Transcript Endocrine Clinical Assessment and Diagnostic Procedures

Endocrine Clinical
Assessment and
Diagnostic
Procedures DKA
Charnelle Lee, RN, MSN
Objectives
• Identify the components of an endocrine history.
• Describe clinical findings of a patient with
pancreatic and posterior pituitary dysfunction.
• Explain the clinical significance of laboratory
and diagnostic tests in pancreatic dysfunction.
• Explain the clinical significance of laboratory
and diagnostic tests in posterior pituitary
dysfunction.
Overview
• Neuroendocrine stress associated with critical illness
• Disorders of three major endocrine glands
o Pancreas
o Posterior pituitary gland
o Thyroid gland
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Endocrine Function
FIGURE 23-1 Location of endocrine glands with the hormones they produce, target cells or organs, and hormonal actions.
Stress
and Critical Illness
• Acute neuroendocrine response to critical illness
o Hypothalamic–pituitary–adrenal (HPA) axis in critical illness
• Release of ADH (vasopressin)
• Release of catecholamines (norepi, epi)
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Stress
and Critical Illness (Cont.)
• Acute neuroendocrine response to critical illness
(Cont.)
o
o
o
o
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Serum cortisol level
Cosyntropin stimulation test
Corticosteroid replacement
Liver and pancreas in critical illness
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Stress
and Critical Illness (Cont.)
• Hyperglycemia in critical illness
o Clinical practice guidelines related to blood glucose management in
critically ill patients
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Endocrine Assessment
• Systematic process incorporating history and
physical examination
• Endocrine glands inaccessible to clinical
examination
• Assessment is indirect
Health History Endocrine
System
• Current health status
• Description of current illness
• Medical history
• General endocrine status
• Family history
Pancreas
• Function
• Dysfunction usually
presents as
hyperglycemia
• Dx: Type I or Type II
Stress
and Critical Illness (Cont.)
• Insulin management in the critically ill (Cont.)
o Transition from continuous to intermittent insulin coverage
o Corrective insulin coverage
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Stress
and Critical Illness (Cont.)
• Hypoglycemia management
o Discontinue continuous infusion of insulin.
o Blood glucose concentration is monitored every 15 minutes until blood
glucose has risen above 70 mg/dL.
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Stress
and Critical Illness (Cont.)
• Insulin management in the critically ill
o Frequent blood glucose monitoring
o Continuous insulin infusion
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Stress
and Critical Illness (Cont.)
• Nursing management
o
o
o
o
o
Monitor hyperglycemic side effects of vasopressor therapy.
Administer prescribed corticosteroids.
Monitor blood glucose, insulin effectiveness, avoid hypoglycemia.
Provide nutrition.
Educate patient and/or family.
• Collaborative management
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Diabetes Mellitus (DM)
• Diabetes
Mellitus
o Type 1 Diabetes
• B cells no longer secrete
insulin
• Autoimmune disease
• Insulin dependent diabetes
o Diabetic
ketoacidosis
(DKA) occurs
without insulin
Diabetes Mellitus (DM)
• Diabetes Mellitus
o Type 2 Diabetes
• Majority of people are adults
• Body mass index > 30%
• Imbalance between insulin
production and use
• Oral medications for most
patients
o Complication of
Type 2 diabetes
is:
Hyperglycemic
Hyperosmolar
Nonketotic
Syndrome
(HHNS)
Patient Compliance
• Only 40% with Type 1
Diabetes
• Only 26% with Type 2
Diabetes
• Monitor their blood
glucose at least once a
day.
Hyperglycemia
• Subjective
Complaints
o Blurred vision,
headache,
weakness, fatigue,
drowsiness, anorexia,
nausea, abdominal
pain
Knowledge check
• Three hours after surgery, the nurse note that the
breath of the client who is a type 1 diabetic has a
“fruity” odor. What is the nurse’s best first action?
1. Document the finding as the only action.
2. Increase the IV fluid flow rate.
3. Call the physician for a arterial blood gas order
4. Perform oral care.
Hyperglycemia
•
•
•
•
•
•
Inspection
FLUSHED SKIN
POLYURIA
POLYDIPSIA
VOMITING
Fluid volume ?
Amb what defining
characteristics.
Hyperglycemia
Abdomen
Subjective:
Hunger then anorexia
NV
Abdominal Cramps
Hypoactive Bowel
sounds
• Palpation – Abdominal
Tenderness
•
•
•
•
•
•
Lab Tests
• How Long Have I had
Diabetes?
