Vipoma Complete

I. INTRODUCTION

The most important thing in illness is never to lose heart.

~Nikolai Lenin

There is nothing more terrifying in life than facing an illness; especially if that illness

inflicts a very young person who did not even experience life yet. That very young

person inflicted with an illness may not see the effects of her illness in her life, but her

loved ones will. What is very essential with a person afflicted with an illness is her

support system. It necessary for the support system to have a positive attitude in facing

an illness with the patient. It is believed that positive thinking can do great effects on the

part of the patient. People who are more optimistic when faced with an illness tend to

have more faith in cure. It gives enlightenment to the persons involved that the illness

will be treated.

Maintaining a positive attitude is needed more when faced with a very rare

disease. One such rare disease is having a pancreatic endocrine tumor. Pancreatic

endocrine tumors (PETs) are also called islet tumors or islet cell tumors; however,

because the cell of origin of most is unknown, the general PET is preferred. PETs

frequently are classified as functional or nonfunctional depending on whether a clinical

syndrome resulting from the autonomously released hormone is present (gastrinoma,

insulinoma, glucagonoma, VIPoma, somatostatinoma, GRFoma, ACTHoma).

Nonfunctional PETs frequently release hormones and peptides (pancreatic polypeptide,

neurotensin, α- and β-subunits of human chorionic gonadotropin, neuron-specific

enolase, chromogranin A and breakdown products) that cause no distinct clinical

syndromes (Goldman and Ausiello, 2008, p. 1482).

Islet cell tumors are either sporadic and can occur in association with other

known genetic syndromes, such as multiple endocrine neoplasia type1. Sporadic tumors

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occur at any age but most commonly are detected between 40 to 69 years of age. The

diagnosis can be confirmed by obtaining tissue during surgical resection or by needle

biopsy (Goldman and Ausiello, 2008, p. 1765).

A more specific type of pancreatic endocrine tumor is VIPoma. VIPoma (also known as

pancreatic cholera) is characterized by profuse watery diarrhea, marked fecal loss of

potassium and bicarbonate, hypokalemia, and low or absent gastric acid secretion

(Greenspan and Baxter, 1994, p. 565). Inappropriate secretion of vasoactive intestinal

polypeptide (VIP) by vipomas causes the watery diarrhea, hypokalemia, and

achlorhydria (WDHA) syndrome, also called Verner-Morrison syndrome. Although VIP is

the most likely mediator of the WDHA syndrome, other hormone-like substances such as

the peptide histidine methionine may also be involved (Flethcer, 2007, p. 1129). Death

may result from renal failure or cardiac arrest caused by volume depletion and acidosis

(Ferry, 2008).

In the adult, the vast majority of vipomas are of pancreatic origin. Exceptions are

some rare VIP-producing pheochromocytomas and intestinal endocrine tumors

(Flethcer, 2007, p. 1129). Pancreatic vipomas are usually solitary large tumors (mean

size 4-5 cm). These tumors are usually not multiple, 50-75% are in the pancreatic tail,

and 37 to 68% have hepatic metastasis at diagnosis (Kasper, et. al., 2005). In children

<10 years, WDHA syndromes have been reported in association with VIP-secreting

ganglioneuromas and ganglioneuorblastomas, which are less malignant and account for

10% of VIPomas in adults (Kasper, et. al., 2005). The WDHA syndrome has also been

attributed to islet hyperplasia. These reports are difficult to interpret because, in the

normal adult human pancreas, VIP is only present in autonomic nerves but not in islet

cells (Flethcer, 2007, p. 1129).

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VIPomas are very rare cancers. Each year very few new cases of VIPoma are

reported (0.05 to 0.2 cases per million adults). Even fewer cases in children are

reported. VIPomas are the third most common neuroendocrine tumor of the pancreas

(15%), after insulinomas (50%) and gastrinomas (30%). When VIPomas occur in adults,

they appear most commonly between the ages of 40 and 50 years (Ferry, 2008).

The diagnosis requires the demonstration of an elevated plasma VIP level and

the presence of large-volume diarrhea (Kasper, et. al., 2005).

The most important initial treatment is to correct their dehydration, hypokalemia,

and electrolye losses with fluid and electrolyte replacement. If a tumor has been

identified, complete surgical excision is the primary form of treatment. If the tumor

cannot be removed completely, surgical debulking may have palliative benefit. In one

series, surgical excision of the primary pancreatic tumor relieved all symptoms in 17

patients (27%) (Vinik, 2006). Because 37 to 68% of VIPomas have metastatic disease in

the liver at presentation, a significant number of patients cannot be cured surgically. In

these patients, long-acting somatostatin analogues such as octreotide or lanreotide are

the drugs of choice (Kasper, et. al., 2005). Other drugs reported to be helpful in small

number of patients include prednisone (60 to 100 mg/d), clonidine, indomethacin,

phenothiazines, loperamide, lidamidine, lithium, propranolo, and metoclopramide.

Treatment of advance disease with embolization, chemoembolization,and chemotherapy

may also be helpful (Kasper, et. al., 2005).

An article by David, et. al. entitled “Multi-visceral resection of pancreatic VIPoma in a

patient with sinistral portal hypertension” shows a patient who have undergone multiple

resection of the pancreas with flying colors. A 46 year old women presented with

abdominal pain and diarrhea. A three-dimensional (3-D) pancreas protocol computed

tomography scan revealed an 18 × 12 cm pancreatic VIPoma abutting the liver,

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stomach, spleen, left adrenal, colon that also invaded the distal duodenum – proximal

jejunum at the ligament of Treitz in association with sinistral portal hypertension.

Following preoperative proximal splenic artery embolization, the patient with underwent

successful en bloc resection of the locally advanced VIPoma in conjunction with a

diaphragmatic resection, total gastrectomy, splenectomy, left adrenalectomy, as well as

small and large bowel resection. The estimated blood loss was 500 ml. All margins were

negative (R0 resection). The patient is alive and disease-free. This case illustrates the

role of aggressive resection of pancreatic neuroendocrine tumors and highlights several

key technical points that allowed for successful resection.

This type of aggressive treatment is only possible under advanced medical

equipment and highly skilled surgeons. The treatment has shown a great improvement

on the patient who have undergone the surgery. However, patients have different

reactions to surgery and it is not assured that if the surgery was successful in one

patient, it would also be successful in another patient. Special precautions should be

made in administering this type of treatment to other patients.

The study “Amelioration of Symptoms and Reduction of VIP Levels after Hepatic Artery

Chemoembolization in a Patient with Sandostatin Resistant VIPoma” by Shaib, et. al.

report a successful treatment of VIPoma with hepatic chemoembolization of a metastatic

hepatic lesion evidenced by a reduction of VIP levels and resolutions of symptoms in a

patient with pancreatic VIPoma unresponsive to increased doses of an octreotide

analog.

This is another treatment alternative to clients with VIPoma who are not

responsive to the octreotide. It is done by injecting a chemotherapeutic drug directly into

the blood vessel feeding a cancerous tumor and an embolic agent is placed inside the

blood vessel feeding the tumor trapping the chemotherapy in the tumor. This treatment

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is effective and durable as a treatment modality for patients with metastatic VIPomas (or

other neuroendocrine tumors) who are clinically symptomatic from the effects of

hormone hypersecretion. It is applied as a palliative technique in symptomatic patients

with unresectable hepatic metastasis. This is a less invasive treatment rather than

undergoing surgery. It provides high successful rates to patients who have undergone

this procedure.

Nowadays, lifespan of humans continuously decreases as time passes by. Many

individuals are suffering diseases due to lack of consciousness on how they can avoid

acquiring such diseases. However, some diseases occur sporadically and are very rare.

One very rare disease is VIPoma.

The study was chosen because it was the first time of the nurse researcher to

encounter this illness. She was interested in the pathophysiology and management of

clients with VIPoma. Such knowledge can be use to formulate health teachings that

could be rendered to clients hence may help them in the management of such condition.

Moreover, with the increased in information, people will know how to approach this very

rare disease.

A case of VIPoma is very rare and as a nurse, it is also very rare to handle such

case. For a disease process that entails proper understanding, to handle such case is a

superb opportunity to fully understand the physiology of the disease process, and thus

knowing the cause of the client’s VIPoma. Furthermore, the knowledge about the

pathophysiology and the treatment regimen for these diseases can help her become an

effective nurse. By being equipped with such knowledge, the researcher can be assured

that she can properly execute her functions whenever in the future she encounters

another case of a client with VIPoma.

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Lastly, curiosity is one of the main reasons why the researcher chose such case.

This study is to boost and broaden her awareness and understanding on how such kind

of condition arise and how does it affect the clients especially their physical wellness.

Through research and studies, the researcher will be able to discover more about some

scheme and method that she can apply and adapt to clients with VIPoma. More facts

and information can be learned through continuous study and reading books and

magazines related to health care. Being a health care provider is not an easy task; it is a

continuous study and discovering new trends about different approach in helping clients

to cope up with their illnesses. And as a member of the health care team, it is only

necessary to be a patient advocate and participate in the medical management of clients

with VIPoma.

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A. OBJECTIVES

1. Nurse-centered

General Objectives:

After completion of the study, the nurse researcher shall be able to:

Establish a good working relationship to the client and her family.

Encourage participation and compliance from the client and her family.

Perform comprehensive assessment.

Explain the medical management.

Provide appropriate interventions.

Understand the concept of Vipoma.

Determine the treatment for VIPoma.

Specific Objectives:


Explain purpose of the case study and its importance to the client/ family.

Gain the client’s/ family’s trust regarding health matters.

Monitor and recorded vital signs.

Perform initial physical assessment needed.

Perform comprehensive assessment with regards to the signs and

symptoms of the disease.

Obtain necessary information like demographic data, family history,

personal history, socio-economic, cultural information from the family.

Gather the past and present health history of the client.

Identify the present medical management of the patient and diagnostic

and laboratory procedure done to the client

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Identify abnormal diagnostic findings that are significant to the

identification of the disease condition.

