Flashcards: med surg 2 Endocrine/Oncologic Emergencies

1. Metabolic: sepsis- septic shock, syndrome of inappropriate antidiuretic hormone (SIADH), hypercalcemia, tumor lysis syndrome (TLS)

2. Obstructive: Superior vena Cava syndrome, Spinal cord compression

1. Morbidity and mortality rates have decreased, however monitoring for infection is still crucial.

2. Common sites for infection include: pharynx, skin, perianal area, urinary tract, respiratory tract, and catheters.

3. Predisposing factors include: immunosuppression, chemo/radiation, malignancy, age >85

4. Most infections arise from endogenous flora of the patient: E coli (gram neg), Strep/staph (gram pos), Candida albicans (fungal)

1. Typical signs of infection may not be present due to decreased WBCs and diminished local inflammatory response.

2. Fever and shaking chills (shake and bake)

3. N/v/d

4. hr < 90

5. RR > 30

6. Elevated or Decreased WBC (leukopenia is all wbcs down)

7. low bp - significant drop from baseline (20 pts in 24hr period)

8. Elevated or decreased temp

9. Reduced LOC

10. FEVER in a patient with neutropenia IS ALWAYS an medical emergency.

1. Infection

2. Bacteremia - infection moves into bloodstream and spreads throughout the body

3. Systemic Inflammatory Response Syndrome (SIRS) - can occur in things that aren't infection. lethal

4. Sepsis

5. Severe Sepsis

6. Septic Shock - cannot maintain cardiac output, (severe vasodilation, hypotension)

7. Multiple organ dysfunction syndrome - MODS

1. Alveolar edema

2. Decrease in surfactant

3. Increase in shunting

4. V/Q mismatch - not good gas exchange between oxygen and carbon dioxide.

5. End result: ARDs - increased RR (!=gas exchange), decreased lung compliance, severe dyspnea, refractory hypoxemia

1. Acute kidney failure: hypoperfusion, release of mediators, activation of renin-angiotensin-aldosterone system.

2. BUN often near 100 mg/dL (8-24)

3. CR >= 3.5 mg/dL (0.6-1.2)

4. Urine output often less than 15 mL/hr

1. GI - motility decreased: abdominal distension and paralytic ileus, decreased perfusion: risk for ulceration and GI bleeding, Potential for bacterial translocation.

2. Hepatic - bilirubin > 2, increased ammonia levels leads to hepatic encephalopathy, elevated liver enzymes, increased prothrombin times, DIC.

3. Hypermetabolic state: hyperglycemia/hypoglycemia state, insulin resistance, lactic resistance, lactic acidosis, electrolyte imbalances

1. Myocardial depression and massive vasodilation

2. Hypotension and decreased SVR (massive vasodilation)

3. Baroreceptors respond to enhance CO

4. Albumin and fluid move out of blood vessels. (third spacing, not enough pressure to maintain fluids in the vessels)

5. Once sepsis reaches Cardiac/CNS systems prognosis is poor.

1. Mental status changes: due to hepatic encephalopathy (liver isn't removing toxins), due to poor cerebral perfusion/hypoxemia, inflammatory mediators

2. Often early sign of MODS

3. May see seizures

1. WBC <4000 or >11,000 (wbc function often impaired in cancer pts and may not work at all)

2. Neutrophils decreased (leukopenia = dec in all wbcs)

3. Bands

4. Elevated Lactate

5. ABG - pH 7.22, pCO2 45, pO2 74, bicarb 12, O2 sats 90%

6. Electrolytes, renal studies, liver studies, and glucose levels are indicators, but of later stages of septic shock.

1. Broad-spectrum antibiotics are given once infection is suspected. (maybe antifungals for fungal inf)

2. Specific antibiotics are given after organism is identified - AFTER cultures are obtained!

3. Volume management - vasopressors to help with massive vasodilation, fluids.

4. O2 - balance supply and demand

5. Hemodynamic support(severe/ICU): EKG monitoring, Swan Ganz or pulmonary artery catheter.

1. See chart 12-6 for clinical practice pg. 348

2. Prevention and early recognition are key! - handwashing, oral care, teaching patients s/s to report. Assess neutropenic patients early and frequently

