Republic of the Philippines

University of Northern Philippines

Tamag, Vigan City

College of Nursing

A Case Study on Non-Insulin Dependent Diabetes Mellitus

In partial fulfilment

Of the requirements

Of the course

Nursing Care Management:

Curative and Rehabilitative Nursing Care

Related learning Experience

Hospital Duty

Presented to:

Madeline C. Villanueva, R.N.

Clinical Instructor

Presented by:

Kimberly Ruth Ramos

BSN-III Bromeliads

JANUARY 2012

TABLE OF CONTENTS PAGE FRONTPAGE TABLE OF CONTENTS i ii

I. II.

INTRODUCTION AND OBJECTIVES PATIENTS PERSONAL DATA (NURSING HISTORY OF PAST AND PRESENT ILLNESS)

III. IV. V. VI.

PEA/RSON ASSESSMENT DIAGNOSTIC PROCEDURE ANATOMY AND PHYSIOLOGY PATHOPHYSIOLOGY A. ALGORITHM B. EXPLANATION

VII.

MANAGEMENT A. MEDICAL-SURGICAL B. NURSING CARE PLAN C. PROMOTIVE AND PREVENTIVE

VIII. IX. X. XI. XII.

DRUG STUDY DISCHARGE PLAN UPDATES ORGANIZATION BIBLIOGRAPHY

I. INTRODUCTION AND OBJECTIVES

According to Department of Health as derived from its book, Public Health Nursing, Diabetes is one of the leading causes of disability in persons older than 45 years old. In this statement, it is evident that Type 2 diabetes mellitus is more common than its counterpart. Diabetes mellitus is a metabolic disorder characterized by hyperglycemia in more than one blood sugar measurement at different visits. It is a disorder in which the primary problem is uncontrolled blood sugar level secondary to impaired insulin production or insulin resistance, thus, classifying diabetes mellitus into Type 1 and Type 2 DM, formerly Insulin-Dependent (IDDM) and NonInsulin Dependent diabetes mellitus (NIDDM) respectively. The latter nomenclature is no longer used today to avoid confusion because the former name signifies literally the treatment not the cause. This has led to confusion because type 2 DM also adds insulin in its pharmacologic therapy. This disorder is a major health threat since it causes macrovascular problems (CAD, CVA, PVD, etc.), microvascular problems (retinopathy and nephropathy) and neuropathy or the loss of sensation. These complications basically resulted from poor circulation s/t increased blood coagulation. Meanwhile, in type 1 DM, the beta cells of the pancreas are destroyed by autoimmunity thus there is little or no insulin production at all. On the other hand, in type 2 DM, the pancreas produces enough insulin but the body has resistance to its effects secondary to increased fat deposits. Thats why obesity is the most common cause of type 2 DM. In line with this, this case study focuses on Type 2 Diabetes Mellitus. It commonly occurs after the age of 30 thus, calling it as adult-onset DM. It is assumed by many as mild because of its slow and gradual occurrence of signs and symptoms and its degree of treatment, but the complications are as dangerous as type 1 DM. Its like transforming your disease into a riskier type if left unguarded and untreated. Persons at risks are the following:
obese

has familial history has previous gestational diabetes The hallmark of type 2 DM is fasting hyperglycemia (high levels of blood sugar even without eating) characterized by the 3 Ps (Polyuria, Polydypsia and Polyphagia), blurred vision, drowsiness, fatigue, glucosuria, UTI and poor healing wound. Its major complication is Hyperglycemic Hyperosmotic Non-Ketotic Syndrome (HHNK). It is non-ketotic because the body still produce insulin thus glucose is still utilize though 4

not all. However, type 2 DM can complicate into type 1 if the pancreas cannot accommodate the insulin needs of the body. The tendency is when the body creates resistance to insulin, it also tries to compensate by increasing the release of the hormone. If more glucose is absorbed in the intestine and produced by the liver, the pancreas tends to wear out. Type 2 DM is reversible as long as diet is modified and exercise is incorporated in the daily lifestyle because the main problem here is insulin resistance. Fat deposits cause insulin resistance and fat comes from dietary intake. However, it really takes time. This study was under the consent of the said patient, thus all of the data used in this study are under legal circumstances. The data were gathered through an assessment conducted on the dates of duty at the said hospital. Nursing interventions were also rendered limitedly within the shift.
This case study was organized having the following objectives:

II.

