CCP 348 Endocrine Emergencies Flashcards

1
Q

main differences in management between peds DKA and adult DKA

A
  1. adults require large volumes of IVF as part of initial resuscitation. large volumes of fluid are harmful in peds DKA (cerebral edema). Fluid resuscitation in peds DKA is more conservative, drawn out over time .
  2. The second important difference is the administration of insulin. While insulin is bloused in the adult patient, insulin boluses are contraindicated in the pediatric patient with DKA.
  3. Monitoring and correction of K+ is heavily stressed in the adult patient with DKA. In children however, IV fluids are started prior to insulin administration, and a K+ level will always be available prior to initiating insulin.
  4. With respect to the acidosis, bicarbonate is indicated in adult patients who are profoundly acidotic. In contrast, sodium bicarbonate is not indicated in children outside of an arrest situation
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2
Q

discuss Sodium Bicarbonate in Pediatric DKA

A
  1. Bicarb is not indicated for routine management of peds DKA
  2. Canadian Diabetes Association (CDA) peds guidelines say “consider in cardiac arrest”
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3
Q

DKA PATHOPHYSIOLOGY

💵💵💵MONEY SLIDE💵💵💵

A
  • metabolic effects of insulinopenia
  • ↓ glucose uptake into muscle, fat, liver
  • ↑ gluconeogenesis, ↑ glycogenolysis, ↑ lipolysis, ↑ ketogenesis
  • hyperglycemia, obligate diuresis
  • ↑ stress hormones aggravate situation
  • metabolic acidosis: ketones, lactate
  • huge losses of H2O, Na+, K+, HCO3–, Pi
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4
Q

BCCH DKA PROTOCOL 2019: GENERAL PRINCIPLES

💎💎💎MEGA PEARL💎💎💎

A
  • 10–20 mL/kg fluid push up front, repeat if CVS status not improved
  • assume 5–10% dehydration (7% for most)
  • nice, even, balanced rehydration over 24–36 h
  • use of 0.45–0.9% NaCl‐containing fluids
  • avoid use of bicarbonate
  • no insulin in the initial 1–2 h of treatment
  • continuous insulin infusion, glucose to match
  • continued use of the “two‐bag” method
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5
Q

BCCH DKA PROTOCOL 2019 BASICS

A
  • on admission: weight, vitals, assessment and stabilization
  • first 30–60 minutes: fluid resuscitation
  • 60 min–36 h: fluid replacement, insulin infusion, addition of glucose
  • throughout: careful monitoring, reassessment, titration of fluids, electrolytes, glucose, insulin
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6
Q

BCCH DKA PROTOCOL: 1st 60 MINUTES

A
  1. give 1st bolus of NS 10 mL/kg IV over 30 min (initial resuscitation)
  2. most really sick patients require a 2nd NS bolus of 10 mL/kg IV over 30 min
  3. the sickest patients may require even more NS to stabilize HR and ↑ peripheral perfusion
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7
Q

best methods for assessing dehydration in kids

🧙🧙🧙ESOTERIC WISDOM🧙🧙🧙

A
prolonged capillary refill (>1.5–2 sec)
abnormal skin turgor
abnormal respiratory pattern
weak pulses
cool extremities
tachycardia
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8
Q

shitty methods for assessing dehydration status in kids

A

dry mouth
urine output
blood pressure
weight

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9
Q

mild dehydration in infants (% BODY WEIGHT)

A

5%

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10
Q

moderate dehydration in infants (% BODY WEIGHT)

A

10%

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11
Q

severe dehydration in infants (% BODY WEIGHT)

A

15%

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12
Q

mild dehydration in kids (% BODY WEIGHT)

A

3%

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13
Q

moderate dehydration in kids (% BODY WEIGHT)

A

6%

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14
Q

severe dehydration in kids (% BODY WEIGHT)

A

9%

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15
Q

BCCH DKA PROTOCOL: 60 MINUTES–36 HOURS

A
  1. begin even rehydration over 36 h, estimating 10% dehydration:
    o 5–10 kg BW: 6.5 mL/kg/h
    o 10–20 kg BW: 6 mL/kg/h
    o 20–40 kg BW: 5 mL/kg/h
    o >40 kg BW: 4 mL/kg/h, max 250 mL/h
  2. start with NS + 40 mEq KCl/L, assuming patient is urinating
  3. at 60–120 min after start of 1st fluid bolus, begin insulin infusion:
    o 0.05–0.1 Units/kg/h
  4. when BG is <25 mmol/L and falling >5 mmol/L/h, add dextrose to IV fluids using the “two‐bag” method
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16
Q

