Diabetes Mellitus

Physiology of Energy Metabolism

All body cells use glucose for energy. To maintain this constant source of energy, blood glucose levels must be kept between 3.3-6.1 mmol/L. Several hormones, help to maintain this level between 3.3-6.1mmol/L, include insulin, glucagon. The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver. The glucagon is released when blood glucose levels decreased (e.g. between meals and over the night) and stimulate the liver to release stored glucose.

Insulin

Diabetes is a disease which deals with insulin. A healthy pancreas releases 40-50 units of insulin daily, still keeping several hundred units available in storage to be released if the blood glucose levels rise. When insulin enters the bloodstream, it binds to insulin receptors on the membranes of the liver, muscle, and fat cells. In these cells, insulin encourages glucose uptake by causing a shift of another insulin sensitive glucose transporter, GLUT 4, to the surface of cells.

Pathophysiology of Diabetes Mellitus

Diabetes mellitus is not a single disease but a complex syndrome characterized by hyperglycemia resulting from altered carbohydrate, fat, and protein metabolism. This altered metabolism is secondary to insulin insufficiency, insufficient insulin activity, or both. Because of the altered fuel metabolism, diabetes is characterized by vascular and neurologic changes throughout the body. Absence of insulin or ineffective insulin activity prevents glucose from entering liver, muscle and fat cells

Pathophysiology of Diabetes Mellitus

As the blood glucose level approaches 10mmol/L, the ability of the kidney to reabsorb glucose is surpassed, and glucose is excreted into the urine. Because it is an osmotic diuretic, glucose causes the osmosis of large amounts of water and electrolytes into the tubules, causing frequent urination in large quantities (polyuria), notably at night (nocturia). Dehydration, hunger, and fatigue follow.

Classical manifestations of diabetes

Polyuria increased urination Polydispia increased thirst, which occurs as a result of excess loss of fluid associated with osmotic diuresis. Polyphagia increased appetite which results from the catabolic state induced by insulin deficiency

Types of diabetes

Type I Type II Gestational diabetes

Type I

This is characterized by the destruction of the pancreatic beta cells and early onset The destruction of the beta cells results in decreased insulin production, unchecked glucose production by the liver and fasting hyperglycemia. Glucose derived from food is not stored in the liver but remains in the blood stream and contributes to postprandial (after meals) hyperglycemia

S&S

Increased thirst Frequent urination Fatigue Excessive weight loss Nausea and vomiting Having dry, itchy skin Feeling of numbness and tingling in the feet Blurry eyesight Constant hunger Abdominal pain if DKA (Diabetic Ketoacidosis) have occurred

Type II

This the most common form of diabetes, often associated with older age, obesity, family history of diabetes e.t.c. In type 2 diabetes, the pancreas is usually producing enough insulin, but for unknown reasons the body cannot use the insulin effectively, a condition called insulin resistance. After several years, insulin production decreases. So thus glucose builds up in the blood and the body cannot make efficient use of its main source of fuel These patients are not prone to the development of DKA.

S&S

Fatigue Frequent urination Increased thirst and hunger Blurred vision

Gestational diabetes

Gestational diabetes is a type of diabetes that occurs in non-diabetic women during pregnancy. It is any degree of glucose intolerance with its onset during pregnancy or late in pregnancy. This form of diabetes usually disappears after the birth of the baby.

Risk factors of gestational diabetes

Over the age of 30 Obesity Family history of diabetes Having previously given birth to a very large child (over 9 pounds, 14 ounces), having previously given birth to a stillborn child or a child with a birth defect Having too much amniotic fluid Having gestational diabetes in a previous pregnancy Having high blood pressure

S&S

Generally, gestational diabetes may not cause any symptoms; however, the woman may experience Excessive weight gain, Excessive hunger or thirst, Excessive urination Recurrent vaginal infections

Diagnosis of diabetes
DM is indicated by typical S&S and confirmed by measurement of plasma glucose. Fasting plasma glucose (FPG): measurement after an 8-12h fast. Oral glucose tolerance testing (OGTT): 2h after ingestion of a concentrated glucose solution. OGTT is more sensitive for Dx DM and impaired tolerance but is more expansive and less convenient and reproducible than FPG. It is rarely used routinely, except for Dx of gestational DM. HbA1c : testing for glycosylated hemoglobin. HbA1c levels reflect glucose control over the preceding 2-3 months. HbA1c is not considered as reliable as FPG or OGTT testing for Dx DM and used mainly for monitoring DM control.