Provide information about the disease process, present signs and

symptoms, its management, and its complications.

Formulate nursing care plans to manage the existing problems of the

patient.

Encourage client/ family to participate in formulating the nursing care

plans.

Provide health teachings with the family regarding prevention of illness

and promotion of wellness and health.

Render the appropriate interventions for patients with Vipoma.

Emphasize the importance of health teachings given and compliance to

treatment regimen.

Determine and understand the etiology, risk factors, assessment findings,

manifestations, pathophysiology, and treatment regimen of Vipoma.

Identify the cause of Asthma of the client in the study.

Present the nursing care plans to the client/ family.

Explain the necessary interventions and their rationales.

Involve the client/ family during the implementation phase of the care

plans.

Evaluate the interventions made in comparison to the objectives set by

the nurse and client/ family.

Monitor the hydration status of the client continuously.

Monitor the progress of the client.

Monitor the intake and output of the client.

Prevent injury and complications of Vipoma.

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Encouraged continuous support of the client at home.

Reassure regarding the characteristic of the course of the disease, with

emphasis on the importance of long-term care, needs to be provided to

parents and the client.

Emphasize the dietary restrictions and needs of the client.

2. Client-centered

General Objectives:


Establish and maintain rapport with the nurse researcher throughout the

nurse-patient interactions.

Participate in the study.

Understand the interventions and management.

Comply with the treatment management.

Specific Objectives:


Express approval and cooperation with the treatment regimen.

Understand the importance of adherence for continuous treatment

regimen of the client.

Participate in the assessment phase and provide the needed information

of the nurse researcher.

Provide the needed information to the nurse researcher.

Participate and impart views on the nursing care plans.

Participate in the implementation of the nurse researcher.

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Understand intervention and management such as compliance to

medications, diet, exercise and lifestyle given by the nurse researcher.

Verbalize current health problems that the client does not know how to

manage.

Verbalize understanding of health teachings regarding prevention of

illness and promotion of wellness and health.

Verbalize understanding of the information regarding the disease

process, signs and symptoms, management and complications.

Comply with the prescribed management, diet, and medications.

Identify and demonstrate behaviors that could prevent complications.

Manifest increased activity tolerance and good hydration status.

Demonstrate ways on how to prevent dehydration.

Identify the medications given after discharge, the route, the time and the

amount that should be taken.

Recognize measures to promote normal activities of daily living.

II. NURSING ASSESSMENT

A. Personal History

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1. Demographic Data

Vipsy, a 2 year-old single female, was born on January 30, 2008 via normal

spontaneous delivery in a private hospital in the City of San Fernando. She is the only

child of Daddy Vips and Mommy Vips. She is a natural born Filipino citizen. Vipsy is

currently residing in Camachiles, Dau Mabalacat, Pampanga. She is the first child of

Mommy and Daddy Vips. Mommy Vips was 16 years old when she got pregnant with

Vipsy and Daddy Vips was 20 years old then. The parents of Vipsy are not married.

They had Vipsy after having a relationship of six months and they were separated by the

parents of Mommy Vipsy.

Vipsy had persistent loose watery stools and loss of appetite which prompted her

mother to seek medical advice and her mother was advised to admit Vipsy. She was

admitted at a private hospital in Angeles City last March 24, 2010 5:20 PM with an

admitting diagnosis of To Consider Vipoma. After five days of confinement, Vipsy was

discharged in the institution last March 28, 2010 at 3 o’clock in the afternoon with the

final diagnosis of Vipoma.

2. Socio-Economic and Cultural Factors.

In the Philippines, the family is a complex network of relatives by blood and affinity.

Affinity may come through marriage or Catholic rituals like god parenting newly baptized

children or newly married couples or even living under the common law.

The Vips family is classified under the extended type of family. Vipsy lives with

Mommy Vips, the mother of Mommy Vips (Grandma Vips), Grandma Vips’ (Sister Vips)

sister and the two siblings of Mommy Vips. Before December 2009, Grandma Vips was

in Iraq and she was working in a laundry shop which makes Sister Vips as the

companion of Mommy Vips, her siblings and Vispy. Mommy Vips is separated from

Daddy Vips. Mommy Vips is 18 years old while Daddy Vips is 22 years old. According to

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the Grandma Vips, she did not like Daddy Vips that is why they separated Mommy Vips

and Daddy Vips. Vipsy is the first born child of Mommy Vips and Daddy Vips. Grandpa

Vips is not living with them as of the moment. He works in Lakuna and he goes home at

least once a week. Mommy Vips has two siblings. Vipsy Boy is 16 years old and Vipsy

Girl is 14 years old.

The Vips Family suffices their needs with the income of Grandma Vips and Grandpa

Vips since Mommy Vips is still a high school student. Grandpa Vips is a personal driver

of the vice mayor in Lakuna. He works six days a week which gives him time to go home

on Sundays. Sometimes, he does not have time to go home during Sundays. His salary

is around Php 20,000.00. Grandma Vips works in Iraq as an employee in a laundry

shop. She has been working abroad for almost four years. Her salary is around Php

30,000.00 per month. Grandma Vips only went home last December 2009 because her

granddaughter is sick and Mommy Vips needs her mother to help her in taking care of

Vipsy.

With the income of Php 50,000.00 per month, they allot Php 4,000 for their daily

food expenditure, Php 2,000 for their electric bill, Php 600 for their water bill. Their

groceries account to Php 7,000, Php 3,000 for the transportation of Vipsy Boy and Vipsy

Girl. Vipsy Boy and Vipsy Girl are fetched by a school service. They also allot Php

7,000.00 for the allowance of Mommy Vips, Vipsy Boy and Vipsy Girl dividied into Php

3,000 for the allowance of Mommy Vips, Php 2,000.00 each for Vipsy Boy and Vipsy

Girl. Mommy Vipsy’s allowance is Php 150/ day while Vipsy Boy and Vipsy Girl’s

allowance each is Php 100/day each. Also, Php 2,000.00 is spent on the milk of Vipsy.

Their total monthly expenditure is Php 25,600.00. The rest of their budget is saved for

their tuition fees and for their extra expenditures.

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As to their economic status, the Vips’ family is considered not poor because their

monthly budget is Php 50,000.00 and when divided into 4 is Php `12,500. And according

to the basis given by NEDA wherein there are two categories of economic status: poor

and not poor. Families who have Php 2,768.60/month/ individual and higher fall under

Not Poor category, and those below the standard amount falls under Poor citizens.

Therefore, the Vips’ family financial assets are adequate as compared to their

expenditures. As shown on the breakdown of their expenses, they allotted budget for

health emergencies. However, their previous monthly budget has been lessened

because Grandma Vips went home from her work from Iraq. Consequently, Grandma

Vips stated that her stay here in the Philippines is only temporary and she will come

back to Iraq this year.

Vipsy does not go to school yet. Sister Vips and Mommy Vips teach her how to

talk, count and sing. She can sing her ABCs and can count up to 10. Vipsy is talkative

according to Mommy Vips; however, she still cannot complete a sentence.

The Vips Family is affiliated with the Roman Catholic. They see to it that they

attend mass every Sundays. Vipsy is baptized as a Catholic when she was 3 months

old. The Vips family prays the rosary at least once a month usually every first Fridays of

the month.

As Filipinos, we are very much concerned when it comes to superstitious or

cultural beliefs. They believe in superstitions. They believe that one should not clean the

house at night because it brings bad luck. When Vipsy was only months old, Sister Vips

puts a touch of lipstick on the forehead of Vipsy to prevent “asug”. They also believe in

herbolarios. They sought a herbolario when Vipsy’s diarrhea was consistent for almost 2

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weeks. “Tawas” was made by the herbolario and interpreted that Vipsy’s stomach is full

of gas. They sought a herbolario because Vipsy’s diarrhea did not stop. However, their

first consultation whenever an illness is present is with their private physician. They only

consult a herbolario if the signs and symptoms of illness are consistent. They also

believe in “nuno” and “tawas” and in offering sacrifices, such as eggs and chicken, to the

“punso”. The family also believes in “ambon” and “pasma”. Whenever Vipsy goes out at

night, Mommy Vips see to it that she wears a cap or Vipsy’s head is covered to prevent

“ambon”. Mommy Vips believe that “ambon” can cause cough and cold. Grandma Vips

does not allow her family members to take a bath if they are tired and after ironing the

clothes. They also self-medicate when one of their members gets sick. They use

Biogesic, Carbocisteine, Solmux and Nafarin for fever, cough and colds. They also do

tepid-sponge bath for members with fever.

Vipsy usually wakes up at around 6 AM. She would have her breakfast then she

would start watching Barney or Dora on the television. She eats Cerelac in the morning

and she still bottle feeds every 3 to 4 hours. She usually consumes 2 to 3 oz of milk

every time she bottle feeds. At 12 noon, she would have her lunch. She eats half cup of

rice with different viands every day. Her favorite viand is fried chicken. Sister Vips

usually cooks Tinola, Sinigang, Caldereta, and Fish. Vipsy is not very particular when it

comes to her food. She usually eats what is served. However, she could not consume

her full meal. She usually consumes ¾ of her meal and she would just be given her milk.

After eating, she would play or watch television. At 2 PM, Sister Vips bathes Vipsy then

puts her to sleep thereafter. She would sleep for three to four hours. When she wakes

up, Mommy Vips would play with her daughter while Sister Vips is cooking dinner. At

6:30 PM, they would have their dinner. After dinner, Mommy Vips would give Vipsy

bananas or apples as her dessert. Vipsy’s sleeping time is usually 9 PM to 10 PM. She

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would usually watch television with her mother or her mother would teach her the ABCs.

Before Vispy’s sleeping time, she would be given milk and water after her feeding and

would go to sleep.

The environmental condition plays a significant role in the development and health of the

family members. The Vips Family lives in Camachiles Dau, Mabalacat, Pampanga. Their

house is located in an urban area in Pampanga.

