Assessing the hyperglycemic patient

  1. 0
    Hi all, I'm a new grad in emerg. Today was my first day on the floor with my own patient load. I had a pt admitted with critically high blood glucose level. Pt was known IDDM x 11 years with an insulin pump. Normally her glucose is well controlled.

    For the life of me I had no idea what to assess beyond her glucose results and her complaints of feeling shaky and unwell. I asked another nurse for help and she fired off a lot of useful things to assess such as hyperventilation, ?polyuria, recent illness, changes in diet or activity, etc. But she listed off things so quickly that I have since forgotten half of what she said and I wanted to develop a plan for the next time a hyperglycemic patient comes in. School taught me well about hypoglycemia but kind of left me hanging in managing the acutely hyperglycemic patient (we talked mostly about teaching patients the importance of prevention).

    If anyone could share a focused assessment for hyperglycemia, I would really appreciate it. Or if you could point me towards any links that would be wonderful too! Thanks a lot

    ETA: The nurse suggested I start a NS bolus and draw CBC, lytes, and glucose on her. Is there anything else I should add to my mental checklist?
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  3. 11 Comments so far...

  4. 1
    EKG, K+ level, respiratory rate and depth, acid/base balance are all the first things I'd be concerned with. You'd also want to know what might have caused this; infection is usually what comes to mind first.
    flyingchange likes this.
  5. 1
    Google Hyperosmolar hyperglycemic state (HHS) and Diabetic ketoacidosis (DKA). Look at the difference in labs. You will have high blood sugars with each, but generally much higher with HHS. Compare the HCO3, osmolarity, Ph, etc and see what you see. Usually DKA turns around fairly quickly with fluids and insulin, HHS is a little trickier.

    Any number of things can cause elevated blood sugars. Steroids, infection, defective pump, stress, etc. can be the culprit.
    flyingchange likes this.
  6. 3
    Diabetic Ketoacidosis DKA..... is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes. DKA is defined clinically as an acute state of severe uncontrolled diabetes associated with ketoacidosis that requires emergency treatment with insulin and intravenous fluids

    Nausea and vomiting usually occur and may be associated with diffuse abdominal pain, decreased appetite, and anorexia. Altered consciousness in the form of mild disorientation or confusion can occur. Although frank coma is uncommon, it may occur when the condition is neglected or if dehydration or acidosis is severe.

    Among the symptoms of DKA associated with possible intercurrent infection are fever, dysuria, coughing, malaise, chills, chest pain, shortness of breath, and generalized aches and pains,.

    Symptoms of hyperglycemia associated with diabetic ketoacidosis may include thirst, polyuria, polydipsia, and nocturia.
    Signs of acidosis may include shallow rapid breathing or air hunger (Kussmaul or sighing respiration), abdominal tenderness, and disturbance of consciousness. Although these signs are not usual in all cases of diabetic ketoacidosis (DKA), their presence signifies a severe form of DKA.

    Signs of dehydration include a weak and rapid pulse, dry tongue and skin, hypotension, and increased capillary refill time.

    Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored:
    • Correction of fluid loss with intravenous fluids
    • Correction of hyperglycemia with insulin
    • Correction of electrolyte disturbances, particularly potassium loss
    • Correction of acid-base balance
    • Treatment of concurrent infection, if present
    It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis
    Medscape: Medscape Access medscape requires registration but it is free they are a huge resource for you.

    HNS....... the term hyperosmolar nonketotic state (HNS) is preferred to denote an acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Criteria for HNS include serum osmolality of 320 mOsm/kg, plasma glucose level greater than 600 mg/dL (>33.3 mmol/L), profound dehydration, no ketoacidosis, pH of 7.3, HCO3 greater than 15 mEq/L, and the absence of severe ketosis.

    HNS is the initial presentation of DM for 30-40% of patients. Most cases of HNS occur in patients with type 2 DM, characterized by insulin resistance and defective insulin secretion. HNS has been reported in patients with type 1 DM, in whom diabetic ketoacidosis (DKA) is more common. Both HNS and DKA may occur in the same individual, which suggests these 2 states of uncontrolled DM differ only in the magnitude of dehydration and the severity of acidosis.

    HNS usually evolves over a period of days to weeks, as opposed to DKA, which develops over the course of a few days. Increasing thirst with polyuria, polydipsia, and weight loss characterize HNS. To quench their thirst, many patients consume beverages containing glucose, including juices and soda. Attempt to quantitate the volume ingested over the preceding 24 hours to try to estimate the degree of diuresis with which the patient is presenting.

    All patients with HNS require hospitalization, and most should be admitted directly to the intensive care unit (ICU). When available, an endocrinologist should direct the care of these patients. The main goals of treatment are to (1) vigorously rehydrate the patient while maintaining electrolyte homeostasis; (2) correct hyperglycemia; (3) treat underlying diseases; and (4) monitor and assist cardiovascular, pulmonary, renal, and CNS function.
    Hyperosmolar Coma Workup
    Medscape: Medscape Access

    I hope this helps.
  7. 4
    This is something you will see frequently in the ED. Diabetes is a tough disease to manage as it requires major lifestyle changes, diligence, and can be associated with significant out-of-pocket costs for meds, glucometers & supplies.

    As previous posters have said, when a patient with previously well-controlled diabetes presents with hyperglycemia we need to a) treat the hyperglycemia and b) determine if there is an underlying cause such as infection. Sometimes it's more straightforward, though ... as in "I've been out of my insulin for 5 days".

