XAVIER UNIVERSITYATENEO DE CAGAYAN

A CASE STUDY ON A 34 YEAR OLD MALE PATIENT DIAGNOSED WITH ACUTE RESPIRATORY FAILURE

SECONDARY TO SEPSIS SECONDARY TO ACUTE NECROTIZING PANCREATITIS AND DIABETES

MELLITUS TYPE II SECONDARY TO ACUTE NECROTIZING PANCREATITIS

Submitted to:Ms. Geraldine Lacar, RN

Mr. George Gordon Lim, RNMrs. Leonora Sumaylo, RN

Fourth year Clinical Instructor

Submitted by:Absin, Mary GraceAbuzo, Ana Kris

Ardiente, Robbie JayCoraler, TC May

Cue, Marc AnthonyDial, Mia Joy

Guzman, Van RyanIlagan, Leah Elizabeth

Lawan, GailManus, Gretta Carmel

Murillo, Joaquin IIPasoquin, Joyce DaneTaal, Mary AnnerizaVega, Angela PaulaYap, Lionel Bryan

BSN 4NC and NGGroup AA2

September 22, 2007

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TABLE OF CONTENTS

I. Introduction……………………………………………………………3

General objective…………………………………………………5

Specific objectives………………………………………………..5

Scope and limitations……………………………………………..6

II. Assessment

Patient demographic data…………………………………………7

Assessment tool…………………………………………………..8

Laboratory results………………………………………………..15

III. Anatomy and physiology……………………………………………16

IV. Pathophysiology

Narrative form……………………………………………………22

Schematic Diagram………………………………………………24

V. Medical management

General management…………………………………………….25

Drug study……………………………………………………….30

VI. Nursing management ………………………………………………61

VII. Discharge planning………………………………………………..72

VIII. Prognosis…………………………………………………………76

IX. Conclusion…………………………………………………………77

X. Recommendation……………………………………………………78

XI. Bibliography……………………………………………………….79

XII. Appendix………………………………………………………….81

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INTRODUCTION

This is a case of patient RP, 34 years ols, male, admitted on august 10, 2007, with the

presenting diagnosis of Acute Respiratory Failure secondary to sepsis secondary to acute

necrotizing pancreatitis; Diabetes Mellitus type II secondary to acute necrotizing pancreatitis.

Under the care of the XUSN4 of block NC and NG during the I.C.U. rotation in Maria Reyna

Hospital.

Acute pancreatitis is defined as an acute inflammatory process of the pancreas with

variable involvement of other regional tissues or remote organ systems. In acute pancreatitis,

protease trypsinogen enzyme, produced by the exocrine pancreas, converts into active trypsin;

the enzyme most responsible for auto-digestion of the pancreas, causes primarily the pain and

complications of pancreatitis.

Acute pancreatitis is classified further into mild and severe forms. Mild acute pancreatitis

is associated with minimal organ dysfunction and uneventful recovery. Severe acute pancreatitis

is associated with pancreatic necrosis and may lead to organ failure or local complications.

The International Symposium on Acute Pancreatitis in 1992 defined pancreatic necrosis

as the presence of one or more diffuse or focal areas of nonviable pancreatic parenchyma, which

is often associated with peripancreatic fat necrosis. By definition, pancreatic necrosis represents

a severe form of acute pancreatitis.

Type 2 diabetes mellitus, 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 insulin resistance or reduced insulin sensitivity (defective

responsiveness of tissues to insulin), which almost certainly involves the insulin receptor in cell

membranes. In short, Type 2 diabetes occurs when your pancreas does not make enough insulin

or is unable to use the insulin effectively. When the body does not make enough insulin or has

trouble using insulin, the cells do not absorb enough sugar from the blood - leading to high blood

sugar levels and diabetes.

This disease condition occurred from pancreatic insulin producing beta cell damage. Beta

cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans.

They make up 65-80% of the cells in the islets. These cells are responsible in making and

releasing insulin, a hormone that controls the level of glucose in the blood.

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Respiratory failure is a syndrome in which the respiratory system fails in one or both of

its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory

failure is defined as a PaO2 value of less than 60 mm Hg while breathing air, or a PaCO2 of more

than 50 mm Hg. Furthermore, acute respiratory failure is characterized by life-threatening

derangements in arterial blood gases and acid-base status.

Acute renal failure (ARF) is the rapid breakdown of renal (kidney) function that occurs

when high levels of uremic toxins (waste products of the body's metabolism) accumulate in the

blood. This disease condition occurs when the kidneys are unable to excrete the daily load of

toxins in the urine.

The above mentioned disease conditions is a brief overview of the presenting diagnosis

of the patient. Thorough discussion of the presenting diagnosis shall be reflected in Anatomy &

Physiology and in Pathophysiology.

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General objective

At the end of one hour of case presentation, we will be able to improve our knowledge in various

concepts related to our patient’s condition, and skills in careful assessment and rendering of

nursing interventions involved in the management of our client’s case; and develop positive

attitudes by cooperation and sense of teamwork as we accomplish our case study using concepts

that we have acquired from our NCM 104 classes and previous related subjects in the BSN and

AHSE curriculum.

Specific objectives

1. Perform a thorough assessment and careful gathering of data that are clinically significant

and will be utilized as reliable cues for our care plans.

2. Further completion of data that will supplement our assessment, such as laboratory

results, doctor’s orders and monitoring sheets.

3. Trace and familiarize the pathophysiology of our patient’s disease process.

4. Design individualized nursing care plans based on nursing diagnoses that are suitable and

feasible to carry out.

5. Carry out nursing interventions that are effective, reality based, time-bounded, achievable

and beneficial for our client.

6. Come up with a medical management, a prognosis, and a discharge plan that are suitable

and individually designed as well as clinically and scientifically based.

7. Develop a sense of teamwork in coming up with the case study by division of labor and

merging of ideas to establish data consistency.

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SCOPE AND LIMITATION

The study focuses on the assessment, anatomy, and pathophysiology and its diagram,

medical management-both ideal and actual, nursing care plans, ideal discharge plan, prognosis,

recommendation and conclusion revolving around the diagnosis of the patient which is Acute

Respiratory Failure secondary to sepsis secondary to acute necrotizing pancreatitis; Diabetes

Mellitus type II secondary to acute necrotizing pancreatitis. Noted complications in the

Respiratory System and Urinary System were also taken into consideration to better understand

the said disease condition.

This study is limited only to the available records found on the patient’s chart and the

information being provided for by the family members present at the patient’s room during the

time of assessment. Other factors that will also be considered as limitations to this study would

include the short-duration of time given for ICU rotation.

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Patient demographic profile

Name of patient: RP

Age: 34 years old

Sex: Male

Address: B-37 L-20 Grand Europa Lumbia Cagayan de Oro City

Civil status: Single

Height: 5’11”

Weight: 72.7 kgs

Language spoken: Visayan, Filipino

Religion: Roman Catholic

Nationality: Filipino

Occupation: unemployed

Income: None

Chief complaint: change in sensorium

Admission diagnosis: Acute Respiratory Failure secondary to sepsis secondary to

acute necrotizing pancreatitis; Diabetes Mellitus type II

secondary to acute necrotizing pancreatitis

Date of confinement: August 10, 2007

Name of attending physician: Dr. Valmores, Dr. A. Sison, and Dra. Solas

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College of NursingXavier University

Ateneo de Cagayan

LEVEL IVNURSING HISTORY & ASSESSMENT RECORD

NAME OF PATIENT: RP CHIEF COMPLAINT: Change in SensoriumAGE: 34 DIAGNOSES: Acute respiratory failure secondary to sepsis and acute necrotizing pancreatitis; Diabetes Mellitus type 2

secondary to acute necro- tizing pancreatitis;hypoalbuminemia

acute necrotizing pancreatitis;Hospital acquired pneumonia;Pulmonary edema; Acute renalFailure sec. acute necrotizing pancreatitis; hypokalemia sec. to insulin drip.

DATE: 8/10/07

TIME: ( / ) AM10:00 ( ) PM

NAME OF ATTENDING PHYSICIAN:Dr.Valmores, Dr. Sison, Dra.Solas

ADMITTED BY: ADMITTED FROM:( ) Ambulatory ( ) Wheelchair ( ) Home( / ) Stretcher ( / ) ER

Temperature:37.7 36.3

Pulse:119bpm 86bpm

Respiration: MV18cpm

Blood Pressure: 100/70 mmhg

Height:5’11” Weight:72.7kgs

Language/Dialeect spoken: Visayan dialect(/) Oriented to unit ( ) Not Oriented Reason: ( ) Confused ( ) Comatose ( ) Critical ( ) Language BarrierReligion: Roman Catholic Status: SingleINFORMANT: ( ) Patient ( ) Others (specify) Friend and younger sisterCHIEF COMPLAINT/REASON FOR HOSPITALIZATION:

1 day PTA, Pt. was noted to be sleeping most of the time without food/fluid intake. On the day of admission, the patient becomes so hypotensive with a blood pressure of 60/40mmhg, thus prompted for admission in Maria Reyna Hospital.Duration/Onset of problem: 1 day PTA (Aug. 9,2007)Treated for symptoms before: (/) No

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ALLERGIES:(/) None known ( ) Yes (Specify Allergen)RP’s younger sister verbalized, “ Wala mana sya’y allergies sa pagkaon og tambal.” MAJOR ILLNESS, OPERATIONS, AND HOSPITALIZATIONSMedical History: ( ) Heart disease ( ) Renal disease

( ) Hyperrtension ( ) Cancer ( ) Stroke (/) Substance Abuse:

Alcohol and cigarette ( ) Lung Disease ( ) Others

Comments: RP’s younger sister verbalized that,” kusog kayo gyud na sya manigarilyo, Makahurot na syag mga isa ka pack taga adlaw.” She then added, “ grabe kayo japon na sya gainom.”

Family History: ( ) Heart disease ( ) Renal disease ( ) Hypertension ( ) Cancer

( ) Stroke ( ) Substance abuse ( ) Lung disease ( ) Others: Diabetes MellitusComments: RP’s younger sister verbalized that, “karon lang gyud mi nakabalo na diabetic man diay akong papa,”

SURGICAL HISTORY/HOSPITALIZATIONS ( INCLUDE DATES): As written on the RP’s chart, he undergone craniotomy last March 2005, due to gunshot wound.

NUTRITION/METABOLIC PATTERNMeal pattern: Usually, RP eats three times a day. However, on our first assessment, RP is on NPO status. He is getting nutrition through TPN.On our second assessment, RP is fed per NGT 6 times a day.

Appetite: ( ) Good ( ) Fair ( ) Poor ( /) NAChanges in eating habits: ( ) No ( ) Yes ( / ) NAAppetite changes: ( ) No ( / ) Yes Time period: 1 day PTA, RP was observed to be sleeping without food/ fluid intake.Weight loss/gain: (+) weight loss; from 78kgs to 72.7kgs in one week Special diet: On our first assessment, RP is

on TPN_Kabiven(1400 kcal). On our 2nd assessment, RP is on NGT feeding of 1800 kcal/day in 1000 cc water in 6 divided doses + 6 egg whites/day.

Comments: RP’s younger sister verbalized that, “ grabe gyud ang iyang pagniwang,tambok mani sya sauna.” Imbalanced nutrition: Less than body requirements; weakness was also noted,and pale conjunctiva and mucous membranes.

TEETH (/ ) Own Comments: Yellowish white in color. RP’s younger sister verbalized that,”kumpleto pa man na iyang ngipon, wala pud na sya gagamit og bisag unsa para ngipon.”

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ELIMINATION PATTERNBLADDER ( / ) CatheterComments: RP is on urinary catheter draining well to a yellow colored urine. RP’s latest intake was 740 cc and his latest output was 860 cc. Polyuria was noted.BOWEL ( / ) DiaperComments: RP’s younger sister verbalized that, “ makalibang na sya mga kausa sa usa ka adlaw, ako may ga ilis sa iyang diaper.” His stool is yellowish brown in color, soft, and in moderate amount.