They own their home and as described by Mommy Vips, their house is concrete,

made up of cement, from wall to wall, roof is made from galvanized iron sheet and

ceiling is fixed with plywood. Their house measures approximately 300 m2. They have a

two-storey house. Their house has three bedrooms, one master bedroom for Grandma

and Grandpa Vips, one for Mommy Vips, Vipsy Girl and Vipsy and the other room is

Vipsy Boy. Their home has a sala, dining room, and kitchen with two windows each

room and two bathrooms. Mommy Vips mentioned that they have good ventilation since

their home is surrounded by plants.

According to Mommy Vips, they have a closed drainage system. The source of

their water is through the jetmatic. Their source of electricity is from a private

corporation. They buy their drinking water from water refilling stations. They have

different appliances like television, refrigerator, electric fans for each room, DVD player,

and a gas range.

In their living room, a set of sofa, and television, an electric fan, and different

room designs like picture frames and figurines would be found. Every room has 2

windows measuring approximately 2x2 meters, where the light and air pass at day time.

It is covered with a curtain but they usually tie it at daytime. There are no other

obstructions other than that for the light and air to pass through. In the bedrooms, they

only have one window in each bedroom.

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Their kitchen is situated at the right side of the dining room with a round glass

table and six chairs. They have their own utensils, which they use when eating and

cooking. They cook by using stove and LPG tank. They use fluorescent bulbs.

Their home is near a supermarket. There is also a church that is a jeepney ride

away from their home. They have a car. However, since Grandpa Vips is the only one in

their family who knows how to drive, they only use their car when he is present. They

use jeepneys and tricycles as their means of transportation. They use cellphones as a

mean of communication.

B. Pediatric History

Growth and Development

1. Erik Erikson

Stage 1: Trust vs. Mistrust

The development task for infants is learning trust versus mistrust. Infants whose

needs are met when those needs arise, whose discomforts are quickly removed, who

are cuddled, played with , and talked to, come to view the world as a safe place and

people as helpful and dependable. However, when their care is inconsistent, inadequate,

or rejecting, it fosters a basic mistrust: infants become fearful and suspicious of the world

and of people (Pillitteri, 2007, p. 815).

According to Mommy Vips, Vipsy’s needs were always met in a consistent

manner. They would feed her every two to three hours. They would cuddle her whenever

she cries. Mommy Vips have a schedule of when to feed Vipsy, her nap time, her play

time, and the time of her bath. During her infancy years, Vipsy always smiles whenever

someone other than her caregivers plays with her. She developed stranger anxiety when

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she was about 9 months old. By that time, only her caregivers are able to cuddle her;

otherwise, she would cry and look for her caregivers.

Stage 2: Autonomy vs. Shame and Doubt

Autonomy builds on children’s new motor and mental abilities. Children take

pride in new accomplishments and want to do everything independently, whether it is

pulling the wrapper off a piece of candy, selecting a vitamin tablet out of the bottle,

flushing the toilet, or replying, “No!” (Pillitteri, 2007, p. 816).

Vipsy as observed by the researcher love to say the word “ayaw”. When asked to

state her name, she would reply “ayaw”. According to Mommy Vips, “ayaw” is her

favorite word. As stated by her mother, Vipsy can already tell her mother that she would

like to pee. Vipsy would say “wiwi” so that she can go to the comfort room. After that,

she always flushes the toilet without the help of her mother. Vipsy at this age loves to do

things independently such as eating her bubble gum. She would open the wrapper by

herself and throw the bubble gum by herself.

2. Sigmund Freud

Oral Phase

Freud termed the infant period the “oral phase” because infants are so interested

in oral stimulation or pleasure during this time. According to this theory, infants suck for

enjoyment or relief of tension, as well as nourishment (Pillitteri, 2007, p. 814).

When Vipsy was in her infancy stage, she loves to put everything in her mouth

according to Mommy Vipsy. Whatever object she touches, she would put in her mouth to

play with. She has her teething toys which she used always. Caregivers usually provide

her with a pacifier. If Vipsy has no pacifier, she would thumb suck and usually fall

asleep.

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Anal Phase

Freud described the toddler period as the “anal phase” because during this time,

children’s interests focus on the anal region as they begin toilet training. Elimination

takes place on new importance for them. Children find pleasure in both the retention of

feces and defecation. This anal interest is part of toddlers’ self-discover, a way of

exerting independence (Pillitteri, 2007, p. 814).

Vipsy can only tell her mother that she is about to urinate by saying the word

“wiwi”. However, she still cannot control her defecation because of her illness.

3. Jean Piaget

Sensorimotor Stage (Coordination of secondary reactions)

Sensorimotor intelligence is practical intelligence, because words and symbols for

thinking and problem solving are not yet available at this early stage. At the beginning of

infancy, babies relate to the world through their sense, using only reflex behavior. As

infants progress through this stage (which includes the schemas of primary and

secondary circular reactions and coorination of secondary reactions), they learn the

basic concept that people are separate entities from objects. In the primary circular

return, infants repeat what they tend to enjoy such as sucking. There is repetition of

behavior. The secondary circular return refers to activities that are separated from the

child’s body. Infants learn that objects in the environment are permanent and continue to

exist even when out of sight. During the final phase (coordination of secondary

reactions), infants begin to demonstrate a goal directed behavior. After noticing that

hitting a mobile makes it move, infants then reach for and hit a music box nearby, in this

way actively seeking new experiences (Pillitteri, 2007p. 818).

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During this stage, Vipsy discovered permanence. She knows that when her

mother disappears, her mother would come back again. When her mother is out of sight,

she would cry continuously because she knows that her mother is present even if she is

out of Vipsy’s sight. She also has a toy that has a button. If that button is pressed, the

toy would vibrate and make sounds. When Vipsy’s mother presses the button, the toy

would vibrate and make sounds; when the toy stopped, the baby pressed the button

again to make it vibrate again and again. Vipsy also loves to play peek-a-boo with her

caregivers during her infancy years.

Tertiary Circular Reaction

The toddler period is one of transition as children complete the final stages of the

sensorimotor period as tertiary circular reaction and begin to develop some cognitive

skills of the preoperative period, such as symbolic thought and ego-centric thinking. In

the tertiary reaction schema, children use trial and error to discover new characteristics

of objects and events. The child is able to experiment to discover new properties of

objects and events. Child uses memory and imitation to act.

According to Mommy Vips, Vipsy can count from one to ten and can sing her

ABCs with the guidance of her caregivers. Vipsy also loves watching Barney and she

can sing with the songs being played. As observed, Vipsy loves to eat bubble gum.

When she eats bubble gum, she only chews it for one minute and throws it. Then she

would get another gum, chew it for one minute and discard it again. She loves to talk

with her caregivers, however, she still babbles and she cannot complete a sentence.

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C. Family-Health Illness History

Legend:

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VIPSY2 y/o

Vipsy Boy16 y/o

Grandma Vips49 y/o

Vipsy Girl

14 y/o

89 y/o 2008DM

GrandpaVips (HPN)

47 y/o

Mommy Vips

18 y/o

2008Old age

66 y/oHPNDM

Daddy Vips20 y/o

Female

Male

Deceased

Client

The diagram shows the family health history of Vipsy. Family health history taking is very

crucial in determining hereditary factors that contributed to the disease of the client. The

information came from Grandma Vips’ narration.

Vipsy have a history of Diabetes Mellitus and Hypertension. Grandpa Vips has

hypertension. Grandma Vips have no diagnosed illness. The father of Grandma Vips

died last 2008 and the death was due to old age. The mother of Grandma Vips is still

alive with no diagnosed illness. On Grandpa Vips’ side, her mother died also last 2008

due to complications of Diabetes Mellitus. Grandpa Vips’ father is diagnosed to have

Hypertension and Diabetes Mellitus. Mommy Vips have no known disease as well as

Daddy Vips. The siblings of Mommy Vips are not diagnosed of any illness.

*Family history of Daddy Vips was not included because Grandma Vips does not want to

talk about the father of Vipsy since they are not married and Mommy Vips got pregnant

with Vipsy when she was only 16 years old. Also, Mommy Vips is not familiar with the

family health-illness history of Daddy Vips.

D. History of Past Illness

Vipsy is diagnosed to have a Glucose-6-Phosphate Dehydrogenase deficiency.

She had her newborn screening after she was born in a private hospital in the City of

San Fernando. Mommy Vips wants to confirm the diagnosis so they went to Manila to

have a second opinion regarding her diagnosis. After testing, it was confirmed that Vipsy

has G6PD. Mommy Vips was given education regarding the diet and food restrictions

with regards to clients with G6PD. Vipsy occasionally has fever, cough and colds. She

had two medical consultations with regards to her fever, cough and colds and she was

prescribed to have Paracetamol and Loviscol and Salinase for her cough and colds.

Mommy Vips religiously followed the prescribed medications for Vipsy.

21

E. History of Present Illness

The history of present illness of the client was discussed by Grandma Vips.

According to her, Vipsy’s first episode of diarrhea started last Novermber 2009. She had

watery stools three to four times per day. At the onset of her diarrhea, they immediately

consulted her private physician and she was prescribed to take OMX, Zinnat, Pediachlor

and Chlorocare. The physician diagnosed her to have an Acute Gastroenteritis

Medications were given to Vipsy then her signs and symptoms would subside for one

week. After that week, she would have episodes of diarrhea again. Consultation is done

and same medications were given. Grandma Vips stated that they have been consulting

their private physician almost every week. Mommy Vips mentioned that her diarrhea

started when Vipsy started to eat solid foods. She was bottle fed for more than one year

before solid foods were introduced. Before, she did not have any episodes of diarrhea

until she began to eat solid foods.