• Diabetic Control – Yes/No
• (4%-6%) Normal Value
• Provides information
about the average
amount of glucose
present in the
bloodstream over the
past previous 3 to 4
months. Most accurate
test about either new
onset or patient’s level of
control of their sugar
• Which of the following
cells give us this
laboratory test value
•
•
•
•
•
Leukocytes
Thrombocytes
Erythrocytes
Granulocytes
Lymphyocytes
Glucose Laboratory
Levels

Laboratory Studies
Fasting serum glucose (FSG)
•70 to 100 mg/dL – normal
•100 to 125 mg/dL – prediabetic
•>126 mg/dL – diagnostic of diabetes
•140-180 mg/dL – target for critically ill patient
•<70 mg/dL – hypoglycemia
•<40 mg/dL – severe hypoglycemia
 Urine glucose
•Not recommended

(continued)
Blood Ketones
• Blood ketones
o 2 to 4 mg/dL – normal
o Elevated in acute illness,
fasting, type 1 diabetes with
lack of insulin, illness, starvation
Urine Ketones
• Presence of urine
ketones is an early
warning sign before the
onset of ketosis
• Should not be present
in a healthy individual
• Exceptions- dieting,
exercise, starvation
and fasting
o Normally ketones are not
present in the urine
o Elevated in diabetic
ketoacidosis
Diabetes Mellitus
• Diabetic
Ketoacidosis
(DKA)
o 20% DKA newly diagnosed
Type 1 diabetics
o 80% DKA in known Type 1
diabetics
Diabetes Mellitus
• Diabetic
Ketoacidosis
(DKA)
o Characteristics
• Hyperglycemia – blood
glucose >250 mg/dl
• Ketosis –
• Acidemia- Arterial ph < 7.3
• Bicarb level < 18 mEq/L
• Decreased insulin
availability
• Role of counter-regulatory
hormones
Major Cause of DKA
• Infection #1
• Changes in Insulin
dose, type
• Increased metabolic
demand
• Growth spurts
• Surgery
• Trauma
• Eating disorders
Lab Value
Diabetic Ketoacidosis
(DKA)Assessment
• Clinical Findings
o Headache
o Polyuria
o Malaise
o Polydipsia
o Nausea and vomiting
o CNS depression and
decreased LOC, stupor
o Coma
o
o
o
o
o
o
Dehydration
Flushed dry skin
Tachycardia
Hypotension
Kussmaul air hunger
“Fruity” odor of acetone
DKA
• Diabetic Ketoacidosis
(DKA)
o Assessment and
Diagnosis
• Diagnosis
• Bedside finger
stick
o Urine ketones
o ABG
o Serum osmolality
o Hematocrit
o Electrolyte panel
o BUN and Creatinine
DKA
o Collaborative
Management
• Hydration
• Insulin
Administration
• Intravenous
Glucose
• Potassium and
Phosphorus
Administration
• Diabetic Ketoacidosis
(DKA)
o
Medical Management
• Goals
o Reverse
dehydration
o Restore insulinglucagon ratio
o Treat and prevent
circulatory
collapse
o Replenish
electrolytes
o Reverse
ketoacidosis
Fluid Volume Deficit r/t
osmotic diuresis
• Fluid deficit of up to 6liters can
occur
o Isotonic saline 0.9% is infused immediately to
reverse vascular deficits and hypotension.
o Fluids after this are based on serum osmolarity
and serum sodium.
o Low sodium – 0.9% saline
o High sodium – 0.45% saline
o K+ is added after fluid volume deficit has
been partially reversed and insulin has been
started.
Hydration Assessment
Assess
• Report
Intervene
Collaborate
Reassess
Body weight
Hourly intake
and output
Patient
complaint of
thirst
Pulse strength
Blood pressure
changes
Gradual
increase from
subnormal to
baseline
Tachycardia to
normocardia
Condtion of
mucous
membranes
Insulin Drip
• Patient is NPO
• IV bolus of ______ insulin
0.1 units/kg is
administered.
• Continuous drip of 0.1
units per kg/hour is
infused with other fluids.
• Goal is to decrease
blood sugar by 50-70
mg/dl q1h until it
reaches 200
Rationale for moderation
in blood sugar decrease
• Cerebral edema can
occur with too rapid of
a reversal
• Notify physician of
rapid drops as well as
elevations in blood
sugar.
• Symptoms of cerebral
edema are:
Nursing – Administration
Fluids/Insulin/Electrolytes
• Rapid IV infusion via pump
• NPO until the blood glucose
is < 200
• Blood sugar checks are
hourly
• Sliding scale insulin is
administered per drip
• Labs are drawn q2h in the
initial 24 hours until the
patient sugar stabilizes and
acidosis resolves.