SLEEP OR REST PATTERN( ) No difficulty ( ./ ) Yes (describe) According to the patient’s sister RP has difficulty in sleeping. He could not sleep continuously and seems to be awake most of the time during the day. “Sige ra og mata-mata, sugod buntag padulong hapon”.

Use of sleeping aids ( /) No ( ) Yes

Comments/Nursing Problem Identified : As observed patient RP seems to be disturbed easily, whenever people would come across or visit him, he would open his eyes.

ACTIVITY/EXERCISEActivities of Daily Living (I= Independent, A=With Assistance, D=Dependent)Eating: (D) Bathing: (D) Dressing: (D) Grooming: (D) Toileting: (D) Ambulating: (D)

ACTIVITY LEVEL ( ) Active ( / ) Sedentary

Comments/Nursing Problem Identified: RP is currently on complete bed rest and is dependent in all activities of his daily living. He is taken cared by his “yaya” and his siblings. According to his sister the patient does not have work and he usually stays at home and helps with the household chores.

BEHAVIOR PATTERNBEHAVIOR ( ) relaxed ( ) mildly anxious

(/ ) moderately anxious ( ) very anxious

Psychiatric History: Upon assessment patient is moderately anxious and irritable. According to his sister RP had episodes of psychosis after he under went craniectomy because of a gunshot. “Paghuman atong napusilan siya, naa na dayon times na makalina iyang storya, mura siyag bata.” Og “naa gyud usahay mutukar na siya saputon lang kalit og di kaila.” As verbalized by his sister.

SUBSTANCE ABUSETobacco ( ) no ( / ) yes Cigarette/Cigar/Pipe 1 pack /day/wkDrugs ( / ) no ( ) yes Type:____________Alcohol ( ) no ( / ) yes Amount: 3 long neck/week

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Comments/Nursing Problem Identified: As verbalized by his “yaya” the patient is a smoker he can consume 1 pack of cigarette a day. RP is a chronic drinker,makahurot na sya og mga tulo ka long neck sa isa ka semana”, “balay ra man na siya, gatambay2x lang, inom og manigarilyo pud dayon” as verbalized by significant other.

SEXUALITY/REPRODUCTIVE PATTERNComments/Nursing Problem Identified: As observed and verbalized by the significant other patient has scrotal inflammation with minimal white discharges.

PHYSICAL ASSESSMENT

NEUROLOGICAL ASSESSMENT

On the first assessment, patient was conscious and able to respond by nodding. He

manifested weak lower extremities and because of this, pillows are placed under the legs to

prevent any further discomfort. He was oriented to the place but not the time. His speech and

swallowing is compromised because of the presence of a mechanical ventilation. Pupils were

4mm in size with the Right pupil sluggish and Left pupil briskly reactive to light

accommodation.

Upon second assessment, RP had no mechanical ventilation attached to him however

patient still had difficulty in vocalization with episodes of irritability and disorientation because

he could not identify some of his relatives. Both pupils briskly reactive to light accommodation

and 3mm in size. Weakness still noted in extremities.

RESPIRATORY ASSESSMENT

On the first assessment, patient RP was hooked on mechanical ventilator but is not fully

dependent on it; the mode was set only to assist and control. Crackles noted on both lungs , there

was deep labored breathing accompanied by the use of accessory muscles.

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On the second assessment, crackles still present and RP is coughing ineffectively due to

post-extubation and white secretions noted in RP’s oral cavity. Lips and mucous membranes are

pale but respirations are normal.

CARDIOVASCULAR ASSESSMENT

RP has a heart rate of 119bpm and was noted with sinus tachycardia.

PERIPHERAL-VASCULAR ASSESSMENT

Partial range of motion noted in the lower extremities. Weak and thready pulse was noted

especially in the lower extremities.

GENITOURINARY ASSESSMENT

RP was on a Foley Bag Catheter with urine clear and color yellow. Based on lab results,

presence of ketones was noted (40mg/dL). There was scrotal inflammation with minimal whitish

discharges.

Upon second assessment, there was an increase in urine output noted (O=870cc,

I=740cc). RP still on catheter and on diaper. Blister formation noted at the scrotal and sacral

area.

MUSKULOSKELETAL ASSESSMENT

There was full range of motion in RP’s upper extremities but with the lower, only partial.

Weakness was noted on the lower extremities.

SKIN ASSESSMENT

Oral mucosa was noted to be dry and lips were scaly and dry. Skin is intact except on the

right arm due to the presence of CVP catheter and on the three toes of his right leg due to

presence of blisters with sizes ranging from 6mm-8mm in diameter.

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On the second assessment, blisters were still evident on the R toes but with additional

blister formation on the Right heel, scrotal and sacral area. Skin is dry.

CURRENT MEDICATIONS

Bactidol oral care TID

1 neb duavent + ½ neb azmavent q6h

Pantoprazole (ulcepraz) 40 mg IVT OD

Citicholine 500mg IVT slow q12h

Furosemide to run in 2-3 hours q12h

Ciprofloxacin 200mg IV drip q12h

Hydrocortisone 100mg vial IVTT q8h

Imipenem and Cilastatin (Tienam) 500mg IVTT q12h

Cefepime 1g IVTT slow q12h

Tranexamic acid (Hemostan) 500mg/amp q8h

Ianzoprazole (Prevacid) 30 mg 1 tab OD/NGT

Glargine Insulin (Lantus) 30 “u” SQ before 8am

Ranitidine 50 mg IV q12h

Dopamine 2gm with D5NSS 300cc

Sodium Bicarbonate 50mg IVTT 4 vials with D5W at 10gtts/min

Tazobactam (Tazocin)4.5 IVTT now then 2.75 mg q12h

Insulin Aspart (Novorapid) 10 “u” SQ before each feeding

Potassium Chloride,60 mg IVTT

-patient RP has no knowledge on the medications prescribed in his treatment regimen.

ROLE RELATIONSHIP PATTERN AND DISCHARGE PLAN

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RP is fully dependent on the mother who resides in Germany due to the fact that he has

no work and has been unemployed for quite some time. He lives in Gran Europa with his 5

siblings and their families. They will also be the ones assisting RP when at home. Patient seems

to anticipate in returning home however, no order was made yet for any discharge due to further

evaluation and treatment. Patient RP is not in need of a social welfare service because the mother

who works abroad is able to compensate for the medical services.

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LAB0RATORY

EXAMINATION

RESULTS REFERENCE

VALUES

INTERPRETATION

ARTERIAL BLOOD GAS

> PaCO2 43.3 35 – 45 Normal

> HCO3 14.2 22 – 26 Low Metabolic Acidosis

> pH 7.2 7.35 – 7.45 Acidic

> PaO2 82.3 % 95% – 100% Low

CBC

> WBC 19.6 x 10^3/ uL 5 – 10 X10^3/uL High

> Platelet 80 x 10^6/ mm3 140 – 440

x10^6/mm3

Low

URINALYSIS

> BUN 58 mg/dL 8 – 20 mg/dL High

> Creatinine 3.2 mg/dL .8 – 1.5 mg/dL High

> Ketones 40 mg/dL Ketonuria

> Albumin Fraction 1.9 g/dL 3.5 – 5 g/dL Hypoalbuminemia

BLOOD CHEMISTRY

> Potassium 3.0 mmol/L 3.5 – 5.1 mmol/L Hypokalemia

HGT (Latest result) 151 mg/dL 60 – 110 mg/dL High

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ANATOMY AND PHYSIOLOGY

The Pancreas

The pancreas is an endocrine and exocrine organ located retroperitoneally in the upper

abdomen overlying the spine. It is a glandular organ that secretes digestive enzymes and

hormones. In humans, the pancreas is a yellowish organ about 7 in. (17.8 cm) long and 1.5 in.

(3.8 cm) wide. It lies beneath the stomach and is connected to the small intestine at the

duodenum. The pancreas is supplied by the gastroduodenal arteries and by branches of the

splenic artery. The splenic vein and artery run superiorly and posteriorly; the mesenteric vein

lies in the angle between the head and body of the gland. At this point the superior mesenteric

vein and splenic vein join to form the portal vein.

Most of

the

pancreatic tissue consists of grapelike clusters of cells that produce a clear fluid (pancreatic

juice) that flows into the duodenum through a common duct along with bile from the liver.

Pancreatic juice contains three digestive enzymes: tryptase, amylase, and lipase that, along with

intestinal enzymes, complete the digestion of proteins, carbohydrates, and fats, respectively.

Scattered among the enzyme-producing cells of the pancreas are small groups of endocrine

cells, called the islets of Langerhans, that secrete two hormones, insulin and glucagon. The

pancreatic islets contain several types of cells: alpha-2 cells, which produce the hormone

Figure 1. Relationships and blood supply of pancreas.

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glucagon; beta cells, which manufacture the hormone insulin; and alpha-1 cells, which produce

the regulatory agent somatostatin. These hormones are 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; glucagon has the

opposite action. Failure of the insulin-secreting cells to function properly results in diabetes,

which can occur in two major forms, the division being between juvenile onset and onset in

maturity.

The exocrine portion of the pancreas accounts for about 80% of the total glandular

volume. It consists of at least two functional units: acinar cells, which secrete primarily digestive

enzymes; and centroacinar or ductal cells, which secrete fluids and electrolytes. Pancreatic

secretion is regulated by several peptides that are released from the gastrointestinal tract. Some

of these peptides, such as secretin and cholecystokinin (CCK), stimulate pancreatic secretions,

whereas somatostatin and pancreatic polypeptide inhibit their release. The pancreas secretes

about 20 digestive enzymes and cofactors. Some enzymes are activated in the duodenum by

enterokinases and calcium. These enzymes account for most of the intraluminal digestion of

dietary proteins, triglycerides and carbohydrates. They are also important in the cleavage of

certain vitamins (such as A and B12) from carrier molecules, thereby allowing them to be

absorbed efficiently. Because pancreatic enzymes are secreted in great excess, maldigestion and

serious nutritional deficiencies occur only when over 90% of the gland has been destroyed.

The Cardiovascular System

The heart is the pump responsible for maintaining adequate circulation of oxygenated

blood around the vascular network of the body. It is a four-chamber pump, with the right side

receiving deoxygenated blood from the body at low pressure and pumping it to the lungs (the

pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping

it at high pressure around the body (the systemic circulation).

The myocardium (cardiac muscle) is a specialized form of muscle, consisting of

individual cells joined by electrical connections. The contraction of each cell is produced by a

rise in intracellular calcium concentration leading to spontaneous depolarization, and as each cell

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is electrically connected to its neighbor, contraction of one cell leads to a wave of depolarization

and contraction across the myocardium.

This depolarization and contraction of the heart is controlled by a specialized group of

cells localized in the sino-atrial node in the right atrium- the pacemaker cells.

1. These cells generate a rhythmical depolarization, which then spreads out over the atria to

the atrio-ventricular node.

2. The atria then contract, pushing blood into the ventricles.

3. The electrical conduction passes via the Atrio-ventricular node to the bundle of His,

which divides into right and left branches and then spreads out from the base of the

ventricles across the myocardium.

4. This leads to a 'bottom-up' contraction of the ventricles, forcing blood up and out into the

pulmonary artery (right) and aorta (left).

5. The atria then re-fill as the myocardium relaxes.

The 'squeeze' is called systole and normally lasts for about 250ms. The relaxation period,

when the atria and ventricles re-fill, is called diastole; the time given for diastole depends on the

heart rate.

The Respiratory System

The respiratory system is

situated in the thorax, and is

responsible for gaseous exchange

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between the circulatory system and the outside world. Air is taken

in via the upper airways (the nasal cavity, pharynx and larynx)

through the lower airways (trachea, primary bronchi and bronchial

tree) and into the small bronchioles and alveoli within the lung

tissue.

The lungs are divided into lobes; The left lung is composed of the

upper lobe, the lower lobe and the lingula (a small remnant next to

the apex of the heart), the right lung is composed of the upper, the

middle and the lower lobes.

Mechanics of Breathing

To take a breath in, the external intercostal muscles contract, moving the ribcage up and

out. The diaphragm moves down at the same time, creating negative pressure within the thorax.

