal tubules - holding onto a lot of fluid →
Retention of free water in blood →
Concentrated urine, Dilutional hyponatremia, ↓ serum osmolality (not concentrated), ↑ urine osmolality (highly concentrated)
causes of SIADH
Anything that is causing swelling or pressure against the pituitary gland
Malignancies - Small cell lung cancer
Pulmonary Disorders - Pneumonia
CNS Disorders - Inflammatory conditions: Encephalitis, Meningitis, TBI, increased ICP, brain tumors &/or removal
Medications
assessment findings of SIADH
Soaked Inside
Stops Urination - Decreased urinary output (oliguria possible-<400 ml/24 hours)
Sticky and thick urine - ↑Urine specific gravity (>1.025)
Pulmonary congestion - Low sats, crackles
Low and Liquidity Labs - Hyponatremia (Na+ <115mEq/L) & Serum Osmolality is low
what s/s might you see with hyponatremia in SIADH
CNS changes r/t osmotic shift of water into brain cells causing cerebral edema
Lethargy, headaches, irritability, ↓DTR, disorientation, Change in LOC
Progresses to ↓responsiveness, seizures, coma
SIADH interventions
Stop all fluids - Fluid restriction
Give Salt - Correct Hyponatremia
Drug therapy with vasopressin receptor antagonists (vaptans) & diuretics
Hypertonic saline (3% NS) - highly concentrated bag of saline
Monitor for fluid volume overload in response to treatment
Place PT in seizure precautions with therapy
fluid restriction in SIADH key fx
Restricted to as little as 500-1000mL/24 hours
Strict I&O, daily weights to assess degree of restriction needed
Oral care to distract from restriction
how to correct hyponatremia in SIADH
Raise serum sodium no more than 12 mEq in 24 hours.
If it is raised too quickly, then the myelin sheath around nerves in pons area will be destroyed and can cause brain and nerve damage
Aim at maximum serum sodium of 125-130 mEq/L
vasopressin receptor antagonists and diuretics tx for SIADH key fx
Meds below only given in hospital setting (ICU) – must monitor serum Na+ levels
Tolvaptan (Samsca), conivaptan (Vaprisol)- promotes water excretion without sodium loss
Loop diuretics with saline - helps pull fluid off PT with FO
how to administer hypertonic saline in SIADH
Given in the presence of neurologic manifestations (Na+ <120mEq/L)
Must be given SLOWLY and through central venous catheter
DI vs SIADH Chart
Diabetes Insipidus – Dry Inside | SIADH – Soaked Inside |
|---|---|
ADH Deficiency | ADH Excess |
High urinary output: output > intake | Low urinary output: output<intake |
↓ urine specific gravity (<1.05) | ↑ urine specific gravity (>1.025) |
Low body water | Too much free water |
Hypernatremia | Dilutional hyponatremia |
S/S: Extremely dilute urine | S/S: Concentrated urine |
Risk: Hypovolemic shock | Risk: Seizures |
Treatment: DDAVP (ADH) | Treatment: Vaptans, Hypertonic saline (3%) |
Hormones of the Adrenal Glands Chart
Hormones of the Adrenal Glands | |||
Adrenal gland | Associated hormones | Chemical class | Effect |
Adrenal cortex | Aldosterone | Steroid | Increases blood Na+ levels |
Adrenal cortex | Cortisol, corticosterone, cortisone | Steroid | Increase blood glucose levels |
Adrenal medulla | Epinephrine, norepinephrine | Amine | Stimulate fight-or-flight response |
adrenal glands key fx
Make life-sustaining hormones that control blood pressure, stress response, and energy use.
Not primarily response for sex hormones, but it does produce androgens, which contribute to secondary sex characteristics (body hair & sexual development).
Additionally, they produce chatecolines (adrenaline), which is rapidly introduced when we are in acute stress. This helps your body prepare for immediate physical reaction.
what life-threatening problem can occur with the adrenal glands
pheochromocytoma
rare tumor of the adrenal medulla
it produces epinephrine and norepinephrine
it can be life threatening because if the epi and norepi are released from this tumor, then it can lead to hypertensive crisis, stroke, kidney disease, and seizures)
cortisol key fx
The body’s stress hormone (fuel manager/stress responder).
