Diabetes, DKA, HHNK

How do you calculate the anion gap?

(Na+)-(Cl- + HC03-)=12 normal gap. If with K+, 14=normal.

What are some causes of DKA?

(Think acute). Could be due to non-compliance with meds, expensive meds, didn't know they had diabetes, trauma, infection (pneumonia/UTI/gastroenteritis/sepsis), pregnancy, pancreatitis, stress, excess alcohol intake, cocaine, infarction

What are s/s DKA?

**K can be high OR low!!!** If glucose has trouble entering the cells, K will as well (both enter cells insulin mediated). Polyuria (>2.5L day), abd pain (ketoacids or sodium level), polydipsia (serum osm high, 330+ osm), vomiting, flushed, decreased skin turgor, acitone (fruity) breath, tachycardia (Pulse 116), Kussmauls breathing (respiratory compensation), SOB, respiratory distress, lethargy, temp elevated, RR 28 (elevated), confusion, tiredness, Na+ not necessarily elevated. Ex: P02=100, PC02=25, bicarb=12.5 (anion gap) Ex: Temp, hunger, thirst, 82/52 (MAP too low, not perfusion, less than 70 or 60 only main organs). Glucose 880, K 2.8 (hypokalemia), osm 368, no ketoacidosis, Na+ 128 (hyponatremia, dilutional) **Usually hypernatremic and polyuria (false hemo-concentration), if hyponatremic, caught it early.**

Hyperglycemia

*Abnormally high blood sugar (above 125 or 200) Can be caused by spike in glucose intake/sickenss, stress, pancreas malfunction, trauma, pregnancy, pancreatitis. *Hyperglycemia impairs immune function (decreases white blood cell function), promotes inflammation, increases blood viscosity, favors the growth of yeast organisms and is associated with blood vessel wall changes resulting in increased risk for infection, microvascular, macrovascular complications and foot ulcers.

What are nursing assessments and interventions for DKA?

*Assessment: The most important aspects of physical examination include monitoring of vital signs, assessment of dehydration, level of consciousness, symptoms of hypovolemic shock, and signs of infection (WBC--not fever). Fever will lead you to assess for an underlying infection so check lung sounds, sputum production- color, amount, consistency. Look at the urine; is it cloudy- do they have symptoms of dysuria, frequency, urgency? Look also for sinus infection, ear infections, and/or abscesses. Labs: glucose, electrolytes, ketones, CBC--infec, BUN/creatinine--RFTs, and arterial blood gas (ABGs). An EKG must be done on admission with continuous monitoring (tele) until the crisis is resolved (*chest x-ray may be done to evaluate pulmonary pathology). *Intervention: 1. only bicarb if pH less than 7.0, will make them alkalosis, will hold onto 02 and it won't leave RBC, not good. 2. No D5W! 3. No insulin until hydrated (MAP stable) 4. K only if K lower than 5.0 (start K first if below 3.5) **PC02 will be low due to Kausmal's respirations (repir compensation), metabolic will tank first. pH is always acidotic. • FVD treat first (or K first if it is VERY low, below 3.5, once 3.5 can begin IV fluids)--NS 20cc/kg for 1st hr infuse fluids (1-2L in 1-2 hrs, then 1L 3-4 hrs). Too much fluid=cerebral edema! • Start K if was at 3.5+, but <5, will drop with fluids (Q1-2 hr lab work). 1st hour. o ****NS drops sugar by dilutional effect alone, don't start insulin 1st hr!!!**** o Monitor renal function Q1hr with K supplement, or could become hyperkalemic and go into acute renal failure. 10mEq K goes up by 0.1, **can't go over 40mEq per L (.4 increase). 10mEq in 100cc typical, bring up by .1—20mEq in 100cc separate line, would bring up by .2). • When MAP up, change to ½ NS infusion. • Insulin regular IV drip, 0.1mg/kg/hr=70kg=7 U per hr 2nd hour •Regular insulin via IV, half-life=9 minutes, steady state reached w/in 45 minutes. • Bolus administration insulin increases the risk of hypokalemia! • When BGL 250mg/dl change to D5W 1/2NS to prevent hypoglycemia. o Monitor with finger sticks (drops quickly w/ just NS), drop in BGL per hr should be **80-100mg less** to prevent cerebral edema due to BBB flooding--if over 100mg difference, H20 will rush to brain if drop too fast. Slow and steady! If it drops too much, cut insulin by 1/4 or 1/2 rate and recheck.