The lungs are held to the thoracic wall by the pleural membranes, and so expand outwards as

well. This creates negative pressure within the lungs, and so air rushes in through the upper and

lower airways.

Expiration is mainly due to the natural elasticity of the lungs, which tend to collapse if

they are not held against the thoracic wall. This is the mechanism behind lung collapse if there is

air in the pleural space (pneumothorax).

Physiology of Gas Exchange

Each branch of the bronchial tree eventually sub-divides to form very narrow terminal

bronchioles, which terminate in the alveoli. There are many millions of alveoli in each lung, and

these are the areas responsible for gaseous exchange, presenting a massive surface area for

exchange to occur over.

Each alveolus is very closely associated with a network of capillaries containing

deoxygenated blood from the pulmonary artery. The capillary and alveolar walls are very thin,

allowing rapid exchange of gases by passive diffusion along concentration gradients. CO2 moves

into the alveolus as the concentration is much lower in the alveolus than in the blood, and O 2

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moves out of the alveolus as the continuous flow of blood through the capillaries prevents

saturation of the blood with O2 and allows maximal transfer across the membrane.

Control of Respiration

0ur respiratory rate changes. When active, for example, respiratory rate goes up; when

less active, or sleeping, the rate goes down. Also, even though the respiratory muscles are

voluntary, we can't consciously control them when we are sleeping.

The rhythmicity center of the medulla:

controls automatic breathing

consists of interacting neurons that fire either during inspiration (I neurons) or expiration

(E neurons)

o I neurons - stimulate neurons that innervate respiratory muscles (to bring about

inspiration)

o E neurons - inhibit I neurons (to 'shut down' the I neurons & bring about

expiration)

Apneustic center (located in the pons) - stimulate I neurons (to promote inspiration) Pneumotaxic

center (also located in the pons) - inhibits apneustic center & inhibits inspiration

 Factors involved in increasing respiratory rate:

Chemoreceptors - located in aorta & carotid arteries (peripheral chemoreceptors) & in the

medulla (central chemoreceptors)

Chemoreceptors (stimulated more by increased CO2 levels than by decreased O2 levels)

> stimulate Rhythmicity Area > Result = increased rate of respiration

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NARRATIVE PATHOPHYSIOLOGY

Acute necrotizing pancreatitis is the acute inflammation and necrosis of pancreas

parenchyma and focal enzymic necrosis of pancreatic fat and vessels. It is known to be

precipitated by chronic alcoholism. Other factors such as obesity and sedentary lifestyle are also

known to contribute to the development of the condition. It is common in people 30-40 years of

age and in those who take drugs such as Thiazide diuretics and steroids for drug therapy.

Given these factors, there will be partial obstruction of the sphincter of Oddi which leads

to obstruction to the outflow of pancreatic enzymes and leakage of these enzymes to pancreatic

tissues. Along with premature activation of these enzymes, autodigestion occurs, leading to acute

necrotizing pancreatitis.

Pancreatic enzymes may also leak into the blood stream and circulate into the lungs and

kidneys, prompting the release of proinflammatory mediators. These pancreatic enzymes and

mediators such as kinins increase vascular permeability and dilate blood vessels, further leading

to loss of plasma volume and increased permeability to protein. Increased permeability to protein

can lead to loss of albumin causing hypoalbuminemia. Loss of albumin stimulates lipoprotein

synthesis by the liver leading to hyperlipidemia.

Increase in vascular permeability also causes loss of plasma volume which leads to

decrease in blood volume and decreased renal blood flow resulting to ischemia. Toxic oxygen-

free radicals are generated, promoting swelling, injury and necrosis of nephrons. Acute tubular

necrosis occurs leading to decrease in filtration pressure and decrease in GFR resulting to acute

renal failure.

On the other hand, pancreatic enzymes circulating in the blood goes to the lungs causing

injury to the capillary endothelium further leading into disruption of surfactant production by the

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alveoli and increased capillary permeability. Increase in capillary permeability causes movement

of fluid and plasma protein from capillary to interstitial space (alveolar septum) and alveoli.

Decrease in blood volume (hypovolemia) and pleural effusion then occurs. Pleural effusion

results to pulmonary edema which impairs gas exchange. Blood oxygen level is then decreased

(hypoxemia), resulting to acute respiratory failure.

Another result of acute necrotizing pancreatitis is damage to the alpha and beta cells of

the islet of Langerhans. There is decrease in insulin production and increase in glucagon

production. Decrease in serum insulin level can cause significant increase in blood glucose level,

a condition known as diabetes mellitus type 2. In DM II there is increase in osmolarity and

chronic elevation in blood glucose level. The increase in osmolarity will then lead to increased

capillary permeability leading to increased urine output and decreased body fluids. This will

trigger the thirst mechanism of the body resulting to polydipsia. Chronic elevations in glucose

level, on the other hand, will cause glycoprotein deposits in the cell wall leading to three possible

conditions namely: diabetic neuropathy, diabetic nephropathy and impaired immune function.

Thus, increasing the client’s susceptibility to infection.

Production of excess glucagon results to production of glucose from protein and fat stores

(gluconeogenesis). There is wasting of lean body mass and serum ketones (byproduct of

gluconeogenesis) that promote ketosis.

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MEDICAL MANAGEMENT

The medical management of patient RP’s condition focused on alleviating of the

symptoms and treating its underlying causes. The following is a table presenting the ideal

management of the patient’s condition as well as the actual management given to the patient

during his hospital stay.

IDEAL MANAGEMENT ACTUAL MANAGEMENT

MANAGEMENT FOR ACUTE NECROTIZING PANCREATITIS:

1. Restoration of circulating blood volume with IV crystalloid or colloid solutions or blood products

2. Invasive monitoring in severe pancreatitis

3. Maintenance of adequate oxygenation reduced by pain, anxiety, acidosis, abdominal pressure, or pleural effusions; and adequate respiratory care because of the risk for elevation of the diaphragm, pulmonary infiltrates and effusion, and atelectasis.

4. Pain control to alleviate pain and anxiety, which increases pancreatic secretions

5. Rest of the GI Tracta. Withhold oral feedings to decrease

pancreatic secretionsb. Nasogastric intubation and suction

to relieve gastric stasis and distention

6. Maintenance of alkaline gastric pH with H2 antagonists and antacids to

- Venoclysis of PNSS 1 L, moderate fast drip then regulated at 40 drops per minute, followed by Lactated Ringer’s solution and regulated according to patient’s requirement at left arm

- Venoclysis of Lactated Ringer’s solution @ right arm

- CVP insertion at patient’s bedside, reading was 9 cm H2O

- Endotracheal intubation of the patient- Mechanical ventilation- O2 inhalation of 5 L/min following

endotracheal extubation- Chest X-ray PA- Monitoring of the patient’s Arterial

Blood Gas

- No pain management given

- Patient was NPO temporarily

- Intubation of the patient with a French 16, opened to drain

- Administration of Bactidol (Hexetidine) TID for oral care

- Administration of Ranitidine 50 mg IVTT q12h

25

suppress acid drive of pancreatic secretions and to prevent stress ulcer complications of illness.

7. Nutrition provided with parenteral feedings, as needed

8. Pharmacotherapya. Electrolyte replacement as needed

and Sodium bicarbonate to reverse metabolic acidosis

b. Regular insulin to treat hyperglycemia

c. Antibiotic therapy for sepsis

- Administration of Ianzoprazole (Prevacid) 30 mg 1 tab OD / NGT

- Administration of Pantoprazole (Ulcepraz) 40 mg IVTT OD

- Nasogastric feeding with Osteurized Formula, 60 cc

- Administration of Potasssium Chloride 60 mg IVTT to treat hypokalemia

- Administration of NaHCO3 50 mEq in 3 vials IVTT

- Administration of NaHCO3 drip: 4 vials with 250 cc D5W at 10 drops/ minute

- Insulin Aspart (Novorapid) 10 “u” SQ before each feeding

- Insulin Glargine (Lantus) 30 “u” SQ before 8 am feeding

- Administration of Ciprofloxacin (Ciprobay), 200 mg IV drip q12h

MANAGEMENT FOR ACUTE RESPIRATORY FAILURE

1. Oxygen therapy to correct hypoxemia

2. Mobilization of secretions

3. Bronchodilators to reduce bronchospasm

4. Corticosteroids to reduce inflammation

- Endotracheal intubation of the patient- Mechanical ventilation - O2 inhalation of 5L/min following

endotracheal extubation

- Suctioning of the Oral Cavity and Endotracheal tube PRN

- Administration of Duavent 1 nebule plus ½ nebule Asmavent q6h

- Administration Hydrocortisone 100 mg vial IVTT q8h

MANAGEMENT FOR DIABETES MELLITUS TYPE 2

1. Dieta. Dietary control with caloric

restriction of carbohydrates and saturated fats to maintain ideal body weight

2. Exercise Regularly scheduled exercise to

promote the utilization of carbohydrates, assist with weight

- Full diabetic diet at 1800 kcal/g in 3 meals and 2 snacks, with the following specifications:a. CHO 60 %b. CHON 20 %c. Fat 20 %

26

control, enhance the action of insulin, and improve cardiovascular fitness

3. Medicationa. Oral antidiabetic agents if glucose

control is not achieved with diet and exercise only

b. Insulin therapy when unresponsive to diet, exercise and oral antidiabetic therapy

4. Monitoring of control blood glucose

- No oral antidiabetic agent was administered

- Administration of the following Insulins:a. Insulin Glargine (Lantus) 30 “u”

SQ before 8 am feedingb. Insulin Aspart (Novorapid) 10 “u”

SQ before each feeding- Hemoglucose tests TID, pre-breakfast,

pre-lunch and pre-dinnerMANAGEMENT FOR HOSPITAL ACQUIRED PNEUMONIA

1. Antimicrobial therapy upon laboratory identification of causative organism and sensitivity to specific antimicrobials

2. Oxygen therapy if patient has inadequate gas exchange

3. Pulse oximetry and Arterial Blood Gas Analysis to determine the need for oxygen and to evaluate the therapy

- Administration of Ciprofloxacin, 200 mg IV drip q12h

- Administration of Cefepime 1g ICTT OD

- Administration of Imipinem + Cilastatin (Tienam) 500 mg IVTT q12h

- Administration of Piperacillin- Tazobactam (Tazocin)4.5 IVTT noe then 2.75 mg q12h

- Endotracheal intubation of the patient- Mechanical ventilation- O2 inhalation of 5L/min following

endotracheal extubation- Patient was constantly hooked to a

pulse oximeter- Arterial Blood Gas Analysis was

conductedMANAGEMENT FOR PULMONARY EDEMA

1. Treatment of underlying disorder

2. Oxygen therapy to correct hypoxemia

3. Administration of morphine to reduce anxiety and control pain

- Management of acute necrotizing pancreatitis

- Endotracheal intubation of the patient- Mechanical ventilation- O2 inhalation of 5L/min following

endotracheal extubation- No pain management

27

MANAGEMENT FOR ACUTE RENAL FAILURE

1. Maintenance of fluid balance. Be alert for and correct underlying fluid excesses or deficits

2. Restore maintain blood pressure

3. Maintain nutrition.

4. Hemodialysis, peritoneal dialysis or continued renal replacement

5. Diuretic agents to control fluid volume

- Intake and Output monitoring and recording every shift

- Measurement of central venous pressure, 9 cm H2O

- Administration of Dopamine 2 grams WITH 300 cc D5NSS

- Correction of hypotension through the administration of:a. 1.5 L Lactated Ringer’s solution at

moderate fast drip then regulating @ 60 drops per minute

b. Administration of 1 L Normal Saline Solution at 40 drops per minute on the left arm after administered IVF was consumed

c. Administration of 1 L Lactated Ringer’s Solution at 50 drops per minute as follow-up to administered intravenous fluid

- Total Parenteral Nutrition after temporary NPO then

- Nasogastric feeding with Osteurized Formula, 60 cc

- No dialysis or renal replacement was indicated for the patient

- Administration of Furosemide (to run for 2 hours) BID

MANAGEMENT OF HYPOKALEMIA1. Restoration of potassium levels

a.administration of 40 to 80 mEq/ Day of potassium

- Incorporation of 40 mEq Potassium Chloride to patient’s intravenous fluid STAT

- Administration of Potassium Chloride,60 mg IVTT

MANAGEMENT OF HYPOALBUMINEMIA1. Correction of low albumin levels - Administration of Albuminar 25% 50

cc stat- Addition of 6 egg whites to daily food

intake

28

DRUG STUDY

Generic Name: ALBUMIN 25 % Brand Name: ALBUMINAR 25Classification: BLOOD DERIVATIVE Dosage/ Administration/ Route: 50 cc STAT

INDICATIONS

THERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Treatment of hypoalbuminemia

Restoration of albumin to normal levels

Provides intravascular oncotic measure in a 5:1 ratio, shifting fluid from interstitial spaces to the circulation and slightly increasing the plasma protein level.

