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Critical Care > Adult Endocrine > Flashcards

Adult Endocrine Flashcards

1
Q

Diabetes Insipidus
Etiology/Patho

A

Results from an ADH deficiency, ADH insensitivity or excessive water intake
- Nephrogenic: ADH Insensitivity (chronic renal insufficiency, hypercalcemia, hypokalemia)
- Neurogenic: ADH Deficiency (most common)
- Primary Cause: traumatic injury to the posterior pituitary or hypothalamus because of head injury or surgery (to remove pituitary tumor)
- Severe head trauma

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2
Q

Diabetes Insipidus
Assessment/Clinical Presentation

A

Clinical Presentation
Onset of symptoms
- Neurogenic occurs suddenly with an abrupt onset of polyuria
- Nephrogenic has gradual onset
- Pale, dilute urine
- Polydipsia (only if patient is conscious and the thirst mechanism is intact)
Signs of hypovolemia if patient unable to replace water lost
- Hypotension
- Decreased skin turgor
- Dry mucous membranes
- Tachycardia
- Weight loss
- Low right atrial and pulmonary artery occlusion pressures
Signs of hypernatremia
- Altered mental status
- Weakness
- Focal neurological deficits
- Ataxia

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3
Q

Diabetes Insipidus
Lab Evaluation
Water Deprivation Test

A

Classic Signs: low urine osmolality, decreased urine specific gravity, and high serum osmolality
CBC
- ↑ Hemoglobin and Hematocrit
CMP (nephrogenic cause)
- ↑ Sodium
- ↑ Calcium
- ↓ Potassium
- ↑ BUN
Urinalysis
- ↓ Specific Gravity
- ↓ Urine osmolality
- ↑ Serum osmolality
Water Deprivation test
- All water is withheld, and urine osmolality and patient’s weight are measured hourly
- Diagnosis of DI is made when the serum osmolality increases and there is no resultant increase in urine osmolality
- May not be an appropriate for critically ill patient

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4
Q

Complications of Diabetes Insipidus
Actual and Potential Complications

A

Actual
- Dehydration
- Hypovolemia
- Hypernatremia
Potential
- Circulatory collapse
- Neurologic complications secondary to hypernatremia (confusion, seizures, coma)
- Fluid overload if too much treatment

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5
Q

Diabetes Insipidus
Medical Management

A

Volume Replacement
- Oral replacement when capable
- If patient shows symptoms of hypovolemia, IV fluids
- D5W: Corrects hypernatremia and replaces water losses
Hormone Replacement for Neurogenic DI
- Desmopressin (DDAVP): a synthetic analog of ADH (Vasopressin)
- Side Effects: headache, nausea, mild abdominal cramps
- Monitor for: dyspnea, hypertension, weight gain, hyponatremia, headache, drowsiness
Sodium Restriction for Nephrogenic DI

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6
Q

Diabetes Insipidus
Nursing Interventions

A
  • Strict VS and I&O monitoring
    *Lack of ADH leads to excessive water loss with resulting decrease in blood pressure and increase in heart rate as a compensatory mechanism.
    *Fluid replacement is largely dependent on the volume of urine output secondary to lack of ADH
  • Maintain IV access
    *In patients with a decrease in level of consciousness, IV fluids are usually indicated.
    It is important to maintain vascular access because placement of an IV catheter in a profoundly hypotensive patient is difficult.
  • Administer medications as directed
    *Desmopressin
  • Provide adequate oral fluids when appropriate
    *If patient is alert and oriented
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7
Q

Diabetes Insipidus
Patient Education

A

*Pathogenesis of DI
*Medication use, side effects, etc.
*Parameters for contacting their provider
*Importance of monitoring daily weight
- Contact provider for weight gain or loss of greater than 2 lbs per day
*Importance of drinking according to thirst and to avoid excessive drinking
*Clinical manifestations of fluid overload

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8
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Etiology/Patho

A

Causes
- Head injury
- Surgery
- Small cell carcinoma of the lung
- Medications
Patho
- Excess secretion of ADH caused by failure in the negative feedback mechanism

