A CASE PRESENTATION OF

DIABETES MELLITUS TYPE 2 UNCONTROLLED;

NON- HEALING WOUND

PREPARED BY: ASHRAL R. CABUGATAN

 II. TABLE OF CONTENTS

Title page

Table of contents

Introduction

Nursing theories

Patient’s data

History of present illness

Review of systems

Physical assessment

Course in the ward

Review of related literature

Anatomy and physiology

Pathophysiology

Laboratory and diagnostic procedures

Drug study

NCP

Bibliography
 III. INTRODUCTION

The case study that is to be presented features a patient who has a Type 2 Diabetes Mellitus
Uncotrolled; Non- healing wound.

The pancreas is an elongated, tapered organ located across the back of the abdomen,
behind the stomach. The right side of the organ (called the head) is the widest part of the organ
and lies inthe curve of the duodenum (the first section of the small intestine). The tapered left
side extendsslightly upward (called the body of the pancreas) and ends near the spleen (called the
tail)Somatostatins are hormones secreted directly into the bloodstream, and together, they
regulate the level of glucose in the blood. Insulin lowers the blood sugar level and increases the
amount of glycogen (stored carbohydrate) in the liver; Diabetes mellitus is a metabolic disorder,
specifically affecting carbohydrate metabolism. It is a disease characterized by persistent
hyperglycemia (high glucose blood sugar). It is a metabolic disease that requires medical
diagnosis, treatment and lifestyle changes. The World Health Organization recognizes three main
forms of diabetes: type 1, type 2 and gestational diabetes (or type 3, occurring during
pregnancy), although these three "types" of diabetes are more accurately considered patterns of
pancreatic failure rather than single diseases.

I as a nursing student is involved in learning what type of nursing interventions that I will
apply to this type of patient. Beyond understanding the relevant health issue, this case study will
also explore other factors that can enhance my knowledge in the field of our nursing practice.
This is also the primary reason why I choose this case study because I know that it is highly
beneficial aside from it is being considered unique.

Included with the case study are the discussions of the anatomical parts, through physical
assessment of the patient, laboratory results and their corresponding findings. Added to this I also
have a discussion of the patient’s daily activities and nursing care plans.

IV. NURSING THEORIES

Dorothea Orem
 "Self-Care Nursing Theory"

Self-Care Nursing Theory or the Orem Model of Nursing was developed by Dorothea Orem
between 1959 and 2001. It is considered a grand nursing theory, which means the theory covers a
broad scope with general concepts that can be applied to all instances of nursing.

OREM’S GENERAL THEORY OF NURSING

Major Concepts of the Self-Care Deficit Theory
 Nursing
is an art through which the practitioner of nursing gives specialized assistance to persons with
disabilities which makes more than ordinary assistance necessary to meet needs for self-care.
The nurse also intelligently participates in the medical care the individual receives from the
physician.
 Humans
Humans are defined as “men, women, and children cared for either singly or as social units,” and
are the “material object” of nurses and others who provide direct care.
 Environment
The environment has physical, chemical and biological features. It includes the family, culture,
and community.
 Health
Health is “being structurally and functionally whole or sound.” Also, health is a state that
encompasses both the health of individuals and of groups, and human health is the ability to
reflect on one’s self, to symbolize experience, and to communicate with others.
 Self-care
Self-care is the performance or practice of activities that individuals initiate and perform on their
own behalf to maintain life, health, and well-being.

Self-care Agency

Self-care agency is the human’s ability or power to engage in self-care and is affected by basic
conditioning factors.
Therapeutic Self-care Demand
Therapeutic Self-care Demand is the totality of “self-care actions to be performed for some
duration in order to meet known self-care requisites by using valid methods and related sets of
actions and operations.”

 Self-care Deficit

Self-care Deficit delineates when nursing is needed. Nursing is required when an adult (or in the
case of a dependent, the parent or guardian) is incapable of or limited in the provision of
continuous effective self-care.

 Nursing Agency

Nursing Agency is a complex property or attribute of people educated and trained as nurses that
enables them to act, to know, and to help others meet their therapeutic self-care demands by
exercising or developing their own self-care agency.

 Nursing System

Nursing System is the product of a series of relations between the persons: legitimate nurse and
legitimate client. This system is activated when the client’s therapeutic self-care demand exceeds
available self-care agency, leading to the need for nursing.

 Theories

The Self-Care or Self-Care Deficit Theory of Nursing is composed of three interrelated theories:
(1) the theory of self-care, (2) the self-care deficit theory, and (3) the theory of nursing systems,
which is further classified into wholly compensatory, partial compensatory and supportive-
educative.

 Theory of Self-care

This theory focuses on the performance or practice of activities that individuals initiate and
perform on their own behalf to maintain life, health and well-being.

 Self-care Requisites

Self-care Requisites or requirements can be defined as actions directed toward the provision of
self-care. It is presented in three categories:
  Universal self-care requisites

Universal self-care requisites are associated with life processes and the maintenance of the
integrity of human structure and functioning.

The theory of nursing systems describes how the patient's self-care needs will be met by the
nurse, the patient, or by both. Orem identifies three classifications of nursing system to meet the
self-care requisites of the patient: wholly compensatory system, partly compensatory system, and
supportive-educative system.

Orem recognized that specialized technologies are usually developed by members of the health
care industry. The theory identifies two categories of technologies.

The first is social or interpersonal. In this category, communication is adjusted to age and health
status. The nurse helps maintain interpersonal, intra-group, or inter-group relations for the
coordination of efforts. The nurse should also maintain a therapeutic relationship in light of
pscyhosocial modes of functioning in health and disease. In this category, human assistance
adapted to human needs, actions, abilities, and limitations is given by the nurse.

The second is regulatory technologies, which maintain and promote life processes. This category
regulates psycho- and physiological modes of functioning in health and disease. Nurses should
promote human growth and development, as well as regulating position and movement in space.

Orem's approach to the nursing process provides a method to determine the self-care deficits and
then to define the roles of patient or nurse to meet the self-care demands. The steps in the
approach are thought of uas the technical component of the nursing process. Orem emphasizes
that the technological component "must be coordinated with interpersonal and social pressures
within nursing situations.

The nursing process in this model has three parts. First is the assessment, which collects data to
determine the problem or concern that needs to be addressed. The next step is the diagnosis and
creation of a nursing care plan. The third and final step of the nursing process is implementation
and evaluation. The nurse sets the health care plan into motion to meet the goals set by the
patient and his or her health care team, and, when finished, evaluate the nursing care by
interpreting the results of the implementation of the plan.

V. PATIENT’S DATA

GENERAL DATA:

NAME: Mr. A.S

MALE: Male
AGE: 45
ADDRESS: City Of Antipolo, Rizal

OCCUPATION: Delivery boy

MARITAL STATUS: N/A

RELIGION: Roman Catholic

ADMITTING DIAGNOSIS: DM TYPE 2 Uncontrolled; Non Healing Wound

DATE OF ADMISSION: June 23 2019

SOURCE OF INFORMATION: Patient

Weight: 53 kg (116lbs)

Height: 5’1”

BMI: 22.1

CHIEF COMPLAINT:

“Ang sakit po ng paa ko dahil sa sugat ko” As verbalized by the patient.

VI. HISTORY OF PRESENT ILLNESS

A year prior to admission (year 2018) patient observed less sensation on his feet and body
weakness but he did not seek any medical attention immediately and no medication was taken.

5 months prior to admission (January 2019) patient had a boil on right lower leg that lasted
for 2 months. He stated that he also experienced fever. He only took medicine with mefenamic,
paracetamol and other unrecalled OTC medications, no consultation was done. He tried to
relieve the pain by rest.

