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N332 > DIABETES EMERGENCIES > Flashcards

DIABETES EMERGENCIES Flashcards

1
Q

Causes of DKA/HHS?

A

Precip factors = situations that increase the amount of stress hormone production: infection, MI, or surgery. Rec drug use (E, ketamine, coke, etc)
Alcohol binges
New diabetes cases or poor insulin management
Error in dosage + admin of insulin, erattic compliance + eating difficulties common cause in young adults

From slides: 
Usually a stressful event that causes the release of glucagon, cortisol and catecholamines
- Infection
- MI
- Treatment errors with insulin
- Diarrhea and vomiting 
- Stroke
- Trauma
- Pancreatitis 
- Unknown etiology
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2
Q

Who usually gets DKA?

A

More often T1DM (or type 2 if critically ill)

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3
Q

Signs + symptoms of DKA?

A

polyuria and polydipsia, vomiting, abdominal pain (with tenderness on palpation, diminished BS) and shortness of breath

Signs are non-specific and relate to dehydration and acidosis, including tachycardia, hypotension, hyperventilation (Kussmaul breathing), the smell of ketones on the breath and drowsiness or coma.

If severe: Reduced consciousness.
Hyperventilation, HoTN, Reduced bicarb

From slides: Polyuria, Polydipsia, Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion),anorexia, nausea, vomiting, abd pain, acetone breath, hyperventilation, mental status changes

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4
Q

Who usually gets HHS?

A

Typically occurs in older (60+)
Often in undiagnosed Type 2 DM cases
predominately associated with type 2 diabetes managed by diet and/or oral medication.

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5
Q

What does HHS stand for?

A

hyperglycemic hyperosmolar state

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6
Q

Signs + symptoms of HHS?

A 
Usually grossly elevated blood glucose
– 34mmol/litre or higher 
Polyuria – osmotic diuresis 
Tachycardia associated with fluid loss 
Polydipsia 
Glucose in urine positive 
Acidosis present – pH not less than 7.30

From slides:
Hypotension, profound dehydration, (dry mucus membranes, poor skin turgor) , tachycardia, varying neurological signs

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7
Q

How does onset of HHS + DKA usually differ?

A

HHS: Insidious onset, days to weeks
DKA: Often rapid onset (<24hrs)

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8
Q

WHich has higher mortality, HHS or DKA?

A

HHS

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9
Q

How do HHS + DKA differ with regard to acidosis/presence of ketones?

A

DKA: positive –> smell acetone in breath
HHS: Serum ketones usually mild or absent, urine ketones negative

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10
Q

How do respirations differ in DKA + HHS?

A

DKA: Kussmaul breathing (deep + rapid…blowing off CO2)
HHS: Shallow rapid resps

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11
Q

How does neurological status differ in DKA + HHS?

A

DKA: Can be alert or drowsy, coma in severe case

HHS: Stupor/coma more likely due to hyperosmolar state. Neurological problems such as seizures
or transient haemiparesis

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12
Q

How are NA+ and K+ altered in DKA + HHS?

A

DKA: Increased or decreased serum sodium
• Initially increased serum potassium

HHS: Serum sodium elevated
Serum potassium normal or slightly low

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13
Q

Is abdominal pain present in both DKA + HHS?

WHy is it seen?

A

DKA: Abdominal pain typically present – related to the metabolic acidosis

HHS: Abdominal pain can be identified in some cases but not a typical presentation

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14
Q

When is DKA seen in type 2 DM pts?

A

Occurs in patients with type 1 diabetes, but it may also occur in those with type 2 diabetes during severe concurrent illness, such as sepsis, myocardial infarction or corticosteroid treatment

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15
Q

Criteria for diagnosis of DKA?

A

include:
o Raised bg >22mmol/L (may be low if already given insulin or hasn’t eaten)
o At least moderate ketonuria or blood ketone levels >3mmol/L
o Significant acidosis (HCO3- <15mmol/L or arterial pH <7.3)

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16
Q

What kind of insulin admin is associated with development of DKA?

A

• Assoc with continuous insulin pumps (but this is getting better); can occur more rapidly in those w pumps if infusion interrupted d/t smaller depot of subcut insulin

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17
Q

Is DKA often fatal?