    Their course in the ED is generally to check CBC, BMP, & urine, hydrate with 1-3 liters of NSS, and possibly administer insulin. For a presenting glucose > 450 I'd also get a venous blood gas and a lactate if it appears there is an infectious process going on.
  8. 3
    Without knowing age, temp and some other S&S, lifestyle, diet and meds, this is tough. Altra's post is informative for me, a LTC person. In LTC, somebody has new onset hyperglycemia, we think UTI. Temp = UTI, change in mental status = UTI, back pain, abdominal pain, poor appetite, feeling punky, etc. = UTI, UTI, UTI, UTI. Infection upsetting the metabolism is usually my #1 suspect. The wbc would be my clue to follow while addressing the management of the blood sugar. I guess like the ER, treat and investigate to further treat.
    Pixie.RN, flyingchange, and Altra like this.
  9. 2
    My best advise for you is to get the ER core corriculum, or a good CEN or CCRN review guide. That way you get ALL the info, assessment, labs, intervention stuff you need. It will serve you well your first year as a critical care nurse (yes, in the ER you are a procedure nurse AND a critical care nurse). This will also help you understand why we do what we do, and prepare you for your eventual CEN and CCRN certifications = ]
    Pixie.RN and flyingchange like this.
  10. 1
    Quote from equestriRN
    If anyone could share a focused assessment for hyperglycemia, I would really appreciate it. Or if you could point me towards any links that would be wonderful too! Thanks a lot

    ETA: The nurse suggested I start a NS bolus and draw CBC, lytes, and glucose on her. Is there anything else I should add to my mental checklist?
    Other posters have left some great information so I will try not to re-post. Here are some highlights of things I believe are improtant:
    • Almost every single patient that comes in with critical high BGL levels are severely dehydrated. Expect all the changes that come with dehydration and plan for a large fluid bolus.
    • If the patient is in DKA they may be in severe acidosis. The treatment of choice for this is fluid boluses. If the pH is critical low (usually less than 7.0) then possibly a bicarb drip BUT this will cause a drop in potassium on top of all the insulin they are getting. Montior the potassium levels closely as they get treated.
    • As for labs the two numbers that will closely guide your treatment are: BGLs and Co2 levels on the BMP. The lower the initial Co2 level, the sicker they are. A more accurate way is to look at anion gap (some labs generate this automatically on the print out, otherwise epocrates has a good anion gap calculator). The higher the anion gap, the sicker they are. These numbers will trend very accurately in the opposite direction as treatment is given. It is helpful to understand the entire picture that the labs present, but those are your two "quick look" items.
    • When BGL drops to less than 250 or so (hopefully you have shipped them to the unit, but you never know) the IV fluid must be changed to either D5 1/2NS or a D10 drip needs to be added. The cells in the body are starved for sugar, the treatment involves "pushing sugar in" with the insulin and later insulin with D5, etc.
    • Remember to check serial BMPs!!! Potassium will fall dramatically with an insulin drip. Be very wary of an intial K of less than 5 when you start a drip. I promise it will be < 3 in 4-6 hours. We chase K for days in the unit.
    I hope this helps. Again, I cut out alot of the important stuff that was already posted. Good luck in your nursing career!

    Matt
    flyingchange likes this.
  11. 1
    Sorry if any of this was already mentioned... i'd also draw a venous blood gas w/lactate (gives you their ph & if the cause is d/t infection they may have elevated lactate), BOHB, mag & phos. Remember that your sodium and potassium may be elevated but mag & phos will decrease.
    Electrolyte & acid-base imbalances can be confusing until you have more experience & can relate the values to your patient's symptoms.. I'll try to explain how I personally remember the main points & hopefully it will help you understand it..

    I think of sodium as if its a glass of saltwater; the more water you add, the more diluted it becomes (I.e. fluid overload patients have low Na+), as the water evaporates it becomes more concentrated (pts with dehydration/vomiting/diarrhea/dka have high Na+ levels)
    Potassium levels are a reflection of how much potassium is OUTSIDE of the cells (extracellular). K+ levels are affected by the pH outside of the cells, and will follow acidosis. in acidosis I.e. DKA, sepsis, the K+ is drawn out of the cell which = high K+. In alkalosis the K+ goes back in the cells = low K+, insulin also pushes K+ back into the cells which lowers serum K+ levels. * this is why hyperkalemia isn't always treated if pt is hyperglycemic.
    Causes of DKA; The six I's:
    Infection, Ignorance (noncompliant diabetics), Infarction, Ischemia, Intoxication, Implantation (gestational diabetes)

    Both DKA and NKHS will present w/symptomatic hypoglycemia: polyuria, polydipsia, tachycardia, orthostatic hypotension, flushed face, irritability, tachypnea, possibly confusion, poor skin turgor, dry mucous membranes, etc.
    DKA is treated w/fluids, insulin drip, poss. Bicarb & KCL, monitor lytes, anion gap & ketoacidosis.
    NKHS is treated w/fluids, insulin ivp or SubQ, KCL and monitoring of lytes & lactic acidosis

    Hopefully this helps make sense of it all!
    flyingchange likes this.
  12. 1
    One more thing... their blood gas may also show low CO2 which is a result of tachypnea or kussmaul resps b/c the faster they breathe, the more CO2 they blow off. The body does this to compensate for the metabolic acidosis (co2 raises the pH, so lowering its level helps to neutralize the ph)
    flyingchange likes this.


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