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Flashcards in Endocrine Emergencies Deck (34):


1. Body’s response to cellular starvation (NOT organism starvation)
2. Relative insulin deficiency
3. Counterregulatory excess (think glucagon)


DKA: Why does one become acidotic?


1. Relative insulin deficiency (not enough
to drive glucose into cells)

leads to

2. ellular starvation (cell requires
something other
than glucose for energy)

leads to

3. Lipolysis with subsequent fatty
acid transport to hepatocytes
and formation of ketoacids

leads to

4. Ketonuria, Anion gap metabolic acidosis with compensatory
tachypnea, and vomiting


DKA why does one become dehydrated?


1. Relative insulin deficiency (not enough
to drive glucose into cells)

leads to

2. Increased serum levels of glucose (hyperglycemia) increases osmotic load
and spills in urine (glycosuria)

leads to

3. Water drawn out of cells (intracellular
dehydration) via oncotic pressure

leads to

4. Impaired consciousness, shock


Why would we have hypotension if we are pulling fluid into the vascular compartment with the osmotic load?

Initially there is an increase in volume in vasculature compartment

Then, as glucose starts to spill into urine there is a massive osmotic diuresis (Carries water with it resulting in cellular dehydration and vasculature depletion!).


DKA presentation

1. Hyperglycemia
2. Acidosis from ketoacids
3. Volume loss


How will the following present in DKA:
1. Hyperglycemia? 2
2. Acidosis from ketoacids? 2
3. Volume loss? 3

1. Hyperglycemia

2. Acidosis from ketoacids
-Tachypnea (to diminish CO2 and restore pH)
-Fruity odor of breath

3. Volume loss
-Dehydration signs
-Dry membranes, poor skin turgor,
-delayed capillary refill, mental confusion.


What about abdominal pain
nausea, and vomiting: what is it due to?

Unclear, but thought to be
related to prostaglandin release


DKA: Approach to Management?
1. Mainstay of therapy?
2. Bedside labs? 3
3. Other labs? 4

1. ***Aggressive fluid therapy initiated if DKA suspected even prior to receiving laboratory results and Insulin

4. Bedside
-urine dipstick,

-Electrolytes along with phosphate and magnesium
-Venous or arterial blood gas
-Blood cultures and other lab tests as indicated


DKA: Approach to Management:

Fundamentals of treatment include? 5

1. Volume repletion
2. Reversal of metabolic consequences of insulin insufficiency
3. Correction of electrolyte and acid-base imbalances
4. Treatment of precipitating cause (if applicable)
5. Avoidance of complications


WHAT is the single most important initial step in the treatment of DKA?

***Rapid fluid administration


1. Which fluid choice?
2. Use of this prevents what?
3. After initial resuscitation recommendation is then to?
4. What will begin to fall after fluid administration and before implementation of any other therapeutic modality (rise in GFR allows for glucose and ketone body clearance)? 2

5. What facilitates the action of insulin?

1. Normal saline most frequently recommended fluid for initial volume repletion
2. Use of NS prevents excessively rapid fall in extracellular osmolality (what could happen if we used a “free water” equivalent with regards to this?)
3. After initial resuscitation, recommendation is then to alternate NS with 0.45%NS
4. ***Blood glucose and ketone concentration

5. Increased tissue perfusion facilitates the action of insulin


DKA Approach to Management:
Insulin Therapy
1. Administered at what dose?
2. Ideal way of administering this?
3. Why? 2
4. What administration should be avoided? 2

1. Administered at 0.1 units/kg per hour after initial fluid bolus
2. “Ideal way” is by continuous intravenous infusion of small doses of regular insulin through an infusion pump
-Less complications
-Allows flexibility in adjusting dose

4. Intramuscular and Subcutaneous administration should be avoided (absorption erratic in volume-depleted patient)


DKA: Approach to Management:
Potassium Therapy
1. What causes K deficiency? 3
2. Initial serum concentration usually normal or high due to the following? 3
3. Large amounts are necessary for replacement for first ____ hours?