BCCH DKA PROTOCOL: 60 MINUTES–36 HOURS

describe the process for titrating therapy according to the coveted “two bag method”

🧙🧙🧙Esoteric Wisdom!!🧙🧙🧙

A

when BG is <25 mmol/L and falling >5 mmol/L/h, add dextrose to IV fluids using the “two‐bag” method

  1. aim to keep BG in the ~8–12 mmol/L range by titrating the rates of the two Bags A and B
  2. a general rule is to make changes of approximately 10–20% of the total rate every hour
  3. if the patient’s BG is lower than desired, despite maximal dextrose infusion from Bag B, you may (in order of safety):
    o cut the insulin infusion rate by ~25%, provided the acidosis is correcting
    o give the patient a small amount (1–2 mL/kg) of juice or 2–4 dextrose tablets (being mindful of the overall fluid balance)
    o change the insulin Bag C to D10/NS
    o in institutions with intensive‐care capabilities, consider placing a central line and
    using a higher concentration of dextrose (e.g. D20) in Bag B
  4. at 4–6 h after initial fluids and if corrected Na+ is ≥145 mmol/L, stable or increasing:
    o switch Bag A to ½NS + 40 mEq/L KCl
    o switch Bag B to D10/½NS + 40 mEq/L KCl
  5. if unable to get K+ >3.5 mmol/L with IV fluids: consider PO/NG KCl
  6. may give 50% of K+ as phosphate (order by the mmol of K+)
    o may prevent ensuing hyperchloremia, but no clear evidence of benefit
  7. bicarbonate: rarely if ever needed
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17
Q

ongoing monitoring for peds DKA

A
  1. BG by meter q30–60 min (may need lab BG if >30 mmol/L)
  2. Na+, K+, Cl−, HCO3−, anion gap, urea, creatinine, venous pH q2–4 h
  3. Ca2+, Mg2+, Pi q2–4 h if giving phosphate
  4. β‐hydroxybutyrate (preferably) or urine ketones q2–4 h
  5. neurovital signs/GCS q30–60 min
  6. corrected Na+ = [measured Na+ + 0.36×(BG−5.6)]
  7. active osmolality = [BG + 2×(Na++K+)]
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18
Q

MECHANISMS OF CEREBRAL INJURY (peds DKA)

A
  1. vasogenic edema: leakage across altered BBB
    - hypoxia
    - cerebral hypoperfusion/reperfusion
    - neuroinflammation (IL‐6, etc.)
    - ketones (altered BBB)
    - hypocapnia (↓ cerebral blood flow)
  2. other possible factors:
    - role of Na+–H+ antiporter‐3 (insulin) and Na+–K+–Cl− cotransporter‐1
    - continued absorption of H2O from GI tract
    - vasopressin, atrial natriuretic peptide
    - cellular edema: osmotic shifts across cell membrane
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19
Q

cerebral injury epidemiology (peds DKA)

A
  • can be present at diagnosis before treatment
  • usually occurs in first 12–24 hours of treatment
  • DKA still has ~0.5–1% risk of cerebral injury
  • ~25% mortality rate, ~35% serious morbidity rate
  • 70–80% of diabetes‐related deaths in kids <12
  • greatest contributor (~50%) to mortality of DKA, not hyperglycemia or shock
  • subclinical CI with subtle sequelae may be frequent in DKA
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20
Q

cerebral injury signs and symptoms (peds DKA)

A
  • severe headache
  • change in sensorium: irritability, confusion, inability to arouse
  • dilated pupils, papilledema, cranial nerve palsies
  • posturing, incontinence
  • decreased O2 saturation
  • Cushing’s triad (bradycardia, hypertension, irregular respirations)
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21
Q

cerebral injury treatment (peds DKA)