PATIENTS PERSONAL DATA NAME: Maxima Fenol Quiba GENDER: Female CIVIL STATUS: Widowed AGE: 90y/o ADDRESS: Anonang Mayor, Caoayan, Ilocos Sur DATE OF BIRTH: Setember 22, 1921 NATIONALITY: Filipino RELIGION: Roman Catholic OCCUPATION: Unemployed ADMITTED AT: Ilocos Sur Medical Mission Group and Hospital ATTENDING PHYSICIAN: Dr. Manuel Cajigal DATE AND TIME OF ADMISSION: November 21, 2011 @ 9:30 AM

To expand knowledge regarding NIDDM. To gather appropriate and sufficient data to trace the history of the present illness. Describe the symptoms of type 2 diabetes mellitus. State the criteria for diagnosis of diabetes mellitus. State the management goals for a patient with diabetes mellitus. List the target goals for blood glucose, blood pressure and lipids. Discuss the role of medical nutrition therapy and the benefit of increased activity. List the types of oral medications for type 2 diabetes and their mechanisms of action. Describe the short-term and long-term complications of diabetes mellitus. Discuss the role of diabetes self-management education in assisting patients with type 2 diabetes to make the necessary behavioural changes to manage their disease. Describe the routine primary care follow-up for a patient with type 2 diabetes. To be aware of the new advances, researches, studies and updates regarding the condition. To evaluate effectiveness of the treatment regime

DATE AND TIME OF DISHARGE: November 27, 2011 @ 12:00 NOON CHIEF COMPLAINT: Body Weakness ADMITTING DIAGNOSIS: DM Type 2, Diaper rash FINAL DIAGNOSIS: Type 2 DM

HISTORY OF PAST ILLNESS: According to the patient, her common illness was cough and colds. No home treatment was provided. It will just subside if time comes as she said. She couldnt remember her immunizations. Her family has histories of hypertension and diabetes. According to her laboratory results, she has dyslipidemia, and often experiences positional vertigo but manages it with prescribed medications. She has non-healing diaper rashes on her perineal area since January 2011 and recurrent body weakness that had brought her to seek medical attention.

HISTORY OF PRESENT ILLNESS: Prior to admission, she complains of body weakness for 2 days. She had difficulties of sleeping at night, and complains of irritating pain on her perineal area due to rashes. On admission, her vital signs were as follows: BP: 120/70, T: 36.5, RR: 24cpm, and PR: 72 bpm. PLRS 1L plus BComplex was infused to her as ordered, and instructed to have complete bed rest. Laboratory tests were ordered: HGT result reflected initially as 129 mg/dl, and Glimeperide 1mg 1 tab OD before breakfast was ordered. Antibiotics were also ordered ANST, as well as multivitamins and prescribed diet.

III.

PEA/RSON ASSESSMENT

P (personal) (psychosocial) (psychosexual) (physical) E

A/R

1ST DAY (November 27, 2011) hospitable and talkative at times conscious and coherent appears weak and sleepy with noted non-healing diaper rash on perineal area noted presence of redness and swelling on perineal area complaints of tolerable pain upon initial contact has (-) bowel movement on Bisacodyl suppository OD after breakfast as ordered voided twice, yellowish and aromatic odor as claimed, during the 8-hour shift no IFC inserted lies in bed most of the time goes to comfort room with assistance, ambulatory cannot sleep well as complained the bed has no side rails the ward is not that congested wears clean clothes that fit her size wears slippers upon ambulation has initial respiratory rate of 20 cpm, shallow and regular no dyspnea observed initial BP = 120/70 mmHg the ward is not well ventilated with poor skin turgor afebrile with an initial temperature of 36.9 C received on bed with PLRS 1L plus BComplex @ 20-22 gtts/min on diabetic diet with fair appetite with no sweet beverages nor food were seen in the bedside table

2nd DAY (November 28, 2011) conscious and coherent appears weak and sleepy still with noted non-healing diaper rash on perineal area still with redness and swelling on perineal area still with bearable pain initially

has (+) bowel movement voided twice with same characteristics

lies in bed most of the time goes to comfort room with assistance, ambulatory cannot sleep well as complained the bed has no side rails the ward is not that congested wears clean clothes that fit her size wears slippers upon ambulation initial RR = 20 mmHg initial BP = 130/80 mmHg ward is still poorly ventilated still with poor skin turgor afebrile initially

same assessment as yesterday

IV.

DIAGNOSTIC PROCEDURE

IDEAL EXAMINATION

A. Urine Glucose Testing

urine is checked for the presence of glucose

due to the excessive amount of blood sugar, the kidney is not able to filter all the glucose thus glucosuria is present in a diabetic pt. not an accurate tool because the result does not reflect the exact amount of glucose in the blood. PROCEDURE:

a. Apply urine over the surface of the reagent strip. b. Wait till color changes. c. Match the color with the standard color chart.
B. Blood Glucose level Measurement

1. Random Human Glucose Test

uses a glucometer blood can be drawn at any time throughout the day, regardless of when the person last ate.