3. Fluids - 0.9% NS 2-3 Liters IV

3a. IV antibiotics (ON TIME)

4. Arterial and/or central line placement

5. Vasopressor support: dopamine drip, epinephrine/norepinephrine drip. (Levophed last line vasoconstrictor, detrimental long term use to small blood vessels)

1. Private room

2. Limit visitors to healthy adults

3. Staff will not care for patients with transmittable dx and neutropenic patients concurrently

4. Dedicated vitals equipment

5. No fresh flowers or plants - eliminate sources of stagnant water

6. No rectal temps or rectal meds

7. Neutropenic diet: no raw meats, fresh fruit or vegetables, no deli foods, no raw or partially cooked eggs.

1. Growing tumor mass expands into epidural space - compress spinal cord, surrounding epidural venous plexus.

2. Mechanical destruction of spinal cord: tumor erodes and collapses vertebral body. Displaces bone fragments into epidural space.

3. Direct expansion of tumor or paraspinal lymph node into epidural space: Without destruction of bone - least common.

4. Mostly associated with solid tumors that metastasizes to bone: breast, lung, prostate, multiple myeloma.

1. Back pain - Never ignore back pain in a oncology patient! (Medical Emergency)

2. Neuro deficits: numbness, weakness, tingling, paralysis-usually permanent.

1. Early recognition and treatment is key: CT scan of torso, MRI of spine, comprehensive neurological exam.

2. High-dose corticosteroids - reduce swelling

3. High-dose radiation - done emergently

4. Surgery: may or may not be indicated to remove tumor. External back or neck braces to reduce pressure in spinal cord. (laminectomy can restore function to spine, removing vertebral bone)

1. Mobilize - rehab to maximize function

2. Monitor for sensory deficit (hot vs cold)

3. Elimination

4. Skin integrity maintenance

5. Prevent injury/safety

6. Pain relief

7. Prevent neurological damage

8. Prepare for surgery

9. Education

10. Emotional support and discharge planning.

1. Hypercalcemia is a metabolic oncologic emergency resulting from elevated levels of Ca.

2. Malignant tumors produce a protein that acts like PTH, stimulating the release of calcium from the bones into the blood. (lungs, breast, and multiple myeloma)

3. Metasis (bone metasis, breaks down releasing more Ca)

4. Non-cancer causes are dehydration, renal failure medications, excessive use of Ca and Vit D.

1. Mild > 10.4

2. Mod - 12-14

3. Severe 14-16

4. Life threating > 16

5. Mild/mod: fatigue, confusion, muscle weakness, constipation, nausea, vomiting, pain, polyuria, thirst

6. High: anuria, HTN, tachycardia, arrhythmias, lethargy, stupor, coma

1. Hydration - IV and oral (excretes and dilutes)

2. Loop diuretics

3. Bisphosphonates

4. Calcitonin

5. Steroids

6. Hemodialysis if severe

7. Controlling the malignancy is the most effective treatment

1. IO, daily weights

2. provide hydration

3. max safety

4. Monitor CO changes

5. Evaluate neurological status

6. Minimize constipation

7. Analgesia for bone pain

8. Maintain level of mobility

9. Do not give multivitamins or antacids

1. A structural oncologic emergency caused by impaired venous return to the heart can be caused by a tumor infection, clot, or fibrosis.

2. SVC is compressed or invaded - has thin wall, low pressure, collapses easily, and is enclosed in a rigid anatomic compartment.