A

• ~5% mortality rate

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18
Q

Outline the Patho of DKA

A
  • Result of absolute or relative insulin def –> glucose can’t enter cells (muscle, liver, adipose) + gluconeogenesis suppressed in liver –> tissues starved of glucose
  • Body responds by inc prod of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone), which inc glucose levels in blood
  • Ketones used for energy as glucose can’t be used
  • In DKA, ketones produced faster than used or excreted
  • Hepatic gluconeogenesis + glycogenolysis inc + lipolysis inc production of free fatty acids (FFAs) d/t insulin deficiency + prod of counter reg hormones
  • Liver uses FFAs for energy –> accum of ketones (end metabolites)
  • Ketones accum –> metb acidosis (drop in pH + bicarb)
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19
Q

Which organs can use ketones for source of energy?

A

•Ketones used in starvation, source of energy by brain + kidneys

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20
Q

With accum of ketone bodies, how does body compensate?

A

• Compensation: Kussmaul breathing (resp rate inc) to excrete ketone bodies

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21
Q

What is the effect of ketones in terms of physical symptoms?

A
  • Ketones cause nausea + vom further fluid + electrolyte loss
  • Hyperglycemia Na+ and H2O loss dehyd third + abm pain
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22
Q

How and why do K+ shifts occur in DKA?

A

• As H+ moves into cells, K+ moves out –> K+ loss through urine + vomit K+ depletion (though will be seen as normal or high in blood as being drawn out into there). Levels fluctuate greatly during DKA, esp as insulin admin pulls back into cells

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23
Q

WHat is the average fluid loss in DKA? How does this change kidney fx?

A

Ave body water loss = 5L in DKA ECV dec –> kidneys can’t excrete ketones + glucose

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24
Q

Key components of tx in pt with DKA?

A
  • IV fluids, insulin + lyte replacement
  • NG tube if pt unconscious
  • Catheter if unconscious, incontinent or anuric after 2 hours
  • Poss thromboprophylaxis in older adult or high-risk pt
  • Hourly monitoring of fluid balance
  • Hourly BG + capillary blood ketone estimation
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25
Q

What lab results will nurse need to check for pt with DKA?

A

• Nurse to check: capillary + lab bg levels, ketones in blood + urine, urea + lytes (recheck after 2 hours, then q 4hrs), ABGs + bicarb, CBC
o Others that may be needed: troponin T amylase (may be elevated, not necc pacreatitis), blood + urine cultures, throat swab, CXR, electrocardiogram, lumbar puncture + CT brain scan

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26
Q

What fluid admin change typically will occur as your rehydrate a DKA pt?

If pt becomes hyperglycemic after this change, what will you do?

A

o Switch to 5-10% glucose over 8 hours once BG <15mmol/L

o May keep NS as well if volume needed. If BG raises, don’t take glucose soln away, just inc insulin dose

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27
Q

Which pt’s are particularly prone to insulin deficiency?

A
  • preg + obese
  • In these pt’s insulin level will need to be titrated appropriately
    + depending on usual insulin levels received by pt
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28
Q

Is bicarb replacement tx usual in DKA?

A

• HCO3- replacement controversial, not generally used but may be if cardioresp collapse imminent

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29
Q

When/how to stop IV insulin in tx in DKA?

A
  • IV insulin d/c once pt able to eat + drink normally + ketones negative or trace (< or equal to 0.6mmol/L
  • Recommends keeping basal SC insulin while getting IV so still established when IV stopped (prevents going back to DKA)
  • IV insulin should not be stopped until 30 minutes after subcutaneous insulin has been given with a meal (other source says 1-2hrs).
  • Reestablish usual insulin regime. Establish cause of DKA.
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30
Q

What are the possible complications of DKA tx?

A

• Hypoglycemia + hypo/hyperkalemia (insulin, carb + K+ intake adjusted as required)
• Renal failure – need strict fluid balance
• Aspiration – NG tube in unconscious pt to prevent this
Cerebral edema
Thromboembolitic (DVT, stroke)
Adult RDS

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31
Q

What would you see if pt has cerebral edema?

What is the tx?

A

•headache, bradycardia, rising BP, dec LOC, restlessness, convulsions. Need to exclude hypoglycemia when see these things.

Sent to ICU, Mannitol 20% 5ml/kg given IV over 20 mins + CT scan done

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32
Q

What might be done to prevent thromboembolitic complications in DKA pt?

A

Anticoags

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33
Q

Why might adult RDS occur in DKA tx?