A
  • elevate head of bed
  • reduce fluid rate by ⅓
  • mannitol 20% 0.5–1 g/kg (2.5–5 mL/kg) IV over 15 min
  • HTS 3% 3–5 cc/kg IV over 15 min
  • intubate if pending respiratory failure
  • mild hyperventilation
  • no known role for dexamethasone
  • early Dx and Rx improve outcome
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22
Q

complications of DKA

A
  • hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia
  • hyperchloremic acidosis (NaCl fluid loading))
  • hypoglycemia
  • peripheral venous, dural sinus, basilar artery thrombosis
  • pulmonary embolism, pulmonary edema, PTX, aspiration pneumonia, ARDS
  • rhabdomyolysis
  • acute pancreatitis
  • intracranial hemorrhage, cerebral infarction
  • acute kidney injury
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23
Q

HYPERGLYCEMIC HYPEROSMOLAR STATE define and describe

A
  • hyperglycemia: glucose >33.3 mmol/L
  • hyperosmolality: osmolality >320 mOsm/kg
  • small ketonuria, absent‐to‐small ketonemia
  • absence of significant acidosis: arterial pH >7.30, venous pH >7.25, HCO3– >15
  • obtundation, combativeness, seizures (~50%)
  • seen in T2D, obese, FN/black/south asian
  • also seen in T1D drinking lots of pop
  • can have mixture of DKA and HHS
24
Q

HHS characteristics vs. DKA

🥼🥼🥼PIMPABLE🥼🥼🥼

A
  • ↑ hyperosmolality, ↑ hyperglycemia
  • ↑ dehydration, ↑ fluid needed
  • ↑ electrolyte loss
  • ↓ acidosis, ↑ HCO3–
  • may not need much or any insulin
  • ↑ risk of shock, thrombosis, rhabdomyolysis
  • ↓ risk of cerebral injury
25
Q

HHS treatment pathway

A
  • assume 12–15% dehydration
  • fluids: 20 cc/kg NS, then balance Na+ content: (intravascular needs vs. lowering osmolality)
  • K+: 20 mEq/L KCl + 20 mEq/L KPhos
  • insulin: 0.025 U/kg/h if BG won’t ↓ with fluids
  • lower Na+ by ~0.5 mmol/L/h
  • lower glucose by ~3–5 mmol/L/h
26
Q

Peds DKA can be easy to miss!

These should lead to a suspicion of peds DKA

A
Abdominal pain
Isolated vomiting
Polyuria or polydipsia
Fatigue
Headaches
Known diabetes
Specific high risk groups (ie. Teenagers, children on insulin pumps and those from lower socio-economic status).
27
Q

symptoms of diabetes

A

polyuria, polydipsia, enuresis ,weight loss

28
Q

Important Pathophysiology of DKA

🥼🥼🥼PIMPABLE🥼🥼🥼

A
  1. DKA = most commonly seen in DM1 since the disease is defined by insulin deficiency
  2. ↓ insulin prevents glucose from being used as energy source → free-fatty acids being used as the primary energy source.
  3. Consumption of free-fatty acids → formation of keto-acids and precipitates AGMA
  4. The acidosis shifts K+ into cells → relative hypokalemia
  5. The lack of insulin also → a surge of stress hormones. An ↑ in stress hormones causes ↑ production of glucose
  6. The fact that the body is not consuming glucose and continuing to produce it → a further ↑ in serum levels
  7. Rising glucose levels precipitate an osmotic diuresis leading to dehydration
29
Q

important differences between the management of DKA in pediatrics compared to adult patients.

💵💵💵MONEY SLIDE💵💵💵

A
  1. adults require large volumes of IVF for initial resuscitation. large volumes of fluid are harmful in pediatric DKA. The administration of IV fluids should be done very judiciously in the pediatric population.
  2. insulin is bolus dosed initially in the adult patient, insulin boluses are contraindicated in the pediatric patient with DKA (↑ risk of CI). insulin should always be started after 1-2 hours of IVF resuscitation. Target 0.05-0.1U/kg/hr infusion.
  3. In peds DKA it is permissible to start insulin before having a K+ level back on your patient. If the initial potassium <5.5mmol/L and the patient has urinated (not in full blown renal failure), add 40kcl to IV NS infusion.
  4. HCO3- is indicated in adult patients who are profoundly acidotic. HCO3- is not indicated in peds DKA outside of cardiac arrest
30
Q

2019 BCCH initial approach to fluid resuscitation in peds DKA patient

(based on Results from the PECARN DKA FLUID Study)