3. Obstructs blood return from head and upper body - syndrome of venous congestion

4. Cardiac output is reduce - decreased blood return to the heart.

5. Chest malignancies near the SVC or surrounding lymph nodes - most associated with lung cancer and multiple lymph node chains

6. Thrombus around central venous catheter or within the SVC

1. Edema - face (around eyes), upper chest, right arm

2. Venous distension of neck veins

3. Dysphagia, cough hoarsness

4. Tightness of shirt collar

5. New onset chest pain

6. Hypotension and diminished pulses- decreased cardiac output

7. Hemorrhage

8. Skin mottling

9. Mentation changes - CRITICAL!

1. Diagnostic tests- spiral CT with contrast or MRI of chest - tumor location, level of invasion, presence of thrombus, ECG

2. Treatment goal is symptom relief and maintain airway: radiation therapy, chemo, thrombolysis, stent placement, O2 use

1. Elevate HOB

2. Assess for progression and resp distress

3. Assess for progressive edema

4. Assess for changes in tissue perfusion

5. Assess for changes in neurological status

6. Avoid IV lines in chest/hands

1. A potentially fatal metabolic complication that results from the rapid destruction of tumor cells leading to hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia.

2. Happens in cancers with high proliferation rate. (grows quickly)

3. Hematologic Malignancy: burkitt lymphoma, Hon-hodgkin lymphoma, acute leukemia

4. Chemo sensitive tumor

5. Large tumor burden: mediastinal mass, intra-abd mass

1. Rapid breakdown of cells in response to anticancer treatment

2. Intracellular contents released into circulation (doing damage)

3. Body unable to maintain normal homeostasis because of excess cellular by-products.

4. Metabolic imbalances and multisystem dysfunction may result.

1. Symptoms related extent of metabolic abnormalities

2. Neuromuscular - muscle weakness, twitching, lethargy

3. Cardiovascular - arrythmias, bradycardia, V tach, V fib, cardiac arrest

3. GI - anorexia, n/v, abd cramps, diarrhea, hyperactive BS

4. Renal - oliguria, anuria, crystals in urine, flank pain, acute renal failure

5. Hyperphosphatemia - n/v, lethargy, seizures

6. Hyperkalemia - nvd, muscle weak, paresthesia's, arrhythmias ekg changes

7. Hyperuricemia - nvd, hematuria, flank pain, oliguria, fluid overload (RF)

8. Hypocalcemia - agitation muscle cramping, twitching, tetany , cardiac arrythmias.

1. Prevention is key

2. IV Hydration and diuresis (immediately): iv fluids prior to chemo, maintains renal blood flow, promotes urinary excretion of uric acid and phosphate, 3-6 L/day, no potassium in IV.

3. If severe, may need dialysis

4. Medication: allopurinol (prevent) and rasburicase (prevent and treat), urine alkalinization - sodium bicarbonate.

1. Max safety

2. Institute seizure precautions

3. Monitor labs

4. I/Os

5. Maintain adequate oral fluid intake.

1. HSCT is a therapy in which healthy stem cells are infused into a recipient for the purpose of resorting normal bone marrow function in patients who have a hematologic malignancy or bone marrow failure.

2. Allows patients with cancer to receive higher doses of chemotherapy than the bone marrow can usually tolerate.

3. Autologous - from pt's own blood or bone marrow

4. Allogeneic - from donor

5. allows for higher doses of chemo

1. mucositis

2. Severe pancytopenia (low wbc, platelets, rbc)

3. Graft-versus-host (donor stem cells attack recipitant)

4. Graft failure

1. System communicates to the body via HORMONES and plays a role in reproduction, growth and development, and regulation of energy and metabolism

2. The GLANDS of the endocrine system produce, store, and secrete hormones that travel though the body to specific target cells.

1. know location of glands.

1. Negative feed back - opposite reaction of initial action

2. Positive feedback - reinforcement of same action

3. Complex feedback - multiple variables, ripple effects throughout entire system.

4. Nervous system control - FOF, catecholamines released determine which hormones need to be excreted.

5. Rhythms - circadian rhythm, hormones fluctuate throughout day.

1. Health history

2. Chief complaint

3. General: changes in energy level/fatigue, tolerance to heat and cold, recent weight changes, sleep pattern, body proportions/muscle mass

4. Dermatologic - pruritus', color changes, wounds

5. Cardiovascular - palpitations

6. pulmonary - dyspnea

7. Neurologic: changes in mood memory, and concentration, voice changes, visual, HAs, loss of smell, nervous, tremors, seizures, confusion, agitation, delusion ,paranoia, depression.