Diagnosis of diabetes (cont)

Diagnostic criteria for DM and impaired glucose regulation
Test CBG FPG Normal Impaired glucose regulation Diabetes

3.3-6.1mmol/L <5.6mmol/L 5.6-6.9mmol/L

>7.0mmol/L

OGTT <7.7mmol/L HbA1c 3%-6%

7.7-11.0mmol/L >11.1mmol/L >7%

HbA1c

Glucose sticks to the haemoglobin to make a glycosylated haemoglobin molecule, called haemoglobin A1c or HbA1c. The more glucose in the blood, the more haemoglobin A1c or HbA1c will be present in the blood. Red cells live 120 days before they are replaced. By measuring the HbA1C it can tell you how high your blood glucose has been on average over the last 8-12 weeks. A normal non-diabetic HbA1C is 3.5-5.5%. In diabetes about 6.5% is good. The HbA1C test is currently one of the best ways to check diabetes is under control; the HbA1C is not the same as the glucose level.

Management of Diabetes

Good Diabetes Management

Regular Blood Glucose Monitoring

Healthy Nutrition

Regular Exercise

Nutrition

There isn't one "diabetes diet." The amount of food you can eat daily depends on: Age -Body size -Activity level -Gender -Pregnancy or breastfeeding Meal plan should be individualized for each client With the help from a dietician, a diet is planned based on the recommended amount of calories, protein, carbohydrates, and fats. A meal plan is a guide that tells you what kinds of food you can choose at meals and snack time and how much to have. For most people with diabetes (and those without, too), a healthy diet consists of 40% to 60% of calories from carbohydrates, 20% from protein and 30% or less from fat.

Nutrition (cont)
1500-1800 calorie is the ideal of amount that diabetes diet should have. This should include simple and healthy foods like whole grains, vegetables, fruits, low fat meats, non-fatty dairy products and fish but avoid foods like pastries, candy bars and pies. Note: This does not include people, like pregnant women, those with eating disorder and children under 16 should seek medical advice before modifying their diet to adopt 1500-1800 calorie diabetes diet. Carbohydrates (50-55% of energy), like whole grains, fruits, vegetables, milk, high fiber foods. Proteins (15-20% of energy). Fat (<30% of energy) Example of 1500 calorie diabetes diet: 6 oz. lean meat/protein 6 servings bread/starch 4 servings fruit 5 or more servings vegetables 2 servings dairy (low fat preferred) 3 servings fat

Exercise

Exercise: Before diabetic patients engage in exercise program, they should consult with their healthcare provider because they need to have a complete history and physical examination Exercise includes anything that keeps them move Exercise (total of about 30 minutes a day, at least 5 days a week) lowers blood sugar levels by improving cell uptake of glucose, causing the body to process glucose faster.

Oral Anti-diabetic Agent

Biguanides-Metformin (Glucophage) Lowers glucose by decreasing liver glucose release and by decreasing cellular insulin resistance Alpha-Glucose Inhibitors: (Precose)-Slows digestion and absorption of carbohydrates to maintain normal blood glucose levels. Meglitinides: (Prandin)-Stimulates pancreas to secrete insulin Thiazolidinediones: (Avandia, Actos)-Increases insulin sensitivity at receptor sites on liver, muscle, and fat cells. The medication works by helping make your cells more sensitive to insulin. The insulin can then move glucose from your blood into your cells for energy.

Insulin
Type+(Trade Name) Rapid-acting (Clear) Insulin Lispro (Humalog) + Insulin Aspart (Novorapid) Short Acting/Regular Insulin (Novolin ge Toronto (R) or Humulin R) (clear) Intermediate-acting (NPH/Lente) (cloudy) Ultra Lente and Glargine (clear) Premixed: 10/90, 20/80, 30/70, 40/60, 50/50 (cloudy) Onset of Action 10-15min Peak 60-90min Duration 4-5hrs Nursing Intervention Take with meals or may be taken before or after meals

30-60

2-4hrs

5-8hrs

Take 30 min before meals

1-4hrs

4-12hrs

18-24hrs

4-8hrs

18hrs

24-38hrs

Note: Glargine can not be mixed with any other insulin

ideal time to give patients with their premixed? 30 min before their meal, with their meal and after their meal Drawing up Insulin: Clear then cloudy to avoid contaminating the clear insulin

Methods of delivery insulin

Intravenous (IV) Syringes (SC) Pens Jet injectors Insulin pumps

Site Selection: Where can I give the Injections?

