10/22- Cases: Diabetes Flashcards Preview

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Flashcards in 10/22- Cases: Diabetes Deck (21):

- A 57-year-old engineer with diabetes mellitus for seven years is brought to the emergency room in a semi-conscious state by his wife.

- He had suffered from the “flu” for the past four days and had not gone to work. Yesterday he was unable to eat because of abdominal pain and repeated vomiting.

- The wife states that the patient had taken his glyburide daily during his illness.

- Capillary blood glucose is measured as > 400 mg/dl in the emergency room. IV isotonic saline has been started at 125 ml/hr. You perform a physical examination.

Physical Exam

- Vital signs:  BP 94/60 supine, 70/50 sitting; P 124 regular; R 18; T 99°F. 

  • Orthostasis indicative of volume depletion
  • Slightly tachypneic

- He is a lethargic African-American male who is oriented only to person. 

- There is clinical evidence of volume depletion. 

  • This could include something like dry mucous membranes, skin tenting...

- Eyes:  pupils equal and reactive; discs flat.  There is evidence of background retinopathy

- Throat red, without exudates. 

- Respirations are deep and rapid

  • Suggestive of Kussmaul respirations

- Chest is clear to percussion, and coarse rhonchi are present throughout. Cardiac normal. 

- Bowel sounds are hypoactive, and there is mild diffuse tenderness with guarding but no rebound. 

- Stool is guaiac positive for occult blood

- The neurological examination reveals no focal motor or sensory deficits but there is evidence of peripheral neuropathy of the lower extremities

- Blood is sent for counts and electrolytes, and an arterial blood gas is ordered. 

- The patient is catheterized for a urine specimen which is tested in the ER (4+/lg for glucose and ketones). 

- The patient vomits some coffee-ground material, strongly guaiac positive. 

- The lab calls:  pO2 85; pCO2 = 14 mm; pH = 7.2. 

  • Metabolic acidosis

- Insulin is ordered, the IV rate is increased, and the patient is admitted to the intensive care unit.

Laboratory data:

- Glucose 850 mg/dL

- HCO3  5 mEq/L

- BUN  37 mg/dL

- Serum ketones positive at 1:32 dilution

- Na 124 mEq/L

- Hematocrit  54%

- K 6.0 mEq/L

- Hemoglobin  15.8 gm/dL

- Cl  82 mEq/L

- WBC  25,700/mm3

What is his diagnosis? What makes you think this?

Diabetic ketoacidosis


Does this person of type I or type II diabetes?

In the past, if someone came in with DKA, you could say definitively that they had type I diabetes

- Recently, it's gotten more complicated

Now we use different classification systems, such as ketosis prone diabetics

- No matter what the underlying cause (type I, II, autoimmunity, lack of beta cell function, etc.) if the patient presents with DKA, they are acutely insulin deficient and should be given insulin


What will be seen in (relative) insulin deficiency?

Describe the vicious cycle.

What will be seen in (absolute) insulin deficiency?

- Relative insulin deficiency (type II) -> Hyperglycemia

  • Osmotic diuresis and glucosuria
    • Hypovolemia
      • Decreased renal clearance/GFR
        • Further hyperglycemia

- Absolute insulin deficiency (type I) -> Increased lipolysis

  • Increased ketones

Amount of insulin needed to suppress ketosis is much less than hyperglycemia. Thus, you can get hyperglycemia without ketosis (ketosis/DKA happens rarely in type II diabetics because have some small level of insulin... classically)


What could be the cause of his upper GI bleeding?

Mallory Weiss tear from excessive/violent, repeated vomiting


What are the possible etiologies of the elevated WBC?

Elevated WBC count in DKA is very common

Want to ask what provoked the DKA:

- In a known type I diabetic population, the most common reason to develop DKA is mediation non-compliance

- Other provocative factors


What is the most common cause of DKA in type I diabetics?

In a known type I diabetic population, the most common reason to develop DKA is medication non-compliance

- (Or got sick and weren't able to use medication effectively/correctly)


Estimate the true serum sodium concentration (why is it not the lab value given)?

Given serum sodium = 124

- Need to correct for glucose

Glucose corrected serum sodium = 

Nameasured + 1.6(glucose-100)/100

- If you actually calculate this, you get 136

  • Don't want to correct an apperent hyponatremia; here it is caused by osmolar contributions of glucose


What is the anion gap?