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9
Q

SIADH
Assessment/Clinical Presentation

A

Neurologic
- Weakness
- Lethargy
- Mental confusion
- Restlessness
- Headache
- Seizures
Gastrointestinal
- Nausea and vomiting
- Anorexia
- Muscle cramps
- Decreased bowel sounds
Cardiovascular
- Edema
- Increased BP
- Elevated central venous pressure
Pulmonary
- Increased respirations
- Dyspnea
- Crackles
- Pink, frothy sputum

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10
Q

SIADH
Labs/Diagnosis

A

CBC
- ↓ Hemoglobin and Hematocrit
CMP
- ↓ Sodium
- ↓ Serum osmolality
- ↑ Urine osmolality
Urinalysis
- ↑ Urine specific gravity
Diagnosis is based on the presentation of ↓ urine output and ↑ urine specific gravity with a ↓ in serum sodium and serum osmolality

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11
Q

Complications of SIADH
Actual and Potential

A

Actual
- Fluid volume excess
- Pulmonary edema
Potential
- Symptoms of hyponatremia
- Seizure and coma
- Cerebral edema

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12
Q

Medical Management of SIADH `

A

Goals of therapy: treat the underlying cause, eliminate excess water, increase serum osmolality
Fluid Management
- Fluid restriction
- Less than 1000mL/day
- Liberal salt and protein intake
Medications
- 3% Saline HIGH RISK
- Diuretics to increase urine output
- Demeclocycline to increase water excretion by the kidneys

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13
Q

Nursing Considerations for Administration of 3% Saline

A
  • Administer via central line (NOT PERIPHERAL)
    USE A PUMP
  • Rate should not exceed 50 mL/hour
  • Monitor sodium levels every 4 hours
  • Hold infusion if sodium level exceeds 155 mEq/Luld
  • Should not increase more than 12 mEq within first 24 hours
  • Wean solution rather than stopping abruptly
  • Monitor for changes in mental status (cerebral edema or worsening hyponatremia)
  • Monitor lung sounds for crackles (pulmonary edema)
  • Hourly I&O monitoring
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14
Q

SIADH Nursing Interventions

A
  • Vital Signs and strict I&O monitoring
    *Monitor for signs of fluid overload
  • Monitor for signs of fluid overload
    *Tachypnea, Neck vein distention, Tachycardia, Crackles, Increased pulmonary artery occlusion or right atrial pressures, Declining level of consciousness
  • Monitor electrolyte imbalances
    *Decreased serum sodium
  • Seizure precautions
    *Risk of seizures increases with hyponatremia
  • Adherence to fluid restriction
    *Fluids are restricted to concentrate serum sodium.
  • Monitor for skin breakdown
    *Fluid reabsorption may result in skin tautness.
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15
Q

SIADH Patient Education

A
  • Disease process and management
  • Fluid restriction
  • Signs of fluid overload
  • Weigh daily at same time (contact for weight gain >2lbs per day)
  • S/S of cerebral edema
  • Monitor Intake/Output
  • NSAIDS can cause SIADH…AVOID NSAIDS
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16
Q

Thyrotoxic Crisis (Thyroid Storm)
Etiology/Patho

A

Occurs when thyroid hormone levels rapidly rise in untreated or inadequately treated patients with hyperthyroidism
Causes
Often precipitated by stress due to:
- Underlying illness
- General anesthesia
- Surgery
- Infection