4 major areas: Arms-posterior surface Abdomen-avoid 1 inch area around navel Thighs-anterior surface Hips Note:

Systematic rotation of injection sites within an anatomic area to prevent lipodystrophy. Administering each injection 0.5-1inch away from the previous injection.

Storing and Handling Insulin

Stored at room temperature (15 to 30C). If stored in a refrigerator, unopened bottles are good until the expiration date printed on the bottle. Opened bottles that are stored in a refrigerator should be used within one month of being opened. Protect your insulin (bottles, pens, and cartridges) from extremes of hot and cold. Never store your insulin in the freezer - once insulin is frozen, it loses its potency.

Diabetes Mellitus
Case Study

Patient profile
Name: J.P . Age: 68 Sex: Male Ethnicity: Algonquin Canadian Ht: 57 Wt: 276 lb (BMI 43.2, obese) Medical Hx: Type II diabetes for 5 years hypertension, A-fib hypercholesterolemia and chronic bronchitis Family Hx: Father died of CVA. Mother died of End-stage renal failure due to complications of diabetes. Social Hx: Elderly, lives alone Sedentary lifestyle Poor understanding of diabetes and non-compliance of medication

Risk factors for diabetes

Being: A member of a high-risk group (Aboriginal, Hispanic, Asian, South Asian or African descent) Overweight, or obese Having: A parent, brother or sister with diabetes Health problems e.g. renal, hepatic Given birth to a baby that weighed more than 4 kg (9 lb) Had gestational diabetes (diabetes during pregnancy) Impaired glucose tolerance or impaired fasting glucose High blood pressure High cholesterol or other fats in the blood

Assessments on arrival in ER
V/S: T: 38.5C ; HR: 145bpm; RR: 21; BP: 80/45 mmHg (lying) SaO2: 88% RA CBG: 34.0 mmmol/L Integumentary: poor skin turgor, cracked lips and very dry mucosa membrane; very dry and flaky skin on both feet and up to knees, the skin on the lower leg and feet is red and shiny in characteristics. One pea-size lesion on the side of baby toe of right foot. Mental Status: Lethargy, confused and disoriented, audio and visual hallucination poor on people, place and time. Neurology: unable to feel left side of body, sensation of right side of body present. c/o dizziness and mild generalized headache. Blurry vision. Pulmonary: respiration shallow. Lungs clear. Decreased AE to both lower lobes of lungs. Cardiovascular: rapid, thready and irregular pulse, cool extremities; peripheral pulses present and weak. GI: Abd distended and firm. No c/o pain on palpation. Decreased and faint bowel sounds . Last BM unknown.

**Doctor ordered diagnostic tests: CT scan of brain, Cardiac marks, BUN, Creatinine, Chemical Routines, Electrolytes, CBC, and UA STAT.

Selected Lab Values

Lab Tests
CBG HbA1c CT of brain CK

Lab values
34.3 mmol/L 14% No structural or anatomic abnormalities are noted 105 units/L

Normal Values (>60 years)

3.3-6.1 mmol/L 4%-7%

38-174 units/L

Troponin
Myoglobin BUN Creatinine Urinalysis (Dipstick)

0.28mcg/
74 mcg/L 25 mmol/L (H)

<0.35 mcg/L
<90 mcg/L 2.9-8.2 mmol/L 62-115 umol/L Negative Negative Negative Negative Negative 4.5-5.9 X10^12/L 14-17.5 g/dL 41.1%-50.4% 4.4-11X10^9/L 280-300 mOsm/L 136-145mEq/L 3.5-5.1 mEq/L 97-107 mEq/L 8.6-10.0mg/dL 1.5-2.3 mg/dL

170 umol/L (H) Glucose: present Bacteria: positive (dipstick) Ketones: absent Protein: Present Bacteria: >10^5/ml (positive) 6.2 X10^12/L (H) 18.8 g/dL (H) 55% (H) 15X10^9/L (H) 350 mOsm/L (H) 125 mEq/L (L) 2.9mEq/L (L) 85 mEq/L (L) 7.8mg/dL (L) 1.5 mg/dL

Urine C&S RBC Hgb Hct WBC Serium Osmolality Electrolytes: Na+ K+ CL Ca++ Mg+

Acute Complications of Diabetes Mellitus

Acute complications of diabetes

Hypoglycemia Hyperglycemia DKA Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

Hypoglycemia

Hypoglycemia can result from Skipping meals, an excess of either insulin or oral diabetes medication. CBG 2.7-3.3mmol/L Usually, hypoglycemia can be managed by consuming a sugar product or fruit juice. Most hypoglycemic reactions are mild, and people with diabetes and their families are trained to recognize them and self-administer the sugar needed to correct the situation. In the case of severe low blood sugar resulting in coma the use of glucagon and/or the assistance of a health professional may be required.

