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Acute Complications of Diabetes Mellitus

Review insulin/Glucose Utilization


o Insulin moves glucose into cell
o If insulin not present cells deprived of glucose which is needed for
energy
o Without insulin, glucose levels in the blood begins to rise
o As cells are deprived of glucose, the liver produces glucagon
o Glucagon increases BG by breaking down stored glucose in the liver
(glycogenolysis)
o Eventually, non carbs (fats & proteins) are converted to glucose
(gluconeogenesis)

The Polys
Polyuria: excessive urination (with glycosuria)
Polydipsia: excessive thirst (from dehydration and hyperglycemia)
Polyphagia: excessive hunger (from using non-CHO sources for energy)
Ketoacidosis
Without insulin, fat is used for energy (gluconeogenesis)
Ketones result from breakdown of fatty acids
3 specific ketone bodies are produced
o Acetone (fruity breath)
o B hydroxybutyrate
o Acetoacetate
Ketones & Acid Base Balance
As ketones breakdown produce H+ ionsdrop in pH
Serum bicarbonate decreases in attempt to maintain pH
Result is severe metabolic acidosis
Ketoacidosis
As bicarbs decrease, breathing becomes deep and rapid (Kussmaul respirations) to
release acid in form of CO2
Acetone: doesnt cause acidosis (eliminated in lungs fruity breath)
Ketones eliminated in urine:ketonuria
Ketones in blood: ketoneumia
Two major complications
DKA: Diabetic Ketoacidosis (Type 1 DM)
HHNS: Hyperglycemic hyperosmolar state (Type 2 DM)

o Also called HHNKS: Hyperglycemic, hyperosmolar non-ketotic syndrome


Similarities:
o Both most often caused by infection/stress
o Both have elevated blood glucose
o Both present with dehydration, polyuria, polydipsia, and electrolyte loss
o Both have altered mental status
Differences
DKA
HHNS
BG >300 (300-800)
BG >600 (600-2000)
Serum & urine ketones
No ketones
Fruity acetone breath
No fruity breath
Acidosis (pH <7.30)
No acidosis
Kussmaul respirations
No Kussmaul respirations
Bicarbonate <15
Bicarb >20
Treatment
1. Rapid rehydration
o fluid deficit
as much as 6 L in DKA or 7-10 L (HHNS)
1 L NS fluid bolus
Further replacement depends on DKA or HHNS
With HHNS may give 10 L in 10 hrs
As BG approaches 200-250 mg/dl
Change IV fluid to D5.45 NaCl at approx 250-500 ml/hr
2. Gentle insulin administration IV
o Initial insulin bolus (regular insulin)
o Continuous IV infusion approx. 7-10 U/hr
o Goal is to decrease BF 50-70 mg/dl each hour. Once BG approx. 200
mg/dl change rate 3-6 U/hr
o Too fast BG correction cerebral edema
3. Monitor/restore electrolyte loss
o Restore electrolyte balance
K+ shifts with acidosis
As H+ (from ketones) more H= moves into cell from
vascular space
As H+ moves into cell K+ moves out (to maintain ion
balance) serum K+ increases
Also, insulin is needed to move K+ into the cell
Without insulin, K+ remains outside of cell
Net result: RELATIVE hyperkalemia
What does this mean?
Ex. Patient with type I DM presents with BG 350 mg/dl, pH
7/20, HCO3 15 and K+ 3.9 mEq

Some protocols: Need K+ > 3.5 before giving initial insulin


bolus
Why? Usually pH corrects itself with adequate hydration
and insulin replacement

o Hyponatremia
Na loses from:
Osmotic diuresis
Vomitting/diarrhea
Correct with infusion of 0.9 NaCl
- need to do all three of these simultanenously

Nursing Care
Monitor!
o Response to therapy
Fluid volume status: hourly urine output
Insulin levels: monitor BG hourly
Electrolytes (Na & K)monitor hourly
Mental status & LOCsudden complaints of HA may signal
cerebral edema. Hyponatremia may cause mental status changes
Cardiac statuscontinous EKG monitoring because of K probs
Patient and Family Education
o Listen: to gain insight into possible cause of hyperglycemic episode
o Possible issues: cost/availability of meds, not able to recognize stress/
infection, drug holiday, knowledge deficit, apathy or memory probs
(older adults)
Diabetes oral meds all rely on the insulin the body makes (so they will not be useful in
patients with type 1 diabetes. Most of these meds can be used in combo with each
other and with insulin
Oral medications

Medications

Action

Advantages

Possible side effects

Meglitinides

Stimulate the release

Work quickly

Severely low blood sugar

Repaglinide

of insulin

(hypoglycemia); weight gain;