1. GI: changes in appetite, weight gain or loss, n/v, abdominal pain, constipation or diarrhea, incontinence, polyphagia, polydipsia

2. GU: polyuria, oliguria, nocturia, incontinence, decreased libido, menstrual irregularities

3. Musculoskeletal: muscle and joint pain or aching, muscle weakness, muscle cramping.

1. Past health history: trauma, ischemia or infarction, neoplasm, inflammation, or infection, AIDs or immune condition, family hx, social hx

2. Medications - RX and non-RX

3. Surgery and other treatments

1. Mental-emotional status

2. General appearance and head-to-toe assessment

3. Palpitation: thyroid - goiter or nodules?

4. Other: temperature change, pulse rate/rhythm (can cause tachycardia), orthostatic hypotension, hypertension, respirations change in rate and rhythm, weight changes.

1. Hormone levels in blood (TSH, T3, T4)

2. Water deprivation test (dx diabetes insipidus, NPO for 6 hours, administer ADH check urine osmolarity)

3. MRI, CT and US - to evaluate gland size and nodules, find tumors (should be pea size)

4. Radioactive Iodine Tests for Thyroid

5. Cortisol Stim Test (30-60min recheck, should inc level)

6. Fasting blood glucose and glucose tolerance tests (usually preg women)

1. Symptoms of endocrine disorders are often missed in the elderly because they are similar with aging (fatigue, constipation, insomnia, mental impairment)

2. As you age: metabolism, in glucose tolerance, sensitivity to insulin, in thyroid hormone production from atrophy of the thyroid gland, menopause, test in men

1. "Master Gland of the endocrine system"

2. The CNS connects to the pituitary via the hypothalamus.

3. There are three lobes: anterior, posterior, intermediate.

4. Located on the inferior aspect of the brain.

1. Produces TSH, ACTH, GH, FSH, LH

2. TSH - stims the thyroid to produce thyroid hormone, aka thyrotropin

3. ACTH - stims the adrenal cortex to produce cortisone

4. GH - controls body growth

5. FSH / LH - follicle stim hormone and luteinizing hormone.

1. Actions: stims protein anabolism, mobilize fatty acids, conserves carbohydrates, stims bone and cartilage growth

2. Releasing Factors: GRH - growth hormone releasing hormone - from hypothalamus in response to exercise, starvation, decreased amino acid levels, stress and hypoglycemia.

1. Target: all body cells capable of growth, especially muscle, bone and cartilage cells.

2. Hypersecretion: gigantism in children, acromegaly in adults.

1. Enlarged supraorbital ridge

2. Thickened ears and nose

3. Paranasal sinus enlargement

4. Thickening of the tongue and soft tissue - resulting in speech difficulties and hoarseness

5. Sleep apnea - upper airway narrowing

6. May have HTN and cardiomyopathy

7. Enlargement of hands and feet

8. Usually begin to develop in 3rd- 4th decades of life.

1. Dwarfism in children

2. Panhypopituitarism (Simmonds's disease) - is total absence of all pituitary secretions

3. Sheehan's syndrome - postpartum pituitary necrosis - of anterior pituitary. Possible decrease in organ weight in adults.

1. GH response to an oral glucose challenge

2. MRI to dx pituitary tumor

3. CT with contrast to locate tumors

4. Eye exam

5. Plasma GH and somatomedin C (insulin like growth factor) 1; IGF binding protein 3 levels.

1. Usually not malignant

2. Their location and effects on hormone production by target organs can cause life-threatening effects.

1. Growth hormone excess: return to normal level, surgical therapy: transsphenoidal approach, hypophysectomy, goal remove only the GH secreting adenoma.