A client is brought to the emergency room in an unresponsive state, and a diagnosis of hyperglycemic hyperosmolar nonketotic syndrome is made. The nurse would immediately prepare to initiate which of the following anticipated physician's orders?

1. Endotracheal intubation 2. 100 units of NPH insulin 3. Intravenous infusion of normal saline 4. Intravenous infusion of sodium bicarbonate 3. Why? The primary goal of treatment in HHNK is to rehydrate the client to restore fluid volume and to correct electrolyte deficiency. Intravenous fluid replacement is similar to what administered in diabetic ketoacidosis (DKA) and begins with IV infusion of normal saline. Intubation and mechanical ventilation are not required to treat HHNK. REGULAR insulin (faster acting), NOT NPH would be administered ***(can only admin reg IV)***

A student with type 1 diabetes tells the nurse she is feeling light-headed. The student's blood sugar is 60 mg/dL. Using the 15-15 rule, the nurse should:

1. Give 15 mL of juice and give another 15 mL in 15 minutes. 2. 3. Give 15 g of carbohydrate and retest the blood sugar in 15 minutes. 4. Give 15 g of carbohydrate and 15 g of protein. 5. Give 15 oz of juice and retest in 15 minutes. 4. The 15-15 rule is a general guideline for treating hypoglycemia where the client consumes 15 g of carbohydrate and repeats testing the blood sugar in 15 minutes. Fifteen grams of carbohydrate equals 60 calories and is roughly equal to ½ cup of juice or soda, 6 to 8 lifesavers, or a tablespoon of honey or sugar. The general recommendation is if the blood sugar is still low, the client may repeat the sequence.

A client with type 1 diabetes mellitus has diabetic ketoacidosis. Which of the following findings has the greatest effect on fluid loss?

1. Hypotension. 2. Decreased serum potassium level. 3. Rapid, deep respirations. 4. Warm, dry skin 4. Due to the rapid, deep respirations, the client is losing fluid from vaporization from the lungs and skin (insensible fluid loss). Normally, about 900 mL of fluid is lost per day through vaporization. Warm dry skin due to hypotension

Oral meds for type 2 DM

1. Metformin=decrease glucose release from the liver, increase insulin sensitivity (don't use w/impaired renal function or contrast) 2. DPP-4 inhibitors (-a)=prolong the action of GLP-1 resulting in a glucose dependent insulin secretion Very few side effects, rhinitis Safe in renal failure 3. Sulfonylureas (-ides): Primary action is to increase insulin release from beta cells in pancreas. Possible side effects: low blood glucose and weight gain 4. Thiazolidinediones (TZD): Primary action is to increase body's sensitivity to insulin Precautions: CHF, decreased liver function Example: pioglitazone (Actos) 5. GLP-1 Analogs: Primary action is to Increase insulin production (glucose dependent) Increase satiety Decrease glycogen breakdown Considerations: risk for pancreatitis Examples: Byetta, Victoza, Bydureon

At what level is the BGL for kidney function surpassed?

180. Kidneys notice at 120-130 but there no changes in function until 180.

How much of CO goes to the kidneys each hr?

25% CO

What is DM Type 1?

5-10% of DM pts. Insulin insufficiency or lack of insulin. Could be an acute infection/illness along with genetic disposition that causes it. Ketosis common. An autoimmune response occurs and body attacks its own beta cells (insulin producing cells in the islet of langerhans in the pancreas). Not enough insulin is produced. Insulin is secreted when BGL rise, and triggers the cells to allow G to enter. *When BGL levels are very high, insulin causes G to be: stored as glycogen in the liver, muscle and fats cells, AA synthesis, fat synthesis and metabolic energy. *When there is not enough intracellular G, the pancreas is stimulated to release glucagon, which stimulates glycogenolysis, and gluconeogenesis = glycogen --> glucose released (happens in the liver) for the body's cells to use as fuel. Fats are broken down for energy as well, and byproduct is ketones (build up and cause metabolic acidosis). *Catelcholemines (androgenes) also stimulate the liver to release glucagon during a stress response. When there is not enough insulin, insulin cell receptors on the cell membranes do not allow G to enter via transport channels, and G remains in the blood, and levels rise. Cells are starved, so liver release glucagon and BGL rise even further.