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17
Q

Thyrotoxic Crisis (Thyroid Storm)
Assessment/Clinical Presentation

A

Abrupt onset
Most prominent clinical features are severe fever, marked tachycardia, heart failure, tremors, delirium, stupor, and coma
Thermoregulation Disturbances
- Fever as high as 106°F**
- Warm, moist skin
Neurological Disturbances
- Agitation
- Delirium**
- Psychosis
- Tremulousness**
- Seizures
- Coma
Cardiovascular Disturbances
- Palpitations
- Tachycardia** (always order EKG and thyroid panel)
- Widened pulse pressure
- Atrial fibrillation**
- Prominent S3
- Systolic murmur
Pulmonary Disturbances
- Increased respiratory rate
- Respiratory muscle weakness
- Hypoventilation
- CO2 retention
- Respiratory failure
Gastrointestinal Disturbances
- Abdominal pain
- Nausea/vomiting
- Diarrhea
- Jaundice
Musculoskeletal Disturbances
- Muscle weakness and fatigue

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18
Q

Lab Evaluation of Thyroid Storm

A

CBC
- ↑ WBC
- ↓ RBC
CMP
- ↑ Sodium
- ↑ Glucose
- ↑ BUN
- ↑ Calcium
Thyroid Hormones
- ↓ TSH
- ↑ T3 and T4 (elevated, but no higher than levels found in uncomplicated hyperthyroidism)
ABGs

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19
Q

Medical Management of Thyroid Storm

A

Antagonism of Peripheral Effects of Thyroid Hormones
*Beta-Blockers: Propranolol
Inhibition of Thyroid Hormone Biosynthesis
*Propylthiouracil or Methimazole (Tapazole)
- Not available in IV form, but may be given via NG tube
- These medications LACK IMMEDIATE EFFECT
Blockage of Thyroid Hormone Release
*Saturated Solution of Potassium Iodide (SSKI)
- Given orally or sublingually
- Must be administered 1-2 hours AFTER antithyroid medications (propylthiouracil/Methimazole)
*Glucocorticoids
Supportive Care
*Identify and treat precipitating cause
*Fever control
- Acetaminophen
- Do not give salicylates (Aspirin, Ibuprofen, etc)**
- Cooling blankets
- Administer Oxygen
- Fluid and electrolyte management as needed

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20
Q

Thyroid Storm
Nursing Interventions

A

Vital sign and I&O monitoring
*Hypermetabolism results in elevated heart rate, increased respiratory rate, and elevation in temperature
Seizure precautions
*Increased risk for seizure activity linked to hyponatremia and elevated temperature associated with hypermetabolism
Eye lubricant
*To prevent irritation from exophthalmos
High calorie, high protein diet
Frequent BG checks
Monitor electrolytes
Implement cooling measures with elevated temperature

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21
Q

Nursing considerations/education for thyroidectomy

A

Pre-procedure:
*Potassium Iodide to reduce vascularity of thyroid gland (decreases size of thyroid, reduces risk of bleeding)
Post-surgical management
*Monitor for airway compromise, hemorrhage, AND hypocalcemia (secondary to removal of parathyroid gland tissue)
*Hematoma -> hemorrhage
*Patients should be kept in Semi-Fowler’s position.
*Assess for laryngeal nerve damage.
- Changes in voice quality, hoarseness, or a husky tone
- Voice assessments every 1-2 hours in the immediate post-op period
*Administer humidified air
*SUCTIONING EQUIPMENT, TRACHEOSTOMY TRAY, AIRWAY/OXYGEN SUPPLIES SHOULD BE KEPT AT THE BEDSIDE
*Patient needs to take Synthroid after surgery because there is no thyroid, take as directed every day

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22
Q

Thyroid Storm
Patient/Family Education

A

Identification and prevention of episodes
Consume adequate calories to minimize weight loss
Do NOT take NSAIDS

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23
Q

Myxedema Coma
Etiology/Patho

A

The most extreme form of hypothyroidism causes increased hormone use but there is decreased hormone production -> crisis state
Precipitating factors
- Infection
- Trauma
- Medications

24
Q

Myxedema Coma
Assessment/Clinical Presentation

A

Cardiovascular Disturbances
- ↓ Heart rate, blood pressure, cardiac output**
- Pericardial effusion → distant heart sounds
Pulmonary Disturbances
- Hypoventilation**
- CO2 retention
- Pleural effusion
Neurological Disturbances: All mental status changes in a patient with hypothyroidism should be reported immediately.
- Somnolence
- Delirium
- Seizures
- Coma
- Paranoia/delusions
Thermoregulation Disturbances
- Hypothermia
- If patient in myxedema coma has a temperature of >98.6°F, underlying infection should be suspected**
Skeletal Muscle Disturbances
- Decreased deep tendon reflexes
- Sluggish, awkward movements