Management of Hypoglycemia

Patient should recognize s&s of hypoglycemia (sweating, shaking, weakness, hunger, nausea, irritability and confusion) and know what to do when it strikes In case of hypoglycemia, the patient should drink a glass of orange juice/regular soft drink, two packets of sugar, or 5 or 6 hard candies. If the symptoms are still present after 10-15 minutes, patient should be given again another glass of orange juice. Once the symptoms have improved, the patient should eat longer lasting carbohydrate such as bread or milk.

Management of hypoglycemia

SC or IM Glucagon or IV dextrose is administered (Unconscious Patients/Unable to Swallow)

Note: High-fat foods and high-protein foods should not be used initially to correct hypoglycemia. These food sources are metabolized too slowly to be effective as immediate treatment.

Hyperglycemia

Patient should recognize symptoms of hyperglycemia (high blood sugar): blurred vision, excess thirst, frequent urination, and nauseaetc. Hyperglycemia develops when there is too much glucose, not enough insulin or insufficient insulin activity in the blood stream.

Hyperglycemia
Gastrointestinal absorption of glucose Impaired insulin secretion

Pancreas

HYPERGLYCEMIA

Liver

Muscle

Increased basal hepatic glucose production

Decreased insulin-stimulated glucose uptake

Management of Hyperglycemia

Rehydration-if dehydrated, drink plenty of water. Oral anti-diabetic agent Insulin

Diabetic ketoacidosis (DKA)

This is a life threatening disease caused by the absence of insulin, which results in disorders in the metabolism of carbohydrates, fats, and proteins Most often occurs in type I diabetes

Sequence of events

Serum glucose level rises because most tissues cannot utilize glucose without insulin The high osmotic pressure created by excess glucose leads to osmotic diuresis Polyuria occurs The sympathetic nervous system responds to the cellular need for fuel by converting glycogen to glucose and manufacturing additional glucose As glycogen stores are depleted, the body begins to burn fat and protein for energy Fat metabolism produces acidic substances called ketone bodies which accumulate and lead to metabolic acidosis Protein metabolism results in the loss of lean muscle mass and a negative nitrogen balance.

S&S for DKA

The individual with DKA has hyperglycemia, ketonuria, and acidosis with a pH of less than 7.3 or a bicarbonate level of less than 15mmol/L Early signs of DKA are anorexia, headache and fatigue. As the condition worsens the classic signs of polyuria, polydipsia, and polyphagia occurs. If untreated, the individual becomes dehydrated, weak, lethargic with abdominal pain, nausea and vomiting, fruity breath, increased respiratory rate, tachycardia, blurred vision and hypothermia. Late signs are air hunger, coma, shock and death

Assessments

Blood glucose test (varies from 16.6 to 44.4mmol/L) Blood and urine ketone measurements Arterial blood gas analysis

Treatment

It is aimed at the correction of the three main problems:

Dehydration, Electrolyte imbalance, Metabolic acidosis.

Hyperosmolar Hyperglycemia Nonketotic Syndrome (HHNS)

Is a condition whereby hyperosmolarity and hyperglycemia predominates with alteration in sensorium. The basic defect is lack of effective insulin. The individual persistent hyperglycemia causes osmotic diuresis and glucosuria, dehydration, hypernatremia and increased osmolarity occurs. This condition occurs in the elderly with history of, or undiagnosed type 2 diabetes. In this situation there is insulin present but the level of insulin is enough to prevent fat breakdown but not enough to prevent hyperglycemia, thus there is no production of ketone bodies and no ketoacidosis.