What is a normal fasting blood sugar level?

70-110, 126+ considered diabetes. 100-125=pre-diabetes

If the anion gap is high...

= metabolic acidosis, anions too high. Why? (MEGSLARD-methyline glycol (antifreeze), salicylate (later), lactic acidosis...

Hypoglycemia

Abnormally low BGL (below 70)

Retinopathy

Altered retinal blood flow Nonproliferative changes Microaneurysms Mild - Moderate - Severe - Very severe Proliferative changes Neovacularization Macular Edema Blurring Metamorphosia

Treatment for Type 2?

Always get data/finger stick!!! Some insulin given, lifestyle modification, weight loss. Nursing: • Full PV assessment: neuropathy (decreased sensitivity due to micro/macro changes in arteries!!, in feet). Cool limbs, decreased sensation, no discharge, sweating, ulcers where skin touches skin, no edema, perfectly circular pale ulcers, no drainage (PAD--peripher. vessels occluding). o Foot care • EKG: check to see if coronary arteries are getting narrower • Eye exam—retinopathy (retinas of the eye). Retinal thrombosis (acute). Unilateral or bilateral. • Fungus/skin issues: elevated blood glucose levels, WBC dont work as well, can't fight off infections, deposit pigment • If WBC low, check lungs, urinary and skin infections. o Get a U/A on pt Modest weight loss leads to improved control

Treatment for Type 1?

Always get data/finger stick!!! Treatment with insulin only, can't stimulate the pancreas (With Type II drugs). •Exogenously given •Glucose can't get into the cells Diagnose by blood sugar: oFasting glucose: 126+ oRandom blood screening level: 200+ suspicious, order a fasting blood sample oHbAIC=6.5 or below

s/s of hypoglycemia?

An addict who needs their meds! diaphoresis (sweaty), nervous, tachycardic, shaky, diaphoretic to pass out/unresponsive. No energy for the brain, will shut down. CNS changes, seizures, disoriented behaviors, lethargy. The brain relies almost entirely on glucose for energy. Since the brain cannot synthesize or store more than a few minutes supply of glucose, symptoms of cerebral function deterioration are noted with hypoglycemia. Symptoms of hypoglycemia may occur suddenly unexpectedly

What are HHNK nursing responsibilities?

Assesment: Identify underlying factors such as MI, infection, illness or extreme stress (Burns, trauma etc) or consider iatrogenic treatments such as TPN/PPN, enteral feedings or sympathomimetics for reasons that should be obvious. Name three medications that are known to elevate glucose: diuretics, steroids, diazoxide, treats low BGL) Treatment: Fluid replacement- This is a more profound dehydration, and this is the priority intervention. Hydration alone has been demonstrated to reduce glucose serum levels and improve clearance presumably by dilution effects alone so the priority is finding a vein. *Typically expect to begin with normal saline (rates of 500cc -1000cc per hour for the first two hours are not uncommon). *Expect to move to ½ normal saline at 125-500cc per hour when the blood pressure has stabilized (MAP). *When the glucose falls to 250-300mg/dL be prepared to change the solution to D5 1/2NS. *Potassium is added to IV fluids when urinary output is adequate and is guided by continuous ECG monitoring and frequent laboratory determinations of potassium. *Insulin Therapy - regular insulin IV at a rate of .1u/Kg of body wt per hour. Monitor the serial labs with the goal of reducing glucose by no more than 50-75 mg per hr. If glucose level decreased by over 100 mg/dl in the past hr, immediately decrease the drip rate by 1/4 to ½. --expect decreased insulin needs compared to DKA pts.** It is a priority to assess cardiac and respiratory status for S/S of FVE while treating the patients, close monitoring of volume and electrolyte status is important for FVE, heart failure, and cardiac dysrhythmias. Central venous or hemodynamic pressure monitoring guides fluid replacement.

What are the s/s that begin at BGL 180?

Renals start to eliminate glucose into the collecting duct, which takes H20 with it, so pt becomes polyuria, polydipsia, dehydrated.

What is DKA?