A
  1. It is now recommended that all patients in moderate to-
    severe DKA receive a 10-mL/kg bolus of 0.9% NS over
    30 minutes. Those patients with persistent tachycardia, prolonged cap refill (>2 sec), and cool extremities should receive a second 10-mL/kg fluid push as well.
  2. Once the fluid push(es) have been delivered, and assuming the patient has adequate UO and a normal serum K+, fluid replacement is continued using NS + 40 mEq/L KCl (Bag A), until the patient has been receiving fluids for 2 hours; at that point, IV insulin is started.
  3. Fluid replacement rates are now calculated for a 36-hour period of rehydration, compared to the 48-h period used in the past
31
Q

describe THE “TWO-BAG SYSTEM” for peds DKA

🧙🧙🧙Esoteric Wisdom!!🧙🧙🧙

A
  1. The “two-bag system” consists of two IV bags (A and B) with equal electrolyte concentration (0.45-0.9% NS + 40mEq/L of K+), bag A contains no sugar, bag B 10–12.5% Dextrose.
  2. A + B are administered simultaneously. Total combined infusion rate is determined by the child’s degree of dehydration, according to the BCCH DKA Medical Protocol (line 5).
  3. The insulin infusion (Bag C) will eventually be Y’d into these bags.
  4. In the “two-bag system”, Bag A is generally 0.9% NS + 40 mEq/L KCl, and Bag B is usually D10NS + 40 mEq/L KCl (or D12.5/NS + 40 mEq/L KCl). The BCCH Pharmacy has prepared a “recipe book” for preparing these solutions
  5. The goal is to keep the BG levels in the 8–12 mmol/L range, both to minimize glycosuria and to allow for a buffer against hypoglycemia.
  6. This is most easily achieved by alternately adjusting the rates of the non–dextrose-containing Bag A and the dextrose-containing Bag B, while keeping the insulin infusion rate constant
  7. At the onset, it is recommended having both bags prepared and hung, starting Bag A at nearly the full rate (from line 8 of the BCCH DKA Medical Protocol), and starting Bag B at a TKVO rate (2–5 mL/h).
  8. The insulin infusion rate of 0.05–0.1 U/kg/h (0.5–1.0 mL/kg/h) should not be adjusted until the pH is close to normal
  9. The BG level will fall quite rapidly in the first hour or two with the initial fluid resus, even before insulin is started, 2nd to improved renal clearance + hemodilution. one should aim for a fall in BG of ~3–5 mmol/L/h
  10. once BG starts to approach ~20 mmol/L—sooner if the initial BG drop is >5 mmol/L/h—the rate of Bag A is ↓, and the rate of Bag B is ↑ by an equivalent amount. A general rule is to make changes of approximately 10–20% of the total every hour. This will depend on the rate of fall of the BG level and the patient’s response to these changes.
32
Q

Neonates at risk for hypoglycaemia

A
  1. Born to a mother treated with oral hypoglycemic agents or received a glucose infusion during labour
  2. LBW
  3. Small for gestational age(SGA)/Large for gestational age (LGA)
  4. Infants of Diabetic mothers
  5. Any unwell baby: Respiratory distress, sepsis, perinatal acidemia (pH < 7), APGAR less than 3 at 5 minutes, unable to feed
33
Q

neonates that shouldn’t Feed

A
ACoRn Respiratory score > 5
CVS instability
Seizures or abnormal tone
Neonatal encephalopathy
Surgical conditions
Abdominal distention
Babies < 1800 grams or less than 34 weeks should be augmented with IV fluids for at least the first 24-48 hours of life to decrease the possibility of NEC
34
Q

neonatal Fluid Required (mL/kg/day) on day 0

A

60-80 ml/kg/day

35
Q

neonatal Fluid Required (mL/kg/day) on day 1

A

80-100 ml/kg/day

36
Q

neonatal Fluid Required (mL/kg/day) on day 2

A

100-120 ml/kg/day

37
Q

neonatal Fluid Required (mL/kg/day) on day 3

A

120-140 ml/kg/day

38
Q

neonatal Fluid Required (mL/kg/day) on day 4

A

150 ml/kg/day

39
Q

List two causes of hyponatremia in a newborn

A
  1. SIADH

2. Excessive maternal free water intake

40
Q

List two causes of hypernatremia in a newborn

A
  1. Excessive sodium intake

2. Dehydration

41
Q

List two causes of hyperkalemia in a newborn

A
  1. Sample hemolysis (from aggressive heel poke lab draws)

2. Renal failure

42
Q

List two causes of hypokalemia in a newborn

A
  1. Excess GI losses

2. Dilution

43
Q

What is the highest concentration of dextrose we should be running through a PIV in infants?