Manifestations
Profound dehydration, poor skin tugour, tachycardia and alteration in sensorium Assessments include: - Blood glucose levels - Electrolytes - BUN - Complete blood count - Serum osmolarity - Arterial blood gas analysis - Mental status changes

Comparison of DKA & HHNS

Variables
Plasma glucose level (mmol/L) DKA DKA Moderate DKA

HHNS Mild >13.9

Severe

>13.9

>13.9

> 33.3

Arterial pH level
Serum bicarbonate level (mEq/L)
Urine or serum ketones

7.25 to 7.30

7.00 to 7.24

< 7.00

>7.3 (normal)

15-18

10-15

<10

>15 (normal)

Positive

Positive

Positive

Small or negative

Effective serum osmolality (mOsm /kg) BUN and Creatinine levels Alternative sensoria in mental obtundation

300-350 Elevated

300-350 Elevated

300-350 Elevated

>320 Elevated

Alert

Alert to drowsy

Stupor to coma

Stupor to coma

Comparison of DKA & HHNS (cont)

Characteristics
Pts most commonly affected

DKA
Type I or II, but more common in type I

HHNS
Type I or II, but more common in type II
Infection, surgery, CVA, MI

Precipitating event

Omission of insulin Physiologic stress (infection, surgery, CVA, MI)

Onset
S&S

Rapid (<24h)
-Acetone breath (a fruity odor) -Dehydration -Anorexia, nausea, vomiting, & abd pain -Blurred vision -Hypotension -Kussmauls respiration -Polydipsia, Polyuria, & Polyphagia -Weak, rapid pulse -Weakness

Slower (over several days)

-no change in breath ordor -Profound dehydration -nausea, vomiting, distended abd -Blurred vision -Hypotension -shallow respiration -lethagy, mental status changes -Tachycardia -Neurological deficits, -seizures - Insulin (play a less critical role in tx of HHNS. -Rehydration -correct electrolyte imbalance

Treatment

-Insulin -Rehydration -Correct metabolic acidosis & electrolyte imbalance

Mr. J.P. Has:

weakness, visual disturbance, Nausea and vomiting (but are much less frequent than in patients with diabetic ketoacidosis). lethargy, confusion, hemiparesis (often misdiagnosed as cerebrovascular accident)

Precipitating Factors in Hyperosmolar Hyperglycemic State

Coexisting diseases Acute MI CVA Cushing's syndrome Hyperthermia Hypothermia Pancreatitis Pulmonary embolus Renal failure Severe burns Infection Pneumonia Urinary tract infection Cellulitis Dental infections Sepsis Medications Calcium channel blockers Chemotherapeutic agents Chlorpromazine (Thorazine) Cimetidine (Tagamet) Glucocorticoids Loop diuretics Thiazide diuretics Olanzapine (Zyprexa) Phenytoin (dilantin) Propranolol (inderal) Total parenteral nutrition Non-compliance Substance abuse Alcohol Cocaine Undiagnosed diabetes

The Tx of hyperosmolar hyperglycemic state

Involves five approaches: Vigorous intravenous rehydration Electrolyte replacement Administration of insulin Diagnosis and management of precipitating and coexisting problems

Prevention, prevention and prevention

In ER

IV: N/S 1000ml @ 500 ml/hr continuous infusion. Then given Humulin R. 10U IV bolus, followed by 5U/h continuous infusion in N/S. O2 therapy 3L/min via NP. Indwelling Catheter in. Monitor I&O. Pt. on Telemetry to monitor his heart.
Two hours later

Physicians order:
Meds: IV solution changed to 1000ml N/S with 40 mEq KCL @ 250 ml/hr continuous infusion. IV solution may change to 2/3 &1/3 with 40mEq KCL @125ml/hr when CBG <10 mmol/L. Novolin 30/70 SQ 36U Qam, and 20U Qpm ac meals. S.S. insulin: Humulin R 5U SQ if CBG>15, 10U if CBG>25 Metformin 500 mg po bid with meals Cipro: 400mg q12h infused over 60 minutes. Atorvastatin (Lipitor), 10 mg od Ramipril 5mg od, Digoxin 0.125 mg po od, Coumedin 2mg po od, Furosemide 80mg po od. O2 therapy 3L/min prn ventolin i neb q4h prn T.E.D stocking (Knee high) on both legs V/S q8h if Temp V/S q4h, and CBG (30 min before B,L,S, HS) Diet: Diabetic diet and snacks Activity: AAT Diagnostic Tests: Repeat Electrolyte, CBC, BUN, Creatinine, ECG, PT, INR, and Urinalysis.

