Hyperglycemic Crises Flashcards

1
Q

Normal Physiological Response to Increased Serum Glucose

A

Increased serumglucose
Detected by the pancreatic beta cells and insulinwill be released

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2
Q

insulin will

A

↓glucagonsecretionfrom pancreatic alpha cells
↓gluconeogenesis andglycogenolysis in theliver
↑glucoseuptake by muscle andadipose cells

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3
Q

Hyperglycemia

DKA & HHS

A

Results from problems relating to insulin (absolute deficiency or insulin resistance):
↓glucose utilization by peripheral tissues (muscle and adipose cells)
↑glycogenolysis and ↑gluconeogenesis by the liver

Leads to:
↑plasma osmolality (high solute – glucose) → draws water out of the cells → outside the cell the sodium concentration is now dilute

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4
Q

hyperglycemia

High serumglucose level (> 180 mg/dL) exceeds renal threshold causing

A

Glucosuria
Increase inosmotic pressure of the urine leading topolyuria
Loss of water → dehydration → worsens plasma osmolality (hyperosmolality) → potassium shifts out of cells → ↑ extracellularpotassium, ↓ intracellular potassium
Impaired renal function (AKI)

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5
Q

DKA

Epidemiology

A

More frequently seen in younger patients
Mostly seen inpatients with type 1diabetes
Accounts for ~14% of all hospital admissions for diabetics
Mortality rate of 5% in individuals < 40 years; ↑ mortality with advanced age

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6
Q

HHS

epidemiology

A

Usually associated with older individuals (≥ 65 years)
Patientswill usually have type 2 diabetes
Accounts for < 1% of all hospital admissions for diabetics
Mortality rate: 10%–20%

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7
Q

HHS & DKA

etiology

A

Infections(most common)
Inadequate or noncompliance withinsulintreatment
Acute illnesses (stroke,myocardial infarction,pancreatitis, surgery, trauma)
Medications - corticosteroids
Illicit drugs - cocaine
Alcohol

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8
Q

HHS

etiology

A

Dehydration
Medications – diuretics, beta-blockers
Endocrine disorders: Cushing syndrome

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9
Q

DKA

etiology

A

new onset diabetes - type 1

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10
Q

DKA

Clin Man

Rapid onset of symptoms (over 24 hours)

A

Polyuria
Polydipsia
Nausea andvomiting
Diffuse abdominalpain
Weakness
History ofweight loss → common with a new diagnosis oftype 1diabetes

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11
Q

DKA

PE Findings

A

Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Rapid, deep respirations (Kussmaul respirations) → compensatoryhyperventilation (attempting to blow off carbon dioxide – acid)
Fruity breath → exhaledacetone

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12
Q

DKA and HHS

Evidence of severedehydration

A

Dry mucous membranes
Sunken eyes
Decreasedskin turgor
Decreasedurine output

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13
Q

HHS

Clin Man

Gradual development of symptoms (over days to weeks)

A

Polyuria
Polydipsia
Nausea andvomiting

Neurologic changes:
Lethargy
Delirium
Coma(in severe disease)
Seizures
Sensory deficits
Vision changes

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14
Q

HHS

PE Findings

A

Physical exam findings:
Vitals:
Tachycardia
Hypotension
Hypothermia
Altered mental status, lethargy, or coma

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15
Q

DKA

Dx

A

Serum glucose: >250 mg/dL
Serum bicarbonate: ↓↓ (< 18 mEq/L)
Anion gap: Yes(the higher the more severe the presentation)
Serum osmolality: Variable
Serum ketones (beta-hydroxybutyrate, acetone): Positive
Urine ketones: Positive
Arterial blood gas: pH < 7.3; ↓ pCO2 (increase resp to reduce CO2 and lessen acidosis)

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16
Q

HHS

Dx

A

Serum glucose: > 600 mg/dL
Serum bicarbonate: >18 mEq/L
Anion gap: Generally normal
Serum osmolality: >320 mOsm/L
Serum ketones (beta-hydroxybutyrate): Negative or small
Urine ketones: Negative or small
Arterial blood gas: pH > 7.3

17
Q

Dx

A

both Na will be low, K will be high

18
Q

DKA

IV fluid management

A

Admit patient to the intensive care unit (ICU)

Aggressive intravenous (IV) fluid replacement:
Begin withnormal saline (0.9% NaCl) (1 L/h for the first 1-2 hours, then run at a rate of ~250 ml/h)
If corrected Na is < 135 mEq/L, continuenormal saline
If corrected Na remains normal or elevated, consider changing to 0.45% saline

Onceglucosereaches 200 mg/dL, change todextrose5 % with ½normal saline at 150–250 mL/hr
Reduces risk ofhypoglycemia
Reduces risk ofcerebral edema (results from rapid decrease inglucose)
Monitorurine output andhemodynamics

fluid is to correct fluid osmolality, which should bring down glucose

19
Q

DKA

IV insulin infusion

A

K+ must be > 3.3 mEq/L
Regular insulin 0.1 unit/kg as a bolus, then 0.1 unit/kg/h as an infusion or SQ
Hourly serum glucose monitoring
Repeat bolus if the plasma glucose does not ↓ by 10% in the first hour

Close monitoring of serumelectrolytes andanion gap (every 2–4 hours)
High potassium normal corrects with IV hydration and insulin

Providepotassium supplementation to maintain a K of 4–5 mEq/L

albuterol treatments will also bring K back into the cell.

20
Q

DKA

Sodium bicarbonate(NaHCO3)

A

can be given over 2 hours if the pH is < 6.9

21
Q

DKA

has resolved once..

A

DKA has resolved once the serumanion gap has normalized (< 12 mEq/L) andglucose is 150–200 mg/dL

22
Q

HHS

IV fluid management

A

Admit patient to the intensive care unit (ICU)

Aggressive intravenous (IV) fluid administration:
HHSpatients typically have a significant fluid deficit of ~4-10 L
Begin with anormal saline bolus: 1 L over the 1st hour
If the corrected Na is < 135 mEq/L, continuenormal saline
If the corrected Na remains normal or elevated, consider changing to 0.45% saline

Onceglucosereaches 300 mg/dL, change todextrose5% with ½normal saline at 150–250 mL/hr
Maintainglucose between 250 and 300 mg/dL
Monitorurineoutput andhemodynamics

23
Q

Management of HHS

IV Insulin infusion

A

(K+ must be > 3.3 mEq/L)
Regular insulin 0.1 unit/kg as a bolus, then 0.1 unit/kg/h as an infusion or SQ
Hourly serum glucose monitoring
Repeat bolus if the plasma glucose does not ↓ by 10% in the first hour

Close monitoring of serumelectrolytes (every 2–4 hours)
High potassium normal corrects with IV hydration and insulin
Providepotassium supplementation to maintain a K of 4–5 mEq/L

24
Q

HHS

is considered resolved when..

A

HHS is resolved when the patient’s mental status has improved, serumosmolalityis < 315 mOsmol/kg, andglucoseis 250–300 mg/dL

25
Q
A
26
Q
A