By the third week of December 2009, she had three watery loose stools and no

other signs and symptoms noted. They consulted her private physician and Vipsy was

diagnosed with Acute Gastroenteritis again. She was prescribed with Erceflora and

Hidrasec. After one week, Vipsy continues to have two to three watery stools per day,

hence, consult to a private physican and was advised to continue taking Erceflora and

Hidrasec. The week after her last consult, Vipsy was still having two to three watery

loose stools. They consulted her private physician again and she was given an

additional antibiotic. By the second week of January 2010, Mommy Vips noticed that

Vipsy’s abdomen is distended; they consulted her private physician and ordered for

Vipsy to have an ultrasound of her abdomen. Vipsy’s ultrasound revealed Hydrops of her

Gallbladder. However, no surgery was done since the surgeon was not available. On the

third week of January 2010, Vipsy’s signs and symptoms persisted and was given

22

Pediachlor by her private physician. The day after her consultation she was advised to

have a repeat abdominal ultrasound. The result was the same as the first ultrasound

which reveals Hydrops of the gallbladder. Her signs and symptoms persisted hence her

admission in a private institution last January 21, 2010 with a chief complaint of

abdominal enlargement.

Her admission last January 21, 2010 was her first confinement. She was

admitted from January 21, 2010 with an admitting diagnosis of Hydrops of Gallbladder,

Electrolyte Imbalance and glucose-6-phosphate dehydrogenase deficiency and was

discharged last February 15, 2010 with a final diagnosis of Vasoactive Intestinal Tumor.

During her confinement, she was given Ampicillin IV, Gentamicin IV, Hidrasec sachet,

Clarithromycin syrup, Paracetamol suppository, Metronidazole IV, Unasyn IV, Aeknil IV,

Vitamin K IV, Famotidine IV, Amikacin IV, Nutrillin and Pedzinc + C syrup as her

medications. Antibiotics, Antipyretic, Antidiarrheal and Vitamins were given during her

confinement. Total parenteral nutrition was also administered because Vipsy was kept

on NPO for almost two weeks. Nasogastric tube was also inserted to decompress her

stomach due to the findings from her abdominal x-ray and CT scan. The nasogastric

tube remained in place for almost two weeks. Abdominal x-ray was done which had an

impression of Mild Adynamic Ileus. The abdominal x-ray also showed that there is an

increase in the number of small and large that shows moderate gaseous distention and

multiple air-fluid levels are seen. Chest X-ray was also done with a result which revealed

Atelectasis or pneumonia left retrocardiac area. Ultrasound of the gallbladder was also

done. Results demonstrated that Vipsy has a normal sized gallbladder with sludge ball,

negative for cholecystits and non-dilated biliary tree. Computed Tomography of the chest

was also done to have more clear visualization of the lungs. The CT scan of the chest

revealed that there is a calcified soft tissue mass, left posterior T8-T12 paravertebral

area, primary consideration is posterior mediastinal teratoma. There was an incidental

23

note of moderate gaseous distention of intestine; either due to ileus or obstruction and

the lungs is negative for neither pulmonary infiltrates nor pleural effusion. On February 4,

2010, Vipsy had undergone operation. The procedure was Exploratory Laparotomy

Transabdonminal Biospy (transdiaphragmatic), Laddi Procedure with Appendectomy

and Cholecystectomy. The tumor incised was located in the left paravertebral area

behind the posterior lips of the diaphragm. The tumor was solid, fixed, and hard in

character. The Histopathology Diagnosis of tumor revealed a posterior mediastinal mass

ganglioneuroma. The microscopic description of the tumor stated no nuclear atypia,

mitosis or malignant changes is seen in the tumor. Vipsy’s potassium levels were also

monitored. She was hypokalemic upon admission with a result of 1.94 mmol/L and she

was infused with postassium chloride in her intravenous solution. Sodium results were

determined which revealed low levels (133.7 mmol/L). Ionized Calcium and Chloride

levels were also determined and the results were within normal range. Bicarbonate

determination was done through arterial blood gas test which revealed a low

Bicarbonate level. Fasting and random blood sugar were determined and they were

within normal limits. According to Grandma Vips, serum Vasoactive Intestinal Peptide

was also determined and the results was VIP serum was >400. It was done on an OPD

basis in Manila.

After one month (March 24, 2010), Vipsy was admitted in the same institution

with a chief complaint of loose bowel movement. Four days prior to admission, Vipsy

had colds of watery discharge associated with low grade fever and soft stool (three times

per day) and she was given Paracetamol and Pediatapp by her mother. Two days prior

to admission, they consulted her attending physician and was given Chlorocare.

According to her attending physician, her weight the week after her admission was 12

kg. Few hours prior to admission, Vipsy had loss of appetite, profuse sweating, and

weakness associated with one soft watery stool which prompted her physician to admit

24

her in a private institution. She was then discharged after five days of confinement last

March 28, 2010.

F. Physical Examination

March 24, 2010 (Lifted from the Chart)

Vital Signs:

Temperature: 36.5 oC

Pulse Rate: 100 bpm

Respiratory Rate: 24 cpm

Physical Assessment

General Survey: Anicteric sclera, pale palpebral conjunctiva

Chest & Lungs: symmetrical lung expansion, clear breath sounds

Cardiovascular: Adynamnic Precordium, normal rate regular rhythm

Abdomen: Globular; LBS, soft, (+) slightly tympanic

Extremities: full and equal pulses, (-) edema

Nutritional Status

Age: 26 months (2 years, 1 month, 6 days)

Weight: 11.8 kgs

According to the FNRI table, Vipsy’s weight is within the normal range.

First Nurse- client Interaction (March 24, 2010)

25

General Appearance

The client was awake, cyring and irritable with an ongoing IVF of #1 D5 0.3 NaCl

500 cc x 44-45 ugtts/ min at 400 cc level infusing well on the left hand, with pale nail

beds, pale palpebral conjunctiva, pale lips, appears weak, and slightly sleepy, (-)

vomiting, with good skin turgor, (+) loss of appetite, with 3 episodes of watery loose

stools.

Vital Signs:


Pulse Rate: 112 bpm


Physical Assessment

The Integument

Skin: Fair complexion, uniform in color, (+) Pallor noted; (-) cyanosis

Hair: Evenly distributed short, thin, straight hair. Body hair are evenly distributed

Nails: pale pink nail beds; Short and clean finger nails, capillary refill of 2

seconds, (-) clubbing

The Head

Skull and Face: Head is normocephalic and has a smooth contour. Facial

features are symmetrical with symmetrical facial movements.

Eyes: Hair at the eyebrows is evenly distributed with skin intact. Eyebrows are

symmetrically aligned and equal in movement. Eyelashes are equally distributed

and slightly curled outside. Eyelids have intact skin with no discharge and

discoloration. The eyelids close and open symmetrically. With a normal blinking

reflex and bilateral blinking. The palpebral conjunctiva is shiny and pale. There

26

is no edema or tenderness over the lacrimal gland. Pupils equally round and

reactive to light accommodation. Sclera is anicteric.

Ears: Color same as facial skin, symmetrical and aligned with the outer canthus

of the eye. The auricles are mobile, firm and not tender. Pinna recoils after it is

folded. She was able to hear normal voice tones.

Nose and Sinuses: Nose is symmetrical, uniform in color, (-) nasal flaring. There

is no presence of tenderness and lesions. Clear watery discharge from both

nares. The nasal septum is intact and in midline. The maxillary and frontal

sinuses are not tender.

Mouth: The lips are pale pink in color. With two upper incisor, two lower incisor,

2 upper lateral incisor, and one upper molar teeth, pinkish gums. The tongue is in

central position, pinkish in color, with thin whitish coating, no lesions. It moves

freely without any tenderness. Uvula is positioned in the midline of soft palate,

tonsils are pink, not inflamed with no discharge. With the presence of gag reflex.

Neck

Head centered, coordinated, smooth movements, no palpable lymph nodes. The

thyroid gland is not visible on inspection and ascends during swallowing. No difficulty

in swallowing. No hoarseness of voice.

Chest

Symmetric, skin intact with uniform temperature. Clear breath sounds,

symmetrical chest expansion.

Cardiovascular and Peripheral Vascular Systems

27

Heart: There were no pulsations, with symmetric pulse volumes of the carotid

artery; there is also absence of sound (bruit) heard on auscultation. The jugular

veins are not visible in a semi-fowler’s position.

Peripheral Vascular System: There is a presence of symmetric pulse volume

with full pulsations. No presence of edema.

Abdomen

Abdomen with uniform color, unblemished skin on the right upper part. No

evidence of enlargement of the liver or spleen and symmetric in contour.

Symmetrical movements caused by respirations. Have tympani sound over the

stomach and dull on the liver and spleen. Flabby, soft and nontender; with a surgical

scar on umbilical area, rounded abdomen.

Musculoskeletal

Muscles are equal in size on both sides of the body. There are no tremors, firm,

and smooth coordinated movements with equal strength on each body side. No

presence of deformities.

Extremities: No edema. Full and equal pulses.

Second Nurse-client Interaction (March 25, 2010)

28

General Appearance

The client was on bed awake on a sitting position, with an ongoing IVF of #4 D5

0.3 NaCl 72.5 cc + KCl 1.5 cc = 74 cc every 2 hours at 50 cc level via soluset infusing

well on the left hand, with pale nail beds, pale palpebral conjunctiva, pale lips, (-)

weakness, (-) vomiting, with good skin turgor, with fair appetite, with 3 episodes of

scanty loose stools, and (+) productive cough. She was not irritable and she smiled

at the nurse researcher

Vital Signs:


Pulse Rate: 124 bpm


Physical Assessment

The Integument

Skin: Fair complexion, uniform in color, (+) Pallor noted; (-) cyanosis


Nails: pale pink nail beds; Short and clean finger nails, capillary refill of 2


The Head






29


reflex and bilateral blinking. The palpebral conjunctiva is shiny and pale. There

is no edema or tenderness over the lacrimal gland. Pupils equally round and

reactive to light accommodation. Sclera is anicteric.





is no presence of tenderness and lesions. Clear watery discharge from both

nares. The nasal septum is intact and in midline. The maxillary and frontal

sinuses are not tender.