Mr. J.P. is now transferred to 4 West NBGH

Dx on admission

Hyperglycemia or HHNS (CBG>33.3mmol/L) Uncontrolled type 2 diabetes (HbA1c >7% and by medical hx) UTI

Medical Hx:

Obese (BMI 43.2 kg/m2 ) Hypercholesterolemia Peripheral diabetic neuropathy (distal and symmetrical by exam) Diabetic retinopathy (blurry vision) Hypertension (by previous chart data) A-fib (by previous chart data and ECG)

Nursing Dx:

Deficient fluid volume/risk for imbalanced fluid volume r/t diabetes complications, polyuria, vomiting Self-care management/lifestyle deficits r/t:

Limited exercise Non-compliance of medication. No SMBG program

Knowledge deficits r/t poor understanding of diabetes

Nursing Assessments @ 0400:

V/S: Temp: 38.1 C; P: 150bpm; RR: 28. BP; 170/100 mmHg; SaO2: 88% CBG: 10 mmol/L Pulmonary: Respiration shallow and rapid. Moist fine crackles present throughout all lung fields. Decreased AE to both lungs. Dyspnea on exertion. Cyanosis. Productive coughing with frothy sputum. Cardiovascular: HR 150 bpm pulse bounding and irregular. c/o chest pain. Abdominal: c/o abdominal pain and bloating. GI: Nauesa Integumentary: +1 pitting edema on both feet up to lower calf. Pallor and skin cool to touch. Genitourinary: Foley catheter in place draining <60 ml clear yellow urine for the last two hour. Mental Status: lethargy, confused, disoriented, anxious and agitated.

Nursing Interventions

J.P. was put on High-Fowlers position with legs elevated. O2 via mask @ 15L. Physician notified. IV continuous infusion D/Ced. Saline lock started on the left hand. Nitro-spray x3, five minutes apart. Digoxin 0.125mg IV push. Furosemide 80mg IV push and Morphine 1mg IV push and Gravol 50mg IM administrated as per ordered.

Education, Education, Education

Client Teaching (also involve J.P.s daughter) re: SMBG; Insulin injection, Importance of adherence to medication regime; Appropriate footwear for diabetes, foot care and eye care; Recognition, self-treatment, and prevention of hyperglycemia and hypoglycemia; Know when need to seek for medical attention; Purchase and wear the diabetes medical bracelet; Diet : meal planning with family members; Exercise Family members need to check on J.P. at least once a day

Referrals
Referral to CCAC Nursing visits 5 times per week for the first two weeks. Teaching/Reinforce SMBG and insulin injection. Home care service (groceries, prepare meals and housework) Referral to Kipawa Reserve Health Center, Diabetes Clinic Additional follow-up education on the disease of diabetes and the management of diabetes is arranged with a diabetes clinic educator in Kipawa Reserve Join diabetes support group Join BP and CBG monitoring program.

Chronic Complications of Diabetes Mellitus

Chronic Complications of DM

Diabetic Neuropathies Microvascular Disease

Retinopathy Diabetic nephropathy

CAD CVA PVD

Macrovascular Disease

Infection Lower-limb amputations

Diabetic Neuropathies

A group of diseases that affect all types of nerves: including peripheral (sensorimotor), autonomic, and spinal nerves. The most common cause of neuropathy The most common complication of diabetes The prevalence is similar for type I and type II Most commonly affects the distal portions of the nerves, especially the nerves of the lower extremities. AKA Peripheral Neuropathy.

Diabetic Neuropathies (cont)

Peripheral neuropathy Paresthesias (prickling, tingling, or hightened sensation) on feet and fingers. Burning sensations (especially at night) The feet become numb as the neuropathy progress. Decreased sensations of pain and temperature. (risk for injury and undetected foot infection) A decrease in proprioception (awareness of posture and movt of body and of position and wt. of objects in relatio to the body) A decrease sensation of light touch (may lead to unsteady gait)

Diabetic Neuropathies (cont)

Autonomic Neuropathies
Affecting almost every organ system of the body Cardiovascular : tachy HR; orthostatic hypotension; and silent, or painless myocardial ischemia and MI. GI : Delayed gastric emptying, bloating, nausea and vomiting. Diabetic constipation or diarrhea. Unexplained wide swings in blood glucose levels r/t inconsistent absorption of the glucose form ingested foods secondary to the inconsistent gastric emptying. Renal: Urinary retention, a decreased sensation of bladder fullness. Neurogenic bladder. UTI (due to neurogenic bladder, inability to completely empty the bladder (This is especially in pt. with poorly controlled diabetes, because hyperglycemia impairs resistance to infection)

Diabetic Neuropathies (cont)

Autonomic Neuropathies Hypoglycemic unawareness: due to diminished or absent adrenergic symptoms of hypoglycemia such as shakiness, sweating, nervousness, and palpations associated with hypoglycemia. (autonomic neuropathy of the adrenal medulla) Sudomotor neuropathy: a decrease or absence of sweating of the extremities. Dryness of the feet increases the risk for the development of foot ulcers. Sexual dysfunction: impotence in men. Deceased libido, vaginal infection, UTI in women.