Contraindicated in hypersensitivity to the drug and in those with severe anemia, or cardiac failure.

Directly enters the circulation following IV infusion.

Headache

NauseaVomitingUrticariaRashBack pain

Vascular OverloadHypotensionTachycardiaAltered respirationDyspneaPulmonary edemeChills

Watch for hemorrhage or shock. Rapid increase in blood pressure may cause bleeding from sites that aren’t apparent at lower pressures. Monitor vital signs carefully. Watch for signs of vascular overload (heart failure or pulmonary edema). Monitor fluid intake and output, protein, electrolyte and hemoglobin levels, and hematocrit during the therapy.

29

Generic Name: HEXETIDINE Brand Name: BACTIDOLClassification: ANTIBACTERIAL Dosage/ Administration/ Route: oral care TID

INDICATIONS

THERAPEUTIC EFFECTS

MECHA-NISM

OF ACTION

CONTRA-INDICATIONS AND

CAUTIONS

PHARMACO- KINETICS/ PHARMACO DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

For general oral hygiene

Bacterial cell death

Kills microorganisms in the oral mucosa that are susceptible to the drug; improves integrity of mouth tissue and protects tooth surfaces against formation of decay acids.

Contraindicated if the patient has known hypersensitivity to the drug or its components

Directly enters the circulation following IV infusion.

Warm feeling in the mouth

Altered sense of taste

Aspiration Elevate head of the bed to prevent aspiration. Ensure aspiration precaution measures. Use full strength of the drug. Use padded tongue depressor and soak it in Bactidol when administering to an intubated client.

30

Generic Name: CEFEPIME Brand Name: (no brand name given)Classification: ANTIBACTERIAL; CEPHALOSPORIN Dosage/ Administration/ Route: 1 gram IVTT OD

INDICATIONS

THERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Treatment of hospital-acquired pneumonia

Bacterial cell death

Inhibits bacterial cell wall synthesis, promote osmotic instability and destroy bacteria.

Contraindicated in hypersensitivity to the drug, cephalosporins,or beta-lactam antibiotics.

Cautious use in patients hypersensitive to penicillin because of possibility of cross-sensitivity with other beta-lactam antibiotics.

Absorption: Well absorbed.

Distribution: Widely dirtributed. Enter the CSF only when the meninges are inflamed. Cross the placenta and enter breastmilk in low concentrations.

Excretions: 80 % renally excreted.

Half-Life: 0.7 to 1.2 hours.

AnorexiaNauseaVomitingHeadache

Dizziness ItchingRash

Unusual bleedingDifficulty breathingHivesSore mouth or throat

Check culture and sensitivity of sputum results to ensure that this is the drug of choice for the patient. Monitor renal function before and during the therapy. Ensure that the patient receives the full course of the therapy. Monitor patient for signs of superinfections and adverse reactions to the drug. Monitor IV site. If phlebitis occurs, change site.

31

Generic Name: CIPROFLOXACIN Brand Name: CIPROBAYClassification: FLUOROQUINOLONE Dosage/ Administration/ Route: 200 mg IV drip q12h

INDICATIONS

THERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO

- DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Treatment of hospital-acquired pneumonia; sepsis secondary to acute necrotizing pancreatitis

Bacterial cell death

Inhibits bacterial DNA synthesis, mainly blocking DNA gyrase; bactericidal.

Contraindicated in hypersensitivity to the drug or other fluoroquinolone; severe renal disease; pregnancy; breastfeeding.

Cautious use in patients with CNS disorders, such as severe cerebral arteriosclerosis or seizure disorders and in those at risk for seizures. Drugs may cause CNS stimulation.

Absorption: Well absorbed.

Distribution: Widely distributed. Enter the CSF only when the meninges are inflamed. Cross the placenta and enter breast milk in low concentrations.

Excretions: 50 % unchanged in urine.

NauseaVomitingDiarrheaAbdominal cramps

Flatulence

Headache

DizzinessFatigueRestlessness

InsomniaRashFlushingTinnitusphotosensitivity

utricariaoral candidiasiscrystalluirahematuria seizures

Check culture and sensitivity of sputum results to ensure that this is the drug of choice for the patient. Monitor renal function before and during the therapy. Ensure that the patient receives the full course of the therapy. Monitor patient for signs of superinfections and adverse reactions to the drug. Monitor IV site. If phlebitis occurs, change site.

32

Generic name: CITICHOLINE Brand name: (no brand name given)Classification: CNS STIMULANT Dosage/ Administration/ Route: 500 MG IVTT slow q12h

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATIONS AND PRECAUTI

ONS

PHARMACO- KINETICS/PHARMACO-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILIT

IES

Pancreatitis Stimulates the Reticular Activating System

Act as a cortical and RAS stimulant, possibly by increasing the release of catecholamines from the presynaptic neurons, leading to an increase in stimulation of the postsynaptic neurons

Contraindicated in the presence of known allergy to the drug; marked anxiety, agitation, or tension and severe fatigue or glaucoma; cardiac disease; pregnancy and; lactation.

Use cautiously in patients with a history of

Absorption: rapidly absorbed

Distribution: Unknown.

Metabolism & Excretion: Metabolized by the liver and excreted in urine.

Half-life: 2-15 hours.

Nervousness Insomnia Dizziness Headache Blurred vision Anorexia Nausea Weight loss

Hypertension Arrhythmias Angina Difficulty with

accommodation

Arrange to dispense the least amount of drug possible to minimize the risk of overdosage and drug abuse.

Monitor wight, CBC, and ECG to ensure early detection of adverse effects and proper interventions.

Provide safety measures such as side rails and assistance with ambulation if CNS effects occur to prevent patient injury.

33

drug dependence, including alcoholism and; with hypertension.

34

Generic Name: DOPAMINE Brand name: (no brand name given)Classification:ADRENERGICS Dosage/Administration/Route: 2 g in 300 cc D5NSS

Indications Therapeutic Effects

Mechanism of

Action

Contraindications Pharmacokinetics/Pharmacodynamics

Side Effects

Adverse Reaction

Nursing Responsibilities

> Adjunct to standard measure s to improveBlood pressure, cardiac output, and urine output.

Increased cardiac output, increased blood pressure and improved blood flow.

Tanawa sa ang dosage please

>Tachyarrhythmias >Pheochromocytoma>Hypersensitivity to bisulfites

Absorption: Administered IV only, resulting in complete bioavailability

Distribution: Widely distributed but does not cross the blood brain barrier

Metabolism and Excretion: Metabolized in the liver, kidneys, and plasma.

>Headache> Dyspnea>Palpitations > Nausea> Vomiting

> Mydriasis>Hypotension> Angina

> Monitor blood pressure, heart rate, pulse pressure, ECG, pulmonary capillary weigh pressure (PCWP), cardiac output, CVP.

> Monitor urine output frequently throughout administration. Report decreases in urine output promptly.

> If hypotensionoccurs, administration rate should be increased. If hypotension continues more potent vasoconstrictors (nor-epinephrine may be administered.

35

> Explain to the patient the rationale for instituting this medication and the nee for frequent monitoring.

> Advise the patient to inform the nurse immediately if chest pain; dyspnea; numbness, tingling, or burning of extremities occur.

> Instruct patient to inform nurse immediately of pain or discomfort at the site of administration.

Generic Name: FUROSEMIDE Brand Name: LASIXClassification: LOOP DIURETIC Dosage/ Administration/ Route: (to run for 2 hours) BID

36

INDICATIONS

THERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Acute Renal Faiulre

Treatment of fluid retention or fluid overload

Inhibition of sodium and water reabsorption from the Loop of henle and distal and renal tubules; potassium, magnesium, and calcium may be excreted.

Contraindicated in presence of severe electrolyte imbalances; hypovolemia; anuria; hypersensitivity to sulfonamides and in hepatic coma.

Absorption: Rapidly bsorbed.

Distribution: 95 % is widely distributed; crosses the placenta

Metabolism and Excretions: excreted in urine, some in feces.

Onset: 5 minutes.

Peak: 20-30 minutes

Duration: 2 hours.

NauseaDiarrheaElectrolyte imbalance

VertigoCramping

RashHeadache

Weakness

ECG changes

Blurred vision

Photosensitivity

Severe dehydrationMarked hypertension

Monitor urinary output to determine body or fluid gain or loss. Urinary output should be at least 25 mL/ hour or 600 mL per 24 hours. Check the client’s weight to determine fluid loss or gain. A loss of 2.2 to 2.5 pounds is equivalent to a fluid loss of 1 liter. Monitor vital signs. Be alert for marked decrease in blood pressure. Administer IV furosemide slowly; hearing loss may occur if rapidly injected. Observe for signs and symptoms of hypokalemia (<3.5 mEq/ L), such as

37

muscle weakness, abdominal distention,leg cramps, and/or cardiac dysrhythmies. Check serum potassium levels.

Generic name: HYDROCORTISONE Brand name: (no brand name given)Classification: CORTICOSTEROID Dosage/ Administration/ Route: 1000 mg IVTT q8h

38

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATIO

NS AND PRECAUTI

ONS

PHARMACO- KINETICS/PHARMACO-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITI

ES

Treatment of inflammatory reaction

Suppression of inflammation and modification of the normal immune response

Blocks the action of arachidonic acid, which leads to a decrease in the formation of prostaglandins and leukotrienes. Without these chemicals, the normal inflammatory reaction is blocked. Hydrocortisone also impairs the ability of phagocytes to leave the bloodstream and move to

Contraindicated in active untreated infection; lactation; and known alcohol, bisulfate, or tartrazine hypersensitivity or intolerance.

Cautious use in children; stress; pregnancy and in chronic treatment.

Absorption: Well absorbed.

Distribution: Widely distributed, crosses the placenta, and probably enters breast milk.

Metabolism and Excretion: Metabolized mostly by the liver.

Half-life: 1.5-2 hours (plasma), 8-12 hours (tissue), adrenal

Headache Restlessne

ss Anorexia Nausea Vomiting Acne Decreased

wound healing

Ecchymoses

Hirsutism Petechiae Fragility Weight

gain/ loss Muscle

pain Increased

susceptibility to infection

Depression Euphoria Increased

intracranial pressure

Increased intraocular pressure

Cataracts Hypertension Peptic ulcer Adrenal

suppression Hyperglycemia Fluid retention Hypokalemia Hypokalemic

alkalosis Thromboemboli

sm Thrombophlebit

is Muscle wasting Osteoporosis Aseptic necrosis

of joints

Administer in the morning to coincide with the body’s normal secretion of cortisol.

Taper doses when discontinuing from high doses or from long term therapy to give the adrenal glands a chance to recover and produce adrenocorticoids

Arrange for increased dosage when patient is under stress to supply increased demands for corticosteroids associated with stress reaction.

39

injured tissues. It also blocks the ability of lymphocytes to act in the immune system, including a blocking in the production of antibodies.

suppression lasts 1.25-1.5 days.

Cushingoid appearance

Do not give live virus vaccines when the patient is immunosppuressed because there is an increased risk of infection.

Protectthe patient from unnecessary exposure to infection and invasive procedure because the steroids suppress the immune system and the patient is at increased risk for infection.