(Prandin)

nausea; back pain; headache

Nateglinide (Starlix)
Sulfonylureas

Glipizide (Glucotrol)

Glimepiride
(Amaryl)

Stimulate the release


of insulin

Work quickly

Hypoglycemia; weight gain;


nausea; skin rash

Glyburide (DiaBeta,
Glynase)

Dipeptidy peptidase-4

Stimulate the release

(DPP-4) inhibitors

of insulin; inhibit the

infection; sore throat;

Saxagliptin

release of glucose

headache; inflammation of

(Onglyza)

from the liver

the pancreas (sitagliptin)

Sitagliptin (Januvia)

Linagliptin

Don't cause weight gain

Upper respiratory tract

(Tradjenta)
Biguanides

Inhibit the release of

May promote modest

Nausea; diarrhea; rarely, the

Metformin

glucose from the

weight loss and modest

harmful buildup of lactic

(Fortamet,

liver; improve

decline in low-density

acid (lactic acidosis)

Glucophage, others)

sensitivity to insulin

lipoprotein (LDL), or
"bad," cholesterol

Thiazolidinediones

Improve sensitivity to

May slightly increase

Heart failure; heart attack;

Rosiglitazone

insulin; inhibit the

high-density lipoprotein

stroke; liver disease

(Avandia)

release of glucose

(HDL), or "good,"

Pioglitazone (Actos)

from the liver

cholesterol

Alpha-glucosidase

Slow the breakdown

Don't cause weight gain

Stomach pain; gas; diarrhea

inhibitors

of starches and some

Acarbose (Precose)

Miglitol (Glyset)

sugars

Injectable medications

Medications

Action

Advantages

Possible side effects

Amylin mimetics

Stimulate the release

May suppress hunger;

Hypoglycemia; nausea or

Pramlintide

of insulin; used with

may promote modest

vomiting; headache; redness

(Symlin)

insulin injections

weight loss

and irritation at injection

site
Incretin mimetics

Stimulate the release

May suppress hunger;

Nausea or vomiting;

Exenatide (Byetta)

of insulin; used with

may promote modest

headache; dizziness; kidney

Liraglutide (Victoza)

metformin and

weight loss

damage or failure

sulfonylurea

monitor lipid levels for avandiamust be cautious if pt has past history of


heart failure
alpha inhibitors- believed to help with weight loss, when person ingests a lot
of starches really helps in the breakdown

Drugs for Diabetes Mellitus


What is diabetes? Basically, a lack of insulin or ineffective use of insulin causing
sugar to build up in the blood.

Functions of Insulin:
Allows glucose into cells
Allows glucose to enter liver
Prevents fat breakdown
Stores excess calories as fat
Who gets diabetes?
Type I Diabetes
No insulin, must be given by injection, prefer use of SQ insulin pump
Ketone prone
Autoimmune disease
Type II Diabetes
Insulin resistance
Deficient insulin secretion
Obesity contributes significantly,
resistance

losing

weight

decreases

insulin

Blood sugar control = 70-140 mg/dl. The ADA recommends keeping blood sugar
as close to 110 as possible.
Hemoglobin A1C expressed as a %, reflects the average blood glucose over the
past 3 months.
ADA now recommends that A1C be used to diagnose type 2 and screen for
prediabetes. Normal Hemoglobin A1C =5%.5.7-6.4 pre-diabetic. < 7.0 is the
target for a diabetic..
A1c (%)
6
7
8
9
10

Complications of diabetes mellitus (DM):


Stroke
ESRD (end stage renal failure)
Heart disease
Diabetic Retinopathy, neuropathy
Foot/leg amputation

Blood glucose
(mg/dL)
126
154
183
212
240

Oral Agents for Diabetes


Sulfonylureas-increase insulin secretion
mechanism of action-improves insulin production from functioning beta cells
not a good agent to be used alone; hypoglycemia reaction
*Glyburide(micronase)
should be taken with meals
*Glipizide (glucotrol)
should be taken before meals
end up gaining weight
Biguanides-decrease hepatic glucose production, will not cause hypoglycemia
mechanism of action-while in a fasting state, will diminish overproduction of
glucose from the liver.
-only comes in certain dose ratios
*Metformin(glucophage, glucophage XR)-lactic acidosis serious side effect
Contraindicated with contrast dye - Must HOLD if IV contrast dye given. In order
to use dye must be greater than 1.5

Thiazolidinediones TZDs glitazonesmechanism of action-decreases insulin resistance at the cell level. May cause
fluid retention, use caution with history of CHF.
*rosiglitazone(avandia)-liver function tests required!
pioglitazone(Actos)
BLACK BOX WARNING for Avandia increased risk of heart disease and
stroke. May cause fluid retention/edema, therefore contraindicated in pts. with
CHF.
September, 2010 FDA advised people to stop taking unless they were not able
to lower blood sugar with any other treatment.
In Europe, the FDA equivalent has stopped the use of this drug. (European
Medicines Agency)
Evidence- based Recommendation: TZDs ( avandia and actos) are NOT firstline options. Metformin is first line recommendation.

