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Endocrine Exam 2 > 28 - Diabetic Emergencies > Flashcards

28 - Diabetic Emergencies Flashcards

1
Q

Describe the pathophysiology of deabetic ketoacidosis (DKA)

A
  • Much more common in type 1 than type 2
  • Due to a relative or absolute insulin deficiency
  • You will see elevated glucagon, cortisol and growth hormones
  • There will be an increased glucagon to insulin ratio
  • This increased ratio will cause increased gluconeogenesis, glycogenolysis and ketone body formation
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2
Q

Describe the molecular changes we see in DKA

A

Decreased GLUT4

  • This means there will be decreased uptake of glucose into the cells
  • The result is decreased glucose metabolism in skeletal muscle and fat
  • This means increased reliance on alternative fuel sources
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3
Q

What is the molecular result of increased glucagon and decreased insulin levels?

A

Glucose generation from pyruvate (gluconeogenesis)
- Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as pyruvate

Increased glycogenolysis will also occur
- Glycogenolysis is the breakdown of glycogen (n) to glucose-6-phosphate and glycogen (n-1)

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4
Q

What happens in the liver during ketoacidosis?

A

In the liver, elevated glucagon leads to increased ketone body formation

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5
Q

What else will happen during ketoacidosis?

A
  • Increased lypolysis
  • Release of free fatty acids

VLDL and triglyceride formation will also increase (via the usual pathway for free fatty acids) but less so than ketone bodies

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6
Q

Describe ketone body formation

A
  • There will be a 3:1 ratio of beta-hydroxybutyrate and acetoacetate
  • Both of these ketones can be detected in the serum
  • Acetoacetate will be preferentially found in the urine
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7
Q

What are the symptoms and physical exam findings in DKA?

A

Symptoms

  • Nausea
  • Vomiting
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Abdominal Pain***
  • Dyspnea

Physical exam findings

  • Tachycardia
  • Hypotension
  • Decreased urine output
  • Tachypnea/Kussmaul Respirations ***
  • Abdominal tenderness
  • Altered Mental Status : lethargy, obtundation, coma
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8
Q

What are the two most important and common patient presentations?

A

Abdominal pain and Kussmaul respirations

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9
Q

What are Kussmaul respirations?

A

Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA)

Hyperventilation is occurring in order to breath of the CO2

Patient will be breathing deep, hard and fast

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10
Q

What are the five factors you use to diagnose DKA?

A
  • Serum glucose
  • Serum bicarbonate
  • Presence of SERUM ketones
  • Serum pH
  • Anion gap
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11
Q

Describe the serum levels you are looking for in a DKA diagnosis

A
  • Blood sugar greater than 250
  • Bicarb low - less than 18
  • Presence of ketones (SERUM is more accurate than urine)
  • pH less than 7.3
  • An increased anion gap, meaning there are many more positive ions in the body than negative (acidosis)
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12
Q

Describe the anion gap

A
  • The anion gap will be increased due to increased ketoacidosis
  • This is what causes the bicarb to be low… It is all being used up trying to neutralize all the positive ions in the body
  • This can potentially occur from lactic acidosis or infection, so you need to check more than just the anion gap when diagnosing DKA
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13
Q

What causes DKA?

A

ALWAYS LOOK FOR THE CAUSE

  • This is the most important thing to figure out
  • Since this is a relative or absolute deficiency in insulin, you need to figure out what has caused the change
  • The work up of DKA is considered incomplete without attempting to determine the inciting event
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14
Q

What are things you will want to ask the patient about when trying to determine the cause of DKA?

A
  • Recent sick contacts
  • Illness
  • Medication compliance (run out, stop taking it, not eating so not taking it, etc.)
  • Sexual activity - ask about infection and pregnancy
  • Cough, fever, sweats, diarrhea
  • Chest pain *** (important in older patients, get EKG)
  • Drug use (abuse)
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15
Q

What are the 5 I’s of DKA?

A 
I = infection
I = infarction/ischemia
I = intoxication
I = impregnation 
I = idiocy (didn't take meds)
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16
Q

What are all the lab values you need to get when diagnosing DKA?

A
  • Serum glucose, electrolytes***, ketones, ABG
  • Urinalysis, dipstick for ketones
  • Electrocardiogram (rule out ischemia, especially when the patient is older)
  • CBC with differential
  • Renal function, electrolytes***, liver enzymes
  • Culture - blood, urine, sputum (especially if they have a fever)
  • Chest x-ray, etc
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17
Q

What is the most important lab value?

A

ELECTROLYTES - I put it up there twice because it is so important

18
Q

What is the first step in treating DKA?

A

Fluid resuscitation

  • Patients are dehydrated due to diuresis and vomiting
  • Replace fluids initially with 0.9% NaCl***
  • They may require many liters depending on severity
  • Give an initial bolus of 2-3 liters over the first 1-3 hours then reassess
  • Once the serum glucose is less than 200 you will need to change fluids to D5% or 0.45% NaCl
19
Q

What is the second step in treating DKA?

A

Insulin therapy

  • Insulin is REQUIRED to reverse DKA
  • You have two options, both are with the use of short acting insulin… (1) bolus 0.1 U/kg then give infusion of 0.1 U/kg/hour OR (2) 0.14 U/kg/hr continuous with no bolus
  • The bolus plus continuous is much more common
  • You need to monitor the serum or fingerstick glucose levels every hour and adjust insulin accordingly
  • Do not transition to subcutaneous insulin injections until DKA is resolved
20
Q

How fast do you want to decrease the blood glucose levels?

A
  • 50-70/hour, max of 100/hour
  • Need to do this gradually because the brain can’t keep up
  • BS concentration is high in the brain, so when you drop the systemic BS, water will rush into the brain to equilibrate the concentration and cerebral edema can occur
21
Q

What is the third step in treating DKA?

