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Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP

Education Specialist

LRM Consulting

Nashville, TN

Learning Outcomes

Differentiate between diabetes insipidus and

syndrome of inappropriate ADH.

Analyze management strategies for

hyperglycemic emergencies (DKA & HHNK).

Evaluate the common causes and

management strategies for patients with

adrenal insufficiency.

lrmmiller@msn.com

Defining Characteristics

•uncontrolled hyperglycemia

•profound dehydration

•electrolyte disturbances

•acid - base abnormalities

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Signs & Symptoms

•coma

•abdominal pain

•polydipsia, polyuria

•Kussmaul respirations

•fruity breath

Signs & Symptoms

•N/V, weakness

•weight loss

•hypotension

•ketonuria

•tachycardia

Treatment

•ABCs

•restore fluid balance

–NS

–D5½NS????

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Treatment

•restore metabolism

–regular insulin

•correct acidosis

–? NaHCO3?

•restore electrolyte

balance

Treatment

•Electrolyte Management

–potassium

–phosphate

–sodium

Case Study

• 37 – year – old male

– found stuporous but responsive

to vigorous shaking

– transported to the ED

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• Initial Assessment:

– warm, dry, flushed skin

– poor skin turgor

– rapid, deep respirations

– fruity odor to breath

– finger stick reveals level that exceeds

upper limits of dextrometer

• Management

– physician notified

– IV started – NS wide open

Case Study

• Vital signs:

HR 118/minute

BP 80/40

RR 24/minute

T 37 °C (98.6 °F)

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• Laboratory Data

Sodium 124

Potassium 6.2

Chloride 92

Carbon dioxide 6

Creatinine 1.9

Glucose 704

Case Study

• Laboratory Data:

Hemoglobin 12

Hematocrit 36

WBC 24, 000

Platelets 358,000

Case Study

• ABGs

pH 7.0

paCO2 17

paO2 90

HCO3 4

SaO2 94%

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Case Study

• Laboratory Data - Other

Serum Ketones 45

Urine Ketones +

Anion Gap 26

Carbon dioxide 6

Lungs Clear to

auscultation

Interventions:

–cultures: 2 sets of blood,

urine & sputum

– IV NS

– regular insulin

–electrolyte replacement

Case Study

• Laboratory Data 1515 1615 1715 1815

Creatinine 1.9 2.0 2.0 1.9

Sodium 124 127 129 131

Potassium 6.2 4.5 3.7 3.2

Carbon dioxide 6 8 7 9

Chloride 92 87 92 93

Glucose 704 625 538 387

Urine Output 500 500 250 205

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Case Study

• Laboratory Data 1915 2015 2115

Creatinine 1.8 1.8 1.6

Sodium 131 135 131

Potassium 2.9 2.8 3.1

Carbon dioxide 9 17 19

Chloride 95 100 97

Glucose 300 284 235

Urine Output 205 190 110

Defining Characteristics

•Type II diabetes

•mortality 40 - 60%

•severe dehydration

•profound hyperglycemia

•sodium abnormality

Signs & Symptoms

•N/V, weight loss

•hypotension, tachycardia

•coma

•poor skin turgor

•seizures, hyperreflexia,

disorientation

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Treatment

•ABCs

•restore fluid balance –NS

•restore metabolism –insulin

–treat cause

Treatment

•restore electrolytes

–potassium

–phosphate

•monitor for cerebral

edema

Case Study

•72 – year old female

•admitted to ICU – became

progressively unresponsive at

nursing home

•developed a mild pneumococcal

pneumonia

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Case Study

•PMH

–CAD & chronic CHF for 6 years

–Non – insulin – dependent diabetes

mellitus for 12 years

–Medications: digoxin,

hydrochlorothiazide, potassium,

micronase

Case Study

•Assessment

–LOC: unresponsive; no

verbalization

–GCS: 7

–Pupils: Equal (3 mm), round,

reacts slowly to light

–Seizures – no seizure activity

Case Study

•Assessment

–Pulmonary: diminished

in right lower lobe

–RR: 22/minute

–O2 therapy: intubated;

TV 700 mL, FiO2 0.40

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Case Study

• ABGs Admission 8 hours

pH 7.23 7.38

paCO2 32 39

paO2 77 88

HCO3 17 21

SaO2 92% 94%

Case Study

• CV Status Admission 8 hours

HR 124 88

Rhythm ST, PAC, PVC SR

BP 78/52 108/72 (RA)

102/70 (LA)

CVP 1 5

Capillary refill > 3 sec 3 sec

Case Study

• Renal Status Admission 8 hours

Urine Output < 20 40

Urine Color dark amber clear yellow

Urine Glucose 4+ 4+

Urine Ketones trace negative

Infection: urine culture pending

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Case Study

•Assessment

–GI

–Abdomen: moderately distended,

soft & tympanic

–Bowel sounds: hypoactive

–NG: moderate amount of bilious

drainage, guaiac negative

Case Study

• Lab Values Admission 8 hours

Glucose 1260 620

Sodium 146 140

Potassium 3.5 3.7

Chloride 103 100

Carbon Dioxide 19 23

Magnesium 1.0 1.0

Case Study

• Lab Values Admission 8 hours

BUN 72 52

Creatinine 2.3 1.7

WBC 22,000 17,000

Hematocrit 49% 42%

Digoxin Pending 2.0

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Diabetes Insipidus

Defining Characteristics

•defect in release or synthesis

of ADH (neurogenic)