It keeps blood sugar elevated when we need energy. It breaks down fat and protein for fuel. It helps our blood vessels respond to adrenaline, so our BP stays up. It calms inflammation when we are sick or injured.
When it is missing, the body can’t make enough energy or handle stress. Therefore, our blood sugar and BP drops, we have no energy, it can’t handle stress, and it can lead to shock.
aldosterone key fx
This regulates fluid and electrolytes. It is a thermostat for sodium, potassium, and fluid balance. It normally tells the kidneys to keep sodium and water to maintain BP, and to let go of extra potassium and acid.
When it is missing, sodium and water are lost. Therefore, BP decreases, leads to dehydration, potassium and acid build up (hyperkalemic and metabolic acidosis).
what is adrenal insufficiency
AKA Addison’s Disease
Adrenal gland hypo function. No longer supplies normal levels of glucocorticoids, androgens, or mineralocorticoids
Absent Steroids
causes of Addison’s Disease
Autoimmune disease or infection
Abrupt discontinuation of long term glucocorticoid therapy
A problem with the hypothalamus or pituitary gland
assessment findings of Addison’s Disease
ADDSS
Added Tan - Hyperpigmentation r/t chronic condition because the adrenal gland is damaged. It is a result of elevated melanocyte-stimulating hormone.
Added Potassium (>5)
Decrease weight, N/V/D, abdominal pain
Decreased b/p, hair, glucose, energy - Decreased secondary sex characteristics & blood vessels relaxed
Sodium loss (135 or less) - Can lead to seizures & decreased cognition
Salt craving – craving salty foods because their sodium is low
Addison’s Disease Interventions
ADDDI
Add steroids - “Sone”
Diet high in protein, carbs, and sodium - prevents hypoglycemia and hyponatremia
Don’t “abruptly” STOP steroids – can lead to crisis
Don’t believe this medication will cure you
Indefinite lifelong hormone replacement
indefinite lifelong hormone replacement key fx for Addison’s disease
Correct Aldosterone Deficiency
Dosage adjustments may be required in hot weather with excessive perspiration
Monitor aldosterone excess
Correct Cortisol Deficiency
Oral cortisol is divided doses and taken with food.
Monitor cortisol excess
complications of Addison’s disease
acute adrenal insufficiency - AKA addisonian crisis
Addisonian Crisis causes
severe infection, surgery, trauma, abrupt stop of steroids
addisonian crisis manifestations
Same as for Addison’s Disease but more severe
Severe hypotension (89/40 or less)
Rapid sodium decrease and rapid potassium increase
interventions for addisonian crisis
Always carry an emergency kit with IM steroids
Cortisol Hormone Replacement (priority**)
Hyperkalemia management
Hypoglycemia management
Hourly glucose checks
Administer IV glucose or glucagon as prescribed
how to replace cortisol in addisonian crisis
**Initial dose: IV bolus hydrocortisone 100-300 mg OR IV bolus dexamethasone 4 to 12 mg.
**Follow with a continuous IV infusion (lower dose) x 8 hours
*Volume Replacement: Rapid IV infusion of 0.9% NS or D5NS
H2 Histamine blocker for GI ulcer prevention
how to manage hyperkalemia in addisonian crisis
Rapid acting: IV insulin (20-50 units), & IV D50W (20-50 mg) in NS
Slow: K+ binding resin (Kayexalate) PO or enema
Loop/Thiazide diuretics
Continuous cardiac monitor
Restrict Dietary K+
what is hypercortisolism
AKA Cushing’s disease
Excess secretion of cortisol by adrenal glands
causes of Cushing’s disease
Glucocorticoid therapy (most common)
Problem with adrenal cortex, Anterior pituitary gland or hypothalamus
Malignant Small cell lung cancer
hx assessment of Cushing’s disease
Other health problems that require glucocorticoid use
Weight gain, increased appetite
physical assessment of cushings disease
CUSHH
Cushion - Truncal obesity + Moon Face + Buffalo Hump
Unusual Hair Growth - Hirsutism (hairy suit) r/t increased androgen excretion
Skin is thin - Purple striae (stretch marks) r/t increased muscle mass breakdown
High glucose, b/p, weight
High risk for infections and fractures (lowers lymphocyte and WBC production; inhibits bone formation)
lab assessment of Cushing’s disease
Blood, salivary, and urine cortisol levels