3 weeks prior to admission (May 02 2019)- According to the patient, there was flood in their
area in Marikina. Accidentally, he stepped on a nail. Using a clean fabric, he applied pressure to
stop bleeding from his wound. He thought that it's just a simple wound that will heal
immediately so he didn't seek consultation and no medication was taken. After that incident he
still went back to his activities of daily living and work.

Two weeks prior to admission (May 09 2019)- patient observed that there was a swelling and
pus on the heel part of his right foot. He applied Betadine once a day with no relief. He
experienced fever so he took OTC paracetamol and mefenamic as a pain relievers. His young
brother suggested to use the boiled leaves of bayabas to cleanse his wound. He managed it by
elevating his feet at night until it subsides. No other symptoms felt, no consultation was done.

One week prior to admission (May 16 2019)- according to the patient, he still had a fever. The
swelling and pain are getting worse. So his siblingsdecided to bring him in Amang Rodriguez
Hospistal for check up. Patient stated that he was prescribed antibiotics and other unrecalled
medications. He further advised to comeback if the fever persists after 1 week.

Four days prior to admission- (June 19 2019) The patient had difficulty of sleeping because
of pain. He had high fever that led to a febrile convulsion.

An hour prior to admission (June 23 2019) - According to the patient, pain continued to
gradually increase in severity by pain scale of 9/10 associated with fever. His brothers decided
to bring him to the ER at QMMC.

June 23 2019- Mr. AS 49 y/o diagnosed with DIABETES MELLITUS TYPE 2 Uncontrolled;
Non-healing wound at Quirino Memorial Medical Center. He has no family history of Diabetes.
Because of this diagnosis, he became aware of the signs and symptoms of the disease and found
out that these include less sensation on his foot and delayed healing the wound. He stated that
upon admission, he learned that his blood glucose level was 400 mg/dL which to he knew that
this level is way high above the normal level.
PAST MEDICAL HISTORY
 According to the patient he never had any serious illnesses during his childhood and
he was not hospitalized other than the said hospitalizations above.

FAMILY HISTORY

 (+) Hypertension

 (-) Diabetes

 (-) Cancer

 (-) Stroke

PERSONAL AND SOCIAL HISTORY

 Patient stated that he never smoked and drink alcohol.

 Did not take any prohibited any drugs

VII. REVIEW OF SYSTEMS

(JULY 11 2019) 9:00AM

I. GENERAL:
 “ Namamayat po ako”

(June 2019) From Weight: 60 kg

(July 2019) To Weight: 56 kilos

 “Sakit ng paa ko dahil sa sugat ko”

 “Mataas po ang blood sugar ko”

II. HEAD AND NECK:

“Okay naman, hindi masakit ulo ko, hindi din naman ako nahihilo”

“Maayos naman paningin at pang dinig ko wala naman problema”

“Nagagalaw ko naman ng maayos leeg ko , hindi naman masakit”

III. CHEST AND LUNGS

 “ Wala naman po akong problema sa paghinga at wala naman akong ubo”

 “Wala naman akong ubo”

IV. HEART AND BLOOD VESSELS:

 “Wala naman masakit sa dibdib ko.”

V. GASTROINTESTINAL:

 “Wala naman problema sa paglunok ko”

 "Wala naman masakit sa tyan ko"
 "Normal naman pag pag dumi ko hindi naman ako nahihirapan"

VI. GENITOURINARY:

 “Wala naman po akong problema sa pag ihi"

 “Hindi naman ako ihi ng ihi”
VII. INTEGUMENTARY:

 “Ito lang sugat ko sa kanan paa matagal gumaling”

VIII. ENDOCRINE:

 "Hindi naman ako pinagpapawisan"

IX. PSYCHIATRIC:

 "Medyo na dedepress ako kasi baka tuloyan na ako maputulan ng paa"

X. MUSCOSKELETAL:

 "Hindi ko mailakad itong kanan paa ko dahil sa sugat ko pero naangat ko naman
siya"
 "Itong kaliwa okay naman nailalakad ko pero medyo hindi ko nararamdaman
minsan parang nangangapal "

VIII. PHYSICAL ASSESSMENT

Received patient awake, lying semi-fowler’s in bed appropriately groomed,

Oriented to time and place He appears of weight loss. He with an IV fluid of 0.9 NaCl 1L
regulated 40gtts/min infusing well at dorsal metacarpal.

(JULY 11 2019) 9:00 AM

 Blood pressure: 130/70 mmHg

 Temperature: 37.3°C
Vital signs  Pulse rate: 91 bpm
 Respiratory rate: 19 cpm

General
 Concious and coherent
 Oriented to time, person and
situation.

 No lesions on the head

 Pale conjunctiva
Head  Eyes are symmetrical
 Pupils Equal, Round, Round and
Light Accomodation
 No nasal flaring
 Moist lips and Complete teeth

Chest  No apparent use of accessory

muscles. Chest expands
symmetrically.
 Normal breath sounds.
 No cough

Abdomen  Non-tender and non-distended

abdomen
 No masses

Extremities Right Lower Extremity

 Asymmetric with the Left Lower

Extremity. wound in right heel
 tenderness to palpation. Joints are
unstable. Range of motion and tone
 are limiited.
 Capillary refill more than 3seconds
 numbness
 mild pitting edema +1

Left Lower Extremity

 Appears asymmetric with the Right

Lower Extremity.
 Scar from boil in his left leg.
 No tenderness
 Joints are stable. Range of motion
and tone are within normal limits.
 Capillary refill more than 3 seconds
 Numbness

Skin  Cool to touch

 Lower extremities appears
discoloration.

IX. COURSE IN THE WARD

Day 1 (June 23 2019)

A 45 years old female was admitted Last June 09 2019, accompanied by his
brothers at the Emergency Room of Quirino Memorial Medical Center with a chief
complaint of “Sobrang sakit po ng sugat ko sa paa”

He was admitted under the care of the Doctors of Quirino memorial Medical Center.
Following orders were given.

 Secure consent of admission and management

Laboratory and Diagnostics

 For CBCPC, Na, K, Cl, BUN and Creatinine, Albumin, (Extracted)

Medications/Therapeutics
 PNSS 1Liter regulated at 20 mins gtts/min
 Paracetamol 300 mg TIV q4 for fever and also for pain
Nursing care
 Vital signs are monitored and recorded
 Doctors order are carried out
 Secured consent for management
 Keep right foot elevated
 Avoid pressure on right heel
 Patient’s safety maintained. Side rails up

Day 2 (June 24 2019) 8:45am

Physical examination
 (+) awake and coherent
 (+) fever (Temperature 37.8C)
 (+) Tenderness and swelling right foot.