A

excessive fluid replacement + rapid correction of osmolarity. May need resp support, ventilation

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34
Q

Steps for prevention of DKA (pt teaching)

A

• Advice + sick day rules for type 1 DM include: seek prompt tx if sick (abx, antipyretics), cough + cold remedies should be sugar free, if can’t eat properly, replace carbs with crereals, soups, liquid carbs; drink lots; if vomiting + unable to tolerate liquid carbs, seek medical attn., continue insulin even if not eating usual amounts of food (likely need to inc dose); test BG at least 4 times/day

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35
Q

Special consideration for young women with DKA

A
  • Omitting insulin to become thin common in young women

* Often psychological issues behind it

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36
Q

How does tx of HHS differ from DKA?

A

Management same as DKA except: may give 0.45% saline if Na+ high, risk of thromboembolitic disease high (given anticoag), older pt’s given CVC, lower rates of insulin given, longer term management with oral meds + diet

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37
Q

Summarize changes that occur in HHS (I know this is repetitive but these from another article…thought it summed it up nicely)

A

• Occurs in patients with type 2 diabetes
• characterized by hyperglycemia and high plasma osmolality without significant ketones or acidosis.
• Have high plasma Na+ levels
• BG often extremely high (50mmol/L)
• Often in previously undiagnosed pts (usually 60+yrs)
• Negative or small quantities of ketones in the urine and/or blood.
• Plasma bicarbonate usually ≥18mmol/L.
• Slow onset of hyperglycaemic symptoms.
• Symptoms rarely include abdominal pain, vomiting or Kussmaul breathing
(unless acidotic).

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38
Q

How long after eating does a peak in blood glucose occur?

A

• Peak in BG occurs 30-60mis following meal

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39
Q

Insulin works in 3 ways:

A

1) Promotes the uptake of glucose by target cells and facilitates excess glucose to be stored as glycogen (a quick energy reserve in the liver)
2) Increases protein synthesis (the build-up of proteins)
3) Inhibits gluconeogenesis (synthesis of glucose from non-carbohydrate sources) by preventing fat and glycogen breakdown

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40
Q

Action of glucagon?

A

Glucagon initiates glycogenolysis + promotes gluconeogenesis by transporting amino acids to liver + stimulating their conversion to glucose

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41
Q

Under what condition is glucagon production inhibited?

A

• Glucagon prod inhibited by inc glucose, but only if insulin present…so when DKA + HHS occur, glucagon still secreted + subsequently, BG continues to rise

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42
Q

What is the biochemical triad of DKA?

A

hyperglycemia, hyperketonaemia, metb acidosis

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43
Q

What occurs in type 1 DM?

A

• Autoimmune destruction of beta cells

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44
Q

Is T2DM absolute insulin deficiency?

A

Relative insulin def, insulin resistence

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45
Q

Why do you see an abn inc in blood osmolality in HHS?

A

Dehydration

46
Q

Does acidosis occur in HHS and why or why not?

A

Ketosis minimal in HHS because there are small amounts of insulin present which suppress lipolysis so avert ketone formation

47
Q

Does a counter-regulatory hormone release occur in HHS as it does in DKA? Is this helpful?

A

• Same as DKA in terms of counter-regulatory hormone inc, which worsens issue (more sugar!)

48
Q

How does water loss compare between HHS + DKA (in L’s)

A
  • DKA water deficit = 5-7L

* HHS water deficit = 7-12L

49
Q

How does insulin release affect dehydration (not just about sugars…has effect on specific organ)

A

• Insulin def contributes to H2O in itself b/c Insulin stimulates water reabsorption in the proximal and distal tubule of the nephron

50
Q

What is the renal threshold of glucose?

A

• Renal threshold of glucose = 10–12mmol/L. Once BG higher than this, glycosuria –> osmotic diuresis

51
Q

How is insulin given for DKA + HHS?

A

• Given IV usually; may recommend bolus dose subcut as well (this has longer half life so not as good at control)

52
Q

How does fluid admin change hormone release in DKA/HHS?

A

• Aggressive fluid replacement (even w/o insulin) shown to dec levels of cortisol, catecholamines, aldosterone and glucagon

53
Q

Why is it important to not dec bg levels too quickly with insulin in response to DKA?

A

• **Important BG levels not decreased too rapidly as leads to cerebral edema

54
Q

How often are you going to be checking BG in DKA?

A

• BG monitoring q 30min – 1hr initially

55
Q

How are renal fx and insulin tx related? (not really sure about how this works…an probably not so important)

A

• Replacing adequate fluid volumes and monitoring urea and creatinine levels are fundamental when assessing the effectiveness of insulin therapy (BG levels may not dec if not adequate fluid admin or impaired renal fx)

56
Q

Why is it difficult to assess dehyration in HHS?