Dexamethasone suppression testing - measures cortisol secretion after giving synthetic cortisol -> did the cortisol suppress when it was supposed to
interventions for Cushing’s disease
Restoring fluid balance
Nutrition: “no added salt diet”
Fluid restrictions: modified based on clinical findings and prescription
Preventing infection - Hand hygiene, vaccines, avoid crowds
Preventing injury - Avoid skin breakdown, falls/fractures, GI bleed
Monitor patient response to drug therapy
Weight loss
Increased urine output
Serum sodium and potassium values
surgical management of Cushing’s disease
laparoscopic adrenalectomy
Pre-op: high-calorie, high-protein diet in days prior to surgery
Pre-op, intra-op & post-op: glucocorticoid given to prevent adrenal crisis r/t sudden drop in cortisol level
Post-op Outcome goals: Hemodynamic Stability, Free of infection, free of injury, free of acute adrenal insufficiency
post-op laparoscopic adrenalectomy key fx
Client goes to critical care unit post-op for monitoring of central venous pressure & pulmonary wedge pressure
Assessing the patient every 15 minutes for shock (e.g., hypotension, a rapid and weak pulse, decreasing urine output) during the first 6 hours
Monitoring vital signs and other hemodynamic variables to detect hypervolemia/hypovolemia:
Strict I & O, Daily weights & Serum electrolyte levels
care coordination and transition management for Cushing’s disease
Home care management - Needs assistance r/t muscle weakness and fatigue
Self-management education
Daily weight
For bilateral adrenalectomy: Adhere to lifelong HRT
Prevent infection r/t reduced immunity
Health care resources
Home health
Medical alert bracelet
what is hyperaldosteronism
Increased secretion of aldosterone “mineralocorticoid excess”.
what are the two types of hyperaldosteronism
Primary “Conn’s syndrome”: Adrenal adenoma, bilateral adrenal hyperplasia, Adrenal carcinoma
Secondary (reduced blood flow to kidneys): Renal artery stenosis, Renal artery obstruction, CHF
what does hyperaldosteronism result in
hypokalemia and elevated blood pressure
tx of hyperaldosteronism
Potassium supplements
Potassium sparing diuretics
Adrenalectomy is most common treatment (removal of one or both adrenal glands)
High risk for Addisonian Crisis (if both adrenal glands are removed)
thyroid glands and hormones key fx
Hypothalamus - Releases TRH (thyroid-tropin hormone). It sends the hormone to the pituitary gland to stimulate that release. It is released into the bloodstream and binds and activates to the thyroid to stimulate the production of T3 and T4, which are then released into the bloodstream.
Pituitary Gland - TSH
T3, T4- They help regulate metabolism, body temperature, heart rate, and nervous system response.
Calcitonin - Released from the thyroid gland and helps regulate serum calcium when it needs to be lowered.
what is hypothyroidism
Thyroid cells fail to produce sufficient levels of thyroid hormones (multiple reasons)
Cellular regulation decreased
causes of hypothyroidism
Hashimoto thyroiditis (autoimmune disorder)
Treatment of hyperthyroid state (thyroidectomy or radiation iodine treatment), radiation or trauma to neck
Insufficient excretion of TSH from pituitary gland
hypothyroidism assessment findings
LOW AND SLOW
Hallmark sign is cold intolerance, decreased body temperature
Weight gain
decreased appetite
cold intolerance, increased sensitivity to cold
bradycardia
constipation
fatigue, depression, impaired memory, impaired concentration, mental fog
hair loss, thin nails, dry skin
lab assessment of hypothyroidism
Dramatic reduction of T3 and T4
High TSH in primary; decreased or near normal in secondary
hypothyroidism management
Levothyroxine (Synthyroid) or Liothyromine sodium (Cytomel)
Avoid changing brands
Medication effectiveness: Improved metabolism
Improve gas exchange
Sleep and bowel elimination patterns improve
pt teaching of hypothyroidism
Seek treatment for chest pain or chest tightness (911)
Lifelong therapy -Take on empty stomach, same dose and same time every day
Recognize/report symptoms of hypo/hyper thyroid state
Too much medication can cause s/s of hyperthyroidism
what is hypothyroidism complication
myxedema coma
Life threatening decreased metabolism
causes/triggers of myxedema coma
