case study help - page 2

by ckirkpa 3,309 Views | 41 Comments

I am currently working on the following case study and need a little guidance on which way to go with the info. Any ideas? I think the patient is possibly septic r/t her leg??? I am not sure though. There is so much going on.... Read More


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    Quote from laurensummers
    Most of the pts assessment data, signs and symptoms appear to look like compensatory stage of this shock..in addition WBC are high and Also bands @10% which is also sn indicator
    If they remain hypotensive, tachycardic, tachypnic that are not compensating. With the elevated glucose, altered LOC, dry tenting skin my vote is HHS. The WBC is elevated and they have an infection but in leiu of the glucose and renal failure/acidosis I vote HHS.

    However...your rationale is correct as well. In the real world these co-morbidities are considered and treated simultaneously
  2. 0
    A minor point...

    With hyperglycemia, serum Na levels are artificially lowered. So, with hyperglycemia, it is necessary to get a correct sodium level. While I have found several formulas for this correction one site (there are many) that provides a tool to make such a correction is:

    MDCalc | Sodium Correction for Hyperglycemia


    This may be beyond the scope of this assignment, but it is important for developing the entire clinical picture. So, is this patient hypo-, hyper-, or eu- natremic?
    Last edit by psu_213 on Mar 20, '13
  3. 1
    And one other thing--

    DKA is not restricted to Type 1 diabetes. What test(s) would help you determine if this is DKA versus HHS?

    Case Study: Diabetic Ketoacidosis in Type 2 Diabetes: “Look Under the Sheets”

    Case Study: Diabetic Ketoacidosis Complications in Type 2 Diabetes
    Esme12 likes this.
  4. 0
    And I also agree with a previous post, establishing the exact diagnosis is not your job, however, it would be your job as the nurse to anticipate the treatments and the patient's response to such treatment.

    Someone talked about the treatments for sepsis. What about txs. for the diabetic complications? What do you anticipate will be ordered? Questions to ask yourself: what is the significance of the kidney labs (Cr/BUN/K)? How will that be treated? What about the tachycardia and the hypotension--what is the tx there?

    Finally, the acidosis and hyperglycemia...how will they be treated? How will this tx effect the lab values? A bit more of an advanced question, but an important one for the nurse treating the pt: given the tx for hyperglycemia and acidosis, to which lab value (that I have mentioned in this post) would the nurse pay close attention and why?
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    Im studying this right now in my senior nursing class...what I got from this module and my current experience. . is yes, all the above co-issues must be adressed however...the exact cause must be fixed I.e. ABX ..or if it was hypovolemic shock...fluid resuscitation. ..the Acute renal failure is due to the body sympathetic nervous system responces to vasoconstrict selectively..usually the GI, the KUDNEYS to perfuse more vital organs...this is also a hypermetabolic state causing insulin resistance, hyperglycemia, lactic acidosis (metabolic), liver dysfunction, lytes imbalance,DIC or microemboli, capillary permeability and systemic vasodilation except for the selectives.etc etc...I would interested to see what the ACTUAL MDs did call it? Lol
  6. 0
    Again treat first things first.....what is going to kill this patient first? elevated glucose, elevated K, acidosis (that may correct with lowering of the glucose and fluid replacement) EXTREME DEHYDRATION skin tenting, decreased LOC accompanies HHS......then treat the infection with antibiotics top prevent this state from reoccurring.

    Trust me.....this patient has an infection (lung or leg) that has caused this patient on METFORMIN to go into a hyperosmolar state that needs to be corrected. The BUN of 82 with a Cr that is only 2.3...how much of that BUN is dehydration that is caused by the hyper diuresis (disproportionate urine output as seen with diabetes insipidus/SIADH) caused by the hyperosmolar state induce by the elevated glucose from the stress of illness.

    Glu 550
    K 5.6,
    NA 132,
    Cl 80,
    Cr 2.3,
    BUN 82

    ABGS
    : pH 7.30, Pa0270, PC0247, HC0320mEq/L
    Hematologypanel:HCT 30. %, HGB 10.1 g/dL, RBC 3.9 x 106/L
    WBCwith differential: WBC 17,000/mm, segmented neutrophils 79%, bandneutrophils 10%, monocytes 9%, lymphocytes 30%, eosinophils 4%, basophils 3%
  7. 0
    Quote from psu_213
    A minor point...

    With hyperglycemia, serum Na levels are artificially lowered. So, with hyperglycemia, it is necessary to get a correct sodium level. While I have found several formulas for this correction one site (there are many) that provides a tool to make such a correction is:

    MDCalc | Sodium Correction for Hyperglycemia


    This may be beyond the scope of this assignment, but it is important for developing the entire clinical picture. So, is this patient hypo-, hyper-, or eu- natremic?
    But that changes in the patient in a HYPEROSMOLAR state that is very dehydrated....you need to exhibit extreme caution when re-hydrating for drops in NA and K
  8. 0
    If this patient was dehydrated the Na would NOT be low ..it would be high becsuse of concentration. ..
    and the creatinine would not be as high..not to mention ...skin tenting is indicative in this case of the decrease in hydrostatic capilkary pressure initially in septic shock which causes fluid to shift from interstial space into vasculature as a compensatory mechanism initially until it gets worn out. I have seen this clinical ly in the icu. I pretty sure about this
  9. 0
    *Because
    Last edit by MendedHeart on Mar 20, '13
  10. 0
    Quote from Esme12
    But that changes in the patient in a HYPEROSMOLAR state that is very dehydrated....you need to exhibit extreme caution when re-hydrating for drops in NA and K
    What I'm going to be most worried about in term of dropping the K is the insulin gtt the pt will (presumably) be getting.


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