Mouth: The lips are pale pink in color. With two upper incisor, two lower incisor,

2 upper lateral incisor, and one upper molar teeth, pinkish gums. The tongue is in




Neck

Head centered, coordinated, smooth movements, no palpable lymph nodes. No

difficulty in swallowing. No hoarseness of voice.

Chest


symmetrical chest expansion. (+) productive cough.


30






Abdomen






Musculoskeletal


and smooth coordinated movements. No presence of deformities.


31

Third Nurse-client Interaction (March 27, 2010)

General Appearance

The client on bed asleep on a supine position, with an ongoing IVF of # 38 D5

0.3 NaCl 72.5 cc + KCl 1.5 cc = 74 cc every 2 hours at 70 cc level via soluset infusing

well on the left hand, with pinkish nail beds, pinkish palpebral conjunctiva, pinkish lips, (-)

weakness, (-) vomiting, with good skin turgor, with fair appetite, with 2 episodes of

scanty loose stools.

Vital Signs:


Pulse Rate: 110 bpm


Physical Assessment

The Integument

Skin: Fair complexion, uniform in color, (-) cyanosis


Nails: pinkish pink nail beds; Short and clean finger nails, capillary refill of 2


The Head






32


reflex and bilateral blinking. The conjunctiva is shiny and pinkish. There is no

edema or tenderness over the lacrimal gland. Pupils equally round and reactive

to light accommodation. Sclera is anicteric.





is no presence of tenderness and lesions. The nasal septum is intact and in

midline. The maxillary and frontal sinuses are not tender.

Mouth: The pinkish lips in color. With two upper incisor, two lower incisor, 2

upper lateral incisor, and one upper molar teeth, pinkish gums. The tongue is in




Neck

Head centered, coordinated, smooth movements, no palpable lymph nodes. No

difficulty in swallowing. No hoarseness of voice.

Chest


symmetrical chest expansion. (+) productive cough

33







Abdomen






Musculoskeletal


and smooth coordinated movement. No presence of deformities.


34

G. DIAGNOSTIC AND LABORATORY FINDINGS

Laboratory

Procedure

Date

ordered/

Date

results in

Indication or Purpose Results Normal Values Analysis and interpretation of results

CBC

The CBC and differential count are a series of tests of the peripheral blood that provide a tremendous amount of information

about the hematologic system and many other organ systems. They are inexpensively, easily, and rapidly performed as

screening test.

Hematocrit

DO: 03/

24/10

Results in:

03/ 24/ 10

To aid diagnosis of

anemia, or abnormal

states of hydration

0.40 0.31 – 0.43

The client has a normal hematocrit count. She

has a good hydration status. The client does

not have anemia.

HemoglobinTo measure the severity

of anemia

128 110 – 160 g/LHemoglobin level is normal indicating the

absence of anemia.

Leukocytes

count

To determine infection or

inflammation

4.2 5 – 15.5 x 103 g/L

The leukocyte count is decreased which

indicates a presence of viral infection that may

be the cause of the client’s cough and colds.

Neutorphils To help diagnose 0.36 0.25 – 0.43 The client has normal neutorphil level. The

specific types of illnesses

that affect the immune

system

client has no inflammation.

Lymphocytes

Plays an important role

in the immunity, they are

the one responsible for

the activities of the

immune system.

To assess and monitor

genetic and acquired

immuno deficiency

states.

0.55 0.20 – 0.65

The client has normal lymphocyte level. This

indicates that the client is not

immunocompromised.

Monocytes

To help diagnose an

illness such as infection

or inflammatory disease

0.07 0.00 – 0.05

The levels are increased. This indicates the

presence of infection as in conjunction with the

decrease in leukocyte count.

Eosinophils To determine allergic

reactions or parasitic

0.02 0.00 – 0.03 The client has normal eosinophil count. She

infections has no allergic or parasitic infection.

Platelet

count

To diagnose and monitor

severe thrombocytosis or

thrombocytopenia

285150 – 400 x 103

g/L

The client has normal platelet count. She does

not manifest bleeding or clotting.

Nursing responsibilities:

Prior to:

1. Explain the purpose of the specimen collection and the reason for obtaining the specimen

2. Provide client comfort and safety.

3. Inform client may experience discomfort upon specimen collection

4. Obtain history of the patient’s gastrointestinal, hematopoeitic, immune and respiratory system, as well as results of previously

performed tests, patient’s complaints, including a list of known allergy.

5. Obtain a list of medications the patient is taking including herbs, nutritional supplements and nutraceuticals. The requesting

practitioner and laboratory should be advice if the patient regularly uses these products so that their effects can be taken into

consideration when reviewing results.

6. There are no food or medical, fluid restrictions unless by medical directions.

During:

1. Avoid hemolysis.

2. List on the laboratory slip any drugs that may affect test results.

3. Direct the patient to breathe normally and to avoid unnecessary movements.

After:

1. Apply pressure to the venipuncture site.

2. Document the procedure done.

3. Label and transport the specimen to the laboratory promptly.

4. Report abnormal lab findings to the health care professional in a timely manner consistent with the severity of the abnormal

results and observe venipuncture site for bleeding or hematoma formation. Apply pressure bandage

5. Evaluate test results in relation to the patient’s symptoms and other test performed.

Laboratory

Procedure

Date ordered/

Date results inIndication or Purpose

Result

sNormal Values Analysis and interpretation of results

BLOOD

CHEMISTRY

A number of other tests may be performed on blood serum. These are often referred to as the blood chemistry. It provides

valuable diagnostic cues.

Potassium

DO: 03/ 24/10

Results in: 03/

24/ 10

To evaluate clinical signs of

potassium excess

(hyperkalemia) or potassium

depletion (hypokalemia) 2.68

3.50 – 5.50

mmoL/L

The client has hypokalemia. Due to the

excessive production of VIP, there is also

excessive stimulation of intestinal

secretions and intestinal motility. This

leads to frequent secretory watery

diarrhea of the client wherein potassium is

lost further.

DO: 03/ 24/10

Results in: 03/

25/ 10 (6 AM)

2.04

The client’s potassium level decreased.

Potassium is lost in her stool due the

effects of excessive amount of VIP

produced by the ganglioneuroma. The

intravenous fluids did not increase her

potassium level.

DO: 03/ 25/10 2.34 The client’s potassium level increased

Results in: 03/

25/ 10 (3 PM)

due to the incorporation of potassium in

the intravenous fluid. However, the client

still has watery stools that cause excretion

of potassium in the stool caused by

VIPoma.

DO: 03/ 25/10

Results in: 03/

26/ 10 (6 AM)

2.89

The potassium level increased indicating

that the client is responding well to the

intravenous therapy prescribed to her.

Her intravenous fluid is incorporated with

potassium chloride. Still with the presence

of VIPoma, potassium is being secreted

continuously through her stool.

DO: 03/ 26/10

Results in: 03/

26/ 10 (2 PM)

3.49

The level of the client’s potassium is near

the normal level showing improvement in

her condition.

DO: 03/ 26/10

Results in: 03/

27/ 10 (6 AM)

3.47 The potassium level slightly decreased

since the client had four episodes of loose

watery stools from the night before

extraction. Potassium is lost through her

stool from the effect of excessive

vasoactive intestinal peptide.

DO: 03/ 27/10

Results in: 03/

28/ 10 (6 AM)

3.18

The client’s potassium level decreased

despite the presence of potassium

chloride in her intravenous fluid since she

had 3 episodes of loose watery stool from

the previous day. Potassium was

secreted from the stool because of the

effect of cAMP which was stimulated by

the excessive amounts of vasoactive

intestinal peptide.

DO: 03/ 28/10

Results in: 03/

28/ 10 (2 PM)

3.49

The client’s potassium level is near the

normal level. She responded well to the

intravenous treatment and with her intake

of kalium durule.

Sodium DO: 03/ 25/10

Results in: 03/

25/ 10 (3 PM)

To evaluate fluid-electrolyte

and acid-base balance and

excretion of sodium from the

136.3 135 – 150

mmoL/L

The client has normal sodium level. The

client did not excrete sodium through her

stool stool.

Chloride

DO: 03/ 25/10

Results in: 03/

25/ 10 (3 PM)

To detect acid-base

imbalance (acidosis or

alkalosis) and to aid

evaluation of fluid status and

extracellular cation-anion

balance

106.198 - 107

mmoL/L

The client has normal chloride level. She

does not manifest hypochlorhydria which

is also a manifestation of vipoma.

Nursing Considerations:

Prior to

1. Explain the purpose of the specimen collection and the reason for obtaining the specimen

2. Obtain history of the patient’s complains, including a list of known allergy.

3. Provide client comfort and safety.

4. Inform client may experience discomfort upon specimen collection

5. Obtain a list of medications the patient is taking including herbs, nutritional supplements and nutraceuticals. The requesting

practitioner and laboratory should be advice if the patient regularly uses these products so that their effects can be taken into

consideration when reviewing results.

During

1. Ensure that the patient has complied with the dietary preparations and other pre-fasting restrictions.

2. Direct the patient to breathe normally and to avoid unnecessary movements.

3. Observe standard precautions.

After

1. Report abnormal laboratory findings to the health care professional in a timely manner consistent with the severity of the

abnormal results

2. Observe venipuncture site for bleeding or hematoma formation. Apply pressure bandage.

3. Instruct the client to resume usual diet as directed by the health care practitioner.

4. Evaluate test results in relation to the patient’s symptoms and other test performed.

Laboratory

Procedure

Date

ordered/

Date

Indication or Purpose Results Normal

Values

Analysis and interpretation of results

results in

Urinalysis

Color

DO: 03/

24/10

Results in:

03/ 25/ 10

To determine color of urine Light yellowYellow to light

orange

The client has normal appearance of

urine. She does not manifest

concentrated urine which may indicate as

dehydration which can be a result of

secretory diarrhea from VIPoma.