25
Q

Lab evaluation of myxedema coma

A

CBC
- ↓ RBCs
- ↓ Platelets
CMP
- ↓ Sodium
- ↓ Glucose
Thyroid Hormones
- ↑ TSH (IF cause is PRIMARY hypothyroidism)
- TSH levels will be normal or low of cause is secondary or tertiary hypothyroidism
- ↓ T3 and T4
Adrenal insufficiency may cause low cortisol levels

26
Q

Medical management of myxedema coma

A

Thyroid Replacement
*Levothyroxine (preferred route is IV) – most commonly used
*Liothyronine (Cytomel)
- Avoid in older adults due to risk of angina, MI, cardiac irritability
Fluid Replacement
*Hypotension/shock usually resolves with thyroid replacement
*Cautious volume replacement with NS may be used
Electrolyte Replacement
*Sodium
- Hyponatremia usually responds to thyroid replacement and fluid water restriction
- If sodium is <120 mEq/L OR patient is having seizures, hypotonic saline may be used
*Glucose
- If patient is hypoglycemic, glucose is added to IV fluids
*Cortisol
- If patient has adrenal insufficiency, Hydrocortisone is given
*Potassium
- If hypokalemic
Aggressive symptom management
*Treat hypothermia with a warm room, warm blankets, warm fluids
*Avoid medications that depress respirations
- Patients with hypothyroidism who are receiving sedatives, hypnotics, or narcotics require close observation because the metabolism of the medication is slower, and respiratory compromise may occur with normal dosages. The dose, as well as the interval between doses, may need to be adjusted in the patient with severe hypothyroidism.

27
Q

Myxedema Coma
Nursing Interventions and Patient/Family Education

A

*Vital sign and I&O monitoring
- Decreased body temperature, heart rate, respiratory rate, and blood pressure
*Administer medications as directed
*Monitor for electrolyte imbalances
*Continuous cardiac monitoring
*Warm blanket/bear hugger
*Administer narcotics and sedatives with caution
Patient and Family Education
*Identification and prevention
*Medication use - Take Synthroid (levothyroxine) EVERY morning
*S/S of hypo and hyperthyroidism
*Need for follow-up/routine check ups

28
Q

Acute Adrenal Insufficiency (Addisonian/Adrenal Crisis)
Etiology/Patho

A

Life-threatening absence of cortisol (glucocorticoid) and aldosterone (mineralocorticoid)
Causes
*Primary Adrenal Insufficiency – Destruction of the adrenal gland
- Autoimmune diseases: 50-70% of cases (Addisons)
- Infection: Most common cause of adrenal insufficiency in ICU settings
*Secondary Adrenal Insufficiency Mechanisms that decrease ACTH secretion
- Abrupt withdrawal of corticosteroids: Most common cause of acute adrenal insufficiency
- Systemic inflammatory states: sepsis, sickle cell disease
- Trauma

29
Q

Acute Adrenal Insufficiency
Assessment/Clinical Presentation

A

Cardiovascular (Hypovolemia:↓Water Absorption, ↓Vascular Tone: ↓Effect of Catecholamines, ↑Potassium)
- Hypotension refractory to fluids
- Weak, rapid pulse
- Cold, pale skin
- Dysrhythmias
Neurologic (↓Glucose, ↓Protein Metabolism, ↓Volume and Perfusion, ↓Sodium)
- Headache
- Fatigue
- Severe weakness
- Confusion, lethargy, psychoses
Gastrointestinal (↓Digestive Enzymes, ↓Intestinal Motility, ↓Digestion)
- Anorexia
- Nausea/vomiting
- Diarrhea
- Abdominal pain
Genitourinary (↓ Renal Perfusion, ↓ GFR)
- Decreased urinary output