Combination Drugs
*Glucovance-Glyburide/metformin-sulfonylurea + biguanide
*Avandamet-rosiglitazone/metformin TZD + biguanide

Types of Insulin

Short or Rapid Acting


Lispro (Humalog)- onset 15, peaks 30-1.5hrs.
Aspart (Novolog)-onset 10, peaks 1-3 hrs.
Regular (Humulin R, Novolin R, Regular Iletin II)-onset 30-1 hr, peaks 2-4
hrs.
Intermediate- NPH, Lente
Long Acting-Glargine (Lantus)- peakless, duration 24 hrs.
Combo MixturesInsulin Pumps -3X as many diabetics are now using insulin pumps. Type 1
&2.
Pumps use rapid acting insulinLispro (Humalog), Aspart (Novolog). 50%
delivered at a continuous basal rate, the remaining ia given as a BOLUS at
meals or snacks. Pumps are not for everyone. They are ore expensive and
require more training.
Medicare and most insurers do cover pumps.
Euglycemic protocol- sliding scale insulin used for non-diabetic and diabetic
patients.
Protocol extended beyond the diabetic population
If patients show very high blood sugars after surgery; due to stress
of surgery; used to help them recover quickly
Hypoglycemia recognize signs/symptoms. Including: headache, confusion,
blurred vision, fatigue, hunger, irritability, shakiness
Causes- too much insulin, skipping meals, not eating food,
Treat if blood glucose is < 60 mg/dl. 15 grams of a simple CHO (6 ounces of
juice or fruit juice; regular soda). If not able t o swallow safely1 mg. glucagon
IM or 25 gms. 50% dextrose IV.
-recheck in 15 minutes
-If patient is not responding well and cannot swallowgive IM glucagon; the
patients families are given
Hyperglycemia As blood glucose increases, the blood (intravascular space)
becomes more hyperosmolar

Cellular dehydration occurs as the hyperosmolar intravascular


space draws fluid from the more dilute intracellular and interstitial
spaces
Recognize signs and symptoms:
o Polyuria, polydyspia, unexplained weight loss, sore that is
slow to heal (or doesnt heal)
If doesnt get treated, very high blood sugars can cause disruption
in fluid and electrolyte; causing them to become comatpossibly
have a seizure

Insulin Aspart
Adult, adolescents, child
Intermittent SQ or continuous SQ
Rapid Acting
Onset 10-20 mins
Duration 3-5 hours
2-4 inj daily just prior to meal
Intermittent SQ 50-70% of total daily insulin may be given Aspart; remainder should
be intermediate of long acting insulin
Continuous: external insulin pump via continuous SQ infusion insulin dose should be
based on previous regimen
Insulin Lispro
Adult, adolescence, child
SQ 15 min before meals
Continuous SQ infusion (external insulin pump)
With infusion total daily dose should be based on previous regimen
50% given at meal related boluses remainder in basal infusion
Rapid acting
Onset 15-30 mins
Peak 30 mins to 1.5 hours
Duration 3-5 hours
Insulin Glargine
Adult and child
SQ 10 international units/day
Range 2-10 international units/day
Long acting
Onset 1.5 hours
No peak
Duration >24 hours
Regular Insulin

Adult
IV 5-10 units/hr until desired response then switch to SQ
SQ 30 mins before meal
Short acting
Onset 30 mins
Peak 2.5-5 hours
Duration 7 hours
Whenregular insulin is administered IV monitor glucose, K+, often to prevent fatal
hypoglycemia, and hypokalemia

Side Effects: blurred vision, dry mouth, flushing, rash, swelling, redness, peripheral
edema, hypoglycemia, anaphylaxis
Interactions:
alcohol, beta blockers, anabolic steroids, MAOIs increase hypoglycemia
Thiazides, thyroid hormones, oral contraceptives, epinephrine DECREASE
hypoglycemia
Decrease K+ and Ca+ lab values
Nursing Considerations
Assess urine ketones during illness; insulin requirement may increase during stress,
illness, and surgery
Assess hypoglycemic reaction that can occur during peak time (sweating, weakness,
dizziness, chills, confusion, headache, nausea, rapid weak pulse, fatigue, tachy
Assess hyperglycemia, acetone breath, polyuria, fatigue, polydipsia, flushed, dry
skin, lethargy