AppearanceTo determine presence of

crystalsClear Clear No crystals are present in the urine.

pHTo determine the acid/ base

balance of the patient.6.5 4.6 – 8.0

The client has normal urine pH. Metabolic

acidosis is not present.

Specific Gravity

Indicates the concentration of

urine and reflects the client’s

hydration status as well as

renal function.

1.010 1.005-1.030The result is within the normal range. The

client is not dehydrated.

SugarTo determine presence of

sugar in the urineNegative Negative

Sugar and albumin are not present in the

urine and it indicates normal functioning

of the kidneys and absence of

hyperglycemia which can be manifested

Albumin To detect protenuria Negative Negative

by presence of sugar in the urine.

Pus cells

To indicate presence

bacteria; to determine

presence of infection

1-3/ HPFNone

Pus cells are present in small amount

which indicates presence of bacteria in

the urine.

Red Cells To detect hematuria 1-3/ HPF < 2/ HPF

The client has a slight presence of

microscopic RBC in her urine. This

indicates the presence of microscopic

hematuria.

Epithelial cellsTo detect infection

RareNone

Results indicate that bacteria are present

in the urine.Bacteria Few

Nursing Responsibilities:

Prior to:

1. Explain that this analysis helps to diagnose renal or urinary tract disease and to evaluate overall body function.

2. Inform the relative that the patient need not restrict food and fluids.

3. Notify the laboratory and physician of medications the patient is taking that may affect laboratory results; they may need to be

restricted.

During:

1. Do perineal hygiene.

2. Place the weebag.

3. Handle the specimen container gently to avoid spillage

After:

1. Submit sample to lab with lab order for proper screening


Laboratory

Procedure

Date

ordered/

Date

results in

Indication or Purpose ResultsNormal

ValuesAnalysis and interpretation of results

Stool

Examination/

Fecalysis

DO: 03/

24/10

Results in:

03/ 27/ 10

The examination of feces

provides important information

that aids in the differential

diagnosis of various

gastrointestinal disorders.

Fecal studies may also be used

for microbiologic studies,

chemical determination, and

parasitic examinations.

To determine cause of diarrhea.

Color: Brown Brown The client has normal color of feces.

Consistency:

watery

Soft and

well formed

The client has an abnormal consistency of

feces. This is due to the effects of

excessive vasoactive intestinal peptide

which stimulates overproduction of cAMP

and cause intestinal motility which cause

passing out of watery stool.

Result: No

intestinal

parasites seen

No

intestinal

parasites

seen

The feces does not contain and intestinal

parasites. No infection is seen.


Prior to:

1. Explain the purpose of the study and how it is done.

2. Prepare all the materials to be used.

During:

1. Observe universal precautions in collecting a stool specimen.

2. Collect stool specimens in a clean container that has a fitted cover.

3. Do not mix urine and toilet paper with the stool specimen.

After:

1. Correctly label and deliver stool specimens to the laboratory within 30 minutes after collection. If you are unable to deliver the

specimen within 30 minutes, it may be refrigerated for up to 2 hours.

2. Note that no special care is required following the procedure


Diagnostic

Procedure

Date ordered/

Date results inIndication or Purpose Results Impression

Analysis and interpretation of

results

Chest X-ray

Posterior-

DO: 03/ 26/10

Results in: 03/

The chest x-ray film is

important in a complete

Compared with chest

taken 2-6-10, present

The rest of the

visualized lung

The results show an abnormal

mass in the left retrocardiac area.

Anterior-

Lateral (PAL)

view

26/ 10

evaluation of the

pulmonary and cardiac

systems.

It was used as a

comparison with the chest

x-ray taken when the client

was admitted in the same

institution last February

2010.

study shows

unchanged status of

mass-like opacity with

lobulated margins

measuring

approximately 48.3 (L)

x 31.8 (trans) mm in

left retrocardiac area.

Rule out posterior

meidastinal mass.

Suggest CT scan for

further evaluation.

fields are

clear.

Heart and

great vessels

in normal size

and

configuration.

Other chest

structures are

unremarkable.

This is in conjunction with the

diagnostic done from the first

confinement of Vipsy such as CT

scan, biopsy and x-ray which

indicates the presence of

ganglioneuroma.

The client has no pneumonia.


Prior to:

3. Make sure the patient has signed and appropriate consent form.


5. Explain who will perform the test and where it will be done.

6. Tell the relatives that fasting is not required and the test takes less than 5 minutes.

7. Instruct relatives to remove clothing to the waist and to put on an x-ray gown.

8. Inform the relatives to remove all metal objects (e.g., necklace) so that they do not block visualization of part of the chest.

9. Tell the relatives that the patient will be ask to take a deep breath and hold it while the film the x-ray films are taken.

10. Instruct relatives to have the patient’s ovaries covered, using a lead shield to prevent radiation-induced abnormalitites.

During:

4. After the patient is correctly positioned, tell him or her to take a deep breath and hold it until the x-ray films are taken.

5. Note that x-ray films are taken by a radiologic technologist in several minutes.

6. Inform the relatives that no discomfort is associated with chest radiography.

After:

4. Note that no special care is required following the procedure


Diagnostic

Procedure

Date ordered/

Date results inIndication or Purpose Results Analysis and interpretation of results

15-Lead ECG

DO: 03/ 25/10

Results in: 03/

25/ 10

Electrocardiography graphically

records the electrical current

generated by the heart and

measured by electrodes connected

to an amplifier and strip chart

recorder.

To identify conduction abnormalities

and cardiac arrhythmias

T wave

flattening on

Lead II;

Presence of

U wave on

Leads V4,

V5, V6

Presence of abnormal T wave flattening

and presence of U wave indicates the

presence of hypokalemia. Hypokalemia

causes prolonged myocardial

repolarization function. Hypokalemia

developed due to the secretory effects of

vasoactive intestinal peptide. Cardiac

dysrhythmias are not present.


Prior to:

1. Explain the procedure to the patient and relatives.

2. Tell the relatives that no food or fluid restriction is necessary.

3. Explain to the relatives the need of the patient to lie still, relax and breathe normally during the procedure.

4. Explain that the test is painless and takes 5 to 10 minutes.


6. Explain who will perform the test and where it will be done.

During:

1. Place the patient in a supine or semi-Fowler’s position.

2. Expose the chest, ankles, and wrists.

3. The skin areas designated for electrode placement are prepared by using alcohol swabs or sandpaper to remove skin oil or

debris.

4. Pads with special gel are applied to ensure electrical conduction between skin and electrodes.

5. Place electrodes on the inner aspect of the writs, on the medial aspect of the lower legs, and on the chest.

6. After all the electrodes are in place, connect the lead wires.

7. Press the start button and input any required information.

8. Make sure that all leads are represented in the tracing. If not, determine which electrode has come loose, reattach it, and

restart the tracing.

9. All recording and other nearby electrical equipment should be properly grounded.

10. Make sure that electrodes are firmly attached.

After:

1. Disconnect the equipment, remove the electrodes, and remove the gel with a moist cloth towel.

2. Note that no special care is required following the procedure and document the procedure done.

III. ANATOMY AND PHYSIOLOGY

THE DIGESTIVE SYSTEM

The digestive system

consists of the digestive

tract, a tube extending

from the mouth to the

anus, plus the associated

organs, which secrete

fluids into the digestive

tract. The digestive tract

consists of the oral

cavity, pharynx, esophagus, stomach, small intestine, large intestine, and anus.

Accessory glands are associated with the digestive tract. The salivary glands empty into

the oral cavity, and the liver and pancreas are connected to the small intestine. Inside

digestive tract is a lining called the mucosa. In the mouth, stomach, and small intestine,

the mucosa contains tiny glands that produce juices to help digest food.

Oral Cavity. The oral cavity is bounded by the lips and cheeks and contains the teeth

and tongue. This is the site where food is mechanically digested through mastication.

Mastication breaks large food particles into many small ones and increases efficiency of

digestion. Salivary glands are also found in the oral cavity. The salivary glands secrete

saliva that begins the process of chemical digestion.

Pharynx. The pharynx connects the mouth with the esophagus, consists of three parts:

the nasopharynx, orophayrnx, and laryngopharynx.

Esophagus. It extends from the pharynx to the stomach. It transports foods from the

pharynx and stomach.it contains upper and lower esophageal sphincter that regulates

movement of food into and out of the mouth.

Stomach. It is an enlarged segment of the digestive tract in the left superior part of the

abdomen. It is divided into the fundus(most superior part) and body(largest part). It has

2 openings: cardiac opening (opening from the esophagus to the stomach) and pyloric

opening (opening from the stomach to the small intestine) surrounded by a ring of

smooth muscle (pyloric sphincter). The wall of the stomach consists of three muscle

layers: longitudinal, circular, and oblique. It consists of gastric glands that produce

mucus, HCl, pepsin, gastrin, and intrinsic factor.

Small intestine. It is divided into the duodenum, jejunum, and ileum. It has circular folds,

villi, and microvilli that greatly increase the surface area of the intestinal lining. Goblet

cells and duodenal glands produce mucus.

Liver and Pancreas. The liver consists of four lobes. It receives blood from the hepatic

artery and the hepatic portal vein. Bile leaves the liver through the hepatic duct system.

The pancreas is an endocrine organ and an exocrine gland. Its endocrine function is to

control blood nutrient levels. Its exocrine function is to produce bicarbonate ions and

digestive enzymes.

Large intestine. The cecum forms a blind sac at the junction of the small and large

intestines. The appendix is a blind sac off the cecum. The colon consists of ascending,

transverse, descending, and sigmoid portions. The rectum is a straight tube that ends at

the anal canal.

The functions of the digestive system are to take in and break down food, absorb

digested molecules, provide nutrients and eliminate wastes.

Digestion involves the mixing of food, its movement through the digestive tract, and the

chemical breakdown of the large molecules of food into smaller molecules. Digestion

begins in the mouth, when we chew and swallow, and is completed in the small

intestine. The chemical process varies somewhat for different kinds of food.