2. Radiation

3. Stereotactic radiosurgery

4. 3 types of drugs used to decrease growth hormone secretion: 1. somastatin analogs (octerotide) act on tumor itself, 2. GH receptor antagonists (somavert) block hormone action, 3. Dopamine agonists (dostinex) suppress GH secretion.

1. DO NOT ALLOW ICP TO BE increased

2. Teach: nasal packing for 2-3 days post op, breathe through the mouth, mustache dressing or drip pad, do not brush teeth, no cough/sneezing, straining, lifting

1. Hyposecretion of GH:

2. Replacement therapy with recombinant GH: expensive, major side effect - fluid retention

3. If tumor is cause - surgery and/or radiation

4. Permanent target organ hormone replacement: corticosteroids, thyroid hormone, sex hormones, gonadotropins - for fertility.

1. Secretes: oxytocin and ADH

2. Oxytocin: increases labor, stimulates breast milk

3. ADH (anti-diuretic hormone or vasopressin): controls body water balance

1. Action: increases water reabsorption (inhibits diuresis) by renal tubules and collecting ducts. causes vasoconstriction of arterioles. cause increased peristalsis.

2. Releasing factors responds to: increase in serum osmolality, hypernatremia, hypovolemia, hypoxia, hypotension, pain, trauma, stress, nausea, pharmacological agents.

3. Target - distal renal tubules and collecting ducts, smooth muscle of arterioles and GI tract.

4. Hypersecretion = SIADH

5. Hyposecretion = Diabetes Insipidus

1. Occurs when ADH is released in amounts greater than indicated by the plasma osmolarity.

2. Characterized by: fluid retention, serum, hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine in the presence of normal or increased intravascular volume, normal renal function.

1. Increased ADH

2. Increased water reabsorption in renal tubules

3. Increased intravascular fluid volume

4. Dilutional hyponatremia and decreased serum osmallity.

1. cancer, pulmonary conditions (pneum, tb, lung abscess, PEEP), trauma, subarachnoid hemorrhage and head injury/surgery, CVA, meningitis, guillian-barre, systemic lupus erythematosus (SLE), HIV, drugs (chemo, oxytocin, anesthesia, opioids, antidepressants)

1. Causes: small lung cancer accounts for most cases of SIADH. Ovarian, prostate, pancreatic, stomach, leukemia, and lymphoma, CNS metastases, chemo

2. Management: treat underlying malignancy with radiation/chemo, usual SIADH treatments

3. Nursing Interventions: same as non-cancerous SIADH

1. increased ECF volume from increased renal tubular permeability and reabsorption of water.

2. GFR increases

3. Sodium levels decrease <120

4. urine output is low and concentrated

5. Weight increase, fluid distributed in all spaces

6. Edema

7. If worsens, cerebral edema occurs, change in LOC, patient becomes lethargic, seizure coma death.

1. Simultaneous measurements of: urine / serum osmolality.

2. Dilutional hyponatremia: sodium less than 134, serum less than 280 mOsm/kg, urine osmolality is high and urine specific gravity's is greater than 1.025

3. BUN - decreased

4. Creatinine clearance - decreased

5. HnH - decreased

1. Treat underlying cause first

2. If s/s mild and serum sodium mis greater than 125: restrict fluids 800-1000ml day, may use Lasix for diuresis, this will cause gradual correction.

3. If not enough to improve symptoms or Na is less than 120: give 3% to 5% Saline given SLOWLY IV. fluid restriction to 500mL/day

4. Chronic cases: fluid restriction <1000 mL day, meds like declomycin or lithium to block the action of ADH at the level of distal collecting tubes.