A

Electrolytes

  • This MIGHT come before insulin (FYI)
  • Total body K+ levels will be depleted, so you will need to replace potassium
  • Serum sodium levels will appear low, but this can be a “pseudohyponatremia” meaning that we are diluting them so much that they look like they’re low on sodium, but they’re just diluted
22
Q

What do you need to know about replacing potassium?

A

If the K+ is less than 3.3, need to replace BEFORE starting insulin

There is a “transcellular shift” that may occur making K+ appear falsely elevated… Be on the lookout for this because it is low and you still need to replace potassium

23
Q

What is important to remember about electrolyte lab tests?

A

NEED to follow them closely and take tests every 3-4 hours to monitor during DKA

24
Q

When can we say that DKA has resolved?

A
  • Serum glucose consistently under 200
  • Serum bicarb normal
  • Serum pH normal (>7.3)
  • Anion gap normal (
25
Q

Describe the pathophysiology of hyperglycemic hyperosmolar syndrome (HHS)

A
  • Much more common in type 2 diabetics
  • Higher mortality rate than DKA (this is because HHS patients will be sicker and older than DKA patients, not because it is more severe)
  • Due to a relative insulin deficiency or inadequate fluid intake
26
Q

Describe how the relative insulin deficiency contributes to HHS

A
  • Deficient insulin will cause increased hepatic glucose production
  • Hyperglycemia leads to osmotic diuresis and dehydration ***
  • It is believed that RELATIVE insulin deficiency leads to less counter regulatory hormones (less glucagon, etc.) and therefore it will NOT cause ketoacid production

NOT KETOACIDOSIS in HHS patients **

27
Q

How are patients with HHS going to present?

A
  • Less severe symptoms than DKA
  • Typically seen in elderly patients
  • Symptoms are more insidious (gradual but harmful) with onset over several days to weeks
28
Q

What are the symptoms of HHS?

A

Symptoms

  • Polyuria
  • Weight loss
  • Decreased oral intake
  • Altered mental status (common)
  • Profound dehydration ***
  • Hypotension and tachycardia (caused by profound dehydration)

ABSENCE of…

  • Nausea
  • Vomiting
  • Kussmaul breath (because there is NO acidosis)
  • Abdominal pain

These absences will help you differentiate HHS from DKA

29
Q

How do you diagnose HHS?

A
  • Serum glucose MUCH higher than in DKA (usually 600+, can be 1000+)
  • Hyperosmolarity (>350)
  • Often pre-renal azotemia with ELEVATED BUN & CREATININE ***
  • Acidosis and ketosis are absent or mild
30
Q

Why could acidosis and ketosis be present (but mild) even in HHS with no DKA?

A
  • If the patient has not been eating, they could be in starvation mode, so ketones are produced
  • If the patient has an infection causing their HHS, they could have a lactic acid build up and present with an anion gap acidosis
  • Note that these findings will be MILD compared to DKA ***
31
Q

What can cause HHS?

A
  • Stroke
  • Myocardia infarction
  • Infection/sepsis (pneumonia is common)
  • Decreased fluid intake (lack of access to water)

HHS doesn’t just happen, something CAUSES it –> You NEED to figure out the cause ***

32
Q

How do you treat HHS?

A

Very similar to DKA

  • Start with fluid resuscitation
  • Give insulin
  • Replace electrolytes
33
Q

Describe the fluid resuscitation in HHS

A
  • Volume depletion and dehydration is usually MORE severe in HHS compared to DKA
  • A bolus of 0.9% NaCl is given to stabilize hemodynamics
  • Then you can reverse free water deficit using 0.45% NaCl
  • Need to monitor electrolytes with volume replacement because you are diluting things our really quickly ***
34
Q

Describe the administration of insulin in HHS

A
  • Insulin is needed, bu it is NOT the primary treatment
  • First you must correct the dehydration and stabilize the patient
  • Give a bolus of 0.1 units/kg then 0.1 units/kg/hr infusion
  • Continue until the glucose is improved and the patient is eating
  • At this point you can begin subcutaneous insulin
35
Q

Describe the replacement of electrolytes in HHS

A
  • Similar to DKA, you need to monitor K+ and replace with insulin
  • Na+ may be elevated due to dehydration
  • Need to monitor to avoid overcorrection of hypernatremia
36
Q

How do you know when HHS has resolved?

A

There are no hard rules for when HHS is gone – it is more just a clinical judgement

37
Q

How do we define hypoglycemia?

A
  • Serum glucose less than 70

- Patient will usually have increased catecholamines and glucagon as well

38
Q

What are the symptoms of hypoglycemia?

A
  • Tremor
  • Palpitations
  • Anxiety
  • Tachycardia
  • Sweating
  • Paresthesias
  • Seizure and coma are possible when severe
39
Q

What do you need to consider when a patient presents with hypoglycemia?

A
  • In the setting of diabetes mellitus need to consider accidental or intentional overdose of insulin
  • Did they accidently take too much insulin? Or did they do it on purpose? Suicide?
40
Q

How do you treat mild vs severe hypoglycemia?

A

Mild
- If the patient presents to the clinic with mild and intermittent hypoglycemia (they are getting low throughout the day), you may consider an insulin adjustment

Severe

  • If the hypoglycemia is severe, infuse with dextrose containing fluids until the insulin effect has worn off
  • Glucagon injection can also be used
41
Q

What is important to remember when counseling patients?

A
  • When counseling patients about diabetes, be sure discuss recognition and treatment of hypoglycemia
  • Suggest the patient always have glucose tabs, candy, etc.
  • Asses the patient’s ability to recognize low glucose

** Patient may lose sensitivity to hypoglycemia over time **

Endocrine Exam 2 (18 decks)

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