Macrovascular Disease
Blood vessel walls thicken, atherosclerosis, and become occluded by plaque. CAD The most common cause of death in those with type II, also common in those with type I. MI (coronary artery occlusion) CHF CVA-hypertension; accelerated atherosclerosis, formation of an embolus ** S&S of CVA may be similar to symptoms of acute diabetic complications e.g. HHNS. It is important to rapidly assess the CBG so that testing and tx of CVA can be initiated if indicated. PVD: gangrene occurs. Occlusions of the small arteries and arterioles lead to the gangrene of the lower extremities results in patchy areas of the feet and toes. Amputation of foot or leg.

Microvascular Disease

Persistent exposure to hyperglycemia is an important factor in the development of diabetic microvascular complications. Microvascular changes are unique to diabetes. Microangiopathy (Diabetic microvascular disease) : Thickening of capillary basement membrane results in decreased tissue perfusion. Hypoxia and ischemia of various organs may result from microangiopathy: two areas often affected are the retina and the kidney. (persistent increased blood glucose levels are responsible for the thickening of the basement of membrane) Renal retinal syndrome: the vast majority of individuals with DM have some degree of retinopathy, and retinopathy is closely associated with diabetic nephropathy. Retinopathy Diabetic Nephropathy

Microvascular Disease

Retinopathy

Diabetic retinopathy is the leading cause of blindness in people b/w 20 and 74 years old. A change in vision (caused by the rupture of small microaneurysms in retinal vessels.) Blurred vision (macular edema) Sudden loss of vision ( retinal detachment) Cataracts ( lens opacity)

Diabetic Nephropathy

Renal disease secondary to diabetic microvascular changes in the kidney. A common complication of diabetes. About 20 % to 30% of people with type I or type II diabetes develop nephropathy. With the blood glucose levels elevated, the kidneys filtration mechanism is stressed. The earliest sign is a thickening in the glomerulus, allowing blood proteins to leak into the urine. As a result, the pressure in the blood vessels of the kidney increases. The elevated pressure stimulates the development of nephropathy.

Infections
The individual with DM is at increased risk for infection throughout the body: Diminished sense Microvascular & macrovascular complications cause decreased O2 supply to tissue. The increased content of glycosylated hemoglobin in the red blood cell impedes the release of O2 to tissues. Pathogens are able to multiply rapidly because the increased glucose in body fluids provides an excellent source of energy. Decreased blood supply resulting from vascular changes, leads to decreased supply of WBC to the affected area The function of the WBC is impaired.

Foot and Leg problems

Typical Diabetic foot ulcer

Foot and Leg problems

50%to 75% of lower extremity amputations are performed on people with diabetes. Complications of diabetes that contribute to the increased risk of foot infections:

Neuropathy: Sensory neuropathy leads to loss of pain and pressure sensation, and autonomic neuropathy leads to increased dryness and fissuring of the skin. Motor neuropathy results in muscular atrophy. PVD: Poor circulation of the lower extremities contributes to poor wound healing and the development of gangrene. Immunocompromise: Hyperglycemia impairs the ability of specialized leukocytes to destroy bacteria. Thus, in poorly controlled diabetes, there is lowered resistance to infections.

Management of hospitalized diabetic patients

10% to 20% of general med-surg patients in the hospital have diabetes. This number may increase as elderly patients make up a greater proportion of the population. Often diabetes is not the primary reason for hospitalization, yet problems with the control of diabetes frequently result from changes n the pts normal routine or from surgery or illness.

Management of hospitalized diabetic patients

Avoid hyperglycemia during hospitalization

Assess the pts usual home routine. Try to approximate as much as possible the home schedule of insulin, meals, and activities. CBG monitoring. The insulin doses must not be withheld when CBG are normal. IV antibiotics should be mixed in NS to avoid excess infusion of dextrose. Tx of hypoglycemia/hyperglycemia by following hospital protocol.

