Critical Endocrine Dysfunction

DKA is

due to an absolute lack of insulin, preventing glucose from entering cells and causing cellular starvation.

In response, counter-regulatory hormones (cortisol, glucagon, growth hormone, catecholamines) increase, triggering lipolysis, glycogenolysis, gluconeogenesis.

DKA cont.

• Glycogenolysis and gluconeogenesis → hyperglycemia (> 250 mg/dL)

• Hyperglycemia → hyponatremia and glucosuria, causing osmotic diuresis

• Osmotic diuresis → polyuria, leading to electrolyte loss, dehydration, hypovolemia, hypEROSMolarity, and acidosis

• Acidosis (pH < 7.3) and ketosis (from lipolysis) are the other two defining features of DKA

Main three characteristics of DKA:

1. Hyperglycemia (>250 mg/dL)

2. Acidosis (pH <7.3)

3. Ketosis

HHS is 

a result of a relative lack of insulin.

During HHS, enough insulin is produced to prevent the body from entering lipolysis and ketogenesis, which prevents ketoacidosis.

Even though the pancreas still produces some insulin in HHS, it is not enough for the utilization of glucose by the peripheral tissues, resulting in hyperglycemia.

The main characteristics of HHS are

a blood glucose level of greater than 600 mg/dL, serum osmolality level of greater than 320 mOsm/kg, and a pH greater than 7.3.

Osmotic diuresis occurs with HHS just as in DKA but results in more significant fluid loss due to the longer onset of HHS, which leads to severe dehydration, and, therefore, a concentration of electrolytes.

DKA and HHS Risk Factor

•Injury, illness, infection

•Surgery

•Excessive alcohol use, illicit drug use

•New onset diabetes, elevated HbgA1C

•Noncompliance with insulin therapy

•Corticosteroids, Antipsychotics, Antidepressants

DKA risk factor

•Age 13 to 25

•Female

•Previous episodes of DKA

HHS Risk Factor

•Age older than 65

•Morbid obesity

DKA Presentation

•Metabolic acidosis

•Muscle weakness

•N/V, Polyuria > Dehydration/hypovolemia > Shock

•Loss of electrolytes- Cardiac arrhythmias

•Tachypnea, Kussmaul respirations

•Decreased perfusion to the kidneys

HHS Presentation

•More profound neurological manifestations

•Muscle weakness

•N/V, Polyuria > Profound dehydration/hypovolemia > Shock

•Thromboembolic disease (clot risk)

•Decreased perfusion to the kidneys

•Loss of electrolytes- Cardiac arrhythmias

DKA and HHS: Lab and Diagnostic Studies

•Serum blood glucose: DKA >250, HHS >600

•CBC- WBC

•Electrolytes

•ABGs- pH <7.3, HCO3 <15

•Anion gap- DKA >10 (acidosis), HHS: WNL

•Serum osmolality- HHS > 320

•Urine studies- glucose, osm above range in DKA

•Chest X-Ray- Resp illness (pneumonia)

•ECG- dysrhythmia

•Blood and Urine Cultures- Sepsis

DKA and HHS: Treatments/Therapies

•Assess ABCs

•Obtain vital signs

•Assess glucose and electrolytes

•Medications- IV insulin, electrolytes, fluids

•Assess lab values

•ABGs

Assess body systems DKA & HHS Tx

oCardiac rate, rhythm and perfusion

oRespiratory: work of breathing and oxygenation

oNeuro

oRenal

oFrequent focused assessments

1) Restore circulatory volume

•Ensure client has a large bore IV access or a central line.

•Replace half of the deficit within first 12 to 24 hours.

•IV isotonic fluid to increase intravascular volume

•Monitor sodium levels

•Switch to IV hypotonic solution if Na rises

2) Correct electrolyte imbalances

•When BG is less than 200 mg/dL in DKA and

less than 250 mg/dL in HHS 

switch to 5% dextrose in 0.45% Normal Saline

Fluid administration is weight based (15-20 mL/kg over first hour of treatment).

Isotonic fluids should continue up to 500 mL/hr for 4 hours.

Potassium levels need

need to reach an appropriate level prior to insulin administration.

Add 20-30 mEq of potassium to each liter of IV fluid until goal is reached.

Goals for treating hyperglycemia

•Avoid rapid drop in blood glucose levels

•Bolus of IV regular insulin based on client’s weight (0.1 units/kg)

•Continuous IV regular insulin at 0.1 units/kg/hour

•Goal- decrease blood glucose by 50 to 70 mg/dL/hr (adjust rate if this is not met)

Insulin should only be administered after the client’s potassium level is greater than 3.3 mEq/L to avoid hypokalemia.