- Glucose 850 mg/dL

- HCO3  5 mEq/L

- BUN  37 mg/dL

- Serum ketones positive at 1:32 dilution

- Na 124 mEq/L

- Hematocrit  54%

- K 6.0 mEq/L

- Hemoglobin  15.8 gm/dL

- Cl  82 mEq/L

- WBC  25,700/mm3

Note: DO NOT use corrected sodium

- The correction is to estimate the osmotic effect of the sodium; reassure yourself that hyponatremia is result of the glucose

- For other calculations, use the actual measured sodium

Here, AG = 124 - (5 + 82) = 37

- This is a high-AG metabolic acidosis

- Here, thinking the cause is DKA


What are the unmeasured anions in this high anion gap metabolic acidosis?



What is the delta-delta comparison in this case?

- AG = 37 (calculated)

- HCO3 = 5

- ΔAG = 37 - 12 (normal is 10 +/-2) = 25

- ΔHCO3 = 24 - 5 = 19

The Δ:Δ ratio should be 1 (values increase and decrease together)

- In acutality, bicarb may not drop as much as generated acids since bicarb is not alone in buffering acid in the body

- ΔAG/ΔHCO3 normal is 1-2 (Here, it is 25/19, which is normal)


- What is the scenario in which Δ/Δ > 2

- What is the scenario in which Δ/Δ

Δ/Δ means AG/HCO3

  • Δ/Δ > 2 means smaller change in bicarb than expected (bicarb value higher than expected)

    • Pre-existing metabolic alkalosis

    • Chronic respiratory acidosis

  • Δ/Δ < 2 means greater change in bicarb than expected (bicarb is lower than expected)

    • Co-existing non gap anion acidosis


What is the expected respiratory compensation in this case? Adequate?

- HCO3 = 5

- pCO2 = 14 mmHg

Winter's formula

ECO2 = 1.5(HCO3) + 8 +/-2

Here, ECO2 = 1.5(5) + 8 +/-2 = 13.5 - 17.5

- Thus, adequate compensation

- If actual pCO2 was higher than expected, could indicate additional respiratory acidosis (hypoventilation)


Estimate the serum osmolality

- Glucose 850 mg/dL

- HCO3  5 mEq/L

- BUN  37 mg/dL

- Serum ketones positive at 1:32 dilution

- Na 124 mEq/L

- Hematocrit  54%

- K 6.0 mEq/L

- Hemoglobin  15.8 gm/dL

- Cl  82 mEq/L

- WBC  25,700/mm3

Osmolality = 2(Na) + glucose/18 + BUN/2.8

Here = 2(124) + 850/18 + 37/2.8 = 308

- This is high (normal is ~ 290 mOsm)


Why is the serum potassium level elevated?

- What is total body potassium storage (high or low?)

- Transcellular shift due to acidosis

- Total body potassium stores are actually lower

  • As soon as you stop DKA, potassium will drop precipitously


In what DKA case do you NOT give insulin?


- Potassium normally high in DKA

- If low to start, need to replace potassium first before giving insulin


Describe the findings of background diabetic retinopathy

- Micro-aneurysms

- Cotton wools pots

- Intra--- hemorrhage

- Dilation of vessels

- Macroedema

- Neovascularization


Describe the symptoms and signs of diabetic peripheral neuropathy

- Sensory or motor

- Symmetric or asymmetric

- Location

- Symptoms

Classic is:

- Sensory

- Symmetric

- Affects long nerves first (stocking-glove distribution)

- Patient feels neuropathic burning pain and then loss of sensation

  • Lose vibration first > soft touch > pain


What form of diabetic autonomic nervous system dysfunction does he probably have

Key clue is the orthostatic hypotension

- Can't maintain BP

- Loss of classic vascular response to standing


What would you advise to prevent the chronic complications of diabetes in this patient?

Glycemic control

  • Major reduction in microvascular complications
    • Retinopathy
    • Nephropathy
    • Neuropathy (some already established; not reversible, but can impede progression)
  • Tight glycemic control does not greatly reduce macrovascular endpoints (exessively tight may actually be harmful in some pt ppulations)

Rather, reduce macrovascular risks rather with

  • Lipid management
  • HTN management
  • Diet, exercise

If neovascularization is playing arole already in his diabetic retinopathy, could to laser photoablation

Check feet for ulcers; may need special shoes, etc.


Another patient presents with basically the same clinical findings and chemistries, with these differences:

- Na   141 mEq/L

- Glucose  1000 mg/dL

- Serum ketones: negative

What is this? Who typically gets it?

Hyperosmolar syndrome

- Still going through vicious cycle of hyperglycemia, glucosuria, decreased volume/GFR and increased blood serum levels

- Can correct this by taking in volume

Thus, someone who goes into hyperosmolar syndrome is typically elderly, frail, bed-bound person with AMS or in nursing home, etc.

- Problem volume-regulating


How does treatment for hyperosmolar syndrome differ from DKA?

In hyperosmolar syndrome, fundamental basis of treatment is fluids

- Still give insulin (as in DKA), but much of the correction will be a result of fluid correction