Management of hospitalized diabetic patients (cont)

Avoid hypoglycemia during hospitalization Hypoglycemia in a hospitalized pt. is usually the result of too much insulin or delays in eating. To avoid hypoglycemic reactions caused by delayed food intake, the nurse should arrange for a snack if meals are going to be delayed because of procedures, PT, or other activities.

Management of hospitalized diabetic patients (cont)

NPO For the pt who must have NPO in preparation for diagnostic or surgical procedure, the nurse must ensure that the usual insulin dosage has been changed. Even when no food is taken, glucose levels may rise as a result of hepatic glucose production, especially in pts with type I diabetes. Elimination of the insulin dose may lead to the development of DKA. ** Administering insulin to the patient with type I diabetes who is NPO is an important nursing intervention. Because DKA does not develop when insulin doses are eliminated in type II diabetes pts, skipping the insulin dose may be safe, but close monitoring is essential. Glucose testing and insulin administration should be at regular intervals usually 2-4 times per day. Pts should receive dextrose infusion to provide some calories and limit ketosis. To prevent these problems resulting from the need to withhold food, diagnostic tests and procedures and surgery should be scheduled early in the morning if possible.

Management of hospitalized diabetic patients (cont)

Hygiene Must focus attention on oral hygiene and skin care, because diabetic pts are at increased risk for periodontal disease. Keep the skin clean and dry, especially in areas of contact b/w two skin surfaces (eg, groin, axilla, and in obese women, under the breasts). For the bedridden diabetic pt, nursing care must emphasize the prevention of skin breakdown at pressure points. The heels are particularly susceptible to breakdown. Feet should be cleaned, dried, lubricated with lotion (but not b/w the toes), and inspected frequently. Teach the pt about diabetes self-management, including daily oral, skin, and foot care. Female diabetic pts should also be instructed about measures for the avoidance of vaginal infections, which occur more frequently when blood glucose levels are elevated.

Management of hospitalized diabetic patients (cont)

Diabetes and the risk of blood clots Higher risk of DVT formation than non-diabetic pts. The factors that increase the risk of DVT.

Age: >60 years Recent major surgery Poor circulation: Lack of adequate circulation in the deep veins can lead to a blood clot. Obesity: Being significantly overweight affects your circulation and your activity levels. Infections

Interventions: Anticoagulant e.g. Heparin T.E.Ds Encourage ambulation/leg exercise

References

Beers, M., Porter, R., Jones, T., Kaplan, J., & Berkwits, M. (2006). The Merck Manual of Diagnosis and therapy. Eighteenth Edition. Merck Research laboratories. Canadian Diabetes Association (nd). Diabetes Facts. Retrieved on Oct 2, 2007 from http://www.diabetes.ca/Section_About/thefacts.asp Canadian Diabetes Association (n.d). Foot care: A step toward good health. Retrieved on Oct 12, 2007 from http://www.diabetes.ca/Section_About/feet.asp Demir, I., Ermis, C., Altunbas, H.,& Balci, M. K.(2001). Serum HbA1c Levels and Exercise Capacity in Diabetic Patients. Jpn Heart J. 42 (5), 607-616. Retrieved on Oct. 12, 2007 from http://sciencelinks.jp/j-east/article/200207/000020020702A0062021.php Malarkey, L., & McMorrow M. (2005). Saunders Nursing Guide to Laboratory and Diagnostic Tests. Elsevier Saunders Mayhall, R. (n.d.) Diabetes and the risk of blood clots. Retrieved on Oct. 20, 2007 from

http://www.helium.com/tm/201996/thrombosis-blood-clots-known

McCance, K, & Huether, S.E. (2002). Pathophysiology the biologic basis for disease in adults &children. Mosby.

References

Public Health Agency of Canada (n.d). Diabetes. Retrieved on Oct. 13, 2007 from

http://www.phac-aspc.gc.ca/ccdpc-cpcmc/diabetes-diabete/english/index.html

Smeltzer, S. C. & Bare, B.G.(2004). Brunner & Suddarths textbook of Medical-Surgical Nursing. Lippincott Williams & Wilkins. Stoner, G. D. (2005) Hyperosmolar Hyperglycemic State. American Family Physician 71(9). 1723-1730. Retrieved on Oct 2/07 from http://www.aafp.org/afp/20050501/1723.pdf News Release(November 14, 2002). Health Canada launches diabetes public awareness campaign Retrieved on Oct 2/07 from http://www.hc-sc.gc.ca/ahc-asc/media/nr-

cp/2002/2002_75_e.html