Goals for treating hyperglycemia cont

•Once blood glucose is consistently less than 200 mg/dL for DKA and less than 300 mg/dL for HHS IV insulin rate can be decreased

•Adjust rate hourly to keep blood glucose of 150- 200 mg/dL in DKA, 250-300 in HHS until resolved

•Once DKA or HHS is resolved and client tolerates oral intake, transition to SQ insulin (dose will vary depending on client’s history)

•IV insulin continued for at least 2 hours after the first dose of SQ insulin

Determinants of Resolution for DKA

Blood glucose: less than 200 mg/dL and any Two of the following:

pH: greater than 7.3

HCO3: 15 mEq/L or greater

Anion gap: 12 mEq/L or less

Diabetes Insipidus (DI): Pathophysiology

•Decreased release of antidiuretic hormone (ADH/Vasopressin) or a decreased response to ADH results in the excretion of large amounts of dilute urine.

•ADH low, more urine

•ADH high, less urine

•Diabetes Insipidus causes uncontrolled diuresis, dehydration ,and extreme thirst.

2 types of diabetes insipidus

•Central DI- Results from a deficiency in secretion of ADH (made in hypothalamus) by the pituitary gland (where it’s stored)

•Nephrogenic DI- Result of resistance to ADH by the kidneys

•Central DI (brain issue)

•Head trauma

•Neurosurgery

•Surgery of pituitary gland

•Cerebral aneurysm

•Arteriovenous malformation

•Cardiac arrest

•Dehydration

Congenital is rare

Nephrogenic DI (kidney issue)

•Lithium toxicity

•Hypercalcemia

•Amphotericin B (antifungal)

•Demeclocycline (antibiotic)

•Antibiotics

•Gene mutations

•Renal disease

•Pregnancy

•Hypokalemia

Diabetes Insipidus: Clinical Presentation

•Neurological effects: thirst, irritability, lethargy, weakness

•Urinary effects: increased output of dilute urine with low specific gravity

•Integumentary effects: poor skin turgor, dry mucous membranes

•Cardiovascular effects: hypotension, tachycardia, weak peripheral pulses

•Urine output of greater than 3L of dilute, odorless urine

Clinical manifestations of clients who have DI include

polyuria, polydipsia, nocturia.

For clients who have neurosurgery and receive desmopressin, the nurse should be alert for and report manifestations of cerebral edema.

HypeERnatremia In DI is

a manifestation that develops when thirst cannot be easily or independently addressed with oral fluid intake, for example, in adults with cognitive impairment, in infants or toddlers, and in clients after surgery.

Diabetes Insipidus: Lab and Diagnostic Studies

•MRI

•Water deprivation test- Confirms dx, differentiate between central & nephrogenic DI.

The expected action of water deprivation is that it stimulate secretion of ADH and increase urine osmolality above 850 mOsm/kg H2O.

In Pt who has DI, ADH does not increase over 300 mOsm/kg H2O with water deprivation

Laboratory Tests for Determining DI

•ADH (1-5) (low in central, normal/high in nephrogenic)

•Serum Sodium- greater than 145

•Urine Osmolality- 300-850

•Urine Specific Gravity- less than 1.005

•Serum Creatinine- greater than 1.1 in dehydration

•Serum BUN- greater than 20 in dehydration

•Urine Sodium- less than 40

In water deprivation test

water intake is withheld, and body weight and urine osmolality are measured hourly.

Desmopressin is administered SQ if 2 sequential urine osmolality measurements differ by less than 30 mOsm/kg H2O or if the client’s weight decreases by more than 3%.

A final urine osmolality measurement is performed on a specimen obtained 60 minutes after the administration of desmopressin.

Water deprivation test cont.

Following the administration of desmopressin, the osmolality will rise to greater than 750 mOsm/kg H2O in central DI, and no rise in osmolality will be observed in nephrogenic DI.

Complications of the test include the risk of dehydration because of a decrease in vascular volume.

Monitor clients for early manifestations of dehydration such as dizziness, tachycardia, and postural hypotension.

Diabetes Insipidus: Treatments/Therapies

•Goal is to hydrate and replace electrolytes and normalize ADH levels

•Insert indwelling urinary catheter

•Monitor strict urine output

•Anticipate the need for IV hypotonic fluid

•Medications as ordered

•IV fluids as ordered

•Dietary consult- low protein/sodium

•Skin care

•Oral care

For the Pt unable to

consume enough water orally to replace urinary losses, hypotonic fluids, such as dextrose and water, should be administered intravenously at a maximum rate of 500 to 750 mL/hour.

Desmopressin (DDAVP) DI

Antidiuretic hormone

stimulates vasopressin receptors to control ADH deficiency and resolve polyuriantidiuretic hormone

can cause decreased urine output in 1 to 2 hours

Most effective routes are intranasal and oral.

Carbamazepine DI

Anticonvulsant

triggers the release of ADH to decrease the volume of urine output

used in Central DI

Adverse reactions: N/V, dizziness, drowsiness, ataxia

Chlorpropamide DI

Sulfonylurea

enhances the effect of ADH on the kidney

used in nephrogenic DI

Adverse reactions: HypOglycemia, over-diuresis

Hydrochlorothiazide (HCTZ) DI

Thiazide-type diuretic

Induces volume depletion by decreasing the amount of water collecting in the renal tubule & increases urine osmolality (paradoxical effect)

Adverse reactions are dose-related and include hypotension, HA, dizziness, AKI

Indomethacin DI

NSAID

enhances urinary concentration in the kidney