PROCEDURE: a. b. c. d. Ask patient what finger he wishes to use. Finger must be intact. Massage fingertip in an upward motion. Wipe the lateral side of the fingertip with an alcohol-wet cotton ball. While waiting for skin to dry, insert the testing strip into the glucometer. Make sure the codes are matched. e. Inform patient when you are about to prick because it causes a little sudden pain. f. g. h. i. j. Wipe the first drop of blood with a dry cotton ball. Massage fingertip upward till a drop of blood is seen. Gently touch the tip of the strip on the blood. Small amount may do. Wait for the glucometer to process the blood. Read the measurement.

CRITERIA:

80-120 mg/Dl = Normal > 120 mg/dL = (+) DM in more than 1 reading at different days of
visits. 2. Fasting Blood Sugar can also be done after meals. PROCEDURE:

a. have pt not eat 8 to 12 hours (usually overnight). Water is allowed as

long as it is not mineralized. b. Blood sample is taken from a vein or fingertip.

CRITERIA: 109 mg/dL = Normal

110 - 125 mg/dL = (+) Impaired Glucose Tolerance (IGT) 126 mg/dL if fasting = (+)DM
200 mg/dL if after meals = (+) DM usually repeated on another day to confirm diagnosis.

3.

Oral Glucose Test

the most sensitive test for diagnosing diabetes.

not routinely recommended because it is inconvenient compared to a fasting blood glucose test.

PROCEDURE:
a. b. c. Perform FBS Test. Obtain FBS measurement. Have patient drink 75 g of liquid glucose solution (which

tastes very sweet, and is usually cola or orange-flavoured). d. CRITERIA: 150 mg/dl after 2 hours = normal > 150 mg/dl = DM in more than 1 reading at different days of visits C. Complete Blood Count done to assess the general status of the bone marrow cells to determine the degree of infection since the patient has non-healing wound. PROCEDURE: 2 hours later, a second blood glucose level is measured.

a. Blood is drawn either from a vein or fingertip.

b. c. Blood is processed in a machine. Blood components are measured and compared with the normal values.

ACTUAL EXAMINATION A. Complete Blood Count

Date: 11/25/11

PARAMETER WBC LYMPH # MID # H L H

RESULT 15.4 x 10/L 1.8 x 10/L 1.8 x 10/L

NORMAL VALUE 5.0 10.0 3.0 3.4 0.1 0.9

10

GRAN LYMPH % MID % GRAN %

H L H H

11.8 x 10/L 11.7 % 11.5 % 76.8 %

5.0 7.0 30 40 % 1 9 % 50 70 %

INTERPRETATION:

The blood components that have increased greatly were those responsible for the immunity. So far WBC and granulocytes are trying to fight the infection. However, the lymphocytes are seriously low which means the body has not produced antibody yet and has not attracted much macrophages and other cells to combat the invading microorganism.

Thus, making the patient still susceptible for spread of the infection because WBC and granulocytes will definitely wear out if antibodies and other defense cells are not in action.

B. Routine HGT q6 DATE 11/23/11 6 am 11 am 11/24/11 6 am 11 am 6 pm 12 mn 11/25/11 6 am 12 nn 6 pm 12 mn 11/26/11 6 am RESULTS 129 mg/dL 120 mg/dL 130 mg/dL 190 mg/dL 145 mg/dL 137 mg/dL 130 mg/dL 190mg/dL 175mg/dL 140 mg/dL 121 mg/dL INTERPRETATION H H H H H H H H H H H

RESULT: There is significant rise in glucose levels which suggest the occurrence of hyperglycaemic reactions as manifested in type 2 DM. Moreover, in adjunct to these levels, medications were given as prescribed.

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V.

ANATOMY AND PHYSIOLOGY

Every cell in the human body needs energy in order to function. The bodys primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches).

12

Glucose primarily comes from the diet and the liver. Once the food is ingested, glucose is absorbed into the bloodstream. This stimulates the pancreas, a small gland located behind the stomach, to secrete insulin which is produced by the beta cells of the said organ. The functions of insulin then are as follows: transports glucose into the cell signals the liver to stop releasing glucose stores glucose in the liver thru the form of glycogen as a reserved energy source stores dietary fat in the adipose tissues

During fasting periods (between meals and midnight), the pancreas continuously releases basal insulin and another hormone called glucagon which is responsible in stimulating the liver to break down glycogen into glucose to be used by the body (basal metabolic rate). The basal insulin assists the transport of glucose then. Blood sugar normally is high early in the morning because of the normal increase in growth hormone and corticosteroids (DAWN PHENOMENON). The blood sugar also increases excessively if there is a sudden drop in the blood glucose level as a compensatory mechanism (SOMOGYI EFFECT).

Reference: Smeltzer, S., et. al., Brunner & Suddarths Textbook of Medical-Surgical Nursing, Vol. 2, 10th ed.

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VI.