Diagnostics:
 For CBCPC, Na, K, Cl, BUN and Creatinine (extracted)
 For Culture sensitivity

Diet:
 Diet as tolerated

Nursing notes/care:
 Provision of care
 Safety measures provided. Monitored closely
 Vital signs taken (T=37.8C)
 TSB done
 Given paracetamol 300 mg TIV Q6
 Patienty safety maintained. Side rails kept up

Day 3 (June 25 2019) 8:00am

Diet:
 Diet as tolerated

Doctor’s order:
 For wound debridement of right heel
 Secure consent for procedure.
 Follow up for cultures
 Keep right foot elevated
 Avoid pressure on right foot
Nursing notes/ care

 Vital signs are monitored and recorded

 Doctors order are carried out
 Secured consent for management
 Keep right foot elevated
 Patient’s safety maintained. Side rails up

Day 4 (June 26 2019) 9:00am

ORTHO

Diet:
 NPO
Therapeutics
 IVF of PNSS 30 gtts/min tto be given every 8 hours

Doctor’s order:
 Endo Cleared/ CP Cleared
 For wound debridement right heel
 Secure consent for procedure
 Keep right foot elevated
 Avoid pressure on right heel

Working diagnosis:

#1 DM foot right wound debridement

(+) pain
(+) Intact dressing
(-) Discharge

#2 Type 2 DM Uncontrolled
109-228 mg/dl

Nursing notes/ care

 Vital signs are monitored and recorded

 Doctors order are carried out
 Secured consent for management
 Keep right foot elevated
 Patient’s safety maintained. Side rails up

Day 5 (June 27 2019) 9:00am

The day I received the patient

Procedure: Wound debridement

ANESTHESIA PRE-OP
1:45pm
 Patient was seen and examined
 History, PE and chart reviewed
 Anesthesia plan explained, understood and accepted by patient
 Secure consent for anesthesia
 NPO
 Monitor VS q4

 Treatment:
1. PNSS 1 liter for 100 cc/hr
2. Omeprazole 40mg TIV OD
3. Vitamin K tab q8

3:45pm
 Noted for wound debridement today
 Hold medications
 Follow up cultures
 Continue present management
 Continue CBG monitoring q4 while on NPO

Student nurse care:

 Awake, conscious and coherent
 Vital signs are monitored and recorded. (T= 36.6C BP=120/80 PR=97bpm RR=20)
 Maintained NPO
 Keep right foot elevated
 Patient’s safety maintained. Side rails up

Day 6 (June 28 2019) 8:00pm

ANESTHESIA POST-OP ORDERS

8:00pm
 To PACU
 Hook to O2 via face mask at 4-5 LPM
 Monitor VS q15
 Moderate high back rest
 NPO temporary
 Keep thermoregulated
 IVF PNSS 1 liter for 8 hours
  Treatment:
1. Paracetamol 300 mg q8 x 3 doses
2. Ketorelac 30 mg/ IV q8h x 3 doses (-) ANST
3. Butorphanol 1mg/ IV q6h x 4 doses

ORTHO POST-OP
Status post wound debridement right foot

1:00am

Doctor’s order:
 Resume diet once fully awake
 Continue IVF
 Continue medications

2:25pm
 Transfer to hallway

3:00pm
Doctors order:
 Inquire with IDS, antibiotic continuation
 May resume metformin only
 Hold insulin temporarily
 Follow up update laboratories post op

Student nursing notes/care:

 Safety measures provided. Monitored closely

 Maintained dressing
 Vital signs are monitored and recorded.
 Keep right foot elevated
 Positioned patient to comfortable position
 Encouraged adequate rest and sleep
 Patient’s safety maintained. Side rails up

Day 7 (June 29 2019) 10:00am

 Continue present management

  Maintain dressing
 Keep right foot elevated
 Avoid pressure on right heel
 Refer
11:00am
 Increase metformin 500 mg tab TID
 Follow up updates laboratory
 Provides adequate analgesia

Day 8 (June 30 2019) 9:00am

 Vital signs are monitored and recorded
 IVF PNSS 1 liter at regulated at 30 gtts/min to be give every 8 hours
 Continue present management
 Nursing care done

10:00pm
 To complete ciprofloxacin and clindamycin for 28 days
 Follow up for ortho plans
 Continue present management

Day 9 (July 01 2019) 9:00am

ORTHO
 Continue present management
 Maintain dressing
 Keep right foot elevated
 Plan: for “E” Repeat wound debridement right heel prior to possible flap coverage
 Secure consent for procdure
 NPO by 12 midnight
 Start omeprazole 40mg IV OD while on NPO

Day 10 (July 02 2019) 8:35am

ANESTHIA PRE-OP
 Patient was seen and examined
 History, PE and chart reviewed
 Anesthesia plan explained, understood and accepted by patient
 Secure consent for anesthesia
 NPO
 Suggest connection anemia
 Monitor VS q4
 Treatment:
 4. PNSS 1 liter for 100 cc/hr
5. Omeprazole 40mg TIV OD
6. Vitamin K tab q8

11:20am
 Noted ortho plans, Hold insulin today
 Facilitate “E” wound debridement
 CBG monitoring q4 once on WPO then q1 at OR
 Continue present management

11:40am
 NPO
 Continue IVF
 Medications main secure
 Give omeprazole 20 mg IV OD while on NPO
 Secure content for procedure
 Maintain dressing
 Keep right foot elevated
 Refer

Day 11 (July 03 2019) 6:05am

 Continue present management

 DAT then NPO by 7am
 Continue IVF
 Continue Medications
 Give omeprazole 40mg IV OD while on NPO
 Still for “E” wound debridement, Right heel
 Secure consent for procedure
 Refer
10:00am
 Hold Vitamin K and Metformin
 Start Lantus 10 “u” SQ 6pm, Hold if NPO
 CBG q4h while on NPO
 Start pregabalin 75mg tab PO OD
 Repeat CBCPC, Na, K, PT PTT, Crea, BUN tomorrow 8am
 Keep dressing
2:00pm
 Noted Ortho plan
 Continue present management
 Hold metformin today
 CBG q4 monitoring once on WPO
 D5050 1 vial PRN CBG <100 mg/dL
  D5050 2 vials PRN CBG <70 mg/Dl
 CBG q1 at OR

Day 12 (July 04 2019) 1:55am

 To PACU
 Hook to O2 via face mask at 4-5 LPM
 Monitor VS q15
 Moderate high back rest
 NPO temporary
 Keep thermoregulated
 IVF PNSS 1 liter for 8 hours

 Treatment:
1. Ketorelac 30 mg/ IV q8h x 3 doses (-) ANST
2. Butorphanol 1mg/ IV q6h x 4 doses
 Refer

2:00pm
 Resume diet once fully awake
 Continue IVF
 Continue medications
 Maintain dressing
 Keep right foot elevated
 Repeat CBCPC, Na, K, Cl, BUN, Crea tomorrow AM
 Refer

Day 13 (July 05 2019) 10:00am

ORTHO
 Continue present management
 Maintain splint and dressing
 Plan: For revine sural flap of right heel
 Once with culture negative wound bed or with variable wound bed
 Keep right leg elevated
 Refer
3:00pm
 Noted ortho plans
 Increase insulin to 12 “u” SQ OD PM
 Provide adequate analgesia
5:30pm
 Give K, 4 tabs now
 Repeat K 2 hours post correction
 Noted ortho plans
 refer
Day 14 (July 06 2019) 11:30am
 Continue present management
 Maintain splint and dressing
 For revine sural flap of right heel
 No pressure on right heel
 Refer
10:00pm
 Continue present management
 Noted ortho plans
 Increase pregabalin for BID
 Refer

Day 15 (July 07 2019) 8:45am

ORTHO
 Continue present management
 Maintain dressing
 Plan: For flap right heel once with viable wound bed
 Keep foot elevated
 Continue wound care with dakins solution
 Refer
2:45pm
 Follow up update cultures
 Hold Clindamycin
 Revise tramadol IV to Paracetamol 1 tab PO TID RTZ
 Secure crutches

Day 16 (July 08 2019) 6:00am

 Follow up culture
 Keep right leg elevated

11:00am
 Noted ortho plan
 Increase Lantus to 16 “u” SQ OD today and shift tomorrow
 Start Humulin R 6 “u” SQ pre dinner only
 Continue present management
12:00am
 Continue present management
 Maintain dressing
 Plan: Flap right heel once with viable wound bed
 No pressure on right heel
  Keep right foot elevated
 Daily daikens