1. Strict I/O

2. daily weights

3. Monitor electrolytes, urine studies

4. Mouth care, skin care

5. Seizure precautions

6. Pt education: diet/fluid restrictions.

1. Is a disorder of water metabolism caused by a deficiency of ADH/vasopressin

2. The absence of ADH allows filtered water to be excreted in the urine instead of being reabsorbed

3. The disease causes excessive urination and excessive thirst and fluid intake

4. More common in men.

1. Central or neurogenic: idiopathic, brain tumors(main cause head trauma), removal of pit gland, intracranial surgery, infection or inflammation

2. Nephrogenic - there is adequate ADH but decreased response to ADH by the kidneys due to kidney injury or medications

3. Dipsogenic- a defect in the hypothalamus or damage to the pit gland.

1. Normally ADH is synthesized in the hypothalamus and then stored by the post pit

2. Once released ADH increases the water permeability in the distal and collecting tubules of the kidney leads to water reabsorption

3. If ADH is absent, the filtered water is excreted in the urine instead of being reabsorbed.

1. Abrupt onset of extreme polyuria- 5 to 20 L day of diluted urine

2. Polydipsia (excessive thirst)

3. In severe cases: fatigue and altered sleep related to nocturia and thirst

4. Weight loss

5. Dizzy weak

6. Constipation

7. Increased serum sodium and osmolality.

1. Identify the cause

2. UA- almost colorless urine, low osmolality 50-200 mOsm, specific grav less than 1.005, decreased urine sodium

2. Dehydration test or water deprivation test

3. Serum sodium > 147

4. Serum osmolality > 300 mOsm/kg

1. Eliminate the cause - is the goal of treatment

2. Replace ADH

3. IV therapy - hydration: saline and glucose, in acute DI admin fluids slowly to decrease serum sodium 1 mEq every 2 hours.

3. Electrolyte replacement

1. Central DI tx: admin of adh replacement

2. Prototype drug is: Desmopressin acetate (DDAVP) a synthetic vasopressin analogue (drug of choice)

1. Hypovolemia, shock, severe dehydration, decreased CO, decreased perfusion - particularly to brain and kidney, CNS damage, elderly at risk - can often occur with pts that have impaired or absent thirst mechanisms.

2. Sodium is increased because it is being retained despite dumping of fluid.

1. Early detection

2. Maintenance of adequate hydration iv fluids

3. I/O, daily weights, manage fluids, vital signs

4. Drugs - DDVAP

5. Pt teaching long term monitoring in chronic cases. (hat in toliet to see what urine looks like)

1. There is adequate ADH, but decreased response to ADH by the kidneys so replacement won't help.

2. Dietary measures

3. Limit Na to <3 grams a day

4. HCTZ may help reduce flow to ADH sensitive distal nephrons

5. Indocin increases renal responsiveness to ADH.

1. caused by profound deficiency of insulin

2. Characterized by: hyperglycemia (250-800), dehydration and electrolyte loss, acidosis (6.8-7.3 pH, bicarb 0-15)

3. Most likely occurs in type 1, may be 1st incident of DM.

1. Infection

2. Inadequate insulin dosage (even when sick)

3. Undiagnosed type 1

4. Poor self-management

5. Neglect

1. When supply of insulin insufficient: glucose cannot be properly used for energy. Body breaks down fat stores. Ketones are by-products of fat metabolism. (alter pH balance, causing metabolic acidosis, ketone bodies excreted in urine, electrolytes become depleted)

2. Classic DKA ABG: pH 7.14, CO2 24, HCO3 14, PaO2 70, O2 sat 94%

1. Lethargy/weakness

2. Blurred vision, HA

3. Dehydration: poor skin tugor, dry mucous membranes, tachycardia, orthostatic hypotension

4. Abdominal pain: anorexia, vomiting

5. Kussmaul respirations: rapid deep breathing, attempt to reverse metabolic acidosis, sweety fruity odor.

1. DKA is a life threatening emergency

2. Correct fluid/electrolyte imbalance/acidosis

3. IV infusions of NS (replace 6-10 L in first 24 hrs): flush out glucose, restore urine output and raise blood pressure, switch 1/2 NS after the first few hours.