PATHOPHYSIOLOGY OF TYPE 2 DIABETES MELLITUS

A. ALGORITHM

Obesity Family history

Insulin resistance

Excessive accumulation of glucose in the blood (hyperglycemia)

osmotic diuresis (polyuria)

blood becomes more viscous

polydipsia

poor circulation

cells become hungry

blurred vision fatigue

gluconeogenesis

tingling sensation

polyphagia

production of insulin

beta cells are worn out

/ no insulin production
COMPLICATIONS: Type 1 DM Retinopathy Nephropathy Neuropathy

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A. EXPLANATION

The primary problem in type 2 DM is insulin resistance, not destruction of the beta cells. The latter is actually a complication. Thats why obesity is the main cause of type 2 DM merely because fat deposits resist insulin. Other causes include genetic factor and previous gestational diabetes.Since there is resistance, glucose is not utilized thereby accumulated in the blood. Signs and symptoms of hyperglycemia occur. As a compensatory mechanism, the body excretes glucose via urine leading to glucosuria. This is called osmotic diuresis wherein some electrolytes are also excreted with the glucose. To compensate the electrolyte loss, the patient experiences polydipsia. However, the cells become hungry without transport of glucose, thus the body breaks down proteins and other substances into glucose (gluconeogenesis). Due to this catabolic effect of the body, the patient tends to hunger much, a condition called polyphagia. On the other hand, the blood becomes viscous leading to poor circulation. Signs and symptoms like blurred vision, tingling sensation, fatigue and drowsiness are experienced. The body then is alarmed and signals the pancreas to secrete more insulin in an attempt to counteract insulin resistance. If resistance continues and glucose uncontrollably increases in the blood, the pancreatic cells become worn out, thus little or eventually no insulin is produced. This complication is called Type 1 DM. Other complications like retinopathy, nephropathy and neuropathy are due to poor circulation while CAD and CVA are due to increased blood coagulation secondary to increased blood viscosity. Hyperglycemic Hyperosmolar nonKetotic Syndrome is the most common complication.

15

Meanwhile, on this case study, obesity, family history and previous gestational diabetes predisposed the patient to type 2 DM. Signs and symptoms of hyperglycemia were claimed as stated in the history of present illness. All other signs and symptoms included in the algorithm are negative so far.

REFERENCE: Smeltzer, S., et. al., Brunner & Suddarths Textbook of Medical-Surgical Nursing, 10th ed., Vol. 2 (2004) The Merck Manual of Medical Information, 2nd home edition (2003)

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VII.

MANAGEMENT

IDEAL MEDICAL MANAGEMENT

GOAL: to enhance activity of insulin and maintain blood glucose level within normal range The primary management of type 2 DM is a combination of diet, exercise and weight loss program. If these are ineffective, medicines are prescribed but still lifestyle modification must be adopted for a long time. A. PHARMACOTHERAPY 1. Oral Hypoglycemic Agents used to decrease blood glucose level by either stimulating the pancreas to release insulin or decrease absorption of glucose in the intestines. Types:

CLASS/EXAMPLES Sulfonylureas Glyburide (DiaBeta, Glynase PresTab, Micronase) Glipizide (Glucotrol, Glucotrol XL) Glimepiride (Amaryl) Chlorpropamide

ACTION Stimulate pancreas to secrete insulin

SIDE EFFECTS GI symptoms and dermatologic problems = most common hypoglycemia

SPECIAL CONSIDERATIONS Drug-to-drug interactions: ** hypoglycemic effect o Sulfonamides o Chloramphenicol o Clofibrate o Phenylbutazone o Bishydroxycoumarin ** hyperglymic effect o K+ sparing diuretics o Corticosteroids o Estrogen o Diphenylhydantoin (Dilantin) Drug-food interactions: o Chlorpropamide + alcohol = disulfiram effect fast and short-acting Drug-to-drug interactions: o Meglitinides + Metformin = synergistic effect must always be taken right before meals to avoid hypoglycaemia except Naglitinide which is very rapid in action. It must be taken with meals Drug-to-drug interactions: o Biguanides + Sulfonylureas = synergistic

Meglitinides Repaglinide (Prandin) Naglitinide (Starlix)

Stimulate pancreas to secrete insulin

hypoglycemia

Biguanides Metformin (Glucophage, Glucophage XR)

Facilitates insulin action on peripheral receptors

metallic taste n/v abdominal bloating

17

pain diarrhea lactic acidosis = most dangerous hypoglycemia

Alpha-glucosidase inhibitors Acarbose (Precose) Miglitol (Glyset)

Slow down glucose absorption in the SI

pain flatulence diarrhea hypglycemia

Thiazolidinediones Rosiglitazone (Avandia) Pioglitazone hydrochloride (Actos)

Make body tissues more sensitive to insulin without ing insulin secretion

liver damage = most serious hypoglycemia

effect of ing blood glucose level o anticoagulants o diuretics o contraceptives o corticosteroids must not be given 2 days before any diagnostic test using contrast agent bec. it inc. lactic acidosis tendency. Drug-to-drug interactions: o AGI + Sulfonylureas/Meglitinides = significant hypoglycaemia If hypoglycaemia occurs, sucrose absorption is useless because its absorption is blocked, rather take glucose tablets. take immediately before meals because food interferes its action. HbA1c es indicated for patients taking INS injections and cannot control blood glucose adequately first-line agents in combination with diet to treat type 2 DM

2.