Day 17 (July 09 2019) 8:40am

 Continue present management
 Maintain dressing
 Plan: Flap right heel once with viable wound bed
 No pressure on right heel
 Keep right foot elevated
 Daily daikens

2:00pm
 Still for flap right heel
 Continue present management

Day 18 (July 10 2019) 7:45am

 Continue present management
 Maintain dressing
 Plan: Flap right heel once with viable wound bed
 No pressure on right heel
 Keep right foot elevated
 Daily daikens

10:00pm
 Still for flap right heel
 Secure ortho crutches
 Repeat CBCPC, Na, K, tomorrow AM
 Refer

Day 19 (July 11 2019) 9:20am

The day I received the patient

 Continue present management

 Plan: Flap right heel once with viable wound bed
 No pressure on right heel
 Keep right foot elevated
2:00pm
 Referred to optha for DM Retinopathy screening
  Still for flap right heel
 Increase lantus to 18 “u” SQ OD PM

3:45pm
 Increase Humulin R 18 ‘u” pre dinner only
 Increase insulin to 18 “u” SQ OD AM
 CBG monitoring
9:51pm
 Patient was seen and examined
 History, PE and chart reviewed
 Anesthesia plan explained, understood and accepted by patient
 Secure consent for anesthesia
 NPO now
 Medications: Omeprazole 40mg TIV OD once on NPO
 Hold hypoglycemic agents prior to procedure
 Monitor VS q4 and record

10:30pm
 Patient seen and examined
 History & PE reviewed
 For fluorescing angiography as out patient basis
 (Normal BUN Crea) for baseline evaluation of patients posterior segment
 Ensure strict glucose control
 No immediate optha intervention for now
 Refer back if there new onset optha symptoms
 Advised follow up at Eye center for evaluation with diagnostics
 Eye exam was done

Day 20 (July 12 2019) 9:00am

ORTHO PRE-OP

 NPO
 Continue IVF
 Continue IV medications
 For “E” Repeat wound debridement, right heel
 Secure consent for procedure
 Secure 1 unit PRBC for OR
 Maintain dressing
 Start Omeprazole 40 mg IV OD while on NPO

Day 21 (July 10 2019) 2:00pm

  Noted ortho plans
 Hold insulin today if for or
 CBG Q4 once on NPO Q1 at OR
 Avoid D5 containing fluids
 Continue present management

REVIEW OF LITERATURE

DIABETES MELLITUS

Somatostatins are hormones secreted directly into the bloodstream, and together, they
regulate the level of glucose in the blood. Insulin lowers the blood sugar level and increases the
amount of glycogen (stored carbohydrate) in the liver; Diabetes mellitus is a metabolic disorder,
specifically affecting carbohydrate metabolism. It is a disease characterized by persistent
hyperglycemia (high glucose blood sugar). It is a metabolic disease that requires medical
diagnosis, treatment and lifestyle changes. The World Health Organization recognizes three main
forms of diabetes: type 1, type 2 and gestational diabetes (or type 3, occurring during
pregnancy), although these three "types" of diabetes are more accurately considered patterns of
pancreatic failure rather than single diseases. Type 1 is generally due to autoimmune destruction
of the insulin-producing cells, while type 2 and gestational diabetes are due to insulin resistance
by tissues. Type 2 may progress to destruction of the insulin-producing cells of the pancreas, but
is still considered Type 2, even though insulin administration may be required.

Since the first therapeutic use of insulin (1921) diabetes has been a treatable but chronic
condition, and the main risks to health are its characteristic long-term complications. These
include cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for
dialysis in developed world adults), retinal damage which can lead to blindness and is the most
significant cause of adult blindness in the non-elderly in the developed world, nerve damage,
erectile dysfunction (impotence) and gangrene with risk of amputation of toes, feet, and even
legs.

TYPE 1 DIABETES MELIITUS

Type 1 diabetes mellitus formerly known as insulin-dependent diabetes (IDDM),

childhood diabetes, or juvenile-onset diabetes - is characterized by loss of the insulin-producing
beta cells of the islets of Langerhans of the pancreas leading to a deficiency of insulin.
Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. This
type comprises up to 10% of total cases in North America and Europe, though this varies by
geographical location. This type of diabetes can affect children or adults, but has traditionally
been termed "juvenile diabetes" because it represents a majority of cases of diabetes affecting
children. The most common cause of beta cell loss leading to type 1 diabetes is autoimmune
destruction, accompanied by antibodies directed against insulin and islet cell proteins. The
principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin.
Without insulin, ketosis and diabetic ketoacidosis can develop and coma or death will result.

Currently, type 1 diabetes can be treated only with insulin, with careful monitoring of
blood glucose levels using blood testing monitors. Emphasis is also placed on lifestyle
adjustments (diet and exercise). Apart from the common subcutaneous injections, it is also
possible to deliver insulin via a pump, which allows infusion of insulin 24 hours a day at preset
levels, and the ability to program a push dose (a bolus) of insulin as needed at meal times. This is
at the expense of an indwelling subcutaneous catheter. It is also possible to deliver insulin via an
inhaled powder.
 Type 1 treatment must be continued indefinitely at present. Treatment does not impair
normal activities, if sufficient awareness, appropriate care, and discipline in testing and
medication. The average glucose level for the type 1 patient should be as close to normal (80–
120 mg/dl, 4–6 mmol/l) as possible.

TYPE 2 DIABETES MELLITUS

Type 2 diabetes mellitus is previously known as adult-onset diabetes, maturity-onset

diabetes, or non-insulin dependent diabetes mellitus (NIDDM) - is due to a combination of
defective insulin secretion and defective responsiveness to insulin (often termed insulin
resistance or reduced insulin sensitivity), almost certainly involving the insulin receptor in cell
membranes. In early stages, the predominant abnormality is reduced insulin sensitivity,
characterized by elevated levels of insulin in the blood. In the early stages, hyperglycemia can be
reversed by a variety of measures and medications that improve insulin sensitivity or reduce
glucose production by the liver, but as the disease progresses the impairment of insulin secretion
worsens and therapeutic replacement of insulin often becomes necessary. There are numerous
theories as to the exact cause and mechanism for this resistance, but central obesity (fat
concentrated around the waist in relation to abdominal organs, not it seems, subcutaneous fat) is
known to predispose for insulin resistance, possibly due to its secretion of adipokines (a group of
hormones) that impair glucose tolerance. Abdominal fat is especially active hormonally. Obesity
is found in approximately 90% of Developed world patients diagnosed with type 2 diabetes.
Other factors may include aging and family history, although in the last decade it has
increasingly begun to affect children and adolescents.
Type 2 diabetes may go unnoticed for years in a patient before diagnosis, since the
symptoms are typically milder (e.g. lack of ketoacidotic episodes) and can be sporadic. However,
severe complications can result from unnoticed type 2 diabetes, including renal failure, vascular
disease (including coronary artery disease), vision damage, etc.
Type 2 diabetes is usually first treated by changes in physical activity (usually increase), diet
(generally decrease carbohydrate intake, especially glucose generating carbohydrates), and
through weight loss. These can restore insulin sensitivity, even when the weight loss is modest,
for example, around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. The
next step, if necessary, is treatment with oral antidiabetic drugs. As insulin production is initially
unimpaired, oral medication (often used in combination) can still be used that improves insulin
production (eg, sulfonylureas) and regulate inappropriate release of glucose by the liver (and
attenuate insulin resistance to some extent (eg, metformin), and substantially attenuate insulin
resistance (eg, thiazolidinediones). If these fail, insulin therapy will be necessary to maintain
normal or near normal glucose levels. A disciplined regimen of blood glucose checks is
recommended in most cases, most particularly and necessarily when taking most of these
medications.