A

D12.5

44
Q

Why are babies born from diabetic mothers at higher risk of hypoglycemia?

A
  1. The fetus is accustomed to receiving an abundance of glucose, meaning they have had to up-regulate endogenous insulin production in order to maintain normoglycemia
  2. Once the placental delivery of glucose comes to a halt, the infant will be overproducing insulin for the amount of glucose being produced
45
Q

What three clinical features are necessary for the diagnosis of DKA?

A
  1. Hyperglycemia > 11.1 mmol/L
  2. Acidosis < 7.3 or HCO3 < 15
  3. Ketones in blood or urine
46
Q

Why does gluconeogenesis and glycogenolysis occur during DKA, despite elevated BGL?

A
  1. Astrocytes cannot detect glucose levels d/t insulin deficiency
  2. Without insulin to transport glucose into astrocytes, the brain registers hypoglycemia, and promotes gluconeogenesis and glycogenolysis.
47
Q

What are the three ketones?

A
  1. Acetoacetate, beta-hydroxybutrate (BOHB), and acetone
  2. Acetoacetate is the initial ketone formed. It is reduced to BOHB and hydrogen, or decarboxylated to acetone and CO2
  3. BOHB therefore contributes to acidosis, whereas acetone does not
48
Q

Outline the management of DKA in paediatrics

A
  1. Initial resuscitation Fluid Bolus 10 to 20 ml/kg (this is gonna correct some of your sugar and K+ just through dilution!)
  2. Even rehydration over 24 to 36 hours, assuming 5 to 10% dehydration (Use of 0.45 or 0.9% NaCl)
  3. No insulin in the first 1-2hr of treatment, d/t the ↑ risk of cerebral edema that is likely related to fluid channels in the brain
  4. Target a capBg of 8-12 mmol/L w/ continuous insulin infusion once initiated, using two-bag method with glucose to match
  5. Continue insulin therapy until anion gap or BOHB level resolves
  6. K+ correction in conjunction w/ insulin therapy
49
Q

Explain the fluctuation of sodium in DKA

A
  1. Hyponatremia is caused by water shift into the extracellular space, diluting serum sodium.
  2. Hypernatremia is superimposed from loss of water with glucosuria-induced osmotic diuresis, sparing sodium and potassium
50
Q

Describe the mechanisms that produce hyperkalemia in DKA

A
  1. Solvent drag.
  2. Impaired potassium entry into cells from insulin deficiency.
  3. Intracellular protein and phosphate depletion.
  4. Buffering of hydrogen ions.
51
Q

Explain the fluctuation of phosphate in DKA

A
  1. Both insulin deficiency and metabolic acidosis cause a shift of phosphate out of the cells, producing hyperphosphatemia
  2. Phosphaturia from glucosuria-induced osmotic diuresis results in a total loss of phosphate
  3. Serum phosphate usually returns to normal once insulin deficiency and acidosis are corrected
  4. Hypophosphatemia isn’t a concern and isn’t generally treated. Treating hypophosphatemia creates a risk of hyperphosphatemia, which can produce hypocalcemia
52
Q

What criteria are necessary for the diagnosis of HHS?

A
  1. BGL >33.3 mmol/L.
  2. Hyperosmolality >320 mOsm/kg
  3. Small or absent ketonuria
  4. Absence of significant acidosis
53
Q

Outline the management of HHS

A
  1. Fluids 20 ml/kg NS
  2. Correct glucose, potassium, and sodium levels
    - Glucose lowered by 3 to 5 mmol/hr.
    - Sodium lowered by 0.5 mmol/hr
54
Q

What is the marker of the correction of HHS?

A

Osmolality and glucose back to normal ranges

55
Q

What are the typical symptoms of HHS?

A
  1. Obtundation
  2. Seizures
  3. Dehydration
56
Q

What is the D10W dosage for neonatal hypoglycemia?

A

2 ml/kg bolus, followed by 4 ml/kr/hr infusion