1. Combination of
-osmotic diuresis, and
-vomiting causes potassium deficiency

2. Initial serum concentration usually normal or high due to the following
-Intracellular exchange of potassium for H+
-Total body fluid deficit
-Diminished renal function

3. 24-36


Both K+ and H+ do what? 2

-Both K+ and H+ are positively charged
-Both move freely between the intracellular and extracellular compartments


1. When excess H+ ions are present in the extracellular fluid, they do what?

2. ***Here’s the catch… when the H+ ion does this, another cation does what?

1. move into the intracellular compartment for buffering (the bicarbonate system is not the only buffering system, just the one that can be highly regulated!!)

2. K+ must leave the cell and move into the extracellular fluid


DKA Approach to Management:
Potassium Therapy
1. Remember, initial therapy for DKA may cause serum potassium concentration to do what?

2. If changes occur too rapidly, precipitous hypokalemia may result in what? 4

3. ***Development of what is potentially the most life-threatening electrolyte derangement during treatment of DKA?

1. fall rapidly

- fatal cardiac arrhythmias,
- respiratory paralysis,
- parlytic ileus, and
- rhabdomyolysis

3. severe hypokalemia


DKA K+ Management:
1. Goals of therapy include ? 2

2. K not given blindly with first fluid bolus but amount determined by what?

-maintaining normal extracellular K concentration during acute phase and
-to replace intracellular deficit over a period of days

2. initial measurement of serum electrolytes


DKA Approach to Management:
Other considerations?

1. Role of phosphate replacement during DKA remains controversial

No trials demonstrate significant benefits from routine IV phosphate therapy

Should be withheld unless?

1. concentration less than 1 mg/dL (can be corrected safely with oral replenishment)

Routine use of supplemental bicarbonate in tx of DKA not recommended



Generally speaking, gradual return of normal
metabolic balance is best medicine
to avoid complications

1. Hypoglycemia
2. Cerebral edema
3. Hypokalemia
4. Hypophosphatemia
5. Adult respiratory distress syndrome


Reasons for DKA in the patient who is not a new onset diabetic?

1. Compliance issues
2. Discontinuation of insulin therapy
3. Insults to the body such as infection (often pneumonia or urinary tract infection) or other insult such as MI, pulmonary embolism


Hyperosmolar hyperglyceimc state
1. AKA?
2. Occurs in which pts?
3. Syndrome includes the following? 3

1. Also referred to as Nonketotic Hyperosmolar State or Hyperosmolar Hyperglcemic Nonketotic Syndrome (HHNS)
2. Occurs in patients with poorly controlled or undiagnosed type II DM

-Severe hyperglycemia
-RELATIVE LACK of ketonemia


Hyperosmolar hyperglyceimc state
How is this state defined?

1. Serum glucose usually > 600 mg/dL
2. Elevated plasma osmolality of > 315 mOsm/kg
3. Bicarbonate > 15
4. Arterial pH > 7.3
5. Serum ketones that are negative to mildly positive


Diabetic Ketoacidosis versus Hyperosmolar Hyperglycemic State

1. Many authors propose that these two should be viewed as similar disease processes with the fundamental difference being what?

2. Shared symptoms include? 5

1. in the metabolism of lipids during a period of relative insulin deficiency

-severe volume depletion,
-electrolyte disturbances, and
-***sometimes acidosis (usually due to hypoperfusion, i.e. lactic acidosis)


Hyperosmolar Hyperglycemic State
1. Occurs in which pts?
2. Occurs more or less frequently than DKA?
3. Mortality rates?

1. Occurs in patients with poorly controlled or undiagnosed type II DM
2. Occurs much less frequently than DKA
3. Mortality rates much higher than DKA
-15-30% versus about 5% in DKA
-Increases substantially with advanced age


Hyperosmolar Hyperglycemic State
Who’s at greatest risk? 2

Those patients with free access to water
are often able to prevent profound volume
depletion by replacing lost water
with large free water intake

1. Greatest risk factor is inability to access water
2. Often occurs in nonambulatory nursing home patient

Uncontrolled diabetes ➔ hyperglycemia ➔ attraction of water from intracellular space ➔ initially increases intravascular volume, but then… ➔ increasing serum glucose ➔ glucosuria and profound osmotic diuresis ➔ decreased GFR ➔ further decrease glucose excretion worsening hyperglycemia