SIGNS AND SYMPTOMS OF DIABETES MELLITUS

Type 2 diabetes almost always has a slow onset (often years), but in Type 1, particularly
in children, onset may be quite fast (weeks or months). Early symptoms of Type 1 diabetes are
often polyuria (frequent urination) and polydipsia (increased thirst and consequent increased
fluid intake). There may also be weight loss (despite normal or increased eating), increased
appetite, and unreduceable fatigue. These symptoms may also manifest in Type 2 diabetes,
though this seldom happens for some years, and sometimes not at all. Clincally, it is most
common in Type 2 patients who appear at the doctor with frank poorly controlled diabetes.

Another common presenting symptom is altered vision. Prolonged high blood glucose
causes changes in the shape of the lens in the eye, leading to blurred vision and, perhaps. All
unexplained quick changes in eyesight should force a fasting blood glucose test.
Especially dangerous symptoms in diabetics include the smell of acetone on the patient's
breath (a sign of ketoacidosis), Kussmaul breathing (a rapid, deep breathing), and any altered
state of consciousness or arousal (hostility and mania are both possible, as is confusion and
lethargy). The most dangerous form of altered consciousness is the so-called "diabetic coma"
which produces unconsciousness. Early symptoms of impending diabetic coma include polyuria,
nausea, vomiting and abdominal pain, with lethargy and somnolence a later development,
progressing to unconsciousness and death if untreated.
Signs and symptoms of diabetes mellitus are due to the high amounts of sugar in the
body. The signs and symptoms of Type 1 diabetes develop quicker and become more severe than
those of Type 2 diabetes. However, the symptoms of Type 2 diabetes may not be noticed until a
regular medical checkup. The more severe the diabetes is, the more sugar is in the blood and the
longer high blood sugar levels last. The high amount of sugar in the blood means that more urine
is needed to carry it out of the body. As a result, people with diabetes usually experience a strong
urge to pee, high amounts of urination (peeing), and constant thirst. The strong urge to pee can
occur at night and lead to low amounts of sleep. A high amount of peeing also leads to high
amounts of water and electrolyte loss. Electrolytes are chemical substances that are able to
conduct electricity after they are melted or dissolved in water.
For people with diabetes mellitus, the urine smells sweet because the extra sugar comes
out in the urine flow. Weakness and tiredness occur because the cells in the body are not able to
store or use the sugar that they need for energy. Thus, the body is being starved of one its main
energy sources. The body still gets some energy, however, from breaking down stored fat. The
breaking down of stored fat, in turn, leads to weight loss.
Although people with diabetes mellitus can break down stored fat for energy, the body
has a difficult time doing so. People with diabetes mellitus also have a difficult time breaking
down proteins. The difficulty in breaking down fats, especially when the body does not produce
insulin, can lead to the production of acids and poisonous chemical substances called ketones.
This condition is known as ketoacidosis. Ketoacidosis is a medical emergency because it can
cause coma, severe loss of body fluids, and even death. A coma is a state of deep
unconsciousness in which there are no voluntary movements, no responses to pain, and no verbal
speech. The signs and symptoms of ketoacidosis are nausea, vomiting, abdominal pain,
confusion, deep breathing, and foul-smelling breath. The foul-smelling breath smells like nail
polish remover.
Emergency treatment for ketoacidosis includes giving the person fluids to correct for
fluid loss and to bring back a normal chemical balance in the blood. Insulin injections are
alsogiven to allow cells to better absorb glucose from the blood. Ketoacidosis can occur in
people with Type 1 and Type 2 diabetes. The difficulty with breaking down fats is especially true
for people with Type 1 diabetes (see two sections down for a description) if they miss several
doses of insulin or develop another disease. The reason for this is that developing another disease
increases the body's use of insulin. Other symptoms of diabetes mellitus are blurry vision,
increased hunger, boils, as well as tingling and loss of sensation in the feet and hands. Boils are
inflamed, pus-filled areas of the skin. Pus is a yellow or green creamy substance sometimes
found at the site of infections.

RISK FACTORS OF TYPE II DM

OBESITY

Obesity is a medical condition in which excess body part has occumulated to the
extent that it may have an adverse effect on health, leading to reduce life expectancy. Body mass
index, which compares weight and height, is used to define a person as overweight when their
BMI is between 25 kg/m2 and 30kg/m2 and obese when it is greater than 30 kg/m2 .

The primary treatment for obesity is dieting and physical exercise. If this fails,
antiobesity drugs may be taken to reduce appetite or inhibit fat absorption.

IMPAIRED GLUCOSE TOLERANCE

Several factors have contributed to induce the impairment of glucose tolerance in the
elderly. Especially, changes of body composition with aging, the loss of skeletal muscle mass and
relatively increased fat tissues, could occur the insulin resistance state. Such state would be well
known to accompany with diabetes mellitus and hypertension. Therefore, the treatment of
hypertension with diabetes in the elderly would be very important to prevent not only
microangiopathy but also macroangiopathy. The optimal blood pressure levels to reduce
hypertension – related morbidity and mortality in diabetic elderly have been proposed 130/85.
The first step therapy in this case would be recommended calcium channel blocker, angiotensin
converting enzyme inhibitor, and angiotensin receptor blocker. In addition, comprehensive
geriatric assessment must be important to maintain drug compliance for well controlled blood
pressure levels.
GENETICS/HEREDITARY

In a study of 200 adults with type 2 diabetes, about 2/3 reported atleast one close
relative with diabetes and nearly 50 % had atleast two relatives with the disease. In particular,
people whos mother had diabetes where twice as likely to get the disease as those whos father
had diabetes.

RACE

Diabetes occurs more often in Hispanic/Latino Americans, African-Americans, Native

Americans, Asian Americans, Pacific Islanders, and Alaska Natives.

HYPERTENSION

Hypertension, or high blood pressure, is a major risk factor of diabetes. High blood
pressure is generally defined as 140/90 mmHg or higher. Low levels of HDL ( good cholesterol)
and high triglyceride levels also put you at risk.

SEDENTARY LIFESTYLE

Being inactive – exercising fewer than 3 times a week makes you more likely to
develop diabetes.

AGE

Some doctors advise anyone over 45 to be screened for diabetes. That’s because
increasing age puts you at higher risk of developing type 2 dibetes. It’s important to remember,
though, that people at any age can develop diabetes.

PREVENTION
Maintain body weight and prevent obesity through proper nutrition and physical
activity/exercise.

Encourage proper nutrition – eat more dietary fiber, reduce salt and fat intake, avoid simple
sugars like cakes and pastries; avoid junk foods.

Promote regular physical activity and exercise to prevent obesity,hypercholesterolimia, and

enhance insulin action in the body.

Advise smoking cessation for active smokers and prevent exposure to second hand smoke.
Smoking among diabetes increases risk for heart attack and stroke.

HYPOGLYCEMIA

Hypoglycemia, sometimes called an insulin reaction, can happen even

during those times where you’re doing all you can to manage your diabetes .

CLINICAL MANIFESTATIOS

 Shakiness
 Dizziness
 Sweating
 Hunger
 Pale skin color
 Clumsy or jerky movements
 Confusion

NEUROPATHY
Neuropathy affects all peripheral nerves: pain fibers, motor neurons,
autonomic nerves. It therefore necessarily can affect all organs and systems
since all are innervated.