30
Q

Lab Evaluation for Acute Adrenal Insufficiency
Diagnosis

A

CBC
- Differential: ↑ Eosinophils
CMP
- ↓↓ Glucose
- ↑ Potassium
- ↓ Sodium
- ↑↑ BUN
ABG
- pH <7.25
- Metabolic Acidosis
↓↓ Cortisol (in crisis, plasma cortisol levels are <10 mcg/dL)
ACTH
- ↑ in Primary Insufficiency
- ↓ in Secondary Insufficiency
Cosyntropin Stimulation Test
- Differentiate primary and secondary

31
Q

Actual and Potential Complications of Acute Adrenal Insufficiency

A

Actual
- Hypovolemia
- Decreased tissue perfusion
- Electrolyte imbalance
Potential
- Shock
- Dysrhythmias

32
Q

Medical Management of Acute Adrenal Insufficiency

A

Fluid Replacement
*D5NS
- Reverses the fluid deficit and treats hypoglycemia
Electrolyte Management
*Hyperkalemia will likely resolve with fluid replacement and cortisol replacement
*Acidosis will likely resolve with fluid replacement and cortisol replacement
- Sodium Bicarb may be required if pH is <7 OR bicarbonate level is <10 mEq/L
Hormone Replacement
*Glucocorticoid replacement is most important initially
- If no previous diagnosis of adrenal insufficiency: Dexamethasone (Decadron) IV is given (as this will not interfere with cosyntropin stimulation test)
- If there is known history of adrenal insufficiency: Hydrocortisone sodium succinate (Solu-Cortef) IV is given

33
Q

Side Effects of Dexamethasone and Hydrocortisone
Nursing Considerations

A

Side Effects
- Hyperglycemia
- Cushing’s Syndrome
- Electrolyte disorders
- Euphoria and other psychic symptoms
- Fluid retention
- Masking of infection
- Hypertension
- Peptic ulcers
- Nausea and vomiting
Nursing Considerations
- Corticosteroids can have significant effects on the GI tract, assess for complaints of GI distress and Bleeding
- GI bleeding prophylaxis (Protonix)
- Be aware of multiple drug interactions
- Avoid abrupt discontinuation
- Monitor glucose and electrolyte levels
- Monitor for signs of fluid overload
- Monitor for signs of infection (remember these may be masked)
- Maintain adequate nutrition
- Provide mouth care

34
Q

Nursing Interventions and Patient Education for Acute Adrenal Insufficiency

A
  • Monitor VS and I&O: decreased BP
  • Monitor for signs of GI bleeding
  • Administer medications as directed
  • HOB elevated at 45 degrees
  • Continuous cardiac monitoring
  • Check BG
    Patient and Family Education
  • Educate on precipitating causes of adrenal crisis
  • Preventative measures are key!
  • Use of meds: do NOT stop steroids abruptly
  • S/S of insufficiency and excess (report weight gain)
35
Q

Pheochromocytoma
Patho

A

Rare catecholamine-secreting tumor of the adrenal medulla
- Excessive catecholamines (epinephrine and norepinephrine) may lead to life-threatening hypertension or cardiac dysrhythmias
Catecholamines are released from the tumor leading to:
- Vasoconstriction
- Increased heart rate
- Increased stroke volume
- Increased systolic BP
- Widened pulse pressure
- Hyperglycemia

36
Q

Pheochromocytoma
Assessment/Clinical Presentation

A

Severe headache*
Hypertension*
- Often severe: may exceed 250/140
Tachycardia*
Palpitations
Hyperhidrosis (excessive sweating)
Hypermetabolism
Hyperglycemia

37
Q

Pheochromocytoma
Lab evaluation

A

↑ Blood glucose
Evaluate levels of catecholamines and catecholamine metabolites
- ↑ Plasma free metanephrines and normetanephrines
*Patient must lay down for 30 minutes prior to the collection of blood sample to prevent false elevation
- ↑ Urine metanephrines, normetanephrines and vanillylmandelic acid (VMA)
*Requires 24-hour urine collection
*Patients should avoid bananas, chocolate, vanilla, tea, and coffee prior to and during the collection period

