NUR 3104-002 Nsg Adults & Older Adults: Acute Complications of Diabetes Mellitus

Acute Complications of Diabetes

• Hyperglycemia

• Hypoglycemia

• Diabetic Ketoacidosies (DKA)

• Hypersmolar Hyperglyciemic Syndrome (HHS)

Hyperglycemia

“Hot and Dry, Sugar HIGH”

• Decreased insulin secretion (endogenous)

• Decreased insulin sensitivity (non-response)

• Increased hepatic production

• Decreased peripheral utilixation

Excessive CHO (carb) consumption

—> Possible combination of any

Morning HYPERglycemia: Insulin Waning

Progressive rise in blood glucose from bedtime to morning.

Morning HYPERglycemia: Insulin Waning Treatment

• Increasing evening (predinner or bedtime) dose of intermediate- or long-acting insulin

• Instituting a dose of insulin before the evening meal if one is not already part of the treatment regimen.

Morning HYPERglycemia: Dawn Phenomenon

(Hint – DOWN insulin)

• Relatively normal blood glucose until early morning hours when levels begin to rise.

Dawn Phenomenon Treatment

• Changing the time of injection of evening intermediate-acting insulin from dinnertime to bedtime.

Morning HYPERglycemia: Somogyi Effect

(Hint - SO Much insulin)

• Normal or elevated blood glucose at bedtime, early morning hypoglycemia, and a subsequent increased blood glucose caused by the production of counter-regulatory hormones.

( Extremely low blood sugar in middle of night —> = Somogyi Effect)

Somogyi Effect Treatment

• Decreasing evening (predinner or bedtime) dose of intermediate-acting insulin or increasing bedtime snack.

Diabetic Ketoacidosis (DKA)

Caused by a profound deficiency of insulin

Blood Glucose > 250!

Type 1 Diabetes —> most likely to occur in

Acute/Rapid Onset

Diabetic Ketoacidosis (DKA) Characterization

• Hyperglycemia

• Dehydration

• Acidosis

Diabetic Ketoacidosis (DKA) Precipitating Factors

• Illness

• Infection

• Inadequate insulin dosage

• Undiagnosed Type 1 Diabetes

Clinical Manifestations of Ketoacidosis:

• Dehydration

  • Poor skin turgor

  • Dry mucous membranes

  • tachycardia

  • Orthostatic hypotension

• Lethargy and Weakness early

• Skin dry and loose; eyes soft and sunken

Adverse Clinical Manifestations of Ketoacidosis:

• Abdominal pain, anorexia, nausea/vomiting

• Kussmaul respirations (d/t low pCO2)

• Sweet, fruity breath odor

• Blood glucose level of ≥ 250 mg/dL

• Blood pH lower than 7.30

• Serum bicarbonate level < 16 mEq/L

• Moderate to high ketone levels in urine or serum

• Electrolytes vary according to the degree of dehydration (increased Cr, Hct, BUN)

Diabetic Ketoacidosis (DKA) Less Severe Treatments

• Less severe form may be treated on outpatient basis

Diabetic Ketoacidosis (DKA) Severe Treatments

• Hospitalize for severe fluid and electrolyte imbalance, fever, nausea/vomiting, diarrhea, altered mental state

• IV Fluid Administration (0.9 NSS) (too low BG → administer 5%-10% Dextrose)

• Continuous Regular Insulin Drip (IV) 0.1U/kg/hr

• Monitor BG, renal function, urine output, ECG, electrolytes, VS, and Lung assessment (fluid overload)

Hyperosmolar Hyperglycemic Syndrome (HHS)

A lack of sufficient insulin causes Hypersmolar Hyperglycemia;

• glucose levels (>600 mg/dL)

• ketosis is minimal or absent

Occurs with T2DM—> insulin resistance

Life-Threatening

Slower Onset (several days)

Hyperosmolar Hyperglycemic Syndrome (HHS) Precipitating Factors

• UTIs, pneumonia, sepsis

• Acute illness

• Newly diagnosed type 2 diabetes

• Impaired thirst sensation and/or inability to replace fluids

Hyperosmolar Hyperglycemic Syndrome (HHS) Systemic Effects

• Enough circulating insulin to prevent ketoacidosis

• Fewer symptoms lead to higher glucose levels (>600 mg/dL)