CLINICAL MANIFESTATIONS

 Numbness and tingling of extremities

 Decreased or loss of sensation to a body part
 Muscle weakness
 Difficulty swallowing
 Speech impairment
 Vision changes
  Urinary incontinence

MACROVASCULAR DISEASES

Cerebrovascular disease is a group of brain dysfunctions related to disease of the blood

vessels supplying the brain. Hypertension is the most important cause; it damages the blood
vessel lining, endothelium, exposing the underlying collagen where platelets aggregate to initiate
a repairing process which is not always complete and perfect. Sustained hypertension
permanently changes the architecture of the blood vessels making them narrow, stiff, deformed,
uneven and more vulnerable to fluctuations in blood pressure.

A fall in blood pressure during sleep can then lead to a marked reduction in blood flow in
the narrowed blood vessels causing ischemic stroke in the morning. Conversely, a sudden rise in
blood pressure due to excitation during the daytime can cause tearing of the blood vessels
resulting in intracranial hemorrhage. Cerebrovascular disease primarily affects people who are
elderly or have a history of diabetes, smoking, or ischemic heart disease.

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a

heart attack, is the interruption of blood supply to part of the heart, causing some heart cells to
die. This is most commonly due to occlusion (blockage) of a coronary artery following the
rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty
acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting
ischemia (restriction in blood supply) and ((oxygen shortage, if left untreated for a sufficient
period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

PERIPHERAL VASCULAR DISEASE

In peripheral vascular disease, a diabetic client can develop arterial occlusion and
thrombosis that can lead to gangrene but this can be developed years after you have been
diagnosed of diabetes mellitus and not properly treating it. Both the types of diabetes mellitus
have a risk to develop this type of disease.

CLINICAL MANIFESTATIONS
  Tingling sensation of affected area
 Numbness / loss of sensation
 Pale skin color

DIAGNOSTIC EXAMS

Random blood glucose test (RBS)

For a Random blood glucose test, blood can be drawn at any time throughout the day, regardless
of when the person last ate. A random blood glucose level of 200mg/dl (11.1mmol/L) or higher
in persons who have symptoms of high blood glucose suggest a diagnosis of diabetes.

Fasting blood glucose test (FBS)

Fasting blood glucose testing involves measuring blood glucose after not eating or
drinking for 8 to 12 hours (usually overnight). A normal fasting blood glucose level is <100
mg/dL. A fasting blood glucose of 126 mg/dL (7.0 mmol/L) or higher indicates diabetes. The test
is done by taking a small sample of blood from a vein or fingertip. It must be repeated on another
day to confirm that it remains abnormally high.

Hemoglobin A1C test (HbA1c)

The A1C blood test measures the average blood glucose level during the past 2 to 3
months. It is used to monitor blood glucose control in people with known diabetes, but is not
normally used to diagnose diabetes. Normal values for A1C are 4 to 6 percent. The test is done
by taking a small sample of blood from a vein or fingertip.

Oral glucose tolerance test (OGTT)

Oral glucose tolerance testing is the most sensitive test for diagnosing diabetes and
pre-diabetes. However, the OGTT is not routinely recommended because it is inconvenient
compared to a fasting blood glucose test.

The standard OGTT includes a fasting blood glucose test. The person then drinks a 75
gram liquid glucose solution (which taste very sweet, & is usually cola or orange flavored). Two
hours later, a second blood glucose level is measured.
MANAGEMENT OF DIABETES

 TYPE I Diabetes Mellitus – Insulin

 TYPE II Diabetes Mellitus – Diet, Exercise, OHA (Oral Hypoglycemic Agent)
 Gestational Diabetes Mellitus – Insulin, Diet, Exercise

DIET

DIABETIC DIET

Maintain blood glucose as near as normal as possible, delay or prevent onset of diabetic
complications.

FOODS ALLOWED

Choose foods with low glucose index compose of:

A. 45-55% carbohydrates
B. 30-35% fats
C. 10-25% protein

EXERCISE

Helps burn fats which in excess may lead to obesity that can cause serious complications, Not
allowed during period of stress (illness or surgery).

INSULIN

Insulin increases glucose transport into cells and promotes conversion of glucose to
glycogen, decreasing serum glucose levels. Primarily acts in the liver, muscle, adipose tissue by
attaching to receptors on cellular membranes and facilitating transport of glucose, potassium and
magnesium. Hormone secreted by the alpha cells of the islets of langerhans in the pancreas.
Increase blood glucose by stimulating glycogenolysis in the liver.
  Given subcutaneously, intramuscularly or intravenously .

TYPES OF INSULIN ONSET PEAK DURATION

SHORT – ACTING

 REGULAR
 SEMI LENTE 7 hours
30 minutes 3 hours
 HUMULIN R
to 1 hour
INTERMEDIATE –ACTING

 LENTE
 HUMULIN N
 NPH (NEUTRAL PROTAMINE
HAGEDON) 3 hours 7 hours 21 hours
LONG – ACTING

 ULTRA LENTE
 HUMULIN U
 PZI (PROTAMINE ZINC
INSULIN) 7 hours 21 hours 28 hours

CHARACTERISTICS:

CLEAR – REGULAR, HUMULIN R

CLOUDY – REST OF INSULINS

DO’S AND DON’T’S IN ADMINISTERING INSULIN

 Check the expiration date.

 Never aspirate.
 Never massage the injection site.
  Never inject a cold insulin.
 Rotate the injection site

ORAL HYPOGLYCEMIC AGENT If normal blood glucose levels are not

achieved after 2-3 months of lifestyle modifications, treatment with an oral
antihyperglycemic drug is often prescribed. However, the patient should be
clearly advised that the ability of any drug therapy to improve the health of any
diabetic patient is aided by appropriate changes in diet and activity leve.

XI. ANATOMY AND PHYSIOLOGY OF THE SYSTEM INVOLVED

Every cell in the human body needs energy in order to function. The body’s primary energy
source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates
(sugars and starches). Glucose from the digested food circulates in the blood as a ready energy
source for any cells that need it. Insulin is a hormone or chemical produced by cells in the
pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of
cell and acts like a key to open a doorway in to the cell through which glucose can enter. Some
of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and
saved for later use. When there is not enough insulin produced or when the doorway no longer
recognizes the insulin key, glucose stays in the blood rather entering the cells.

Anatomy of the pancreas:

The pancreas is an elongated, tapered organ located across the back of the abdomen, behind the
stomach. The right side of the organ (called the head) is the widest part of the organ and lies in
the curve of the duodenum (the first section of the small intestine). The tapered left side extends
slightly upward (called the body of the pancreas) and ends near the spleen (called the tail). The
pancreas is made up of two types of tissue:

• Exocrine tissue The exocrine tissue secretes digestive enzymes. These enzymes are secreted
into anetwork of ducts that join the main pancreatic duct, which runs the length of the pancreas.
 • Endocrine tissue The endocrine tissue, which consists of the islets of Langerhans, secretes
hormones into the bloodstream.

Functions of the pancreas:

The pancreas has digestive and hormonal functions:

• The enzymes secreted by the exocrine tissue in the pancreas help break down carbohydrates,
fats, proteins, and acids in the duodenum. These enzymes travel down the pancreatic duct into
the bile duct in an inactive form. When they enter the duodenum, they are activated. The
exocrine tissue also secretes a bicarbonate to neutralize stomach acid in the duodenum.

• The hormones secreted by the endocrine tissue in the pancreas are insulin and glucagon (which
regulate the level of glucose in the blood), and somatostatin (which prevents the release of the
other two hormones.