A

Will see polyuria, rather than oliguria so need to look for other signs of fluid deficit
• Many HHS patients do not respond to the stimulus of thirst because of incapacity or confusion.
• May need CVC to measure intravascular vol

57
Q

Guidelines for fluid admin in HHS…Maureen says really depends so probably don’t need to know this

A
  • No consensus on fluid type (but usually 0.45-0.9 saline, depending on Na+ levels)
  • The overall goal is to replace half of the fluid deficit over the first 8 hours and the remaining fluid over the next 16 hours
  • There is general consensus that one litre of 0.9% saline should be administered over the first hour for both DKA and HHS patients to help replace intracellular and extracellular volume and restore renal perfusion; rest of tx depends on protocol
58
Q

Why do you switch to d5w in treatment of DKA/HHS?

A

to avoid hypoglycemia + replenish stores in liver + muscles

59
Q

K+ levels in DKA/HHS?

A
  • K+ in DKA initially elevated (d/t high H+ levels); total body deficit of K+ often but not observed until fluid admin + insulin therapy established
  • K+ often a bit low in HHS
60
Q

What electrolyte would you want to be particularly diligent in checking prior to admin of insulin + why?

A

• Important to assess k+ prior to insulin admin, as will further red EC levels

61
Q

Important consideration for what to check prior to giving K+?

A

• When giving K+ important to take into account urine output levels
–> assume this is because will accum if not adequate kidney fx to excrete excess

62
Q

WHy does change in LOC occur with DKA/HHS? Which is more likely leading to coma?

A
  • /t dehydration + resulting changes in serum osmolality
  • Higher serum osmolality = greater determioration in sensoria
  • HHS tend to have higher incidence of coma d/t hyperosmolar state (than DKA)
63
Q

nursing response to altered LOC in DKA/HHS?

A
  • Pt w altered LOC should be high visibility area of unit
  • Lower nurse to pt ratio b/c high risk of losing airway
  • Use GCS to monitor
  • O2 admin
  • Monitor for signs of resp distress
  • DKA often exhibit Kussmaul breathing, with deep rapid breaths.
  • Patients with HHS often have rapid shallow breaths, a more typical sign of failing respiratory compensation which lowers further the already reduced oxygen in the blood
64
Q

Guidline for admin of K+ with DKA? (not important)

A
  • Potassium above 5.5mmol/litre – no K+ given
  • Potassium levels 3.3–5.5mmol/litre – Commence potassium therapy at 20–30mmol/litre saline
  • Potassium levels below 3.3mmol/litre - Insulin therapy not given. Commence potassium therapy at 40mmol/litre saline until level reaches 3.5 mmol/litre
65
Q

What is DKA in children most often occurring?

A

• Most often assoc w newly diagnosed type 1 DM

66
Q

What causes most deaths in children with DKA?

A

• Leading cause of morbidity + death in children w type 1 DM – ½ of these deaths d/t cerebral edema

67
Q

4 main causes of DKA in children?

A

1) Delayed diagnosis of type 1
2) omission of insulin
3) delivery failure (device issue)
4) Type 2 DM

68
Q

WHy is diagnosis of T1DM often delayed in children until DKA symptoms appear?

A

Hard to discern symptoms like polyuria + polydipsia in children

69
Q

Omission of insulin in children - why is it an issue?

A

can be mistake or deliberate; adolescents most at risk (rebellion, eating disorders)

70
Q

Why does delivery failure occur in children taking insulin?

A

• device used to admin insulin faulty; DKA twice as likely in insulin pump users (could be set up wrong or don’t understand ramifications of interrupting it)

71
Q

WHy do you need increased insulin in illness?

A

cortisol etc inc + this dec effectiveness of insulin

i believe this is because it causes mobilization of even more sugar from stores?

72
Q

Considerations for fluid admin in treating child with DKA?

A
  • Done according to child’s BSA
  • Given at measured pace as don’t want to cause cerebral edema
  • NS = fluid of choice; changed to 0.45%NS once following rehydration
  • Catheterization not routine but will if severely ill or unconscious
  • Oral hydration replaces IV as child clinical condition improves
73
Q

WHy is fluid admin alone so helpful for treating DKA? (even without insulin)

A

• Inc fluids enhances elimination of glucose + ketones (more output)

74
Q

What factors affect movement of K+ in the body?
Is individual with DKA K+ depleted/

What effect does insulin + fluid admin have on K+ movement?