Generic name: IANSOPRAZOLE Brand name: PREVACID

40

Classification: PROTON-PUMP INHIBITOR; ANTI-ULCER AGENT Dosage/ Administration/ Route: 30 mg 1 tab OD/ NGT

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATION

S AND PRECAUTIO

NS

PHARMACO-

KINETICS/PHARMAC

O-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITI

ES

Prevention of Stress Ulcer complication of Acute Necrotizing Pancreatitis

Diminished accumulation of acid in the gastric lumen, with lessened acid reflux.

Binds to an enzyme in the presence of acidic gastric pH, preventing the final transport of hydrogen ions into the gastric lumen.

Contraindicated in hypersensitivity to the drug.

Use cautiously in geriatric patients; severe hepatic impairment; pregnancy; lactation or; children below 1 year old.

Absorption: 80 % absorbed after oral administration.

Distribution: Unknown.

Metabolism & Excretion: Extensively metabolized by the liver to inactive compounds. Converted intra-cellularly to at least two other anti-secretory compounds.

Headache Diarrhea Abdominal

pain Nausea Rash Dizziness

No known adverse effects

Assess patient routinely for epigastric or abdominal pain and for blood in stool, emesis, or gastric aspirate.

Administer medication before meals.

Crush the medication before administering via the NG tube.

Flush the tube after medication administration.

41

Half-life: Less than 2 hours.

Generic name: IMIPENEM/CILASTATIN Brand name: (no brand name given)

42

Classification: CARBAPENEMS; ANTI-INFECTIVES Dosage/ Administration/ Route: 500 mg IVTT q12h

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATION

S AND PRECAUTIO

NS

PHARMACO- KINETICS/PHARMACO-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITI

ES

Treatment of sepsis secondary to Acute Necrotizing Pancreatitis and treatment of Hospital Acquired Pneumonia

Bactericidal action against susceptible bacteria.

Imipenem binds to the bacterial cell wall, resulting in cell death. Combination with cilastatin prevents renal inactivation of imipenem, resulting in high urinary concentrations.

Contraindicated in hypersensitivity to the drug.

Use cautiously in patients with previous history of hypersensitivity; seizure disorders; geriatric patients; renal impairment; pregnancy; lactation.

Absorption: IV absorption results in complete bioavailabilities.

Distribution: Widely distributed. Crosses the placenta and enters breast milk.

Metabolism and Excretion: 70 % is excreted unchanged by the kidneys.

Half-life:prolonged in renal

Dizziness Somnolen

ce Diarrhea Nausea Vomiting Rash Pruritus Sweating Urticaria Phlebitis

at IV site Fever

Seizures Hypotension Pseudo-

membranous colitis

Eosinophilia Anaphylaxis Superinfecti

on

Assess patient for infection at the beginning of and throughout the therapy.

Obtain a history before initiating therapy to determine previous use of and reactions to penicllins.

Obtain specimen for culture and sensitivity before initiating therapy.

Observe patient for signs and symptoms of anaphylaxis. If present, discontinue the drug and notify the physician.

Infuse slowly

43

impairment, because rapid infusion may result in nausea, vomiting, unusual tiredness or weakness, dizziness or sweating.

Generic name: INSULIN ASPART Brand name: NOVORAPIDClassification: PANCREATIC; ANTIDIABETIC Dosage/ Administration/ Route: 10 “u” SQ before each

feeding

44

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATIONS AND PRECAUTI

ONS

PHARMACO- KINETICS/PHARMACO-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILIT

IES

Prevention of Hyperglycemia after each meal

Control of blood glucose

Lowers blood glucose by increasing its transport into cells and promoting the conversion of glucose to glycogen. It also promotes the conversion of amino acids to proteins in muscles; stimulates triglyceride formation and; inhibits the release of free fatty acids.

Contraindicated in hypersensitivity to the drug.

Cautiously use in patients with infection; in pregnancy and; stress.

Absorption: Rapidly absorbed from subcutaneous administration sites.

Distribution: Widely distributed.

Metabolism and Excretion: Metabolized by the liver, spleen, kidney and muscle.

Half-life: 5-6 minutes but is prolonged in patients with diabetes. Biologic half-life is 1-1.5 hours.

Urticaria Itching Redness Swelling

Hypoglycemia Rebound

hyperglycemia Lipodystrophy Lipohypertrophy anaphylaxis

Assess patient for signs and symptoms of hypoglycemia and hyperglycemia periodically throughout the therapy.

Monitor body weight periodically.

Monitor blood glucose every ---- throughout therapy, more frequently in times of stress.

If hypoglycemia, which is a manifestation of overdose, occurs, administer oral glucose. Severe hypoglycemia is a life threatening emergency and

45

its treatment includes IV glucose, glucagon or epinephrine.

Because medication errors involving insulin have resulted in serious patient harm and death, clarify all ambiguous orders.

Generic Name: INSULIN GLARGINE Brand Name: LANTUSClassification: ANTIDIABETIC Dosage/ Administration/ Route: 30 “U” SQ before 8 am

feeding

46

INDICATIONS

THERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Management of Diabetes Mellitus type 2

Control of blood glucose

Lowers glucose level by stimulating peripheral glucose uptake, especially by skeletal, muscle, and fat and by inhibiting hepatic glucose production.

Contraindicated in hypersensitivity to glargine, preservatives, or additives.

Cautious use during stress, pregnancy and infection.

Absorption: Rapidly absorbed fro SQ administration site

Distribution: Widely dirtributed.

Metabolism and Excretions: Metabolized by the liver, spleen, kidney and muscle.

Half-Life: 5-6 minutes.

Urticaria ItchingRednessSwellingAllergic reactions

HypoglycemiaRebound hyperglycemiaLipodystrophyLipohypertrophyAnaphylaxis

Desired glucose levels as well as the doses and timing of antidiabetic medication must be determined individually. Glucose monitoring is recommended for all patients. The rate of absorption, onset and duration may be affected by exercise and other variables, such as illness and emotional stress. Hypoglycemia is the most common adverse effect of insulin. Early symptoms may be different or less pronounced in patients with long duration of

47

diabetes, diabetic nerve disease or intensified diabetes control. Monitor glucose level closely in these patients because severe hypoglycemia may result before the patient may develop symptoms.

Generic name: MUPIROCIN Brand name: BACTROBANClassification: LOCAL ANTI-INFECTIVE Dosage/ Administration/ Route:

48

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATIONS

AND PRECAUTION

S

PHARMACO- KINETICS/

PHARMACO-DYNAMICS

SIDE EFFECTS

ADVERSE

EFFECTS

NURSING RESPONSIBILI

TIES

Skin Lesion

Bacterial death

Unknown. Thought to inhibit bacterial protein and RNA synthesis

Contraindicated in hypersensitivity to the drug.

Use cautiously in patients with burns or large open wounds and in those with impaired renal function because serious renal toxicity may occur.

Absorption: Penetrates outer layers of skin; systemic absorption minimal through intact skin

Metabolism: Skin: 3% to monic acid

Half-life elimination: 17-36 minutes

Excretion: Urine

Headache Burning Pruritus Stinging Rash Pain erythema

taste perversion

abdomen pain

ulcerative stomatitis

Take note that drug is not for ophthalmic or internal use.

Do not use in prolonged time because it may cause of nonsusceptible bacteria and fungi. Notify the doctor if the condition doesn’t improve o gets orse in 3 to 5 days.

Observe patient for local adverse effects of the medication.

49

Generic name: PANTOPRAZOLE Brand name: ULCEPRAZClassification: GASTRIC ACID PUMP INHIBITOR; ANTI-ULCER AGENT Dosage/ Administration/ Route: 40 mg IVTT OD

50

INDICATION

THERAPEUTIC

EFFECTS

MECHANISM OF

ACTION

CONTRA-INDICATION

S AND PRECAUTIO

NS

PHARMACO-

KINETICS/PHARMAC

O-DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITI

ES

Prevention of Stress Ulcer complication of Acute Necrotizing Pancreatitis

Diminished accumulation of acid in the gastric lumen, with lessened acid reflux.

Binds to an enzyme in the presence of acidic gastric pH, preventing the final transport of hydrogen ions into the gastric lumen.

Contraindicated in patients with hypersensitivity to the drug.

Use cautiously in pregnancy or lactation.

Absorption: well absorbed

Distribution: Unknown.

Metabolism & Excretion: Mostly metabolized by the liver via CYPSystem; inactive metabolites are excreted in urine (71%) and feces (18 %).

Half-life: 1 hour.

Headache Diarrhea Abdomin

al pain Eructatio

n Flatulenc

e

Hyperglycemia

Assess patient routinely for epigastric or abdominal pain and for frank or occult blood in stool, emesis, or gastric aspirate.

Administer over 25 minutes at a rate of 3 mg/min.

Patients receiving IV pantoprazole should be converted to PO as soon as possible.

Administer through filter to remove precipitates that may form when solution is mixed.

51

Generic Name: PIPERACILLIN- TAZOBACTAM Brand Name: TAZOCININDICATION

STHERAPEUTIC EFFECTS

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO

- DYNAMICS

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

Treatment of Bacterial cell Binds to Contraindicate Absorption: Rashes Seizures Check culture and

52

hospital-acquired pneumonia

death bacterial cell wall membrane, causing cell death. Spectrum is extended compared with penicillins.

d in hypersensitivity to penicillins or tazobactams.

Cautious use in renal impairment, sodium restriction, pregnancy and lactation.

Well absorbed.

Distribution: Widely dirtributed. Enter the CSF only when the meninges are inflamed. Cross the placenta and enter breastmilk in low concentrations.

Excretions: 80 % renally excreted.

Half-Life: 0.7 to 1.2 hours.

UrticariaDiarrheaNauseaPhlebitis at IV site

ArrhythmiasCongestive Heart FailureNephritisFluid and Electrolyte imbalancesBleeding, increased bleeding timeMetabolic AlkalosisAnaphylaxisSuperinfectionsDrug-induced nephritisPseudomembranous colitis

sensitivity of sputum results to ensure that this is the drug of choice for the patient. Monitor renal function before and during the therapy. Ensure that the patient receives the full course of the therapy. Monitor patient for signs of superinfections and adverse reactions to the drug. Monitor IV site. If phlebitis occurs, change site.

Classification: ANTI-INFECTIVES; EXTENDED SPECTRUM PENICILLINS Dosage/ Administration/ Route: 4.5 g IVTT now then 2.75 g IVTT q 12 h

Generic Name: POTASSIUM CHLORIDE Brand name: (no brand name given)Classification: MINERAL AND ELECTROLYTE REPLACEMENTS/SUPPLEMENTS Dosage/ Route: 60 mg IVTT

Indications Therapeutic Effects

Mechanism of Action

Contraindications

Pharmacokinetics/

Pharmacodynamics

Side Effects

Adverse Reaction

Nursing Responsibiliti

es

53

>Treatment/prevention of potassium depletion

>Replacement

>Prevention of deficiency

> Maintain acid-base balance, isotonicity and electrophysiologic balance of the cell

> Activator as many enzymatic reactions; essential to transmission of nerve impulses; contraction of cardiac, skeletal, and smooth muscle, gastric secretion; renal function; tissue synthesis; and carbohydrate metabolism.

>Hyperkalemia> Severe renal impairment> Untreated Addison’s disease > Severe tissue trauma>Hyperkalemic familial periodic paralysis> Potassium acetate injection contains aluminum, which may become toxic with prolonged use to high risk groups (renal impairment, premature neonates)

Absorption: Well absorbed following oral administration

Distribution: Enters extracellular fluid; then actively transported into cells.

Metabolism and Excretion: Excreted by the kidneys

Half-life: Unknown.

>Abdominal pain> Diarrhea> Nausea>Vomiting

>Confusion>Restlessness> Weakness>Arrhythmias> ECG changes>Ulecration> Stenotic lesions> Irritation at Ivsite> Paralysis >Paresthesia

> Assess for signs and symptoms of hypokalemia and hyperkalemiaMonitor pulse, blood pressure, and ECG changes periodically during IV therapy.