4. When blood glucose levels approach 300 mg/dL change to D5W

5. Cautious, but timely, potassium replacement

6. Insulin therapy.

7. Priority is IV infusion, d5w, insulin drip, potassium replacement (Order)

1. Insulin therapy

2. Withheld until fluid resuscitation has begun

3. Correct acidosis - don't interrupt continuous infusion until SQ insulin has been started!

4. Bolus followed by insulin drip

5. Regular insulin only one approved for IV - must convert units per hour to IV drip rates

6. Example: 100 units of regular insulin mixed into 500 mL of 0.9% NS, 1 unit of insulin equals 5 mL and there fore 5 units per hour equals 25 mL per hour.

1. K replacement

2. As H+ ions move INTO the cells, K+ moves OUT of the cells, initially causing HYPERKALEMIA. But, with treatment (Insulin and fluids) K+ is forced back into the cells and HYPOKALEMIA is present.

3. The average DKA patient has a total body K+ deficit of 3-6 mmol/kg.

4. K needs to be cautiously replaced (Mg and Phos too)

5. Sodium bicarbonate administered if severly acidotic.

1. Frequent DKA in type 1 diabetic

2. Clinical and emotional issues with insulin therapy that are incapacitating

3. Consistent failure of insulin based management to prevent acute complications.

1. Life threatening syndrome

2. Less common than DKA

3. Often occurs in patients 50-70 years with type 2 DM

4. Precipitating event such as acute illness such as stroke or infection, medications such as thiazides, or treatments such as dialysis.

1. Patient has enough circulating insulin that ketoacidosis does not occur.

2. Produces fewer symptoms in earlier stages.

3. Neurologic manifestations occur because of increase in serum osmolality.

4. Medical emergency

5. High mortality rate

6. Therapy similar to DKA: except HHS requires greater fluid replacement. (6-18 L in 24hrs)

1. hypotension

2. profound dehydration

3. tachycardia

4. neurological signs

5. Lab values: BGL > 600 - 1000, serum osmolality >320 mOsm, absent/minimal ketone bodies.

1. Similar to DKA

2. monitor for fluid overload, HF, and cardiac arrhythmias - typically older patients.

3. IV fluids guided by central venous or hemodynamic pressure

4. Potassium added when urinary output is adequate with ECG monitoring

5. Low-rate IV insulin when glucose reaches 250-300

6. Follow protocols.

1. Less than 70 bgl

2. Simple carb, OJ or coke apple juice, recheck in 15 minutes, if no response 1mg of glucagon IM or SQ, possibly dextrose 15% 20 mL.

3. 15g of carbs, 4 oz of juice/soda.

1. Cushing syndrome - hypersecretion of ACTH

2. Addison's Disease and Adrenal Crisis - hyposecretion of ACTH

1. Action

2. Stimulates growth and function of adrenal gland

3. Controls production and release of glucocorticoid hormones (stress, metabolism, immune)

4. Stimulates mineral corticoid production (FE balance)

5. Stimulates androgen production (sex hormones)

1. A spectrum of clinical abnormalities caused by an excess of glucocorticoids

2. Causes:

3. Commonly caused by excessive corticosteroid (prednisone) administration

4. Excessive glucocorticoid production secondary to hyperplasia of the adrenal cortex.

5. Pit tumor secreting too much ACTH

0. Disease is excessive secretion by adrenal glands (20-40 yrs old)/ pit tumor. Syndrome = excessive admin of steroids

1. truncal obesity, buffalo hump, moon face, hirsutism (excess hair), broad purple striae, thin extremities w/ muscle wasting, thin/fragile skin, thinning scalp hair, bruising petechia, impaired wound healing, electrolyte imbalances.

1. Osteoporosis and pathological fractures

2. Peptic ulcer

3. Lipidosis (a disorder of fat metabolism) usually occurs

4. Increased hepatic gluconeogenesis and insulin resistance

5. HTN from Na and water retention

6. Ischemic Heart disease and failure

7. Menstrual disturbances

8. Sexual dysfunction

9. Immune complications: delayed wound healing, suppression of inflammatory response-mask infections.

1. Three tests used with 2 of 3 being abnormal to diagnose Cushing's.

2. 24 hour urine collection for free cortisol

3. Serum cortisol levels

4. Overnight dexamethasone suppression test: dexamethasone given orally late in evening, plasma cortisol level obtained in AM.