•defect in response to ADH at

the distal tubule (nephrogenic)

Diabetes Insipidus

Etiology

•Traumatic

•Inflammatory

•Pharmacologic agents

–alcohol

–dilantin

–lithium carbonate

Signs & Symptoms

•polyuria

•polydipsia

•dehydration

–dry skin

–confusion

–poor skin turgor

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Lab Tests

•Serum osmolality

–Normal: 285 – 295 mOsm/kg

–Critical values

• <265 mOsm/kg

• >320 mOsm/kg

–(increased in DI)

– > 295 mOsm/kg

Lab Tests

•Urine osmolality

–12 – 14 hour fluid restriction

(> 850 mOsm/kg)

–random sample 50 – 1200 mOsm/kg

–(decreased in DI)

– < 500 mOsm/kg

Diabetes Insipidus

Complications

•dehydration

•bladder hypertrophy

•resistance to vasopressin therapy

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Diabetes Insipidus

Treatment

•correct water & electrolyte

imbalance

•administer vasopressin

•watch for water intoxication

Case Study

•20 – year college student

•waking up 1 – 2 times each

night (started 1 month ago)

•Increased output during day

– attributed to coffee intake

•urine pale and colorless

Case Study

•ED visit

–No abnormalities on PE

–Labs

•Sodium 149 mEq/L

•Serum Osm. 308 mOsm/L

•Urine Osm. 200 mOsm/L

•Glucose 85 mg/dL

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Case Study

•Water deprivation test

–Serum Osm. 315 mOsm/L

–Urine Osm. Unchanged

•DDAVP

–Serum Osm. 290 mOsm/L

–Urine Osm. 425 mOsm/L

Case Study

•MRI

–Idiopathic pituitary

diabetes insipidus

SIADH

Defining Characteristics

•increased secretion of ADH

•results in water intoxication

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SIADH

Etiology

•tumors (extracranial & cranial)

•traumatic

•infections

•pharmacologic agents

–chlorpropamide

–thiazides

–acetaminophen

SIADH

Signs & Symptoms

•water intoxication

–altered LOC

–diminished DTR

–Seizures

SIADH

Signs & Symptoms

•Lab Values –Normal: 285 – 295 mOsm/kg

–Serum osmolality: low

–Urine osmolality: high

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SIADH

Complications

•coma

•seizures

•death

SIADH

Treatment

•fluid restriction

•hypertonic saline

•diuretics

•democlocycline

Case Study

•37 – year admitted to Neuro

ICU with SAH

•Dilantin, nimodipine &

amicar started

•GI ulcer & DVT prophylaxis

•Day 2 surgical clipping

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Case Study

•Postoperatively

–Fluids

•Maintain blood pressure

•Minimize/prevent vasospasm

Case Study

•7th postoperative day VS

T 37.2C

HR 112

RR 24

BP 115/56

CVP 3

Case Study

•Laboratory Data

Glucose 113 mg/dL

Sodium 128 mEq/L

Potassium 4.8 mEq/L

Chloride 100 mEq/L

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Case Study

•Laboratory Data

BUN 21 mg/dL

Creatinine 1.0 mg/dL

Uric Acid 3.0 mg/dL

WBC 7,300

Hct 48%

• Reported in critically ill patients

• Subnormal adrenal corticosteroid production

• Hypoadrenal state without clearly defined defects in HPA axis

• Difficult to define based on serum cortisol concentrations:

– Although cortisol level may be normal, it may remain inadequate for the patient’s metabolic demands

• Rapid improvement on Hydrocortisone therapy

Relative Adrenal Insufficiency

0%

10%

20%

30%

40%

50%

60%

70%

Septic Shock Other ICU Patients

CABG

Dissecting AAA

JCEM (2006) 91: 105–114

Incidence of Relative Adrenal Insufficiency

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CORTISOL

ACTH

CRH

STRESS:

Physical stress

Emotional stress

Hypoglycemia

Cold exposure

Pain

Adrenal Cortex

Anterior Lobe of

Pituitary Gland

Hypothalamus

• Increased sensitivity to pressors

• Anti-inflammatory effect on immune

system

• Maintenance of vascular tone &

endothelial integrity

• Modulation of angiotensinogen synthesis

• Reduction of NO-mediated vasodilation

Cortisol Action

Classical regulators of the axis continue to

be operable in critically ill patients but with significant alterations:

– Hypothalamic hormones

– CRH

– Vasopressin

– Inflammatory cytokines: IL-1, IL-6,TNF-α

– ANS

modulators of HPA function

Anesthesiology (1993) 77: 426–431

HPA Alteration During Critical Illness

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• Impaired hepatocellular

function

• Impaired hepatic blood

flow

• Impaired renal/thyroid

function

J Clin Invest (1958) 37: 1791–1798

• Increased steroid production

•Decreased steroid clearance

Increased Serum Cortisol

(free cortisol level)

Stress

• ACTH and cortisol responsiveness to exogenous CRH is enhanced during critical illnesses

• ACTH = dominant factor stimulating cortisol secretion throughout the critical illness → other factors play a significant modulating influence on the axis

J Inflamm (1996) 47: 39–51

Arginine Vasopressin

Endothelin

Atrial Natriuretic Factor

(ANF)

Variety of Cytokines

(IL-6)

Type & Severity of Illness • Acute phase of illnesscortisol levels proportionate to

degree of stress

• Cortisol levels: major surgery vs sepsis SIMILAR ELEVATION

• Cortisol elevations in sepsis: -wide range

-? don’t correlate with APACHE

-highest levels highest mortality

• Sepsis vs Trauma patients: -similar cortisol elevation

-levels markedly higher in:

– Sepsis,

– Progression to ARDS

– Patients who didn’t survive

• Glucocorticoid resistant patients have higher levels

JCEM (2001) 86: 2811–2816 Intensive Care Med (2001)27: 1584-1591 Clin Endocrinol (2004) 60:29-35.

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Short-Term Stressors vs. Protracted Critical Illness

• Initial phase is characterized by:

» ↑ACTH

» ↑Cortisol

• Protracted critical illness:

» ↓ACTH

» ↑Cortisol

cortisol secretion is being regulated and stimulated by

alternative pathways other than the classical hypothalamic CRH

JCEM (1998)83: 1827-34

J Trauma (1987)27: 384-392

Persistent Hypercortisolism Observed in Protracted Critical Illness

J Trauma (1987) 27: 384–392

Benefits Related To Long Term Complications

Providing energy Hyperglycemia

Maintaining volume Myopathy

Minimizing inflammation Psychiatric alterations

Poor wound healing

Diagnostic Clues in Critically Ill Patients

• persistent hypotension despite

adequate volume resuscitation

• hyperdynamic circulation and low SVR

• ongoing inflammation w/o obvious

source that does not respond to empiric

treatment

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High-Dose ACTH Stimulation Test:

• Can be done at any time of day

• Baseline cortisol 250g ACTH measure cortisol at 30 and 60 minutes

• Non-stressed pt: increase to 18 g /dL R/O AI

• High sensitivity & specificity for primary AI using

threshold value of 15 g /dL

• Less sensitive for secondary AI

Critical Care Clinics (2006) 22 (2): 245-53

Random Cortisol Level

Poor prognosis in septic shock patients:

– extremely HIGH (>34g/dL) total cortisol

– extremely LOW (<25g/dL) total cortisol

N Engl J Med (2003) 348 (8): 727-734 Chest (2002) 122 (5): 1784-1796 Critical care medicine (2003) 31 (1): 141-145

• Unstressed subjects, AI:

– ACTH stimulated cortisol 18-20 ug/dl

• Critically illness, AI:

– random cortisol <15 or 25 ug/dl (if on pressors)

– cortisol increment after ACTH stimulation < 9ug/dl

• Severe hypoproteinemia, AI:

– serum free cortisol < 2 ug/dl or

– ACTH stimulated value < 3.1 ug/dl

N Engl J Med (1996) 335: 1206-1212 N Engl J Med (2003) 348: 727–734

Diagnostic Criteria

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Case Study

• 24-year-old white female

• presented with a 5-day history of

periumbilical abdominal pain,

non-bilious emesis, fatigue, and

intermittent low-grade

temperature

• no significant medical history

Case Study

•VS

T 37.1C

HR 113

RR 14

BP 60/32

capillary refill 5-6 sec

Case Study

•Laboratory Data

Glucose 112 mg/dL

Sodium 126 mEq/L

Potassium 4.3 mEq/L

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Case Study

•Laboratory Data

BUN 33 mg/dL

Creatinine 1.6 mg/dL

WBC 17,000

Hct 16.7

Case Study

• CVP 8 to 11

NS (20 mL/kg) + 5%

albumin (30 mL/kg) over 3

hours

• UO 1.6 mL/kg/hr

Case Study

• Dopamine (10 mcg/kg/min)

• Epinephrine (0.12 mcg/kg/min)

• Norepinephrine (0.18

mcg/kg/min)

No Change in Blood Pressure

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Case Study

•Laboratory Data

Random cortisol (< 1.0 mcg/dL)

normal 5 – 25 mcg/dL

Cosyntropin stimulation test (<

1.0 ug/dL) after 30 & 60 minutes

Case Study • Hydrocortisone 100 mg/m2 IV

• Hydrocortisone 100 mg/m2/day

• BP improved, vasoactive agents

discontinued within 36 hours

• Cultures negative – antibiotics

stopped

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