> Monitor serum potassium before and periodically during therapy

> Symptoms of toxicity are those of hyperkalemia

> If hypokalemia is seconfary to diuretic therapy,

54

consideration should be given to decreasing the dose of diuretic, unless there is a history of significant arrhythmias or concurrent digitalis glycoside therapy.

Generic Name: RANITIDINE Brand name: (no brand name given)Classification: _ANTIULCER AGENTS/HISTAMINE H2 ANTAGONISTS Dosage/Administration/Route: 50 mg IV q 12 h

Indications Therapeutic Effects

Mechanism of

Action

Contraindications

Pharmacokinetics/Pharmacodynamics

Side Effects

Adverse Reaction

Nursing Responsibilities

55

>Maintenance of alkaline gastric pH

> Healing and prevention of ulcers

> Decreased symptoms of gastroephageal reflux

> Decreased secretion of gastric acid

Inhibits the action of histamine at the H2

receptor site located primarily in the gastric parietal cells, resulting in inhibition of gastric acid secretion

> Hyprsensitivity> Cross hypersensitivity may occur> Some oral liquids contain alcohol and should be avoided in patients with known intolerance.

Absorption: 50% absorbed after PO and IM administration

Distribution: All agents enter breast milk and cerebrospinal fluid

Metabolism and Excretion: metabolized by the liver, mostly on first pass, 30% excreted unchanged by the kidneys after PO administration.

>Confusion>Dizziness>Drowsiness >Hallucinations>Headache > Nausea>Impotence

>Arrhythmias >Gynecomastia>Agranulocytosis > Aplastic anemia> Anemia>Neutropenia>Thrombocytopenia >Hypersensitivity reactions > Vaculitis

> Assess patient for epigastric or abdominal pain and frank or occult blood in the stool, emesis, or gastric aspirate.

> Instruct patient to take medication as directed for the full course of therapy, even if felling better. Take missed doses as soon as remembered but not if almost time for next dose. Do not double dose.

> Advise patients taking OTC preparations as to take the maximum dose continuously for more than two weeks without consulting health care professional. Notify health care provider if difficulty swallowing occurs if abdominal pain persists.

56

> Inform patient that smoking interferes with the action of histamine antagonsists. Encourage the patient to quit smoking or at least not to smoke after last dose of the day.

> Advise patient to avoid alcohol, products containing aspirin or NSAIDS, and foods that may cause an increase in GI irritation

> Inform patient that increased fluid and fiber intake and exercise may minimize constipation.

Generic Name: SALBUTAMOL + IPRATROPIUM Brand Name: DUAVENTClassification: BRONCHODILATOR Dosage/ Administration/ Route: 1 neb + ½

neb Asmavent q 6 hINDICATION

STHERAPEUTIC

EFFECT

MECHANISM OF ACTION

CONTRA-INDICATIONS

AND CAUTIONS

PHARMACO- KINETICS/ PHARMACO

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITIE

S

57

S DYNAMICSTreatment of hypoxemia caused by hospital acquired pneumonia

Bronchodilation

Salbutamol binds to beta2-adrenergic receptors in airway smooth muscle, leading to activation of adenyl cyclase and increased level of cAMP

Ipratropium inhibits cholinergic receptors in bronchial smooth muscles, resulting in decreased concentrations of cGMP, causing bronchodilation

Contraindicated in hypersensitivity to drug and in patients peanut/ soy allergy.

Cautious use in cardiac disease, hypertension, hyperthyroidism, diabetes, glaucoma, geriatric patients, pregnancy, lactation, children below 2 y.o., patients with bladder neck obstruction, prostate hypertrophy and during urinary retention.

Peak: 2 hours Metabolism

and Distribution: widely distributed and metabolized by the liver. Enters the breastmilk.

Excretion: excreted in the urine.

Headache InsomniaDizzinessDry and irritated nose and throat

Nasal congestion

NauseaVomitingCoughDyspneaWheezingAltered taste

Increased appetite

Malaise

TremorHypokalemiaBronchospasmBronchitisHypersensitivity reactionsTachycardiaPalpitationMuscle crampsNervousnessHypertensionCNS Stimulation

Monitor the patient’s response to the drug therapy to determine the effectiveness of the dosage and to adjust the dosage as needed. Provide comfort measures including rest periods, a quiet environment, dietary control of caffeine and headache therapy as needed, to help the patient cope with the drug therapy. Watch out for side and adverse effects of the drugs.

Generic Name: SODIUM BICARBONATE Brand name: (no brand name given)Classification: ALKANIZING AGENTS Dosage/Administration/Route: 4 vials in 250 cc

D5NSS

Indications Therapeutic Effects

Mechanism of Action

Contraindications

Pharmacokinetics/Pharmacodynami

Side Effects

Adverse Reaction

Nursing Responsibilitie

58

cs s >Management of metabolic acidosis

>Alkalinization

>Neutralization of gastric acid.

> Acts as an alkalinizing agent by releasing bicarbonate ions.

> Following oral administration, releases bicarbonate, which is capable of neutralizing gastric acid.

> Metabolic or respiratory alkalosis > Hypocalcemia> Excessive chloride loss> As an antidote following ingestion of strong mineral acids > Patients on sodium restricted diets (oral use as an antacid only)> Renal failure (oral use as an antacid only)> Severe abdominal pain of unknown cause, as especially if associated with fever (oral use as an antacid only)

Absorption: Following oral administration, excess bicarbonate is absorbed and results in metabolic alkalosis and alkaline urine.

Distribution: Widely distributed into extracellular fluid.

Metabolism and Excretion: Sodium and bicarbonate are excreted by the kidneys

Half-life: Unknown.

>Flatulence> Gastric distention> Sodium and water retention> Irritation at IV site

> Tetany> Metabolic alkalosis>hypernatremia>hypocalcemia>hypokalemia

> IV: Assess fluid balance

> Report symptoms of fluid overload

> Assess patient for signs of acidosis, alkalosis, paresthesia, tetany, altered brerathing pattern, hypernatremia, or hypokalemia throughout the therapy.

>Avoid extravasation, as tissue irritation or cellulites may occur. If infiltration occurs, confer with physician

59

or other health care professional regarding warm compresses and infiltration of site with lidocaine or hyaluronidase.

> Antacid: Assess patient for epigastric or abdominal pain and frank or occult blood in the stool, emesis, or gastric aspirate.

Generic name: TRANEXAMIC ACID Brand name: HEMOSTANClassification: ANTI-FIBRINOLYTI Dosage/ Administration/ Route: 500 mg amp IVTT

q8h

INDICATION

THERAPEUTIC

MECHANISM OF

CONTRA-INDICATION

PHARMACO- KINETICS/

SIDE EFFECTS

ADVERSE EFFECTS

NURSING RESPONSIBILITI

60

EFFECTS ACTION S AND PRECAUTIO

NS

PHARMACO-DYNAMICS

ES

Prophylaxis for bleeding tendencies /hemorrhage

Hemostasis Stop the natural plasminogen clot-dissolving mechanism by blocking its activation or by directly inhibiting plasmin.

Contraindicated in patients with pronounced thrombotic tendency w/o simultaneous use of anticoagulant and in patients with defective color vision.Use cautiously in renal insufficiency and in massive bleeding o the upper urinary tract.

Peak: 1 to 3 hours

Onset: Rapid

Duration: Duration of infusion

Dizziness Tinnitus Headache Weakness Nausea Cramps Diarrhea Hypotensio

n Malaise

Fertility problems

Elevated serum creatine phosphokinase (CPK)

Monitor clinical response and clotting factor levels regularly, in order to arrange to adjust dosage, as needed.

Offer support and safety measures to prevent patient injury.

Monitor the patient for any signs of thrombosis, in order to arrange to use comfort and support measures, as needed.

NURSING MANAGEMENT

Assessment Nursing diagnosis Objective Intervention Rationale Evaluation

Subjective: “Maglisud man

1) Ineffective Airway Clearance

Short term:At the end of 30

Independent:> position the head midline with >open/maintain airway patency

After 30 minutes, the patient was

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syag ginhawa tungod sa mga plemas nya, unya dili pa gyud nya maluwa” as verbalized by patient’s significant other.

Objective:> attempts to expectorate but can’t do it>crackles present on both lungs upon auscultation>deep and labored breathing>use of accessory muscles

related to retained secretions and impaired gag reflex secondary to presence of mechanical ventilator

minutes, the patient will be able to:-demonstrate and maintain airway patency-demonstrate non- verbalize understanding of causes and it’s management

Long term: At the end of 8 hrs, the patient will be able to:- maintain clear airway and demonstrate techniques that aids in expectorant/suctioning through secretion machine

flexion appropriate for client’s condition

> elevate the head of the bed and change position every 2 hrs

>do suctioning of secretions using suction machine

> reinforce techniques that would help client express his understanding on the information being given like:

a. associate actions or things on which the patient would like/ wanted to expressb.encourage by nodding, raising eyebrows and raising thumb for approval and turning head side-to-side for disapproval

> gravity decreases pressure on the diaphragm and enhancing drainage of ventilation to different lung segments

> helps in evacuation of secretions

> for the client to understand and express what he had wanted to verbalize or say since the patient cant express verbally, association of words into action or things may be a great help to both the nurse and the patient.

able to express non- verbally by association of things like pillow as smooth feeling/ relieved and comfort. Also secretions were improving gradually throughout improving with suctioning and expectorates/suctioned secretions into yellow to green colored at minimal amount,. The patient was as well compliant to procedures and interventions given .

Assessment Diagnosis Objectives Intervention Rationale EvaluationSubjective:“O, galisud man na siya ug ginhawa.” As verbalized

2)Ineffective breathing pattern related to decreased

Short term:At the end of 30 minutes of nursing intervention, pt. will be able to:

Independent:-position patient with proper body alignment.-monitor vital signs including O2 saturation.

-for optimal breathing pattern-for comparative baseline data

-The patient was able to manifest improved respiratory pattern, with an O2

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by SO

Objective:-on mechanical ventilation-HR = 119 bpm-presence of mimimal pleural effusion based on x-ray report-use of accessory muscles-deep and labored breathing-weak lower extremities-speech and swallowing is compromised.

energy and weakness.

-manifest improved respiratory pattern-patient’s SO will verbalize awareness of causative factors and lifestyle changes(i.e.cessation of smoking)

Long term:At the end of 8 hours of nursing intervention, patient will be able to have:-normal O2 saturation(97-100%)-no signs of cyanosis and other symptoms of hypoxia.-normal ABG values

-auscultate chest regularly

-elevate head of bed as appropriate

-suction airway as needed-reposition patient every 2 hours or regularly-provide reassurance and allay anxiety by staying with patient during acute episodes of respiratory distress.-maintain calm attitude when dealing with patient. -encourage adequate rest periods.-encourage patient/SO to develop plan for smoking cessationDependent:Administer bronchodilator such as Salbutamol (duavent 1 neb + ½ neb asmavent q 6 hrs.) as ordered by doctor

Administer O2 (5 L/min)

-to note presence of secretions or character of breath sounds.-to promote physiological ease of maximal inspiration.-to clear secretions-to mobilize secretions and prevent pressure ulcers.-air hunger can produce an extremely anxious state.

-to limit level of anxiety

-to limit fatigue

-to provide optimal recovery of condition.

-this relaxes bronchial muscles which allows the patient to breathe comfortably.-for optimal oxygenation

- for effective oxygenation of the body

saturation of 98% and no signs of cyanosis or hypoxia.

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Assessment Nursing diagnosis Objective Intervention Rationale Evaluation

Subjective:“ Oo.Sige na syag ihi-ihi”

Objective:

3)Deficient Fluid Volume Related to hyperglycemic-induced osmotic diuresis.

Short term:At the end of 1 hour of nursing interventions, the patient’s significant

Independent:> Monitor vital signs, especially noting respiratory status changes or alterations in BP.

> Tachycardia and hypotension are classic symptoms of hypoglycemia. Respiratory changes may occur as the lungs

We were not anymore able to evaluate the patient’s intake and output since

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> dry lips, mucous membranes> weak and thready pulse>imcreased urine output>> intake less than output ( I- 740cc, O-860cc)

others/patient will be able to identify signs and symptoms of hyperglycemia

Long term:At the end of 4 hours of nursing interventions, the patient will be able to have vital signs within normal range and have equal balance between intake and output.