A

• Factors which influence the movement of potassium are: pH, blood osmolarity, fluid replacement and insulin therapy. T

his means that, depending on conditions, serum potassium levels may be low, normal or high. total body potassium is always low because intracellular potassium is depleted

•Fluid recplacement + insulin tx move K+ into cells

75
Q

What is a means by which K+ is lost in DKA?

A

lost through vomit

76
Q

What special monitoring does a child need if they have DKA?

What signals in this monitoring warrant concern?

A
  • Kids in DKA need continuous ECG monitoring

* Changes in QRS complex show important changes r/t K+

77
Q

What occurs in children with DKA with regard to Na+ levles?

A

• First Na+ low as leaves w water. May fluctuate d/t fact that Sodium levels tend to rise as glucose levels fall.

78
Q

When is insulin typically started in the treatment of DKA in children? RIght away?

A

• IV insulin usually started 1-2hrs following IV fluid start (starting earlier = inc risk of cerebral edema)

79
Q

What kind of monitoring will be needed for child receiving insulin for DKA? (2 measures of bg)

Do children receive D5W?

A

• Hourly BG monitoring + urinalysis
• 5% dextrose generally added to the infusion regimen when
the blood glucose has fallen to 14-17mmol/L

80
Q

When are you going to change to subcut insulin in a kid with DKA?

A

• Can change to subcut when BG levels have normalised, oral fluids are established and ketoacidosis and serum bicarbonate levels are no longer causes for concern.

81
Q

What is a prominent symptom of ketosis? What is done about this to mitigate risks?

A

• Vomiting = prominent feature of acidosis. NG tube inserted if semi or unconscious

82
Q

What sort of infections are you looking for in a child with DKA?

A

watch for UTI, gastroenteritis + tonsillitis. Temp may not be present.

83
Q

T/F

Cerebral edema is equal risk in children + adults with DKA?

A

No, more of a risk in chidlren

84
Q

When does cerebral often show during tx of DKA in children?

A

Most commonly seen after tx has commenced + child has shown signs of improvement

85
Q

What are the signs + symptmos of cerebral edema?

When this occurs, does it progress rapidly?

A

• Narrow time frame between onset + brain herniation - Need hourly neuro observations if child is drowsy or not!
• Early signs:Headache, return of vomiting, behavioural changes, reduced LOC,
Elevation in blood pressure and fall in pulse rate. Decreased oxygen saturation.

86
Q

What is the tx of cerebral edema in children with DKA?

A

• If occurs, want to reduce speed of rehydration, admin mannitol (cerebral specific diuretic), hypertonic saline (if mannitol doesn’t work), poss intubation

87
Q

risk factors for hypoglycemia in hospitalized patients include?

A

older age, existing comorbidi- ties, diabetes, receiving more oral antidiabetic agents, tight glycemic control, septic shock, renal insufficiency, mechanical ventilation, and severity of illness.

88
Q

Which 2 infections most commonly lead to DKA?

A

UTI + pneumonia

89
Q

Reasons for insulin omission

A

(1) fear of weight gain with improved metabolic control, (2) fear of hypoglycemia, (3) reduction or elim- ination of insulin doses as a result of limited financial resources, (4) reduction or omission of insulin doses when ill, (5) rebellion against authority, and (6) stress of chronic disease

90
Q

Reasons for insulin pump problems

A

• (1) the infusion set in subcutaneous insulin administration has not been replaced by the patient for more than 3 to 4 days, and the site has poor absorption; (2) the infusion set may have recently been replaced by the patient, but the flow of insulin is impaired as a result of a kinked cannula or tissue obstruc- tion; (3) the pump ran out of insulin; or (4) the pump battery ran out of power supply.

91
Q

Which meds can precipitate HHS + DKA

A

Drugs that affect carbohydrate metb (steroids, thiazides etc), and diuretics, beta blockers, + phenytoin

92
Q

What populations are most prone to idiopathic DKA

A

• DKA cases without a precipitating cause have been reported in subjects with type 2 diabetes, mainly in blacks and Hispanics.

93
Q

Initial laboratory values to be obtained should include ___ with DKA

A

• plasma glucose, blood urea nitrogen, creatinine, electrolytes (with calculated anion gap), serum osmolality, serum ketones or serum β-hydroxybutyrate (if available), calcium and phosphorus concentrations, arterial blood gases, complete blood cell count with differential, and urinalysis. In addition, an electrocardiogram, chest radiograph, and urine, sputum, or blood cultures should be obtained.