Hyperosmolar Hyperglycemic State
Presentation? 4

Symptoms other than those discussed previously may include ? 6

1. Usually elderly and
2. often referred by caretaker for abnormalities in vital signs and/or mental status
3. Often precipitated by acute illness such as pneumonia or UTI (accounts for up to 50% of cases)
4. Great majority have some level of baseline cognitive impairment

1. weakness,
2. anorexia,
3. fatigue,
4. cough,
5. dyspnea, or
6. abdominal pain


Hyperosmolar Hyperglycemic State
Tx? 5

1. Volume repletion
2. Correction of electrolyte abnormalities
3. Identifying and treating precipitating cause
4. Gradual correction of hyperglycemia
5. Judicious management of concurrent illnesses (remember, this is often seen in elderly)


Signs and Symptoms

Neurogenic (Increased autonomic nervous system activity)? 7

Neuroglycopenic (Not enough sugar to feed the brain)? 7

Neurogenic (Increased autonomic nervous system activity)
1. Sweating
2. Pallor
3. Tachycardia
4. Palpitations
5. Tremor/shaking
6. Nervousness/anxiety
7. Tingling, paresthesias (mouth and fingers)

Neuroglycopenic (Not enough sugar to feed the brain)
1. Headache
2. Drowsiness
3. Lightheadedness/syncope
4. Mental dullness/confusion
5. Amnesia
6. Seizures
7. Coma


Hypoglycemia thresholds
Thresholds vary depending on the individual?
In general however, drop in plasma glucose to:
1. 65-68 mg/dL ➔ ?
2. Approx 54 mg/dL ➔ ?
3. Approx 47 mg/dL ➔ ?

1. 65-68 mg/dL ➔ secretion of insulin counter-regulatory hormones glucagon and epinephrine
2. Approx 54 mg/dL ➔ neurogenic symptoms of hypoglycemia
3. Approx 47 mg/dL ➔ symptoms of cognitive dysfunction (neuroglycopenic)


1. ***Poorly controlled diabetes with persistent hyperglycemia results what?

2. What are seen with repeated hypoglycemic episodes?

1. in higher glucose thresholds
2. Lower thresholds


Hypoglycemia Unawareness
1. Definition?
2. PLaces pt at greater risk for what?
3. Patients at greater risk for this are? 3

1. Development of low serum sugar values without physiologic ability to react
2. Places patients at greater risk for coma and other neurologic sequelae

3. Patients at greatest risk for hypoglycemia unawareness are:
-Extremes of age


Hypoglycemia Management- Outpatient:
***Some patients are great at recognizing hypoglycemia, other patients are not
Recommendations for management:

1. Preferred treatment is?
2. Treatment effects should be apparent in how long?
3. Treatment effects may only be transient so how should we make sure this is not the case?

4. What should be prescribed for all patients at significant risk for severe hypoglycemia and does not require a health care professional for its administration?

5. What kind of medication adjustments may be required?

1. Preferred treatment is 15-20g of glucose (although any form of carbohydrate that contains glucose may be used)

2. Treatment effects should be apparent in 15 minutes

3. Treatment effects may only be transient so plasma glucose should be retested in 15 minutes with additional treatments as necessary

4. Glucagon

5. Altering of insulin regimen or dosage adjustment of oral medication may be required


Hypoglycemia Management in the ED
1. Initial management is administration of what? 2

2. Repeat bedside glucose how often?

3. Oral replacement: consists of?

4. What can be used in diabetics or in those in whom intravenous access is not readily obtainable?

5. Response to what generally slower when compared with IV dextrose?

6. What can be given after initial glucuse therapy has been initiated in the patient with sulfonylurea ingestion?

-1 g/kg body weight dextrose, as D50W in adults which can then be
-followed by infusion of D10W at a rate to maintain serum glucose above 100 mg/dL.

2. q 30 minutes for 2 hours

3. (300g carbohydrate given PO)

4. Glucagon, 1 mg IM or IV

5. glucagon

6. Octreotide (somatostatin analogue)


What if the patient is not a diabetic?

Other underlying etiologies include
-ETOH use and
- sepsis