> monitor Intake and Output every 4 hours.

> Assess patient’s mental status and observe for significant changes

>Instruct patient/family members regarding signs and symptoms of hyperglycemia.

Dependent:> Administer Insulin glargine (Lantus) 30 “u” SQ before 8 am(long acting) feeding as ordered. And insulin aspart 10 “u” SQ before each feeding (short acting) as ordered.

attempt to remove acids by creating a compensatory respiratory alkalosis.

>Facilitates accurate measurement and effectiveness of volume replacement and maintenance of adequate circulation fluid volume.

> Mental status changes occur with exceedingly high or low glucose levels, electrolyte imbalances and acidotic states.

> Provides information and promotes more timely identification of complications.

> Increases glucose transport across muscle and fat cell membranes to reduce glucose levels.

the patient was transferred to the private room during/ within our shift.

Assessment NURSING DIAGNOSIS

OBJECTIVES INTERVENTIONS RATIONALE EVALUATION

SUBJECTIVE:

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SO verbalized “Nagniwang gyud na siya sukad nahospital.”

OBJECIVES: Fatigue Weakness Increased

glucose level; Hgt: 151 mg/dL (NV: 60 – 100 mg/dL)

(+) Weight loss: from 78kgs to 72.7kgs in one week

Presence of appetite changes

Dry mucous membrane

Scaly, dry lips

4)Imbalanced Nutrition: Less Than Body Requirements related to insulin deficiency

Short term:At the end of 30 mins. of nursing interventions, the patient/SOs will be able to determine proper diet for the patient, diet low in fats, sodium and carbohydrates.

Long term:At the end of 8 hrs. of nursing interventions, the patient will be able to have intake of appropriate amounts and types of calories and have glucose levels within acceptable range.

Independent: Provid3e

high nutrient liquids as soon as patient is able to tolerate oral intake with progression to solid foods.

Instruct patient/SOs in dietary management, with ideal amount of 60% CHO, 20% fats, and 20% CHON to be divided in designated no. of meals and snacks daily.

Encourage patient to avoid diet rich in fats

- Provides nutrition and helps restore bowel function.

- Complex carbohydrates decrease the amount of insulin needs, reduce serum cholesterol and help to satiate patient. Food should be scheduled for peak effects of insulin as well as patient preference.- Diet high in fats, Na and CHO increases blood sugar level.

At the end of 30 mins. of nursing interventions, the patient/SOs was able to verbalized avoidance of diet rich in fats, sodium , such as dried fish, bagoong, fatty meats, mayonnaise.

At the end of 8 hrs. of nursing interventions, the patient was able to have intake of appropriate amounts and types of calories and have glucose levels within acceptable range, as evidenced by Hgt of 90mg/dL.

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and sodium and reduce intake of carbohydrates.

Dependent: Administer

Lantus 30 “u” SQ before 8am feeding as ordered.

Collaborative: Consult with

a dietician.

- Increases glucose transport across muscle and fat cell membranes to reduce glucose level.

- Assist in facilitating adjustmens to diet for patient’s special needs and facilitates dev’t of workable meal plans.

Assessment NURSING DIAGNOSIS

OBJECTIVES INTERVENTIONS RATIONALE EVALUATION

Subjective:none

Objective:

5)Impaired Skin Integrity related to presence of blisters on right heel, right

Short term:At the end of 30 mins. of nsg. interventions,

Independent: Remove wet

diapers and wet linens promply.

- prevents aggrevating the condition.

At the end of 30 mins. of nsg. interventions, patient will be free

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Blisters on right heel, right 3rd and 4th toes, sacral area and scrotal area

Redness on affected parts

Restlessness

3rd and 4th toes, sacral area and scrotal area secondary to physical immobilization for long hours

patient will be free of itching, as evidenced by absence of restlessness.

Long term:At the end of 8 hrs. of nursing interventions, the patient will display improvement in blisters as evidenced by decreased redness and absence of pus and swelling which are signs of infections.

Clean blisters regularly using normal saline sol’n or antiseptic.

Instruct patient not to touch/ rub affected areas.

Dependent: Apply

Bactroban ointment BID as ordered.

- To promote healing.

- To prevent further damage to skin integrity.

- To promte healing using pharmacologic approach.

of itching, as evidenced by absence of restlessness.

At the end of 8 hrs. of nursing interventions, the patient demonstrated improvements in his blisters as evidenced by decreased redness and absence of pus and swelling.

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Assessment Diagnosis Objectives Intervention Rationale EvaluationSubjective:

“Gamata-mata mana sya permi,dili straight iyang tulog” as verbalized by the informant.

Objective:-frequent yawning-appears weak-with gestures of sleepiness like the eyes wanted to close-RR= 31 cpm, dyspnea-moderately anxious-blisters noted at sacral area

6)Sleep pattern disturbance related to discomfort secondary to attachment of tubings and presence of blisters.

Short term:At the end of 2 hours, the patient will be able :-at least try to sleep undisturbed for two hours straight especially in the evening.-demonstrate and understand tolerable tecniques that would be suitable for sleeping.

Long term:At the end of 8 hours, client will be able to :-sustain 2-3 hours of undisturbed sleep since client maximum of sleeping time is 30 minutes to 1 hour.

Independent:-provide comfortable position during sleep and provide:-well groomed and straightened mattresses and bed covers and pillow.-change patient’s gown into new one-do evening care/morning care, especially the back rubbing.-minimize use of lights if not necessary; maintain quite environment-positioning during sleep in which he could properly breathe,check mechanical ventilation,airway and others.-maintain environment conducive to sleep/rest.-organize nursing care

-limit fluids before bedtime

-this is to give comfort and also avoid pressure ulcer to develop.-to make the patient feel comfortable-this is to let the patient feel fresh and at ease while lying on back; back rubbing allows circulation of blood then promoting comfort

-so as not patient be disturbed during on and off lights.-this may contribute to hindrances during sleeping.

-to promote relaxation

-to promote minimal interruption in sleep or rest-to reduce need for voiding during night

After 8 hours of nursing intervention, patient was able to gradually improving from 1-2 hours of sleeping. It’s a good sign and indication that procedures should be taking cared of seriously especially when client sleep hygiene is abnormal, this may exacerbate other symptoms, which client may experience. is abnormal, this may exacerbate other symptoms, which client may experience.

69

Dependent:Administer sedatives as ordered by the doctor.

-this is to make patient sleep comfortable.

70

Assessment Diagnosis Objectives Intervention Rationale EvaluationSubjective:“sige ra na siya og mata mata sa gabi-i” as verbalized by patient’s sister.

Objective:-restlessness-insomnia-patient was restrained.

7)Mild anxiety related to alteration of health status secondary to present medical condition.

Short term:At the end of 30 minutes of nursing intervention, the patient will be able to:

verbalize awareness of feelings of anxiety

identify 2 healthy ways in dealing and expressing anxiety such as diversional activities and comfort measures.

Long term:At the end of 2 days of nursing interventions, the patient will be able to report and demonstrate decrease anxiety as evidenced by absence of

Independent:1. Monitor physical

responses of the patient.

2. Establish a therapeutic relationship between the patient and the student nurse by conveying empathy and unconditional positive regard.

3. Be available to the patient for listening and talking.

4. Encourage patient to verbalize what he feels and needs.

5. Encourage patient to express feelings through actions.

6. Provide accurate

1. To measure the extent on which the patient can follow instructions.

2. To build rapport with the patient and allay fear and apprehension.

3. To gain trust from the patient and for the patient to be open in expressing what he feels.

4. For the nurse to know and immediate interventions will be given. It is also help release and lessen anxiety.

5. Promote patient’s self-esteem.

6. Helps client to

After 30 mins of nursing interventions pt. SD demonstrated healthy ways in dealing and expressing anxiety i.e (diversional activities and comfort masures)

71

restlessness and appearing relaxed.

information about his condition.

7. Provide comfort measures and diversional activities such as providing a calm and quiet environment, soft music and back rubbing.

8. Include patient’s significant others in the health teachings.

9. Provide health teaching about behaviors that is indicative for mild anxiety such as restless, irritable, wakeful, reports of insomnia and etc.

Dependent:1. Provide anxiolytic or anti anxiety drugs as ordered.

identify what is reality based.

7. It’s a non-pharmacologic approach in dealing with anxiety.

8. It would help client to identify what is reality based.

9. To provide continuity of care.

1. To reduce if not totally eliminate anxiety.

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DISCHARGE PLAN

Medications Exercises Treatment Health teachings Out- patient follow-up

Diet Spirituality

> strict compliance to medications

> maintenance dose should be known

> side effects and drug interactions of medication indicated for DM

> teach patient exercises that only be at tolerable rate like: - passive ROM of upper and lower extremities especially

>proper positioning during sleep or when awake, so as to allow airway and breathing properly

>deep breathing at tolerable pace

>encourage also verbalization of feelings; if able to write provide pen and paper, it

>compliance to medication with supervision, or remind the SO to always be reminded for client’s recovery

>proper timing and duration during procedure like the medication at prescribed time, dosage, route and other rights in administration of medication

>buying/complying of necessary equipments should be followed as prescribed

>social interactions also by significant others plays an important role in the recovery of the

>strict compliance to medication especially administration and maintenance of insulin therapy

>avoidance of food that contains: -caffeinated drinks and food like: coffee, cola, and chocolates and the likes

>limit if not avoid and stop smoking and alcohol consumption, it may exacerbates the condition

>encourage food rich in protein, for collagen synthesis and healing of tissues- like: fish, eggs, meat and other dairy products

>pt. SD and SO should be back on specified time written in their discharge slip

> pt. should be accompanied by significant others for explanation, results, and findings, and even stand as a support for the client emotionally

>also indicate the date, physician’s name in the pts. Card so as not to be confused on when to come back and where to have

>diet should include: -low: sugar, fat, carbohydrate

-20%CHON, 20% HCHO, 60% CHO

-high fiber, it inhibits glucose absorption in the intestines

-also give Ca supplements, to manage hypocalcemia and Vit. D for absorption of Calcium

>pt should always be encourage and emphasized to the fact that, all should be lifted to God alone, that even medication may not be effective if Faith is not being practiced by the Lord.

>reinforce that illness experienced was not brought about by other factors, or a curse from God, he should be reminded that God alone can be the most source of healing in all aspect of human person

73

is exercises on the digitals as well, and even her cognition and mental ability.

client (if not contraindicated and if prescribe by the physician.)

>encourage SO to participate in the course of treatment by being the means of the therapy since SD is dependent on his ADL, medication and other instructions should be emphasize

check- up

74

PROGNOSIS

Early evaluation and risk stratification for patients with acute pancreatitis are

important to differentiate patients with mild versus severe disease because patients with

severe disease often need intensive care treatment. Several scoring systems can predict

the severity of pancreatitis, and recent work has attempted to compare their relative

predictive values.

In most cases, acute pancreatitis goes away on its own after a couple of days with

no complications and no further problems. About 10% of patients develop complications,

such as a pseudocyst or abscess in the pancreas,that may require monitoring or additional

treatment.

Pancreatitis caused by heavy drinking is likely to come back if drinking

continues. Over time, permanent damage may be done to the pancreas, and a chronic

form of the disease may develop

Patients usually recover fully from acute pancreatitis and do not experience

recurrence if the cause is removed. Alcohol consumption should be eliminated even if it

is not the determined as the cause of the disease. Smoking, which stresses the body's

defenses against inflammation, should be stopped. If gallstones were the cause, then

removal of the gallbladder is required to prevent further attacks. For those patients in

whom a cause is not readily identified, there should be consideration of other diagnostic

testing such as endoscopic ultrasound.