94
Q

Explain how an anion gap shows acidosis

I don’t think we need to know this at all except could be handy for real life nursing

A

• As ketoacids accumulate, an increase is found in the anion gap.1 The plasma anion gap is calculated by subtracting chloride and bicarbonate (anions) from sodium (cation). An anion gap larger than 10 to 12 mEq/L indicates metabolic aci- dosis (normal gap = 7-9 mEq/L).12

95
Q

Low normal or low potassium level indicates what in pt with DKA? What should be done about it?

A

that the patient has severe total-body potassium deficiency and requires vigorous potassium replacement with cardiac monitoring.

96
Q

How does osmolality differ between DKA + HHS typically?

A

Osmoloarity variable in all stages of DKA, whereas >320mOsm/kg in HHS (as result of severe dehydration)

97
Q

Does a high WBC count mean infection with DKA?

A

No, see leukocytosis d/t stress

98
Q

How do you differentiate pancreatitis from DKA?

A

• May have elevated lipase in DKA. This can help w differentiating from pacreatitis.

99
Q

Over what period of time should fluid replacement typically occur in DKA?

A

24 hrs

100
Q

If a pt present with hypokalemia, should insulin be given?

A

• If a patient presents with hypokalemia, insulin treatment should be delayed until the serum potassium level is greater than 3.3 mEq/L to avoid life-threatening arrhythmias and respiratory weakness.

101
Q

What are the primary treatment complications of DKA therapy?

A

• Hypoglycemia and hypokalemia are the primary treatment complications (cerebral edema also one but rare)

102
Q

Why is it difficult to detect hypoglycemia in pt being treated for DKA?

A

• Many patients with DKA do not experience adrenergic manifestations of sweating, nervousness, fatigue, hunger, and tachycardia so ensure BG monitored q1-2hr

103
Q

Will a pt with DKA return to prior insulin doses if they were previously managing it at home?

A

• Patients with known diabetes can resume their home insulin regimen if their glucose levels were under control prior to the crisis.

104
Q

When BG drops, 3 critical physiological defences =

How is this changed in pt with diabetes?

A

1) dec in insulin 2) inc glucagon 3) inc in epinephrine

Behavioral defense is ingestion of carbs

• In Type 1 DM + longstanding Type 2, all of these defenses are compromised

105
Q

What is “hypoglycemia unawareness”

A

In diabetes pts:
Even epinephrine response diminished defective glucose counterregulation + impaired sympathetic response, which makes it much harder to detect hypoglycemic episode:

106
Q

Hypoglycemia-associated autonomic failure (HAAF)

A
  • – see defective glucose counterregulation and hypoglycemia unawareness; most often caused by recent antecedent iatrogenic hypoglycemia
  • The increased risk of severe hypoglycemia during intensive insulin treat- ment is 25-fold with HAAF.8
107
Q

What should you ask at risk of iatrogenic hypoglycemia?

A

• Pt at risk of hypoglycemia should be asked if they’re usually symptomatic or asymptomatic. At what BG do they get symptoms? And what symptoms?

108
Q

Risk factors for iatrogenic hypoglycemia =

A

altered nurtiional state, heart failure, renal disease, malignancy, infection or sepsis

  • Critically ill at risk
  • Other risks: sudden reduction of corticosteroid doses, altered ability of the patient to report hypoglycemic symptoms, reduction of oral nutritional intake, emesis, new NPO status, inappropriate timing of short or rapid-acting insulin in relation to meals, reduction of the rate of intravenous dextrose, and unexpected interruption of enteral feedings or parenteral nutrition.
109
Q

What can be done to mitigate the risk of hypoglycemia in those who are critically ill?

A

therefore not going to aim for as tight glycemic control in these groups

110
Q

Does insulin or oral meds place a pt at more risk of iatrogenic hypoglycemia?

A

• Insulin better than oral agents for accurate titrated control of BG in hospital (greater risk of hypoglycemia in oral tx)

111
Q

Older adults at greater risk

A

d/t decline in renal + hepatic enzyme activity (interferes w metb of insulin + sulonylureas), impaired counter-regulatory (glucagon + growth hormone) responses

112
Q

Treatment of hypoglycemia?

A

o Fat containing foods will retard glucose absorption and recovery from the hypoglycemic event.
o Given 15-20g straight glucose
o Glucose monitoring q15 + futher tx until bg >70mg. A carbohydrate snack containing 15 g of carbohydrate, with a protein, is recommended if the patient is not able to eat a meal within the hour
o IV glucose or glucagon injection given if pt NPO or can’t eat
o *Glucagon should only be repeated once!

N332 (8 decks)

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