BGL are 300-600mg/dl *Type I associated.* Metabolic diabetic ketoacidosis. Insulin deficiency precipitates a ↑ in catecholamines and a ↑ in glucagon. The liver's response of gluconeogenesis further compounds this problem. The high glucose concentration causes water to be pulled from the ICF to the ECF in an attempt to decrease the blood's tonicity. The ensuing intracellular dehydration stimulates the brain's thirst center and polydipsia occurs. The renal response to the hyperglycemia is to increase excretion of glucose with resulting polyuria. Build up ketones due to lack of glucose for cells to use as energy (b/c of lack of insulin), the body begins to burn fat for energy, which produces ketone bodies. Ketones are acids that build up in the blood and appear in the urine. DKA can lead to coma and death.

What is HHNK?

BGL are 600mg/dl+ Hyperglycemic Hyperosmolar Non-ketotic coma. This is severe hyperglycemia without ketosis, predominately affects older adults with *Type 2 DM*. More multisystem diseases, have thick blood, poor pump, lactic acidosis can occur, or renal insufficiency (long standing hypertension, GFR not good, serum osm 500, renal failure and acidemia). Sometimes they ARE acidotic, but never because of ketoacids). Higher morbidity rate, blood is very thick (viscous), more likely to develop a clot. Usually occurs slow onset, and after illness or infection. Extreme dehydration! If Cr=3, acidotic; CVP=18 (poor cardiac pump). If high anion gap and HHNK/metabolic acidosis, need to find OTHER causes of acidosis (Cardiac (CO, CVP), renal (RFTs) or COPD—PC02 levels and other s/s), MEGSLARD. Mortality rate ranges from 10% to 50%, usually related to an underlying illness, the vulnerability of the elderly patient, and the severity of HHNS.

What are s/s HHNK?

Blood sugar level over 600 mg/dl (higher than with DKA) 340+ blood osm. Elevated bicarb Dry, parched mouth Extreme thirst (although this may gradually disappear) Warm, dry skin that does not sweat High fever (over 101 degrees Fahrenheit, for example) with infections, decreased with sepsis. **Sleepiness or confusion Seizures, mimic CVA, electrolyte depletion (correct for glucose levels!) *Loss of vision *Hallucinations (seeing or hearing things that are not there) *Weakness on one side of the body High serum osm (very thick blood). If HHNS continues, the severe dehydration will lead to seizures, coma and eventually death. HHNS may take days or even weeks to develop. Slow onset! (as opposed to DKA).

Dogs with DKA

Cerebral edema Hypokalemia Hypoglycemia Cardiogenic and noncardiogenic pulmonary edema Venous thrombosis Undiscovered primary problem DIC- Disseminated Intravascular Coagulation

Sick day rules and insulin

Check BG every 3-4 hours or more Check urine ketones HYDRATION 8 ounces of fluid every 1-2 hours Increased frequency of small meals Call provider for BG > 300 If unable to keep fluids down may require IV

What are some causes of HHNK?

Chronic renal disease, chronic CVD, acute illness, infection, surgery, burns, trauma, tube feedings, drugs (diuretics, steroids, proponolol, diazoxide, chlorpromazine)

Fast acting/regular insulin

Clear. Lispro, humalog, novalog. Immediate acting, within 15 min start to work, peak within 1 hr, used to cover meals.

Disseminated Intravascular Coagulation (DIC)

Complication of DKA. If see bleeding at the IV site, think they might have this. Then, get CBC, platelets, PT/PTT, fibrinogen level, **fibrin split product (means disorder if that is elevated) Decreased fibrinogen levels, decreased platelets, prolonged PT/PTT, increased split fibrinogen levels, blood oozing from wounds, ecchymosis, hypovolemic shock

Order of nursing treatment for DKA...

IV insertion, fluid, Foley, 12 lead EKG, vitals, 02, I/O

What are two side effects of hyperglycemia?

DKA, HHNK

DM is #1 cause of...

ESRD, blindness, amputations, CAD, liver failure in the US

What is polyuria?

Excessive amount of urine production, >2.5L day.

s/s Type 2 DM?

Fatigue and irritability Polyuria, polydipsia, polyphagia Weight loss Chronic infections Vision changes No symptoms at all

How do you calculate Na+ when a pt is DKA and dilutional?

