case study help

[ckirkpa]

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. Thanks for any input!

48year old Mexican American female admitted with fever,difficulty breathing, pleuritic chest pain, weakness, and shaky chills. Hx of flu like symptoms from approximately one week ago, took over-the-counter medications with moderate resolution of symptoms. On the day of admission, pt sleeping more than usual and seemed confused. In ER, pt's chest x-ray revealed left lower lobe pneumonia.

Health History Data:diagnosed with type 2 diabetes and hypertension about15 years ago and a "thyroid problem" for a year or two.

Prescribed Oral Medications:

Glucophage (Metformin) 500 mg twice a day.

Pravastatin(Pravachol) 40 mg daily at bed time

Levothryoxine100 mcg daily

Vasotec(Enalapril) 5 mg twice a day

Diltiazem(Cardizem) 240 mg daily

Reportfrom ER nurse

Vitals:HR 116, BP 88/56, RR 26, T 96.4°F, Wt 180, Ht 5'4",

Neuro:lethargic, responds to verbal stimuli and oriented to self

CV:heart tones distant, S1S2S4audible, capillary refill 3 > seconds

Pul:lungs clear bilaterally

GI:abdomen protuberant, hypoactive bowel sounds in all 4 quadrants

Integ:skin dry with tenting present over sternum, lips and oral mucus membranes dry and cracked, left lower leg edematous and erythematous with serous fluid oozing from lateral aspect of calf.

AdmissionLabs: SerumChemistry:

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/µL

WBCwith differential: WBC 17,000/mm³, segmented neutrophils 79%, bandneutrophils 10%, monocytes 9%, lymphocytes 30%, eosinophils 4%, basophils 3%

[psu_213, BSN, RN]

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

[psu_213, BSN, RN]

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?

[MendedHeart]

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

[Esme12, ASN, BSN, RN]

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/µL

WBCwith differential: WBC 17,000/mm³, segmented neutrophils 79%, bandneutrophils 10%, monocytes 9%, lymphocytes 30%, eosinophils 4%, basophils 3%

[Esme12, ASN, BSN, RN]

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

[MendedHeart]

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

[MendedHeart]

*Because

[psu_213, BSN, RN]

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.

[MendedHeart]

I do agree with the insulin drip however

[psu_213, BSN, RN]

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

But is the Na really that low? Plus, hypovolemic hyponatremia does exist.

Plus, the high Cr and high BUN are indicative of AKI, most likely resulting from dehydration (secondary to both DKA/HHS and sepsis). No one is denying that there is infection/sepsis, but there is definitely a diabetic emergency at work too...it may be secondary to the sepsis, but treatment of the pt is going to be treating both the sepsis and the diabetic issues.

[MendedHeart]

I would hardly say a BGM of 550 is an emergency over the fact that this patient is in SEPTIC SHOCK. ..there is no resson in this stem that would indicate this patient was hypovolemic...and not to mention the K is high but not that high...but the Na is low..135-145 is norm

[MendedHeart]

The point is the labs dont match what your going for and Shock causes AKI