Causes: Untreated or undertreated hypothyroidism or a trigger
Triggers: Acute illness, surgery (thyroidectomy), chemo around neck, sedatives, opioids, discontinued thyroid medication
manifestations of myxedema coma
Non-pitting edema, hypothermia, puffy face and tongue, cardiovascular collapse, coma
Bradycardia, hypotension, Alterations LOC, Hypotension
Hyponatremia, hypoglycemia
Elevated serum TSH & low T4
nursing interventions of myxedema coma
Place tracheostomy/airway kit at bedside
Place PT on cardiac monitor
Monitor ABCs
tx of myxedema coma
Thyroid replacement hormone – lowest dose to start IV levothyroxine 100-500mcg
Rapid Dose increase can result in hypertension, heart failure, myocardial infarction
what is hyperthyroidism
AKA thyrotoxicosis
Excessive thyroid hormone secretion from the thyroid gland
causes of hyperthyroidism
Autoimmune disorder (Graves’ Disease) - Immune system forms antibodies that causes your thyroid to grow and produce excess of thyroid hormone
Toxic multinodular goiter (multiple thyroid nodules)
Excessive thyroid replacement hormones
hx assessment of hyperthyroidism
Weight loss, increased appetite
Hallmark sign: Heat intolerance
Vision changes (double or blurred vision, eye fatigue)
physical assessment of hyperthyroidism
Exophthalmos (Graves Disease) - Due to inflammation and swollen eye tissue that forces eyes out (Educate on use of eye patch to close eye and rest)
Goiter - Prevalent in Graves Disease; Do not palpate because it can stimulate the release of the hormones and cause thyroid storm
Palpitations, Tachycardia
Insomnia, Irritable, Tremors
lab assessment of hyperthyroidism
High T3 & T4, Low TSH (can vary), elevated TRAbs (antibody that can be measured to diagnose Graves disease)
diagnostic assessments of hyperthyroidism
Thyroid scan
Ultrasonography
Electrocardiography (ECG) - Looks at HR to determine if there is any CV problems due to hypermetabolic state
interventions of hyperthyroidism
Monitoring: temperature increase of one degree F° from baseline (cue that PT is possibly going into thyroid storm) -> immediately assess cardiac status and report
Reducing stimulation - Encourage rest, limit visitors, postpone nonessential care
Drug therapy
RAI therapy
drug therapy of hyperthyroidism
Methimazole – Watch out: can cause birth defects, avoid and report pregnancy
Propylthiouracil (PTU)-increases risk for infection
RAI therapy key fx hyperthyroidism
Takes 6-8 weeks for symptom relief, destroys thyroid cells to a degree
Used Preoperatively - decreased vascularity and size of thyroid
complication of hyperthyroidism
thyroid storm
Hyperthyroidism Complication: Thyroid Storm
manifestations of thyroid storm
Fever (>1º F), tachycardia, systolic hypertension, anxious, tremors, abdominal pain, N/V/D
Worsening of condition: Agitation, confusion, seizures, coma, death
tx of thyroid storm
ICU for care & monitoring
Maintain airway, ventilation, cardiac monitoring***
Give antithyroid medications to achieve hemodynamic stabilization
Reduce fever (non-salicylate antipyretics), cooling blanket or ice packs
IV saline to correct dehydration: Maintain adequate hydration
surgical management for hyperthyroidism
partial or total thyroidectomy p
pre-op care for thyroidectomy
Euthyroid state to ↓ decrease size, vascularity and risks
Control B/P, dysrhythmias, & tachycardia prior to surgery
Pt teaching – deep breathing, supporting posterior neck to reduce strain, hoarse voice is common (have to monitor severe changes -> indicate laryngeal complications)
post-op care for thyroidectomy
Place suction, oxygen and tracheostomy trays at BS
Priority ABCs, monitor vital signs, ability to swallow saliva, O2 sats, deep breathe
Position - ↑HOB to semi-fowler’s, pillows to support head & neck, avoid neck extension
Pain control
complication of thyroidectomy
Hemorrhage - monitor dressing & drainage, bleeding under skin
Respiratory distress & impaired gas exchange - edema or spasms can cause stridor indicating resp. distress
Laryngeal nerve damage - laryngeal spasms can impair airway
Hypocalcemia and tetany - If parathyroid glands inadvertently removed or blood supply damaged. Numbness tingling around mouth, fingers or toes, and +Chvostek’s and +Trousseau’s signs