38
Q

Actual and Potential Complications of Pheochromocytoma

A

Actual
- Hypertension
- Tachycardia
- Hyperglycemia
Potential
- Dysrhythmias
- Intracranial hemorrhage
- MI
- Kidney failure
- Adrenal insufficiency (if managed surgically)

39
Q

Medical Management of Pheochromocytoma

A

Blood pressure management
*Sodium Nitroprusside (Nipride) → Vasodilation
- Administer via IV infusion and titrate to effect
*Alpha adrenergic blockers → Vasodilation
- Ex: Doxazosin (Cardura) or Prazosin (Minipress)
*Must give alpha blockers FIRST to allow for vasodilation
Heart rate control
*Beta Blockers → Decrease HR

40
Q

Surgical Management of Pheochromocytoma
PreOp and PostOp care

A

Pre-Op Care
*Alpha-adrenergic blockers for 7-10 days prior to scheduled procedure
- Goal is to maintain BP 120/80 or lower when patient is in a seated position
*Beta-blockers for HR control AFTER the BP has been decreased
*Fluid management
*Administration of glucocorticoid the morning of surgery
Post-Op Care
*Monitoring of BP, HR and glucose
- Patients are at risk for hypotension or hypoglycemia because of the sudden decrease in catecholamines
- VS every 15 minutes
- I&O and daily weights
- Monitor for blood loss
- Re-evaluate plasma and urine catecholamine levels
Patients who have bilateral tumors and undergo bilateral adrenalectomy will require lifetime adrenal hormone replacements → Cortisol Daily

41
Q

Pheochromocytoma Nursing Interventions, Patient Education

A
  • DO NOT palpate the abdomen of a patient with pheochromocytoma, this may cause it to secrete more catecholamines
  • Close VS and I/O monitoring
  • Keep head of bed elevated
  • Maintain a quiet, non-stimulating environment (reduce anxiety)
  • Continuous cardiac monitoring
  • Administer medications as directed
  • Frequent BG checks
    Patient and Family Education
  • Post-op care and monitoring
  • Clinical manifestations of adrenal insufficiency
  • Increased risk for this during times of physiological or emotional stress
42
Q

Diabetic Ketoacidosis (DKA)
Etiology/Patho

A

*DKA is characterized by (1) Uncontrolled hyperglycemia, (2) Increased production of ketones, and (3) Metabolic acidosis
Pathophysiology
*Precipitating factors:
- Stress
- Infection: pneumonia, UTI, sepsis, or abscess (most common)
- Trauma or surgery
*Patho
- Stress response triggers adrenal cortex, adrenal medulla, and pituitary glands
- Decreased insulin, increased cortisol, and glucagon -> increased gluycogen to glucose conversion -> hyperglycemia
- Lipolysis -> Increased Free Fatty Acids -> Increased production of ketones -> Ketoacidosis
- Proteolysis -> Increased amino acids -> Increased BUN
- Ketone bodies and Increased BUN -> Osmotic diuresis -> Polyuria -> Hypovolemia -> Hypotension -> Decreased Cellular Tissue Perfusion -> Shock

43
Q

DKA
Assessment/Clinical Presentation

A

Superficial Vasodilation
- Flushed, dry skin
Dehydration
- Dry mucous membranes
- Decreased skin turgor
- Tachycardia
- Hypotension
- Abdominal pain
Ketoacidosis
- Altered level of consciousness
- Kussmaul respirations
- Acetone breath
Delayed Gastric Emptying
- Nausea
- Vomiting
- Anorexia
Hyperglycemia/Osmotic Diuresis
- Visual disturbances
- Increased thirst (polydipsia)
- Increased urine output (polyuria)