•
Monitor for complications:
hypoglycemia, hypo &
hyperkalemia, hyponatremia,
cerebral edema, infection
Regular Insulin
• Continued until
acidosis, ketonuria, and
fluid volume deficit
have resolved.
• Call physician when
blood glucose is at 200
– at that time D5NS will
be started or D51/2 NS
based on the sodium
level of the patient at
this time.
Potassium & phosphorus
• Will drop as sugar drops
• Administer IV potassium
based on lab results
• Assess for s/s of
potassium imbalance
during acute states of
DKA
• Monitor phosphorus as
well, replace
phosphorus if less than
1 mg/dl.
Knowledge Check
• A client with type 1 diabetes is found unresponsive
in the morning by a family member and is admitted
to the emergency department. On admission to the
emergency department, the client is unresponsive
to stimuli and has fruity, sweet breath with
Kussmaul’s respirations. Laboratory results include
arterial blood gases of pH 7.32, PCO2 34 mm Hg,
and HCO3 11 mEq\L (11 mmol\L) and a plasma
glucose of 518 mg\dl (28.8 mmol\L). The
intervention that a nurse anticipates will be
prescribed initially for the client is
Knowledge Check
• Describe the blood gas in this scenario?
• Fluid replacement therapy in the initial rehydration
hours would be?
• What type of insulin would be given to this patient?
• Based on how fast the sugar should be decreased
to prevent cerebral edema, the blood sugar
measured in the next hour would be?
• A physician orders sodium bicarbonate for this
patient. Nursing action would be:
• Which electrolytes would the nurse monitor closely
in the first 4 hours of rehydration and insulin therapy.
Case Study
• Ms. Baker, a 28 year old unemployed English
teacher is brought in to the ER by her boyfriend
• She is difficult to arouse. Her mucus membranes are
dry, and her skin is warm and dry.
• She has fruity odor to her breath, elevated heart
rate and decreased blood pressure
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Case Study Continued
• The following lab work is obtained on Ms. Baker
• BS – 496
• ABGs – pH 7.16 – PCO2 27- PO2 106 – Bicarb – 11 –Sat
96%
• Her anion gap is 20
• What is Ms. Baker’s probable diagnosis?
• What other tests might be ordered?
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Case Study Continued
• IV fluids are ordered on Ms. Baker. She has a BS of
419 and a K of 5.0
• What type and rate does the nurse anticipate?
• What lab work does the nurse anticipate will be
repeated?
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Case Study Continues
• Ms. Baker is now alert, oriented, with stable vital
signs and is tolerating an ADA diet
• The insulin drip is off and she is receiving sliding scale
insulin coverage for AC and HS finger sticks and
long acting insulin SC
• She informs the nurse that since she lost her job and
insurance she has been unable to afford her
medications
• What discharge plans will she require?
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Hyperglycemic
Hyperosmolar State
• Epidemiology and etiology
o Differences between hyperglycemic hyperosmolar state (HHS) and
diabetic ketoacidosis (DKA)
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Hyperosmolar State
(Cont.)
• Pathophysiology
o Deficit of insulin and excess of glucagon
o Hypovolemia
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Hyperosmolar State
(Cont.)
• Assessment and diagnosis
o Clinical manifestations
o Laboratory studies
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Hyperosmolar State
(Cont.)
• Medical management
o Rapid rehydration
o Insulin administration
• Insulin resistance
o Electrolyte replacement
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Hyperosmolar State
(Cont.)
• Nursing management
o Administering fluids, insulin, and electrolytes
o Monitoring response to therapy
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Hyperosmolar State
(Cont.)
• Nursing management (Cont.)
o Surveillance for complications
o Patient education
• Collaborative management
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Summary
• Stress of critical illness
o The endocrine system is complex. Assessment relies on laboratory tests.
Critical care nurses must understand the intricacies of the endocrine
system.
o Physiologic stress associated with critical illness causes increased secretion
of stress hormones by the HPA pathway. If critical illness lasts longer than 7
to 10 days, suppression of pituitary, thyroid, and adrenal gland function
occurs.
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Summary (Cont.)
• Pancreas: DKA and HHS
o Diagnostic criteria for DKA include a blood glucose concentration
greater than 250 mg/dL, an arterial pH value of less than 7.3, a serum
bicarbonate level lower than 18 mEq/L, and moderate or severe
ketonemia or ketonuria.
o Diagnostic criteria for HHS include a blood glucose concentration
greater than 600 mg/dL, an arterial pH value higher than 7.3, a serum
bicarbonate level greater than 18 mEq/L, a serum osmolality greater
than 320 mOsm/kg H2O (320 mmol/kg), and absent or mild ketonuria.
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