Arterial Blood Gases


pH 7.35-7.45
PaCO2 35-45 mmHg
HCO3 22-26 mEq/L
PaO2 80-100 mm/Hg
O2 sat >95-100%
If pH normal - fully compensated
If pH abnormal, but both systems moving in diff directions partial compensated
CO2 respiratory
HCO3 metabolic
ROMES (Respiratory opposite, metabolic equal)

pH

o A measurement of the acidity or alkalinity in the blood


o Inversely proportional to the number of hydrogen ions (H+) in the
blood
o The more H+ present, the lower the pH will be; the fewer the H+ the
higher the pH
Acidic state (below 7.35)
o Changes in body function in this state
Decrease in force of cardiac contractions
Decrease in vascular response to catecholamines
Diminished response to the effects and actions of certain
medications
Alkalotic state (above 7.45)
o Changes in body function in this state
Interferes with tissue oxygenation and normal neurological
and muscular functioning
pH above 7.8 or below 6.8
o will interfere with cellular functioning and if uncorrected will lead to
death
Normal pH is maintained using delicate buffer mechanisms between the
respiratory and renal systems
o Respiratory Buffer Response
o Renal Buffer Response
Blood pH decreases, the kidnets will compensate by retaining
HCO3 Rises, kidneys excrete HCO3- through the urine

Blood gases
I.

Physiological controls
A. Chemical buffer systems in ICF and ECF
1.
Bicarbonate-carbonic acid
a.
Ratio of bicarb to carbonic acid is 20:1
b.
Responsible for 45% of all H+ buffering
2.
Inorganic phosphates
3.
Plasma proteins
4.
Intracellular buffers - proteins, organic & inorganic phosphates
5.
RBC buffers - hemoglobin
B.
Respiratory - removal of CO2
1.
PaCO2 is an acid, serum CO2 is a base
2.
Rise in PaCO2 is powerful stimulus for increased respirations tidal volume & rate
3.
Consistent PaCO2 > 50 mm Hg desensitizes the respiratory center
4.
Compensation
a.
metabolic acidosis - increased respirations
b.
metabolic alkalosis - decreased respirations
c.
respiratory compensation has limits

C.

II.

III.

Renal regulation
1.
Bicarbonate is reabsorbed from kidney tubules. Kidney
manufactures bicarbonate
2.
Hydrogen ion - excreted during acidosis and retained during
alkalosis
3.
Kidneys can compensate for respiratory imbalances over a period
of days
Tests to measure acid-base
A. Anion gap Na+ - (CL- + HCO2) = 12 -15 mEq/L
1.
Determines if metabolic acidosis is from excessive acid or loss of
bicarbonate
B.
pH - reflects H+ concentration
C.
Total serum CO2 - indirect measure of bicarbonate
1.
Increased in metabolic acidosis
2.
Decreased in metabolic alkalosis
3.
Total CO2 is 95% HCO3 and 5% CO2 gas and H2CO3
D. Blood gases
1.
Normal values
a.
pH 7.35-7.45 (usually fatal if < 6.8 or > 7.6)
b.
PaCO2 35-45 mm Hg
c.
PaO2 80-100 mm Hg
d.
HCO3 22-26 mEq/L
e.
O2 saturation (SaO2) 95-100% - Oxyhemoglobin
dissociation curve
f.
Base excess/deficit -2 to +2 mEq/L
g.
O2 content - 15-23 vol% - measurement of total O2 in
blood, including that bound to Hgb and free dissolved in
plasma)
2.
Pediatric procedures
a.
Transcutaneous pO2 monitoring - 50-100 mm Hg
i.
special heated electrode placed on head, chest or
thigh
ii. warmth causes O2 to diffuse out of capillaries
iii. electrode measures O2 at skin surface
iv.
proportional to capillary O2
b.
Fetal scalp vein pH 7.25-7.40
i.
Helps determine if cesarean section is needed
How to analyze ABGs
A. Determine if acidosis or alkalosis by looking at pH
B.
Determine the primary disturbance
1.
Look at the HCO3 and CO2 - which one goes in the same direction
as the pH? If the CO2 is in the same direction, it is respiratory; if
the HCO3 is in the same direction, it is metabolic.
a.
CO2 > 40 = acidosis
b.
CO2 < 40 = alkalosis
c.
HCO3 > 24 = alkalosis

C.

d.
HCO3 < 24 = acidosis
e.
May have a combined cause
Compensation
1.
Look at the value that is not the same as primary cause. If it is
going in the opposite direction (alkalosis or acidosis) as the
primary problem, then compensation is occurring. Compensation
may be partial or complete. Renal can completely compensate for
respiratory.