Insulin used if OHA cannot control blood sugar level in the shortest period of time used for sudden hyperglycemia dependence to drug depends on the ability of the pancreatic beta cells

TIME COURSE Rapid-acting

AGENT Lispro (Humalog) Aspart (Novolog)

ONSET 10-15 min 10-15 min

PEAK 1h 40-50 min

Short-acting

Regular (Humalog R, Novolin R, Iletin II Regular) NPH (neural protamine Hagedorn) Humulin N (Lente, NPH) Ultralente (UL) Glargine (Lantus)

-1h

2-3 h

Intermediateacting Long-acting Very long-acting

2-4 h 3-4 h 6-8 h 1h

6-12 h 6-12 h 12-16 h continuous

DURATION INDICATIONS 3h used for rapid reduction of 4-6 h glucose level to treat postprandial hyperglycemia to prevent nocturnal hyperglycemia 4-6 h usually administered 20-30 minutes before a meal may be taken with long-acting INS 16-20 h usually taken after meals 16-20 h 20-30 h 24 h

used primarily to control fasting glucose level used for basal dose

Administration Consideration: 1. 2. 3. Main areas of injection site: abdomen, arms, thigh, buttocks Systemic rotation of anatomical sites every day. Injection site must be 1 inches apart within the anatomical area.

18

4.
5.

Insulin syringe needles are G27-G29 that is inch long. Usually prefilled but can be prepared. Roll the container first before

withdrawing. 6. 7. 8. 9. 10. 11. Complications: Hypoglycemia Lipodystrophy Dermatologic allergic reactions Only regular INS may be mixed with other INS. When mixing, withdraw Regular INS first. Administer mixed dose within 5-15 minutes after preparation. Administer 45-90 angle in fat persons and 45-60 in thin persons. Regular INS is the only INS given IV. Place the needle upright or flat to prevent clogging.

B. DIET 1. Diabetic Diet diet with exercise is the primary key or first line in treating type 2 DM. must be low in calorie all food groups have caloric value, its just that carbohydrates have the highest value. must be referred to a dietician. a. Meal Plan 50-60% Carbohydrates 20-30% Fats 10-20% Proteins b. Food Guide Pyramid

represents the base as with the lowest in calories and fats and the highest
in fiber.

19

fats, oils and sweets

milk, yogurt and cheese

meat, poultry, fish, dry beans, eggs, nuts vegetables

fruit bread, rice, cereals, pasta

C. OTHERS 1. Hemoglobin A1C also known as Glycosylated Hemoglobin represents the blood glucose level changes over a prolonged period of time usually 2-3 months. used as a monitoring tool of the effectiveness of OHA and INS, not a diagnostic tool. when blood glucose level is elevated, glucose molecules attach to haemoglobin in the RBC. The longer the amount of glucose in the blood remains high, the more glucose binds to RBC an the higher the HbA1c which is permanent and lasts for the life of RBC usually up to 120 days.

2. Daily Wound Care of the affected leg

involves bed rest, proper hygiene, antibiotic and debridement safety precaution against potential injuries. IDEAL SURGICAL MANAGEMENT A. Possible Amputation

done if treatment is long enough to prevent the spread of infection.

done if wound is poorly healing due to poor circulation without improvement despite interventions.

20

ACTUAL MEDICAL MANAGEMENT Upon admission, the patient received an initial treatment of PLRSS plus B-Complex 1L regulated to 21-22 gtts/min. Her initial blood glucose level was 129 mg/dL and Metformin was administered as ordered. The physician also prescribed her an antibiotic, Ceftriaxone, and was administered accordingly. The patient was on diabetic diet and has fair appetite within the 2 consecutive shifts. During the course of hospitalization, the patients blood glucose level was monitored every 6 hours. Upon discharge, the physician prescribed home medications and advised the patient for follow-up one week after discharge.

SURGICAL MANAGEMENT **None so far.