For every 100mg glucose over normal level, add 1.6 to Na+ level ie: glucose=880 (6x1.6 + 128) Why? Glucose pulls water from ICS-->ECS, and so Na+ will not look elevated even though the pt is dehydrated as a result. Dilutional serum hyperglycemia. Late stage if Na+ is elevated (even more severe dehydration).

What is glucosuria?

Glucose peed out in the urine, occurs at 160-190mg/dl BGL.

What is HbAIc?

Glycated Hemaglobin: It is formed in a non-enzymatic glycation pathway by hemoglobin's exposure to plasma glucose. The more glucose, the higher the Hb1Ac. Shows the average level of blood sugar (glucose) over the previous 3 months. It shows how well you are controlling your diabetes. Normal: Less than 5.7% Pre-diabetes: 5.7% to 6.4% Diabetes: 6.5% or higher. DM goal is below 7 (glucose 154 at 7) The higher the HbA1c, the more likely: Eye disease, Heart disease, Kidney disease, Nerve damage, Stroke. Every 1% drop in A1C=decrease of 21% in DM related end point, 14% risk MI, 12% stroke, 37% microvascular disease

Nursing goals for hyperglycemia?

Goal is to control blood sugar, insulin, diet, monitoring Careful not to cause hypoglycemia

Hypoglycemic unawareness?

Hypoglycemic unawareness=This condition occurs when the normal compensatory response to low blood sugar fails to cause symptoms, thus the patient is unaware of the problem and may experience profound hypoglycemia (pts with diabetes for many years). Hypoglycemia BGL depend on the person and their baseline levels--will start to have symptoms as different levels accordingly.

Hyperkalemia treatment

K over 5. Kayexilate=works slowly, keep Na+ and lose K+. Not good for older pt with HD (do on top of everything else since takes time to work) Insulin with glucose/dextrose Diuretics (not if hypotensive) Alkalinize the cell (give bicarb) Dialyze=6-8hrs

Basal insulin

Lantus, Levemir, NPH (U500), cloudy. Basal insulin (2 hrs to start, peak 4-6 hrs)=coverage all the time.

Type 1.5 DM/LADA

Latent autoimmune diabetes of adulthood Eventually become Type 1 Testing GAD antibodies Islet cell antibodies C-peptide levels

What is a normal serum osm?

Normal 0sm=<300

Treatment DIC

Paxels and NS only!! If bleeding/hemorrhaging. If D5W in IV, flush the D5W out, hang the NS with paxels (1U) If keep giving them (more than 4U), hypocalcemia. Given in a citrate solution, and it binds to Ca++.

What are short term nursing goals for pts with diabetes?

Prevent HHNK, DKA, Infection Poor outcomes during hospitalization Keep glucose levels in check, as normal as possible (based on HbAIC, last 3 months)

Why is it important to control BGL?

Prevents hypo/hyperglycemia Controlling glucose helps to control blood pressure/ cardiovascular health. The higher the glucose, the higher the chance of micro and macrovascular issues (all else controlled)--parasite cells degrade and caps become leaky

What is DM Type 2?

Primary DM in the world, rates increasing. Either resistance to insulin or don't have enough insulin. Among patients with diabetes, findings reveal that glucagon is not suppressed and may experience an inappropriate increase, revealing inherent dysfunction of the pancreatic α-cell (which decrease glucose production in the liver when serum glucose levels are high.) Incretin secretion decreased (helps for person to feel satiated, usually rises after glucose intake, glucose homeostasis). 90-95% of DM pts. Slow onset Obesity (BMI), lifestyle, risk factors can cause Type II. Treatment with oral meds and insulin and lifetsyle change. Ketosis uncommon.

Lactic acid build up as a result of...

protein (lactic acid) and fat metabolism (ketones), kidneys can't filter it out, state of metabolic acidosis