5. Blood chemistry can also indicate Cushing's increased cortisol, increase serum sodium and glucose, decrease serum potassium.

6. MRI/CT- shows pituitary or adrenal tumor.

1. Goal to normalize hormone secretion

2. Treat underlying cause

3. Transsphenoidal hypophysectomy- surgical removal of pit adenoma

4. Adrenalectomy - for adrenal tumors or hyperplasia

5. If surgery - control of HTN and hyperglycemia prior

6. Radiation - may be done instead of surgery or with.

7. Drug therapy

8. Adrenal enzyme inhibitors if syndrome is caused by ectopic ACTH secretion

9. If caused due to prolonged administration of glucocorticoids: d/c of therapy by gradually tapering medication - avoid adrenal crisis. Conversion to alternate-day regimen.

1. Addison's disease involves hypofunction of the adrenal cortex and an insufficiency of ACTH.

2. Glucocorticoids, mineralocorticoids and androgens are all decreased.

3. Causes include autoimmune response, TB, AIDS, metastatic CA, adrenal hemorrhage.

4. In Cushing's disease there is a cushion of ACTH, where in Addison's we need to add some ACTH.

1. Loss of mineralcorticoids - decreased CO due to extracellular fluid deficiency from increased excretion of sodium, chloride, and water and potassium retention.

2. Loss of glucocorticoids - hypoglycemia, muscle weakness, lethargy, anorexia, weight loss, n/v.

3. Hyperpigmentation is an important characteristic - comes from increased levels of ACTH.

4. Patients are not able to withstand food deprivation or stressors to the body (surgery, infection, fasting)

1. Combined measurements of early morning serum cortisol and plasma ACTH

2. Plasma ACTH increased, serum cortisol decreased

3. Hypoglycemia, hyponatremia, hyperkalemia and leukocytosis

4. Cortisol stim test (opposed to suppression)

1. Combating circulatory shock is number one priority: admin fluids and corticosteroids, place pt in recumbent position with legs elevated, tx underlying cause

2. Drugs: mineralocorticoids (fludrocortisone), antacids, magnesium, and aluminum hydroxide (maalox), glucocorticoisteroids - cortisone, hydrocortisone

3. FE balance

1. High cal, protein, sodium and low potassium diet: small freq meals, feed BEFORE steroids, may require high potassium and low sodium while on steroids.

2. Weight daily

3. Change positions slowly

4. Conserve energy - assist with ADL's, provide rest periods.

1. A critical deficiency of mineralocorticoids and glucocorticoids. Mostly commonly related to sudden stopping of steroids.

2. It generally occurs in patients who have chronic adrenal insufficiency or following acute stress, surgery, sepsis, trauma, or omission of steroid therapy.

3. Considered a medical emergency - requires immediate treatment.

1. Hypotension - orthostatic can lead to shock and circulatory collapse

2. Tachycardia

3. Dehydration

4. Hyponatremia

5. Hyperkalemia

6. Hypoglycemia

7. Fever

8. Weakness/confusion

9. GI - nausea, vomitting, diarrhea, abd pain.

1. IMMEDIATE IV Hydrocortisone - 100 mg q6 hrs

2. Fluid resuscitation with 3-5 L of D5NS (reverses shock and hyponatremia)

3. Glucose - for hypoglycemia.

4. Maintain IV for at least 24 hours or until BP is stable.

1. Effects: anti-inflammatory, immunosuppression, maintenance of normal BP (Na retention), influences carbohydrate and protein metabolic effects, opposes insulin, causes glucose intolerance.

2. Complications vary.

1. Patient teaching: why steroids cause bgl changes, follow up with PCP r/t potential for development of DM

2. Take as directed

3. Take with food to reduce GI effects

4. Do not miss dose

5. Taper off - depends on drug/dose/length

6. If > 3 months, osteoporosis - increase Ca, Vit D, walking program

7. Monitor Glucose levels - may require treatment.