REFERENCE: Smeltzer, S., et. al., Brunner & Suddarths Textbook of Medical-Surgical Nursing, 10th ed., Vol. 2 (2004) The Merck Manual of Medical Information, 2nd home edition (2003)

21

NURSING CARE PLAN CUES SUBJECTIVE: Nag-ut-ot unay toy sugat ko. OBJECTIVE: presence of frequent facial grimace diaphoresis with pain scale of 7/10 wound appears red and warm V/S taken as follows: T 38.6 C P 108 bpm R 24 cpm BP 130/80 mmHg NURSING DIAGNOSIS P - Acute pain E - r/t progression of non-healing wound s/t poor circulation S as evidenced by the presence of facial grimace, diaphoresis, pain scale of 7/10, elevated vital signs and pts verbalization SCIENTIFIC BACKGROUND Local tissue damage from injury Initiation of nociceptors to respond to noxious stimulus Transmission of nerve impulses to the brain Pain sensation is experienced Increased metabolic rate GOAL/OBJECTIVES Date:11/20/11 Shift: 7-3 Time: 1:30 PM GOAL: After rendering nsg ix, the pt will verbalize pain relief and demonstrate relaxation and diversional activities. OBJECTIVES: After 30 minutes, facial grimace will decrease from frequent to moderate diaphoresis will stop pain scale will decrease to 6/10 V/S will normalize pt will demonstrate 2/2 relaxation/ diversional activities INTERVENTIONS INDEPENDENT: Obtained V/S Asked patient the degree of pain RATIONALE EVALUATION Date: 11/20/11 Shift: 7-3 Time: 1:30 PM GOAL PARTIALLY MET as evidenced by: facial grimace decreased diaphoresis stopped pain scale decreased to 5/10 V/S stabilized within normal range and taken as follows: T- 37.2 C P- 94 bpm R- 20 cpm BP- 120/80 mmHg pt demonstrated 2/2 relaxation/ diversion activities

to have a baseline data and

to verify pain because it alters V/S. to intervene appropriately. Severe pain already needs pain reliever rather than simple diversional activities. to assess progress of wound focusing on discharges that might have initiated pain or another infection. to normalize temperature. increased in V/S was affected by the ed temp. So if temp normalizes, other V/S follow. to provide better ventilation which will help normalize temperature and respiration. Pain can also be eased by good ventilation. Done if and only if analgesic was administered in order to refocus attention. Diversion activities are useless in severe pain to evaluate effectivity of care and medications

Noted characteristics of
wound Provided TSB and increased hydration

Opened the windows

Diaphoresis, V/S Redness and warmth REFERENCE: Smeltzer, et. al., Brunner and Suddharths textbook of MedicalSurgical Nursing, 10th Edition, Vol 1, pg. 256

Instructed and encouraged

diversional activities such as sleeping, listening to radio or chatting with students and other patients/ SO. Monitored V/S q 15 minutes especially temperature and asked patient about the pain status. DEPENDENT:

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Administered Diclofenac
75 mg IV q8 PRN. Administered Paracetamol 500 mg IV q4 PRN COLLABORATIVE: Monitored laboratory results

to rapidly relieve pain to normalize temperature

To determine progress of condition and obtain cues related to pts diagnosis.

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CUES Subjective: Nabayag atoy sugat kon. Objective: poorly healing rahes on perineal area (+) redness (+) swelling wound site is warm

NURSING DIAGNOSIS P- Impaired tissue integrity E- r/t mechanical trauma of of skin and subcutaneous tissue s/t injury S- as evidenced by presence of poorly

SCIENTIFIC BACKGROUND Injury Destruction of skin layers Initiation of wound healing as a compensatory mechanism (but here, there is slow

GOAL/OBJECTIVES Date: 11/21/11 Shift: 7-3 Time: 8:00 am GOAL: After rendering nursing interventions, the pt will display behaviour and lifestyle changes to promote healing and prevent complications

INTERVENTIONS INDEPENDENT: Noted evidence of tissue involvement Obtained history of condition including color, smell, location and consistency Reinforced knowledge

RATIONALE

EVALUATION Date:11/21/11 Shift: 7-3 Time: 8:00 am GOAL MET as evidenced by: the patient enumerated and observed 2/2 lifestyle changes the patient enumerated

to determine which tissue

is affected which will serve as baseline data for your health teachings. to know the progress of the condition and have a baseline data to plan for nursing interventions

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to touch (+) pain, rated as 5/10

healing wound with redness and swelling as well as pts verbalization

wound healing) Occurrence of the cardinal signs Presence of redness(rubor) in the incision site Sensation of heat(calor) in the incision site Swelling(dolor) is observed Pain(tumor) sensation REFERENCE: Elaine Marieb, Anatomy and Physiology 9th Edition, pg. 463 OBJECTIVES: The patient will: enumerate and observe 2/2 lifestyle changes enumerate and display 3/3 safety precautions against injury

about wound care as observed during doctors round Emphasized the importance of proper food intake especially food rich in fiber and protein such as vegetables and meat Encouraged skin hygiene

to motivate the pt for selfcare upon discharge

and displayed 3/3 safety precautions against injury

fiber promotes tissue

healing and decreases blood sugar level. Iron enhances clotting factors. Maintaining clean, dry skin provides a barrier to infection. Patting skin dry instead of rubbing reduces risk of dermal trauma to fragile skin. to enhance patients knowledge and self-care.