44
Q

DKA
Lab evaluation/Diagnosis

A

CBC
- WBC: mildly elevated
CMP
- Blood glucose: elevated (>250 mg/dL)
- Serum bicarbonate: decreased (≤ 18 mEq/L)
- Serum potassium: usually elevated (*Be careful here! *)
- Serum creatinine: often elevated
- Anion gap: elevated (>10 mEq/L)
β-Hydroxybutyrate – elevated (>3.0 mg/dL)
ABG
- Arterial pH: decreased (≤ 7.3)
- Metabolic Acidosis
UA
- Ketones: Positive
- Glucose: Positive
Cultures (to determine precipitating factors, i.e., infection)
Diagnosis
- Based on the following factors:
- Blood glucose level > 250 mg/dL
- Ketonuria
- Arterial pH of ≤ 7.3
- Serum bicarbonate level of less ≤ 18 mEq/L
- Positive anion gap

45
Q

Complications of DKA
Actual, Potential

A

Actual
- Hyperglycemia
- Metabolic acidosis
- Electrolyte imbalance
- Dehydration
Potential
- Respiratory compromise
- Electrolyte imbalance
- Fluid overload
- Kidney Injury

46
Q

Medical Management of DKA

A

*Support airway and breathing as needed
- Oral airways and oxygen therapy
- May need ventilator support in severe cases
- Prevent aspiration: consider need for NG tube in a patient who is vomiting and has impaired mentation
*Fluid Replacement
- Initial fluid replacement: Normal saline (0.9% NS)
- When serum glucose approaches 200 mg/dL, 5% dextrose is added
*Goal is normovolemia
- Prevent fluid overload from overaggressive fluid replacement
*Insulin Therapy
- IV Insulin
*Potassium

47
Q

Fluid Replacement for DKA
Complications, Nursing Considerations

A

*Prevent fluid overload from overaggressive fluid replacement
*Signs and Symptoms of Fluid Overload
- Tachypnea
- Neck vein distention
- Tachycardia
- Crackles
- Increased pulmonary artery occlusion or right atrial pressures
- Declining level of consciousness…
Cerebral Edema: potentially fatal complication of DKA
- Possibly due to rapid IV infusion and too rapid correction of blood glucose (max rate for BG correction is 35-90 mg/dl/hr)
- Monitor neuro status and place on seizure precautions
- If this occurs: osmotic diuretic (20% mannitol solution)

48
Q

Insulin Therapy and Potassium for DKA
Nursing Considerations

A

IV Insulin
*Check potassium first: should be >3.3 PRIOR to starting insulin
*Initial bolus of 0.1 unit/kg REGULAR INSULIN
*Continuous infusion of 0.1 unit/kg/h to achieve a steady decrease in serum glucose levels of 50/75 mg/dL/h
*Target glucose value is 100/150 mg/dL until acidosis resolves
*May transition to subcutaneous insulin when blood glucose is less than 200 mg/dL or less PLUS TWO of the following:
- Venous pH is > 7.3
- Serum bicarbonate level is >15 mEq/L
- Anion gap is ≤ 12 mEq/L
Potassium
*May drop quickly after insulin therapy is started
*Usually added to maintenance fluids after administration of bolus/insulin (UNLESS initial K+ was less than 3.3)
*Maintain serum K+ between 4 and 5 mEq/L
*Ensure urine output is AT LEAST 30 mL/hr prior to administering IV potassium (CHECK KIDNEY FUNCTION)
*Monitor for EKG changes

49
Q

Nursing Interventions for DKA

A
  • ABCs!!
  • Hemodynamic monitoring
  • Hourly I&O: Increased urine output may be present because of osmotic diuresis secondary to hyperglycemia.
  • Continuous cardiac monitoring
  • Hourly BG checks
  • Administer IV fluids, electrolyte replacement and insulin as directed
  • Monitor for fluid overload
  • Frequent Neuro Exams (cerebral edema)
50
Q