Anatomy of the kidney :

Precipitating Factors:
Predisposing Factors:
 Obesity
 Unhealthy Insulin resistance
 Male
eating  Age 45
 Physical
inactivity
 Exhaustion of beta cell

Impaired insulin
secretion

Decrease absorption of
glucose by the cell

Cell starvation

1st CBG monitoring: UNCONTROLLED

400 mg/dl HYPERGLYCEMIA

Increase serum osmolarity

Increase viscocity of blood

Thickening of blood
vessel walls

Decrease blood flow to

organ and extremities

Sluggish blood
circulation
Microorganisms enter the Delayed wound healing
open wound

Presence of necrotic
Infection tissues on the heel part of
right foot

Disruption of skin
Hyperthermia

Occlusion of plaque Musculoskeletal effects

Blood flow blocked Impaired glucose

absorption in the muscle
tissue
Increase blood pressure

Production glucose
protein and fat stores
Hypertension

Wasting of lean body Fatigue

mass

Weight loss
 LABORATORY AND DIAGNOSTIC
PROCEDURES
QUIRINO MEMORIAL MEDICAL CENTER

CHEMISTRY

Received Lab Checked-in Released Printed

26-June-2019 12:23 AM 26-June-2019 12:42 AM 26-June-2019 1:16 AM 26-June-2019 2:36

TEST NAME RESULT UNIT REFERENCE RANGE INTERPRETATION

HEMATOLOGY
Complete Blood Count

RBC COUNT 4.28 X10^12/L 4.7-6.1 NORMAL

HEMOGLOBIN 124 G/L 120-160 NORMAL

HEMATOCRIT 0.46 VOL % 0.40-0.54 NORMAL

MCV 82.0 FL 80.0-96.0 NORMAL
MCH 27.10 PG 27.0-31.0 NORMAL
MCHC 33.00 % 32.0-36.0 NORMAL

RDW 14 11.-14.6 NORMAL

High platelet
PLATELET 478 X10^9/L 150-450 count may be
COUNT reffered to as
thrombocytosis

High white blood

cell count may
indicate that the
WBC 21.6 X10^9/L 5.0-10.0 immune system is
working to
destroy an
infection
DIFFERENTIAL
COUNT
High neutrophils
is a sign that your
NEUTROPHIL 0.90 0.50-0.70 body has an
infection
 High level of
lymphocytes is
LYMPHOCYTES 0.07 0.2-0.5 associated with
inflammatory
bowel disease.
EOSINOPHIL 0.01 0.0-0.6 NORMAL
MONOCYTES 0.05 0.02-0.09 NORMAL
BASOPHIL 0.00 0.0-0.2 NORMAL

LABORATORY AND DIAGNOSTIC

PROCEDURES
QUIRINO MEMORIAL MEDICAL CENTER
 CHEMISTRY

Received Lab Checked-in Released Printed

26-June-2019 12:23 AM 26-June-2019 12:42 AM 26-June-2019 1:16 AM 26-June-2019 2:36

CLINICAL CHEMISTRY

TEST NAME RESULT UNIT REFERENCE RANGE INTERPRETATION

 GLUCOSE, 19.27 Mmol/L 2.5-7.2
RBS
SODIUM 137.57 Mmol/L 136-145 NORMAL
POTASSIUM 3.28 Mmol/L 3.5-5.1 NORMAL
BLOOD UREA
NITROGEN 8.64 Mmol/L 3.0-9.2 NORMAL
CREATININE 71.04 Umol/L 64-104 NORMAL
CKMB 23.82 U/L 7.0-25.0 NORMAL

TEST NAME RESULT UNIT REFERENCE RANGE INTERPRETATION

LABORATORY AND DIAGNOSTIC

PROCEDURES
QUIRINO MEMORIAL MEDICAL CENTER

CLINICAL CHEMISTRY

Received Lab Checked-in Released Printed

12-June-2019 12:23 AM 12-June-2019 12:42 AM 12-June-2019 1:16 AM 12-June-2019 2:36

CLINICAL CHEMISTRY

Hemoglobin A1C 6.65 % <6.65 HIGH

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 400 700 1100 1100 1100
2-10 500 600 1000 900 900
10-6 500 500 1000 900 900
Date: _06-23-19_ 3100 2,900
INTAKE AND OUTPUT SHEET

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 300 800 1100 300 700
2-10 400 500 900 300 700
 10-6 300 200 500 300 300
Date: _06-24-19_ 2500 2300
INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 300 400 700 700 700
2-10 NPO 1000 1000 1000 1000
10-6 500 300 800 600 600
Date: _06-25-19_ 2500 2300

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 800 1300 800 800
2-10
10-6 500 900 1400 600 600
Date: _06-26-19_ 2600 2200

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 700 600 1300 800 800
2-10 400 900 1300 700 700
10-6 400 600 1000 1000 1000
Date:_06-27-19_ 2800 2500

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 800 500 1200 1000 1000
2-10 500 1000 1000 1000 1000
10-6 300 500 800 900 900
Date: _06-28-19_ 3000 2800

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 400 600 1000 700 700
2-10 400 400 800 700 700
10-6 300 400 700 600 600
Date: _06-29-19_ 2500 2100

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 400 500 900 600 600
2-10 300 700 900 900 900
10-6 400 600 1000 1000 1000
Date: _06-30-19_ 2800 2500

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 1000 800 900 700 700
2-10 400 800 800 600 600
10-6 350 500 800 600 900
Date: _06-01-19_ 2500 2200

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 700 1200 1000 1000
2-10 200 600 800 700 700
10-6 500 700 1000 1000 1000
Date: _06-02-19_ 3000 2700
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 800 1300 700 700
2-10 400 500 900 800 800
10-6 300 700 1000 900 900
Date: _06-03-19_ 2700 2400
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 600 500 1100 1000 1000
2-10 300 1000 1300 1000 1000
10-6 300 500 800 900 900
Date: _06-04-19_ 3200 2900
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 400 900 700 700
2-10 500 500 1000 700 800
10-6 400 500 900 900 900
Date: _06-05-19_ 2800 2400

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 800 500 1200 1000 1000
2-10 500 1000 1000 1000 1000
10-6 300 500 800 900 900
Date: _06-06-19_ 3000 2800
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 300 400 700 700 700
2-10 NPO 1000 1000 1000 1000
10-6 500 300 800 600 600
Date: _06-07-19_ 2500 2300
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 600 500 1100 1000 1000
2-10 300 1000 1300 1000 1000
10-6 300 500 800 900 900
Date: _06-08-19_ 3200 2900

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 700 1200 1000 1000
2-10 200 600 800 700 700
10-6 500 700 1000 1000 1000
Date: _06-09-19_ 3000 2700

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 400 600 1000 700 700
2-10 400 400 800 700 700
10-6 300 400 700 600 600
Date: _06-10-19_ 2500 2100

INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 500 800 1300 700 700
2-10 400 500 900 800 800
10-6 300 700 1000 900 900
Date: _06-11-19_ 2700 2400
 INTAKE OUTPUT
Shift Oral Parenteral Total Urine Drainage Vomitus Total
6-2 1000 800 900 700 700
2-10 400 800 800 600 600
10-6 350 500 800 600 900
Date: _06-12-19_ 2500 2200
 CBG MONITORING