Instructed to avoid injury as much as possible especially in the lower extremities. Activities involved wearing closed slippers, cutting nail into square-tipped and avoiding pedicure and abrasions. DEPENDENT: Administered Ceftriaxone 1 gram IV q12 COLLABORATIVE: Monitor laboratory results

antibiotic helps prevent

spread of infection

to determine changes
indicative of healing; to gain data as a basis for interventions.

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PROMOTIVE AND PREVENTIVE INTERVENTION FOR TYPE 2 DM Since the patient is diabetic, she is more likely experiencing poor wound healing accompanied with pain. Wound can be an entry of infection especially that there is poor circulation. Moreover, if blood glucose level cannot be controlled, complications stated earlier are more likely to happen. The goals of promotive-preventive interventions are to: Promote optimal blood glucose level Proper wound care and prevent infection Prevent complications Interventions are as follows: To promote optimal blood glucose level, the patient has to:

Eat proper diet which is low in calories and lose weight. Foods high in fiber are
recommended to decrease elevated blood glucose level. These include vegetables and fruits.

Exercise regularly as tolerated to burn calories. Be sure that she had taken meals and
medications before doing so to prevent hypoglycaemia and hyperglycaemia respectively.

Take medications religiously and with precautions. OHA must always be taken before
meals so that there will be insulin needed for the food to be digested and utilized into energy.

Avoid food and medications that may alter the actions of her medications. Better consult
the doctor first before taking anything.

To facilitate proper wound care and prevent infection, the patient has to: Take antibiotics religiously.
clean wound with antibacterial soap and wrap it with gauze to prevent exposure to debris. wear protective shoes and observe safety precautions on the affected leg. practice proper hygiene. eat foods high in protein to facilitate wound healing. But this still depends on lowering the blood glucose level in order to improve circulation.

To prevent complications, the patient has to:

avoid injury as much as possible because of slow wound healing which might lead to infection and eventually to amputation. take medications religiously to control blood glucose level. All she has to do is to maintain the blood sugar within normal level so that the blood will circulate properly.

26

 report unusual signs and symptoms such as loss of sensation, spread of infection, and the like to intervene immediately and prevent progress.

27

VIII.

DRUG STUDY NAME/CLASS DOSAGE/ROUTE 1 gram IV q12 MECHANISM OF ACTION Bactericidal and bacteriostatic. Inhibits bacterial cell wall synthesis. INDICATION Treatment of moderate to severe infections of soft tissues and wounds CONTRAINDICATION Hypersensitivity ADVERSE EFFECTS GI symptoms headache vertigo pruritus NURSING RESPONSIBILITY Drug-to-drug interaction: Aminoglycosides and diuretics Ensure safety Encourage to drink lots of water to counteract SE

1. Ceftriaxone
(Antibiotic)

2. Metformin

500mg 1 tab OD

3.Glimepiride (Oral Hypoglycemic Agents)

1 mg/tab 1 TAB OD

Decreases hepatic glucose production and intestinal absorption of glucose. Stimulate pancreas to secrete more insulin

Adjunct to patients with type 2 DM Adjunct with diet for the management of type 2 DM

Hypersensitivity

Hypersensitivity

4. Simvastatin

10 mg 1 tab TID

Inhibits HMG-CoA reductase an early stage in biosynthesis.

To reduce total LDL cholesterol levels

Hypersensitivity

5. VCO Cogel

1 tab OD

Unknown action

Believed to have numerous indications such as vitamins, or reducing risks of CVAs and cancer.

Hypersensitivity

GI symptoms Hypoglycemia Megaloblastic anemia Hypoglycemia headache dizziness n/v GI pain and diarrhea pruritus abdominal pain nausea vomiting, constipation diarrhea No known side effects

Give with meals. Monitor glucose levels regularly. Drug-to-drug interaction: diuretics, corticosteroids, some NSAID Administer right before meals Monitor blood glucose level patient should follow a low cholesterol diet during treatment.

Regularly take the drug for better results.

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IX.

DISCHARGE PLAN

Glimepiride 1 mg/tab 1 tab OD; taken before meals

M (Medications) E (Exercise) T (Therapeutic) Metfrormin 500 mg 1x a day after lunch Simvastatin 10 mg tab HS Diazepam 5mg tab OD at bedtime Buclizine with Fe 1 cap 1 hr before bedtime Erceflora 2x a day for 5 days Can walk around for 30 minutes when tolerated and assistance.

can do household chores as tolerated can talk to healthcare team about worries on present condition upon follow-up can ask assistance from SO when activities or needs are not possible for the patient to

do proper hygiene and cleaning of the perineal area. report to healthcare team any unusual signs and symptoms which can be indicative of complications. These includes: o o H (Health Teachings) o o o loss of sensation progressive loss of vision acetone-smelled urine (progressed into Type 1 DM) chest pain (CAD) slowly healing wound

importance of compliance to drug regimen. monitor blood glucose level by going to a health center since the patient claimed she cant O (OPD) D (Diet) afford to buy a glucometer and its testing strips. follow-up 1 week after discharge . Diabetic diet low caloric diet. Carbohydrates can be eaten in moderation as well as other food groups. high fiber diet which includes vegetables and fruits.