Patient Education for DKA

A

Primary focus is on the prevention of DKA
- Manage glucose levels with diet, exercise, and medication
- Monitor hemoglobin A1c
- Maintain a regular schedule for eating, exercise, rest, sleep, and relaxation
- “Sick day management” (what to do with insulin when sick)
- If using an insulin pump, re educate on pump features, safety, management, and troubleshooting
- Avoid exercise and excessive activities when blood glucose is >240 mg/dL
- Disease process and management
- Dietary management

51
Q

Hyperglycemic Hyperosmolar State (HHS)
Etiology/Patho

A

*Precipitating Factors
- Major illness/infection that causes a stress response (Most Common)
- High calorie tube feedings
- Medications
*Patho
- Characterized by hyperglycemia, hyperosmolality and dehydration WITHOUT significant ketoacidosis
- Occurs when there is sufficient insulin to prevent rapid fat breakdown and ketone release, but not enough to prevent severe hyperglycemia
- Extremely elevated blood glucose levels lead to extreme hyperosmolality, which leads to osmotic diuresis

52
Q

HHS
Assessment/Clinical Presentation

A

Superficial Vasodilation
- Flushed, dry skin
Dehydration
- Dry mucous membranes
- Decreased skin turgor
- Tachycardia
- Hypotension
- Shallow respirations
Electrolyte Abnormalities
- Altered level of consciousness
- Decreased or absent deep tendon reflexes
- Seizures

53
Q

Lab Evaluation of HHS
Diagnosis

A

CBC
CMP
- ↑↑ Glucose
- ↑ Sodium
- ↑ Serum Osmolality
ABG
- pH >7.30
- Bicarbonate >15 mEq/L
Urinalysis
- No or trace ketones
Diagnosis
- Blood glucose level of 600 mg/dL or greater
- Serum osmolality of 320 mOsm/kg or greater
- Profound dehydration
- Serum pH GREATER than 7.3: NO ACIDOSIS
- Serum bicarbonate concentration greater than 15 mEq/L
- Small ketonuria and absent to low ketonemia
- Alteration in level of consciousness

54
Q

Medical Management of HHS

A

Support airway and breathing as needed
- Oral airways and oxygen therapy
- May need ventilator support in severe cases
- Prevent aspiration: consider need for NG tube in a patient who is vomiting and has impaired mentation
Fluid Replacement
- Similar to DKA
- Initial fluid is NS bolus
- Goal is normovolemia
Insulin Therapy
- Per hospital protocol – similar to DKA
- Initial bolus of REGULAR INSULIN IV, followed by an insulin drip
- Glucose levels should be monitored hourly while on insulin infusion
- Target glucose levels of 200-300 mg/dL should be maintained until patient’s mental status improves
- Patient may then be transitioned to Sub-Q insulin
Electrolyte Management
- Similar to DKA

55
Q

Nursing Interventions and Patient Education for HHS

A

Close monitoring of VS
Strict hourly I&O
Frequent neuro checks
Administer fluids, electrolyte replacement and insulin as directed
Monitor for fluid overload
Patient and Family Education
- Disease process and treatment
- PREVENTION measures
- Medication use and adherence
- Dietary guidelines

56
Q

DKA vs HHS
Occurence
Onset
Blood Glucose
Arterial pH
Serum Bicarb
Urine or Serum Ketones
Effective Serum Osmolality
Anion Gap

A

DKA
- Most often seen in type 1 DM, but can occur in type 2, especially with severe stress such as infection
- Rapid onset
- Blood glucose >250 mg/dL
- Arterial pH ≤ 7.3
- Serum Bicarb < 18 mEq/L
- Urine or Serum Ketones Positive
- Effective Serum Osmolality >300 mOsm/kg
- Anion Gap Positive
HHS
- Occurs more commonly in older adults in response to stress or infection
- Gradual onset
- Blood Glucose >600 mg/dL
- Arterial pH >7.4
- Serum Bicarb >15 mEq/L
- Urine or Serum Ketones Negative
- Effective Serum Osmolality >320 mOsm/kg
- Anion Gap Negative

Critical Care (12 decks)

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