Diabetes Insipidus and SIADH Reference Sheet: Normal Lab Values Siadh DI
Diabetes Insipidus and SIADH Reference Sheet: Normal Lab Values Siadh DI
Diabetes Insipidus and SIADH Reference Sheet: Normal Lab Values Siadh DI
Diabetic Crisis
Blood Glucose
High Low
DKA/HHNKS Hypoglycemia
Arterial ph
Normal Acidosis
HHNKS Ketone
Negative Positive
Ketones Ketones
Another type
DKA
of acidosis
Diabetes Insipidus (DI) and Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion are both disorders of
water metabolism. The posterior pituitary gland secretes anti-diuretic hormone (ADH). ADH is responsible for
regulation of water balance and serum osmolality.
SIADH DI
If there is too much ADH secreted from the posterior If there is not enough ADH secreted from the posterior
pituitary gland your body will hold on to water. This pituitary gland, or, your renal tubules are resistant to it,
can lead to water intoxication of not recognized and your body will be unable to conserve water. This leads
treated promptly. to an excessive excretion of urine.
Dilute blood (low sodium and low osmolality) Concentrated blood (high sodium, high
osmolality)
Concentrated urine (high urine sodium and
high osmolality/specific gravity) Dilute urine (low urine sodium, low
osmolality/specific gravity)
Goals of care
Ensure patient and family understanding of long term therapies and treatments needed/diet needs
Hydration status (IV sites, orthostatic vitals, tissue Strict I&O (every 2 hours) Daily weights
perfusion)
24 hour urine collection Dietary restrictions
Cardiac (rhythm abnormalities)
Monitor, report labs/vitals/rhythm changes
Neuro (mental status changes, seizure activity, neuro
checks every 2-4 hours) Fluid therapy/restrictions Falls prevention
I. Definitions
A. Shock: Inadequate tissue perfusion to vital organs that typically manifests itself as
respiratory failure, renal failure, altered mental status, DIC
Decreased tissue perfusion leads to decreased delivery of vital oxygen/nutrients and
energy to cells. This leads to eventual cell necrosis and acidosis and if left untreated can
lead to cell death and organ damage
B. Compensatory mechanisms of shock include:
Massive vasoconstriction: tachycardia, shunting of blood from less vital organs to vital
organs (cool, clammy skin; decreased capillary refill, decreased urine output, hypoactive
bowel sounds; depending on the organs affected)
II. Types of shock:
A. Cardiogenic/Obstructive
1. Impaired tissue perfusion resulting from severe cardiac dysfunction and or
obstruction to blood flow
2. Causes: Papillary muscle rupture, acute valvular dysfunction, trauma, PE, aortic
dissection
3. Signs and symptoms include: Distended neck veins, large differences in extremity
pressures, pulmonary edema, murmurs, distant heart sounds, (tamponade),
elevated CVP
4. Diagnostics: EKG, Echo, CXR, TEE, Cardiac catheterization, labs (ABG, CBC,
Electrolytes, Cardiac enzymes – troponin, CPK)
5. Pharmacology: + Inotropes, vasopressors, anticoagulants, diuretics
B. Neurogenic
1. Impaired tissue perfusion caused by sympathetic nervous system dysfunction
2. Rarest form of shock
3. Causes: Trauma, spinal anesthesia, spinal shock, spinal cord injury
4. Signs and symptoms: Bradycardia, absence of thermoregulation (sweating,
temperature control), paralysis profound hypotension not relieved with
conventional treatment, decreased CVP
Symptoms depend on the level of injury
5. Diagnostics: Radiologic imaging (MRI/CT)
6. Pharmacology: Volume, vasopressors, steroids, atropine
C. Septic
1. Impaired tissue perfusion caused by massive infection
2. Causes: Anything that can cause infection
3. Signs and symptoms: Tachycardia, hypotension, increased WBC,
hyper/hypothermia, decreased CVP, confirmed infection
4. Diagnostics: Radiology (CXR), labs (WBC, lactate)
5. Pharmacology: Volume, antibiotics, vasopressors
D. Hypovolemic
1. Impaired tissue perfusion resulting from decreased intravascular volume
2. Causes: Fluid shifts (burns), hemorrhage, dehydration (vomiting, diarrhea, DKA, DI,
heat stroke), extravascular fluid loss/3rd spacing, ascites, ruptured spleen,
pancreatitis, hemothorax
3. Signs and symptoms: Collapsed neck veins, poor capillary refill, dry/pale/grey skin,
tenting, decreased CVP
4. Diagnostics: CXR, CBC, BUN/Creatinine
5. Pharmacology: Volume, treat the cause
E. Anaphylactic
1. Impaired tissue perfusion related to an allergic reaction
2. Causes: Allergens – contrast dye, drug/food allergies, insects/animal/snake bites
3. Signs and symptoms: Stridor/wheezing, hives, abdominal symptoms, decreased CVP
4. Diagnostics: WBC, CXR
5. Pharmacology: SC Epi, steroids, racemic epi nebulizer, IV Benadryl
III. Assessment and care
A. Primary survey: Is the patient breathing, do they have a pulse, are the awake?
B. Secondary survey: Is the patient breathing effectively/can they maintain an airway, what
are the vital signs, what is their mental status, do they have IV access, what is going on?
C. Positioning: Reverse Trendelenburg for hypotension, or upright/tripod for ease of
breathing
D. Maintain adequate nutrition (TPN needed if NPO for a prolonged period)
E. Infection prevention/infection control
F. Invasive monitoring (Arterial line, CVP monitoring, central line)
G. Treat the underlying cause
H. Nursing care would consist of:
1. Frequent vitals and physical assessment
2. Pulmonary toileting/pulmonary prevention bundle (C&DB, incentive spirometer,
early ambulation)
3. Early and frequent ambulation (improves respiratory status, helps maintain
perfusion, helps decrease risk of complications, improves patient morale)
4. Administration of medications, fluids, blood products, electrolytes
5. Frequent and accurate monitoring of I/O
IV. Goals of care
A. Return patient to their baseline
B. Increase systolic pressure to maintain adequate perfusion (Is the HR/BP in WNL for the
patient?)
C. Maintain adequate oxygenation (Improve pulmonary congestion)
D. Maintain adequate fluid and electrolyte balances
E. Prevent complications and delays in care/treatment
V. References:
Mower-Wade, D.M., Bartley, M.K. & Chiari-Allwen, J.L. (2001). How to respond to shock.
Dimensions of Critical Care Nursing, 20(2), p 22-27.
American Association of Critical Care Nurses. (2010). Core Curriculum for Progressive Care
Nursing. St. Louis, MO: Saunders.