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UPDATES RELATED TO TYPE 2 DM

Study: Lung cancer patients with diabetes mellitus tend to live longer Published on October 18, 2011 at 1:31 AM

Lung cancer patients with diabetes tend to live longer than patients without diabetes, according to a Norwegian study published in the November issue of the Journal of Thoracic Oncology, the official publication of the International Association for the Study of Lung Cancer. Researchers did not speculate on the reason for the effect, but said that the survival benefit warranted more study and that diabetes should not be considered a reason to withhold standard cancer treatment. "Standard therapy should not be withheld from patients with diabetes mellitus provided they are otherwise fit, even if it may be considered a significant comorbidity," researchers wrote in the study. "The survival benefit may be of clinical importance and should be focused on in future studies." Researchers at the Norwegian University of Science and Technology and Trondheim University analyzed 1,677 lung cancer cases from the Nord-Tr-ndelag Health study (HUNT), the pemetrexed gemcitabine (PEG) study and the Norwegian Lung Cancer Biobank study. It was the first cohort study from a well-defined geographical area, with a stable and large number of inhabitants, investigating lung cancer, diabetes and survival. They found that the 1-, 2-, and 3-year survival in patients with lung cancer with and without diabetes mellitus were 43% versus 28%, 19% versus 11%, and 3% versus 1%, respectively. The fact that patients with diabetes mellitus showed a lower frequency of metastatic diseases may partly explain the survival benefit in patients with diabetes mellitus, because the majority of the patients with lung cancer die of metastasis and not of the primary tumor," researchers wrote. "However, as we adjusted for stage of disease in our analyses this potential advantage can hardly explain the observed increased survival in patients with diabetes mellitus. In addition, increased survival in patients with diabetes mellitus was clearly demonstrated in the PEG study where all patients had advanced lung cancer." Source: International Association for the Study of Lung Cancer Reaction:

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Its quite strange at first because most would expect that death rate is higher in patients with lung cancer and diabetes at the same time because these are fatal diseases than in patients without diabetes. Out of the blue, since metastasis occurs through the blood, the increased coagulation and poor circulation in patients with diabetes might have slowed the spread of cancer compared to those who dont. Its one of the possibilitie TRPM2 in pancreatic beta-cells may control insulin secretion levels Published on January 4, 2011 at 11:25 PM The research group led by professor Makoto Tominaga and Dr. Kunitoshi Uchida, National institute for Physiological Sciences (NIPS), found TRPM2 ion channel in pancreatic beta-cells is important for insulin secretion stimulated by glucose and gastrointestinal hormone (incretin) secreted after food intake. Their finding was reported in Diabetes. Diabetes mellitus is a disease caused by lack of insulin secretion from pancreatic cells, or less response to the secreted insulin, which raises the blood glucose levels, and as a result, causes serious disorders. It is said that at least 171 million people worldwide suffer from diabetes mellitus, and its incidence is increasing rapidly. Clarify the mechanisms of insulin secretion is important for the development of diabetes therapy. Here, this research group focused on TRPM2 acting as a body temperature sensor. TRPM2 is a temperature-sensitive Ca2+-permeable channel and expressed in pancreatic beta-cells. They found that TRPM2-deficient mice have shown the higher blood glucose levels with impaired insulin secretion compared with wild-type mice. Furthermore, TRPM2-deficient pancreatic beta-cells showed smaller intracellular Ca2+ increase and lesser insulin secretion stimulated by glucose and incretin. Professor Makoto Tominaga and Dr. Kunitoshi Uchida said,"TRPM2 may control insulin secretion levels mainly by modulating intracellular Ca2+ concentrations. Finding the substance which stimulates TRPM2 effectively could lead to the development of a new therapy for diabetes mellitus." Source: National Institute for Physiological Sciences

BIBLIOGRAPHY

BOOKS:

Merck Medical Manual of Medical Information, 2nd home ed., (2003). Smeltzer, S., et. al., Brunner & Suddarths Textbook of Medical-Surgical Nursing, Vol. 2, 10th ed. (2004). Philippine Pharmaceutical Directory, 14th annual ed., (2007-2008). Grodner, et. al., Foundations and Clinical Applications of Nutrition, 4th Edition (2009). Karch, A., Focus on Nursing Pharmacology, 4th ed., (2008).

ONLINE:

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www. news-medical.net www.nursing-crib.com

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