Insulin

Serum Insulin rises minutes after eating, peaking in 3-5 minutes and returning to baseline within 2-3 hours. 50% of insulin is for basal insulin secretion. Insulin replacement therapy: Most effective! Just b/c insulin dependent, doesn't mean Type I or 2, could be either. Regular acting and short acting. If diabetic and change in mental status, always know it could be related to insulin (too much, hypoglycemic). • Check before the meal, know what it is (basal rate), know that it will jump up after meals • In hospital, giving Lispro (immediate acting, within 15 min start to work, peak within 1 hr)—to cover meals • Also need basal insulin (2 hrs to start, peak 4-6 hrs)=coverage • **If insulin is very high, need to give IV insulin, can only give regular insulin IV*** Kg weight x .2 or .3 (<>200mg/dl)=amount to give (units) • Injecting insulin: Subcutaneous Rotate sites Site prep Disposal Storage Room temperature 30 days once open IV Insulin: To minimize the effect of adsorption of insulin to the IV container or tubing, it is recommended that the nurse "coat the IV line" by flushing the tubing with the insulin solution. When using a standard IV insulin infusion of 100 U of regular human insulin in 100 mL of normal saline, a priming volume of 20 mL is sufficient to saturate the binding sites before connecting it to the patient

What is the anion gap?

The difference btwn cations and anions that we measure (in the body they should be equal). ALways give an anion with a cation! + and - (K+ with Cl-), (Na+ with HC03-), 154mEq Na+ with 154 mEq Cl-

What are HHNK pts not acidic?

There is enough insulin produced by type 2 diabetics to prevent fat catabolism but not enough to prevent hyperglycemia.

Combination of both

To have basal coverage and meal coverage. Clear before cloudy.

Complications from dropping BGL too fast/too rapid IV?

Too rapid administration of IV fluid increases the risk of cerebral edema, and while the patient clinically may present with hypovolemic shock it is essential to monitor the patient closely for avoiding cerebral edema while correcting the fluid volume deficit. Can occur 6-10hrs later, common in peds pts. Treatment: decrease the IV flow rates, watch the hypotonic solutions and expect to prepare a Mannitol infusion.

What is a normal blood sugar level after eating or random?

Under 200, 200+ suspicious, order a fasting BGL.

"Starvation in the midst of plenty."

When high BGL, DM, BGL will continue to rise even though peeing out glucose, because the cells ar starved for glucose/energy, body keeps breaking down glycogen (gluconeogenesis) for glucose, carbs, and proteins to get energy.

s/s hyperglycemia--3 P's

polyuria (peeing), polydipsia (drinking a lot, due to thirsty), polyfasia (eating, body feels starved)

Gestational Diabetes

usually during 3rd trimester high risk groups increases chances of diabetes Type 2 after pregnancy/lifelong, or with other preg. Dx: 1 hour oral glucose tolerance test Confirmed with 3 hour glucose (1st trimester test after 1st preg) tolerance Treatment: diet, insulin, exercise

What should you do as a nurse?

• Have to guess how much glucose they need, if coma, give a bolus of D50W IV, protect airway, if awake and groggy, give glucagon, if awake and can drink, OJ. • Adults get 50% glucose bolus, Neonates 10% glucose bolus, children 25% glucose bolus, must be given IV, confirm placement, slow IV push, then continuous. *Alcohol pts are deficient in thiamine, need it as well as glucose. • For training, ask how the patient felt when hypoglycemic, so they can remember for the next time (pt education)

What are long term goals?

• Prevent cardiovascular damage: check PV function, coronary artery perfusion (12 lead, EKG, stress test), renals (BUN/Cr, Cr best, BUN will be elevated due to dehydrated state/polyuria) • Watch for infections • Check penis function, measure of blood flow (unable to have an erection) • Maintain tight glycemic control—slide 46, know changes, tight HbAIC (normal less than 6.5, less than 7 good--ADA) o RBC + glucose attachment, the more free glucose there is, the more it attaches to RBCs • Exercise is important • Sick day rules: when stressed, increased blood sugar, need to take insulin, start with ½ dose then check. • Foot care: white socks, lambswool, btwn toes, podiatrist, eye glasses, big mirror *Prevention: Microvascular Nephropathy Retinopathy Neuropathy Macrovascular CAD PVD Hypoglycemic unawareness Erectile dysfunction

s/s hyperglycemia

• dehydrated, FVD, thirsty (serum osmolality increases, H20 moves from ICS-->ECS), hungry, blurred vision: as blood sugar rises, glucose coats the crystal lining of the eye, hard to see. Check blood glucose level! • Weight loss, every 500cc lost=1lb (glucose not being stored) • Usually when have type 1 diabetes, don't know, and drink sugary drinks, which also increases blood sugar levels. Blurred vision (glucose and water on lens, changed refractory period of lens)