75

CONCLUSION

Nursing care and management of the client with type 2 diabetes mellitus is both

complex and challenging. Especially that the disease is already severe and with

complications present. Compliance to the medication regimen could be a burden to the

family considering that it needs be strict and lifelong. Having a thorough understanding

of the pathophysiologic changes, knowing what to expect clinically and becoming

familiar with the standards of care, patient education in reference to the nature of the

disease, as well as educating the client’s significant others is essential for the better

understanding of the client’s condition. Hence, patient education in conjunction with the

nursing care could be a great factor in achieving positive outcomes. As student nurses, we

are responsible for developing an individualized plan of care that reflects the client’s

medications, diet and physical activity during the development and progression of

different phases of recovery. Not only would the health teachings be directed to the

patient himself but to the significant others as well.

The group would have had a complete and productive evaluation of patient RP’s

condition and his progress if we were able to conduct a home visit however, due to the

wrong information provided, i.e. address given by SO and as stated in the chart, the group

wasn’t able to do so. Some members of the group went to the specified location (Grand

Europa) but upon arrival to the area, the address particularly the block/street and lot was

not present or in existence. The group also tried calling up the patient or his SO through

the phone information but there were no record of the names of our patient and SO

(sister).

76

Recommendation

The proponents of this case analysis recommend that further study will be made

on the different diagnosis of the patient. In order for the health care providers including

nurses and student nurses will be equipped with knowledge, skills and attitude in

rendering care for patients having this type of diseases. Further study about these diseases

will help the family who have relative’s having this type of multiple disease, will have

better understanding about this condition, In order that they could better take care of their

family member.

This study is also recommended for nursing students who will conduct case

presentation that they will be able to have a flow on the proponents needed for a case

presentation. They will be equipped with knowledge, skills and attitude in conducting a

case presentation especially in making a thorough assessment of their patient.

It is also of high consideration that further evaluation be done to determine the

progress and compliance of the patient to the out-patient treatment regimen like being

able to conduct a home visit. Aside from this, the sources of data for this case

presentation is only limited to the assessments, laboratory results, patient’s chart and

personal interview with the patient, as well as on his significant others thus, other sources

of data, such as personal interview with the patient’s attending physician must also be

done for more information regarding the patient’s condition. Progression of the patient’s

recovery must also be monitored and documented regularly to determine the necessary

changes and improvement of patient’s care. Nevertheless, this case presentation is

recommended to be used as a reference for future studies about type 2 diabetes mellitus.

77

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79

Appendix

Nurses Notes

Date Notes

8-19-07

Ineffective

Airway clearance

NGT

Standard

FBC

Standard

Impaired

Skin

Integrity

> received on bed awake conscious and coherent to

both verbal and tactile stimuli ; with pupils @ 5mm

sluggish, reactive light accommodation; normal

power on both upper and lower extremities; GCS q 4

score 15

> hooked to cardiac monitor on sinus rhythm (-)

arrythmias

> initial v/s taken and recorded BP: 110/70 mmHg;

O2 sat: 98%, HR: 88bpm

> with ET @ 22 cm Lip level to vent: TV: 400ml,

RR: 10cpm, F1O2 35% PS 10 cm H2O on SIMV

mode with minimal yellowish sticky oral secretions

with MOD yellow ETA. Secretions suctioned q hour

and PRN turned to sides q 2 – able to turn with NEB

q 6h; oral care BID

> with NGT for of 166 cc q 4 – tolerated FED with

aspiration precaution and due PO Meds; intake

measured and recorded; standard followed

> with FBC to urobag draining well to moderate

yellowish colored urine - cloudy; output measured

and recorded; standard followed

> with blister @ R heal toes and scrotum area; and

sacral area - apply bactoban

> with Hgt monitoring q 4 7:30 am – Hgt result

relayed to Dr. Lolong = Coverage Lantus 20 units

80

8:00am

9:00am

11:00am

8-19-07

6:00am

7:30pm

8:10pm

and Novorapid given q before feeding

> RR decrease to 10 pressure support 10 for 1 hr –

tolerated

> RR decrease to 8 pressure support decrease 8 for 1 hr – tolerated> patient hooked to T-piece @ 5 L/min saturating

well t o100%

> for possible extubation if weaning tolerated and

labs within normal limit

> extubation hold

> endorsed to pm shift

> received awake on bed; with GCS score of 25/15,

with spontaneous eye opening, obeys command and

oriented to place, time and person; with 4 mm size

on both pupils and sluggishly reactive to light and

accommodation; upper and lower extremities are in

normal power

> initial v/s taken and recorded with BP: 90/60, HR: 99bpm; T: 36> on bladder training 4 hours clamped; 30 minutes –

released; tolerated

> Hgt result 3:30 pm was 151 mg/dl relayed to Dr.

Austria with orders to coverage of insulin

> result was 76 mg/dl relayed to Dr. Austria to hold

covergage

> for possible transport tomorrow

> seen and examined by Dr. Sison with orders

carried out

> encourage oral feeding as ordered

> ICU care rendered; needs attended

> endorsed

> received awake on bed; responsive to all forms of

81

8-20-07 (PM)

FBC

Standard

IVF

Standard

Impaired

Skin

Integrity

DM

Standard

Gen. Notes

stimuli

> initial v/s taken and recorded with BP: 130/90

mmHg. HR: 87 bpm, RR: 12 cpm, and T: 35.6

> hooked to cardiac monitor on sinus rhythm (-)

PACs, (-) PVCs

> with FBC attached to urobag draining yellow

colored urine; outputmeasured and recorded

> FBC standard followed

> with ongoing venoclysis at both arms

> no infiltration observed

> with blister @ R heel, toes, sacral and scrotum

area

> applied bactroban once on affected area

> with Hgt monitoring q4h and relayed result to IM

ROD

> given aspart 10 u SQ pre-feeding

> DM standard followed

> CXR film – for official recording

> decrease BUN and pressure support to 8 at 6am

today

> for possible extubation @ 8 am today

> kept watched for any unusualities

> needs anticipated

> endorsed

> kept HR and BP monitored

82

8- 21-07 (AM)

NGT

Standard

FBC

Standard

DM

Standard

Impaired

Skin

IntegrityIVF

Standard

> provided calm and quiet environment to promote

rest

> with O2 inhalation @ 2 LPM via nasal prong

> turned to sides @ intervals

> placed on MHBR

> O2 sat monitoring, saturating well @ 97-99%

> with NGT for OF 166 cc q4 and due PO meds

given

> may have sips of H2O/ clear soup

> encourage oral feeding

> (-) NGT drainage

> standard followed

> with FBC attached to urobag, draining yellow

colored urine

> output monitored and recorded

> FBC standard followed

> with Hgt monitoring q4h, relayed result to

IMROD and with insulin coverage

> given dose of Xlosarapid 8 u SQ as ordered

> DM standard followed

> with blister @ R heel, toes, sacral and scrotal area

> applied bactroban over affected area

> with ongoing venoclysis @ R arm (CVP line) –

infusing well

> due IVTT meds given

> no infiltration observed

> IVF standard followed

> on bladder training

83

8-21-07 (AM)

9:30am

Gen. Notes

Ineffective

Breathing

Pattern

> 4 clamped and 30 minutes released

> kept watched for any unusualities

> needs anticipated

> endorsed

> received awake on bed, conscious and coherent

> hooked to cardiac monitor on sinus rhythm; no

arrhythmias noted

> placed on MHBR

> turned to sides @ intervals; back tapping rendered

> on O2 sat monitoring saturating well 98-100%

> with due nebulization given

> seen and examined by Dr. Solas with orders to off

O2; remove NGT – done and carried out

> voids per diaper/urinal

> output measured and recorded

> on DM diet – consumed share with fair appetite

with strict aspiration precaution

> with Hgt monitoring pre-feeding

> results relayed to ROD with orders carried out

> for CXR – PA tomorrow am – requested

> needs attended

> Nursing care done

> endorsed

84

Doctor’s Notes

Date ordered Doctor’s Order

8-19-07

6:55am

K=4.1

12:05pm

12:35pm

8:25am

9:00am

11:00am

> BUN and PS at 8am and 6pm tomorrow (8-20-07) for 2 hours

> for possible extubation at 8am tomorrow

> revise insulin administration as follows

30 units glorgine insulin (Lantus) SQ

before 8am feeding

10 units insulin aspart (NOVORAPID)

SQ before each feeding

 > problem: hypohaluis

> HRd extubation

> side drip: to D5W 500cc in q shift follow 90 cc D5W + 10 mg

KCl to MN in 1 hour x 5 cycles

> Repeat K after 5th of KCl drip.

> look back to mechanical vent. At 5L/min

> for extubation – done

> suction excretion ET and Oral

> O2 inhalation at 5 L/ min via nasal canula

> possible trans-out tomorrow

> start bladder training

> may have sips of water/clear soup

> decrease O2 to 2 L/ min

>D/ IC IVF at left arm

85

12:00nn

7:00pm

8:10pm

8-21-07

5:15 am

9:30am

8-21-07

9:30am

> NNO

> IVF TF with PLR 1 L at 10 gtts/min

> hold 7pm dosage of Novorapid

> decrease Dovos qid to * lib SQ before each feeding

> repeat CBC; CREA, K tomorrow

> encourage oral feeding

> include serum albumin on blood reaction

> remove FBC and refer if with out output for 4 hours

>D/C Prevoid once stock is consumed

> inform surg. Resident re = CVP line

> IVF TF with PLR @ 10 gtts/min

> CXR PA in Lab

> Resume NGT

> Off O2

> incorporate 60mg KCl in present IVF

> shift ciprofloxacin IV to P.O 5mg BID

> D/C albumin

> may transfer to referred room of choice

> start diabetic diet at 1800 Kcal/ of single mg and more of

polysaccharide fat; CH 60%, CHO 30%, fat 20%

Trans-out Orders

> may transfer to room of choice under D5S volume 1 L/ O2

> regulated plain LR 1 L + 60 Meg KCl at 10 gtts/ml

> meds: cifloxacin 500g + eb bid – D7# Do

cefeprine1 gm IVTT q OD – D7 to complete 10 days

86

Lantus 30 units SQ before 8 hr feeding

Novo rapid 8 units SQ before lunch and dinner and

breakfast

> Duavent + net q6hrs nebulization

> TPR; v/s q4hrs

> Hgt TID pre-breakfast, pre-lunch and pre-dinner – record in

separate sheet

> full diabetic diet at 1800 Kcal/ gw/ no more of single mgs and

more of polysaccharide fat with the ff: specifications:

HO 60% in 3 meals and 2 snacks

CHON 20%

Fat 20%

> strict aspiration precaution

> I and O qshift

> inform surgery resident

> effective accordingly

> inform APS

> for pt CXR PA in am

87

Progress Notes

8-15-07

A case of 34 Y.O M/ single. Admitted due to sensorial changes on his 5th

Hospital day with P.W.I

1. Acute Respiratory Failure Type II secondary to Sepsis secondary to Acute

Necrotizing Pancreatitis/ Hypotension secondary to Acute Necrotizing

Pancreatitis.

A. Acute Renal Failure

B. Hypoalbuminuria secondary

C. Thrombocytopenia secondary to Pulmonary Edema secondary

to B secondary to A

2. Diabetes Milletus type II; newly diagnosed

3. Hospital Acquired Pneumonia

4. S/P craniotomy

8-17-07

Impression:

Acute Necrotizing Pancreatitis – resolving

Acute Respiratory Failure – resolving

Acute Renal Failure – resolving

Pulmonary Edema secondary to Hypoalbuminemia secondary to

Acute Illness

88

S/P Craniotomy secondary to Gun shot wound – 2005

MODS resolved 8/16

Problem 1 Acute Respiratory Failure – resolving

Pulmonary Edema secondary to Hypoalbuminemia secondary to

Acute Illness

S = Px has no subjective data

O = 100/60

Good coughing reflex

Awake; oriented

+ rates mid to basal area

A = with persistence of the Pulmonary Edema on P5

Symbolized by possibility of fatigue

P = increase serum albumin to 3.0 to 3.8 with albuminar infusion

Problem 2 Diabetes Mellitus type II newly diagnosed

S = none

O = Hgt is for 45 g/dL – 34.29 g/dL

A = with NGT feeding, control of blood sugar level

P = adjust insulin drip accordingly

89