DATE TIME CBG RESULT

06/23/19 11AM 200mg/dl
6PM 242mg/dl
10PM 109mg/dl
06/24/19 6AM 169mg/dl
11AM 129mg/dl
6PM 215mg/dl
10PM 251mg/dl
06/25/19 6AM 109mg/dl-
11AM 122mg/dl
6PM 154mg/dl
10PM 286mg/dl
06/26/19 6AM 150mg/dl-
12PM 176mg/dl
6PM 163mg/dl
10PM 149mg/dl
06/27/19 6AM 196mg/dl -
11AM 158mg/dl
6PM 294mg/dl
10PM 145mg/dl
06/28/19 6AM 171mg/dl -
12PM 191mg/dl
6PM 180mg/dl
10PM 145mg/dl
06/29/19 6AM 159mg/dl
12PM 152mg/dl
6PM 145mg/dl
10PM 171mg/dl
06/30/19 6AM 131mg/dl
11AM 219mg/dl
6PM 213mg/dl
10PM 160mg/dl
06/01/19 6AM 109mg/dl-
11AM 122mg/dl
6PM 154mg/dl
10PM 286mg/dl
06/02/19 6AM 150mg/dl-
12PM 176mg/dl
6PM 163mg/dl
10PM 149mg/dl
06/03/19 6AM 196mg/dl -
11AM 168mg/dl
6PM 294mg/dl
10PM 145mg/dl
06/04/19 6AM 161mg/dl -
12PM 191mg/dl
6PM 180mg/dl
10PM 145mg/dl
06/05/19 6AM 189mg/dl
12PM 152mg/dl
6PM 165mg/dl
10PM 171mg/dl
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION
SUBJECTIVE Impaired skin After 8 hours of INDEPENDENT: 1. Establishes After 8 hours of
DATA: integrity related to nursing interventions cooperative nursing interventions
open wound the patient will be 1. Assessed skin, baseline providing the patient was
“Parang hindi secondary to able to Participate in Noted color, turgor opportunityFor able to Participate in
gumagaling yung impaired circulation prevention and sensation. timely intervention. prevention measures
sugat ko sa paa” As as evidenced by measures and Described wounds and treatment
verbalized by the Disruption of skin treatment program and observed 2. Maintaining program and
patient. and Demonstrate changes. clean, dry skin Demonstrate proper
Swelling of right proper wound care provides a barrier wound care to
OBJECTIVE DATA: foot, Foul odor 2. Demonstrated to infection. Patting
to minimize skin minimize skin
proper wound care skin dry instead of
Disruption of skin breakdown or injury. breakdown or injury.
Drainage from the and good skin rubbing
(+) Swelling of right wound and hygiene.
foot Numbness 3. Wound dressings
3. Provided and protect the wound
(+) Foul odor applied wound and surrounding
dressings carefully. tissues.
(+) Drainage from
the wound 4. . Positioned leg 4. To promote
(+) Numbness elevated proper venous
return
DEPENDENT:
5. Antibiotic
5. Administered
medications are
medication as
widely used in the
prescribed:
treatment and
Clindamycin prevent ion of such
300mg, TIV x 28 infections.
day Q6

6. Assist daily
wound care with
dakins To clean the
7. For debridement wounded area and
as indicated prevents
contamination
ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION

SUBJECTIVE Imbalanced After 8 hours of 1. Monitored and 1. Changes in VS After 8 hours of

DATA: nutrition less than nursing recorded vital signs. Indicate impending nursing intervention,
“Laki ng pinayat ko body requirements intervention, the illness/disease patient was able to
kaysa sa katawan ko related to insulin patient will be able 2.Monitored and verbalize
dati” As verbalized deficiency as to gain weight. recorded I & O 2. To determine understanding and
by the patient. evidenced by recent nutrional and demonstrate
weight loss 3. Weigh weekly as elimination problems selection of meals
OBJECTIVE Weight: 60 kilos ordered and that help in stabilized
DATA: (May 2019) recorded. 3. Weighing serves as weight.
-Weight loss Weight: 53 kilos an assessment tool to
-Poor muscle tone (June 09 2019) 4. Assessed determine the
Weight: 60 kilos causative factors adequacy of
(May 2019) contributing to nutritional intake
Weight: 53 kilos imbalanced
(June 09 2019) nutrition. 4. To determine the
source of the problem
5.Discussed eating and eliminate it to
habits and prevent occurrence of
encouraged malnutrition.
diabetec diet as
prescribed by the
physician 5. To determine what
information to be
provided to patient
6. Educated the
client regarding the 6. Education provides
imporatance of information that the
eating healthy food. patient may not be
aware.

7. Observed signs Hypoglycemia can

of hypoglycemia. occur once blood
glucose level is
reduced and
carbohydrate
.
metabolism resumes
and insulin is being
given. If the patient is
comatose,
hypoglycemia may
occur without notable
change in level of
consciousness. This
potentially life-
threatening.
 ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION

Hypertension and After 8 hours of INDEPENDENT

SUBJECTIVE Decrease cardiac output nursing 1. Changes in BP may After 8 hours of
DATA: Related to increased intervention the 1. Monitored and indicates changes in nursing intervention the
peripheral vascular patient will be recorded blood
“Nahihilo po ako at pressure every 1 patient status requiring patient was able to
resistance as manifested able to verbalize
medyo nanlalabo hour prompt attention. stabilize her blood
by dizziness restlessness an absent of,
paningin ko” as and clammy skin dizziness, pressure from 140/90 to
verbalized by the 2. Assessed patient’s 2. To ensure patients 120/80 and dizziness,
BP= 140/90mmHg restlessness and
patient. dizziness and safety
clammy skin and restlessness and
blurred vision every
BP will 3. For the patient to be clammy skin were
4 hours until absent.
stabilized to relieved.
OBJECTIVE comfortable during
120/80 3. Promote adequate
DATA: therapy.
rest by decreasing
-Dizziness stimuli. 4. Salt retains water
-Restlessnes 4. Provide for thus increasing blood
restrictive diet: Low volume and blood
-Cool, clammy skin salt and low fat diet. pressure
V/S taken: 5. Suggest frequent 5.It may decreases
position changes. peripheral venous
BP = 140/90 mmHg
DEPENDENT: pooling that may be
potentiated by
6. Administered vasodilators and
medication as
prolonged sitting or
prescribed:
Atorvastatin standing
40mg/dl
1 tab OD HS
 ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION

SUBJECTIVE Hyperthermia Short Term: Independent: 1. Vital signs After 4 hours of

DATA: related to bacterial After 4 hours of 1. Monitored and provide more nursing
“Hindi maganda infection as nursing recorded vital accurate indication intervention
pakiramdam ko manifested by intervention the signs of core temperature Patient’s
kasi may lagnat Temperature: patient’s temperature is
ako” as verbalized 2. These decrease
38.6C temperature will 2. Removed warmth and
already in the
by the patient RR: 23cpm decrease to 37C excess clothing range; T= 37.1
increase
flushed skin and covers evaporative cooling Skin is cool,
Warm to touch Long Term: absence of
OBJECTIVE After 8 hours of 3.Promoted a 3. To promote clear flushing skin
DATA: nursing well-ventilated flow of air in the and diaphoresis.
Temperature: intervention the area to patient patiient’s area. One
38.6C patient’s vital way of promoting
RR: 23cpm signs will return to 4. Provided tepid heat loss
flushed skin normal range; with sponge bath.
Warm to touch 4. TSB helps
a temperature of
lowering the body
36.5-37.5C. 5.Advised patient temperature.
to increase oral
fluid intake 5. Fluids help
prevent elevated
6. Maintained bed temperature
rest associated with
dehydration
7. Educated and
advised support Teaching the
system (relative) support system the
right way to do the
to do TSB when
TSB will help in
patient feels hot. knowing what to do
 in case the patient’s
Dependent: increase
8. Administered temperature
antipyretic increases
medication as
prescribed: These drugs inhibit
Paracetamol the prostaglandin
300mg TIV Q4 that serve as
PRN: mediators of pain
and fever