After mastication, food is swallowed. Deglutition or swallowing can be divided into

voluntary phase (bolus is formed and it is pushed by the tongue into the oropharynx),

pharyngeal phase (the soft palate is elevated and closes the passage between the

nasopharynx and the oropharynx and the food is received by the pharynx causing the

epiglottis to cover the opening of the larynx) and esophageal phase (food is moved from

the pharynx to the stomach through peristaltic waves. The action of peristalsis looks like

an ocean wave moving through the muscle. The muscle of the organ produces a

narrowing and then propels the narrowed portion slowly down the length of the organ.

At the junction of the esophagus and stomach, there is a ringlike valve closing the

passage between the two organs. However, as the food approaches the closed ring,

the surrounding muscles relax and allow the food to pass.

The food then enters the stomach, which has three mechanical tasks to do. First, the

stomach must store the swallowed food and liquid. This requires the muscle of the

upper part of the stomach to relax and accept large volumes of swallowed material. The

second job is to mix up the food, liquid, and digestive juice produced by the stomach.

The lower part of the stomach mixes these materials by its muscle action. The third task

of the stomach is to empty its contents slowly into the small intestine.

Two solid organs, the liver and the pancreas, produce digestive juices that reach the

intestine through small tubes. In addition, parts of other organ systems (for instance,

nerves and blood) play a major role in the digestive system.

Several factors affect emptying of the stomach, including the nature of the food (mainly

its fat and protein content) and the degree of muscle action of the emptying stomach

and the next organ to receive the contents (the small intestine). As the food is digested

in the small intestine and dissolved into the juices from the pancreas, liver, and

intestine, the contents of the intestine are mixed and pushed forward to allow further

digestion.

Finally, all of the digested nutrients are absorbed through the intestinal walls. The waste

products of this process include undigested parts of the food, known as fiber, and older

cells that have been shed from the mucosa. These materials are propelled into the

colon, where they remain, usually for a day or two, until the feces are expelled by a

bowel movement.

The Pancreas

The secretions of the pancreas, called pancreatic juice, include various enzymes,

including pancreatic amylase (digestion of starch), trypsin, carboxypepiydase, and

chymotrypsin (proteases), as well as pancreatic lipase (digestion of fats). Sodium

bicarbonate is also produced, making the pancreatic juice alkaline. An alkaline

solution neutralizes the HCl in the chyme and provides an optimal environment for

the action of these enzymes.

Pancreatic juice is produced in clusters of exocrine cells called acini. The

remaining cells in the pancreas (about 1 percent of the total) also form clusters (islets of

Langerhans). These are the endocrine cells that produce the hormones insulin,

glucagon, somatostatin, and pancreatic polypeptide.

Pancreatic

juice collects in

small ducts that

merge to form

two large

ducts. The main

pancreatic

duct (duct of

Wirsung)

exits the

pancreas

and merges with the common bile duct from the liver and gallbladder. This combined

duct, called the hepatopancreatic ampulla (ampulla of Vater), then enters the duodenum.

A smaller, second duct that exits the pancreas, the accessory pancreatic duct (duct of

Santorini), joins the duodenum directly.

Pancreatic Islets Form the Endocrine Pancreas

The islets of Langerhans are scattered throughout the organ and consist of richly

vascularized globular masses of cells. Six distinct cell types are correlated with

specific hormones.

Alpha cells synthesize glucagon and are located in the outer rim of the islets.

They constitute 15 to 20% of the total islet cell population. Glucagon induces

glycogenolysis and gluconeogenesis in the liver, thereby raising the blood

glucose level. Its secretion is stimulated by hypoglycemia and by the ingestion of

a low-carbohydrate, high-protein meal. By virtue of these responses, glucagon,

together with insulin, serves to maintain fuel homeostatis.

Beta cells produce insulin and constitute 60 to 70% of all islet cells. By electron

microscopy, cellular insulin is resolved into characteristic polygonal and

rhomboidal crystals enclosed in secretory vesicles. The major obligatory stimulus

for insulin secretion is the binding of glucose to receptors on the surface of the

beta cell.

Delta cells are subdivided into D and D1 types, secreting somatostatin and

vasoactive intestinal polypeptide (VIP), respectively. They are fewer in number

and slightly larger than alpha cells and, like them, tend to be localized at the

periphery of the islets. Delta cells are situated between the alpha and beta cells,

so that the three cell types are often contiguous. Pancreatic somatostatin, a

peptide identical to the one in the hypothalamus, inhibits the pituitary release of

growth hormone. Somatostatin also inhibits secretion by alpha, beta, and D1

cells, acinar cells of the exocrine pancreas, and certain hormone-secreting cells

in the gastrointestinal tract. Coupled with the topographical cell-cell relations

noted above, these hormonal interactions suggest that somatostatin plays a

regulatory role in glucose homeostatis.

D1 cells are smaller than other islet cell types and are rare in the islets of normal

human pancreas. Its hormone, VIP, also has been localized in ganglion cells and

nerve fibers of the pancreas, gut, and brain. In a manner similar to that of

glucagon, VIP induces glycogenolysis and hyperglycemia and regulated ion and

water secretion by epithelial cells of the gastrointestinal tract.

Pancreatic polypeptide-secreting cells are located primarily in the islets of the

head of the pancreas and synthesize a polypeptide that appears to have variable

and opposed functions. These include stimulation of the secretion of enzymes

from the gastric mucosa and inhibition of a number of functions, such as smooth

muscle contraction in the intestine and gallbladder, production of gastric acid,

and secretion by the exocrine pancreas and biliary system.

Enterochromaffin cells are rare components of the islet cell population in the

head of the pancreas. They synthesize serotonin and peptide motilin, a hormone

that stimulates motility of gastric smooth muscle and increases the tone of the

sphincter at the gastoesophageal junction (Rubin, 2005).

IV. THE PATIENT AND HER ILLNESS

Produce excessive amounts of VIP: ↑ serum

VIP

Tumor in adrenal areaNeuroblastic tumors

GanglioneuromaGanglioneuroblastomaNeurofibroma

Dilation of blood vessels

Vasodilatory hypotension

Severe hypotension

Non-modifiable Risk Factors Gender: M 1: F3 (Adults); M1:F1 (Children) MEN Family History; Somatic mutations of MEN1 gene Age: 40-50 years old

Secretion of calcitrophic peptide

Neuroendocrine islet cell tumor of the pancreas

Primordial neural crest cells

CNS

Coincidental MEN accompanied by

hyperparathyroidism

↑ Blood flow to the corpora cavernosa

Priapism in males

Penile erection

Hypercalcemia

A. Pathophysiology (Book-based) Schematic Diagram

Idiopathic

GIT CV GUT

Profound glycogenolytic effect

S/sx of DM

Steatorrhea

↑ Glucose intolerance

Hyperglycemia

LipolysisRegulation of neuronal activity, differentiation,

and survival in SNS

Embryologic endoderm

VIPoma

Paravertebral mass on chest radiograph

Malignant

Benign

Hepatomegaly

Metastasis commonly in the liver

Facial flushing

Abdominal distention; bloating;

Abdominal pain

Massive secretion of water and

electrolytes (Na, K, Mg, Cl)

Stimulation of cAMP

Secretroy, non-fasting, large

volume diarrhea (dilute tea in appearance)

Bronchial smooth muscle contraction

Colonic dilatation

Dilation of intestinal smooth

muscle & peripheral blood

vessel

Stimulate bicarbonate

secretion

Gallbladder Intestine

↑ Intestinal motility

Dilation of gallbladder

Hypochlorhydria/ achlorhydria

A

Relaxation of lower esophageal sphincter,

gastric fundus, anal sphicter

Stimulate alkaline pancreatic juice

secretion

GIT

Inhibits secretion by exocrine

pancreas and biliary system

Inhibits smooth muscle contraction

Inhibits histamine release &

pentagastrin-stimulated acid

secretion

Vasodilatory effect

Renal failure

Retention of Cl by kidneys

Bicarbonate wasting

Hyperchloremic metabolic acidosis

Hypomagnesemia Tetany

Hypochlorhydria/ achlorhydria;

hypercalcemia

Electrolyte imbalance

Hypokalemia

Large distended

gallbladder

Gallbladder relaxation

Cardiac arrest

Dehydration & weight loss; poor

skin turgor

↑ Conduction of nerve impulses

Fatigue, paresthesia, hyporeflexia,

irritability

Ventricular fibrillation

Hypokalemia

↑ Resting membrane potential

↓ K gradient b/w ICF & plasma

Reabsorb water and Na in kidney; K is

eliminated

↑ Excitability

Anorexia, abdominal distention,

constipation

Slowed smooth muscle contraction

↑ In transmembrane

potential

A

Hypotension & slow peak

pulse

↓ Myocardial contraction

↑ Cellular excitability

Dysrythmia

Depressed & prolonged ST segment, depressed

& inverted T wave, prominent U wave

Prolonged myocardial

repolarization function

Severe hypokalemia

Shallow respirations,

shortness of breath, apnea

Respiratory arrest

Deterioration of respiratory muscular

contractionMuscle

weakness & leg cramps, nephrosis

Tachycardia

Progression of hypokalemia

Vomiting, ileus, urinary retention

Extreme smooth muscle slowing

Dysphasia, confusion, depression,

convulsions, areflexia, coma

Altered nerve conduction

Paralysis

Inhibits the kidney to concentrate urine

Polyuria, nocturia, ↓ plasma osmolality

Baroreceptors stimulate SNS

ADH & aldosterone secretion

↑ Na levels in blood

Increase peripheral vasoconstriction

Osmoreceptors triggers thirst mechanism



Movement of fluid from the periphery to

the circulation

Excess fluid loss & volume depletion

Slowed skeletal muscle

contraction

Synthesis of the Disease (Book-based)

1. General Description of Vipoma

Vipomas are endocrine tumors that secrete excessive amounts of VIP, which causes a

distinct syndrome characterized by large-volume of watery diarrhea, hypokalemia, and

dehydration. This syndrome is also called Verner-Morrison syndrome, pancreatic

cholera, or WDHA syndrome fro watery diarrhea, hypokalemia, and achlorhydria, which

some patients develop. The mean age of patients is 49 years; however, it can occur in

children. (Kasper, et. al., 2005).