• More severe neurologic manifestations because of increase serum osmolality

•Ketones absent or minimal in blood and urine

Hyperosmolar Hyperglycemic Syndrome (HHS) Adverse Effects

• Seizure

• Shocks

• Coma

• Death

Hyperosmolar Hyperglycemic Syndrome (HHS) Treatment

• Therapy similar to treatment DKA

• Fluid replacement: NaCl infusions

• Insulin as needed

• Monitor serum potassium and replace as needed

•Correct underlying precipitating cause

Hypoglycemia:

“COLD and Clammy, needs some candy”

Low Blood Sugar

< 70mg/dl in Adults

Hypoglycemia: Diabetic Causes

• Too much insulin

• Too much diabetes medication

Hypoglycemia: Non- Diabetic Causes

• Eating less/Exercising More

• Medications

• Alcohol

• Reactive

Hypoglycemia: 15-15 Rule

Test Blood Glucose

Eat/Drink 15grams of Fast Acting Carbs

Wait 15 minutes —> Test Again

15g Simple Carbs:

Fruit juice or regular soda, 4 to 6 oz

3-4 glucose tablets

1 tablespoon of sugar

8 oz milk

1 tablespoon honey

Hypoglycemia Symptoms

S/S of Hypoglycemia

• Hunger

• Fatigue

• Shaking

• Sweating

• Pale Skin

• Headaches

• Dizziness

Hypoglycemia Symptoms Severe Symptoms

Severe S/S of Hypoglycemia

• Slurred Speech

• Blurred Vision

• Fainting

• Seizures

• Coma

Hypoglycemia Treatment:

Glucagon Injection

• Inject at 90* angle into THIGH or BUTTOCK

• Glucagon stimulates RELEASE of sugar

Angiopathy

Damage to blood vessels secondary to chronic hyperglycemia

• Leading cause of diabetes-related death

• Macrovascular and microvascular

•Tight glucose levels can prevent or minimize complications

Macrovascular Angiopathy

Diseases of large and medium-sized blood vessels

• Greater frequency and earlier onset in patients with diabetes

• Cerebrovascular disease

• Cardiovascular disease

• Peripheral vascular disease

Microvascular Angiopathy

Thickening of vessel membranes in capillaries and arterioles

• Specific to diabetes and includes

• Retinopathy

• Nephropathy

• Dermopathy

Usually appear 10 to 20 years after diagnosis

Diabetic Retinopathy

Microvascular damage to retina

• Most common cause of new cases of adult blindness

Diabetic Retinopathy Treatment

Laser photocoagulation

• Most common

• Laser destroys ischemic areas of retina

Vitrectomy

• Aspiration of blood, membrane, and fibers inside the eye

Drugs to block action of vascular endothelial growth factor (VEGF)

Diabetic Nephropathy

Damage to small blood vessels that supply the glomeruli of the kidney

• Leading cause of end-stage renal disease

Risk factors:

• Hypertension

• Genetics

• Smoking

• Chronic hyperglycemia

Diabetic Nephropathy Treatment

• Annual screening

• If albuminuria present, drugs to delay progression:

• ACE inhibitors

• Angiotensin II receptor antagonists

• Control of hypertension and blood glucose levels in a healthy range: imperative

Diabetic Neuropathy:

Nerve damage due to metabolic derangements of diabetes

• 60% to 70% of patients with diabetes have some degree of neuropathy

• Reduced nerve conduction and demyelination

• Sensory or autonomic

Diabetic Neuropathy: Distal symmetric polyneuropathy

• Most common form

• Affects hands and/or feet bilaterally

• Loss of sensation, abnormal sensations, pain, and paresthesia

Diabetic Neuropathy Treatment

Managing blood glucose levels

Drug therapy

• Topical creams

• Tricyclic antidepressants

• Selective serotonin and norepinephrine reuptake inhibitors

• Antiseizure medications

Diabetic Ulcers: Risk Factors

• Previous amputation

• Past foot ulcer history

• Peripheral neuropathy

• Foot deformity

• Peripheral vascular disease

• Visual impairment

• Diabetic nephropathy (especially patients on dialysis)

• Poor glycemic control

• Cigarette smoking