VIPomas in adults are usually neuroendocrine islet cell tumors of the pancreas

that produce high amounts of VIP. Other secreted hormones may include secreted

gastrin and pancreatic polypeptide (Ferry, 2008). The cells in pancreatic endocrine

neoplasms are termed amine precursor uptake and decarboxylation (APUD) cells

because they have a high amine content, are capable of amine precursor uptake, and

contain an amino acid decarboxylase. It is believed that these cells develop from

embryologic endoderm (Ong, 2009).

In children and adolescents, VIP is produced mainly by ganglioneuromas,

ganglioneuroblastomas, neurofibromas, or other tumors in the adrenal area (most

common location) (Ferry, 2008). Neuroblastic tumors are derived from primordial neural

crest cells (Kumar, et. al., 2010).

VIP is a 28-amino-acid peptide that is an important neurotransmitter ubiquitously

present in the central nervous system (ie, hypothalamus, hippocampus, cortex).,

respiratory system, urogenital tracts, and gastrointestinal tract. Its known actions include

stimulation of small-intestinal chloride secretion and effects on smooth-muscle

contractility, inhibition of acid secretion, and vasodilatory effects which explain most

features of the clinical syndrome (Kasper, et. al., 2005). Vasoactive intestinal peptide

(VIP) is a peptide hormone with a number of important functions in the regulation of

neuronal activity, differentiation, and survival, particularly in the sympathetic nervous

system. It probably functions as a neuroacrine agent, and its presence in neurons with

processes extending to mucosal cells, smooth muscle, and blood vessels suggests that

VIP affects local secretion, motility, and blood flow (Greenspan and Gardner, 2001).

The most important physiologic actions of VIP in the gastrointestinal tract are

relaxation of vascular and nonvascular smooth muscles specifically relaxation of the

lower esophageal sphincter, receptive relaxation of gastric fundus, relxation of the anal

sphincter, and relaxation of gallbladder. VIP inhibits pentagastrin and histamine-

stimulated gastric acid and pepsin secretion. It stimulates lipolysis, glycogenolysis, and

secretion by the small intestine and pancreas. It stimulates pancreatic bicarbonate

secretion (Greenspan and Gardner, 2001). These effects work together to increase

motility (Bergram RA, 2010). VIP is a potent stimulator of adenosine 3',5'-cyclic

phosphate (cAMP) production by the gut. Thus, overproduction leads to massive

secretion of water and electrolytes, mainly potassium (Ferry, 2008). The action of VIP is

mediated by stimulatory G proteins and activation of adenylyl cyclase Additionally, VIP

increases gut blood flow and is one of the many factors responsible for penile erection.

This causes priapism in males (Greenspan and Gardner, 2001).

The principal symptoms are large-volume diarrhea (100%) severe enough to

cuase hypokalemia (80 to 100%), dehydration (83%), hypochlorhydria (54 to 76%), and

flushing (20%). The diarrhea is secretory in nature, persists during fasting, and is almost

always >1 L/d and >3 L/d in 70% (Greenspan and Baxter, 1994). The diarrhea is caused

by the effects of excessive VIP to increase the motility (Bergram RA, 2010) and the

overproduction of cAMP that leads to massive secretion of water and electrolytes (Ferry,

2008). Steatorrhea (16%) is caused by lipolysis, and the increased stool volume is due

to increased excretion of sodium and potassium, which with the anions, account for the

osmolality of the stool (Kasper, et. al., 2005). Clients frequently have hyperglycemia (25

– 50%) due to the profound glycogenolytic effect of high portal vein VIP on the liver

(Vinik, 2004) and hypercalcemia (25 – 50%). The cause of hypercalcemia is not clear,

but it may relate to dehydration, electrolyte imbalance due to diarrhea, coincidental MEN

accompanied by hyperparathyroidism, or secretion by the tumor of calcitrophic peptide.

Hypomagnesemia also results secondary to diarrhea which is manifested by tetany. The

vasodilatory effects of VIP cause gallbladder distention, facial flushing, dilation of blood

vessels in the cardiovascular system which causes vasodilatory hypotension, and

dilation of intestinal smooth muscle. Dilation of intestinal muscle causes colonic

dilatation which manifests abdominal distention, bloating, and abdominal pain. Severe

metabolic acidosis may be present due to severe bicarbonate wasting (Vinik, 2004).

When excess bicarbonate is lost from the body, the kidneys retain chloride causing

hyperchloremic metabolic acidosis (Black and Hawks, 2005). Death may result from

renal failure or cardiac arrest caused by volume depletion and acidosis (Ferry, 2008).

Approximately 60-80% of VIPomas are malignant and have metastasized at the time of

diagnosis. Metastasis occurs most frequently in the liver, but it may also occur in the

lymph nodes, lung, or kidneys (Tung, 2008).

With dehydration, ADH and aldosterone secretion increase to reabsorb water

and sodium in the kidney. The baroreceptors sense low blood pressure, and the

sympathetic nervous system is stimulated to increase peripheral vasoconstriction and

the heart rate. Vasoconstriction moves fluids from the periphery (legs, gastrointestinal

tract) into circulation. Increasing sodium levels in the blood is also sensed by the

osmoreceptors in the hypothalamus, which triggers thirst mechanism (Black and Hawks,

2005). Aldosterone secretion aggravates hypokalemia since it excretes potassium

(Seeley, et. al., 2007).

The remaining sysmptoms associated with VIPomas are secondary to

hypokalemia (Ong, 2004). When plasma potassium levels decrease, a decrease in

potassium gradient occurs between ICF and the plasma. The decreased gradient

causes the resting membrane potential to increase, thus increasing excitability.

Therefore, cell membranes are more responsive to stimuli. In hypokalemia, muscle

contraction is slowed. Slowed smooth muscle contraction leads to early GI

manifestations, which include anorexia, abdominal distention, and constipation. Slowed

skeletal muscle contract results in muscle weakness and leg cramps. Increased

conduction of nerve impulses secondary to an increase in the transmembrane potential

leads to neurologic manifestations of fatigue, paresthesias, hyporeflexia, and irritability

(Black and Hawks, 2005).

With severe hypokalemia, ECG changes may occur. The depressed and

prolonged ST segment, depressed and inverted T wave, and prominent U wave are due

to the prolongation of myocardial repolarization. Dysrhythmias are common because of

increased cellular excitability. Hypokalemia also leads to a decrease in myocardial

contraction, which is manifested as hypotension and a slow, weakened pulse. Potassium

levels of less than 2.5 mEq/L increase the risk of ventricular fibrillation and cardiac

arrest. Pulmonary manifestations of shallow respirations, shortness of breath, and

apnea, culminating in respiratory arrest, are also from progressive deterioration of

respiratory muscular contraction (Black and Hawks, 2005).

The progressive neurologic consequences of altered nerve conduction are

manifested as dysphasia, confusion, depression, convulsion, areflexia, and coma.

Extreme smooth muscle slowing leads to vomiting and ileus as well as urinary retention.

Skeletal muscle weakness may progress to paralysis. Hypokalemia also inhibits the

ability of the kidney to concentrate urine, which leads to polyuria, nocturia, and a

decreased plasma osmolality (Black and Hawks, 2005).

2. Non-modifiable/ Modifiable Factors (Book-Based)

Non-modifiable Factors

Idiopathic. The etiology of sporadic pancreatic endocrine tumors in largely unknown.

Risk factors have not been identified, but carcinogens may be involved, because

pancreatic endocrine neoplasms can be induced in rats treated with streptozotocin in

combination with nicotinamide. (Fletcher, 2007).

Family history of Multiple Endocrine Neoplasia Type 1. A family history of Multiple

Endocrine Neoplasia type 1 and similar syndromes can also increase one’s risk

(http://www.knowcancer.com/oncology/vipoma/). Multiple Endocrine Neoplasia Type

1hyperfunctioning tumors in all 4parathyroid glands, pancreatic islets (eg, gastrinoma,

insulinoma, glucagonoma, vasoactive intestinal peptide tumor [VIPoma], pancreatic

polypeptide–producing tumor [PPoma]), and the anterior pituitary (eg, prolactinoma,

somatotropinoma, corticotropinoma, nonfunctioning tumors) (Ferry, 2008).

Somatic point mutations on chromosome 11 of the MEN1 gene have been

discovered in sporadic VIPomas and VIPoma cases associated with MEN type 1 (Ferry,

2008).

Age: When VIPomas occur in adults, they appear most commonly between the ages of

40 and 50 years and they usually develop in the pancreas. In children, VIPomas more

commonly arise in or near the adrenal gland

(http://www.novartisoncology.us/education/diseases-conditions/oncology/vip-tumors.jsp).

http://emedicine.medscape.com/article/925341-overview

Gender: Male-to-female ratio in children is approximately 1:1, compared with 1:3 in

adults (Ferry, 2008).

3. Signs and Symptoms (Book-Based)

Increased Serum VIP test. Increased due to secretions of excessive amounts of

VIP by the endocrine tumor. Determined during periods of ongoing diarrhea, the

level of serum VIP in clients with Verner-Morrison syndrome ranges from 225-

1850 pg/mL. The normal serum VIP level is less than 170 pg/mL (Ong, 2008).

Hypokalemia. VIP is a potent stimulator of adenosine 3’,5’-cyclic phosphate

(cAMP) production by the gut. Thus, overproduction leads to massive excretion

of water and electrolytes, mainly potassium.

Hypercalcemia. May relate to dehydration, electrolyte disturbances secondary to

diarrhea, coincidental MEN accompanied by hyperparathyroidism, or secretion

by the tumor of a calcitrophic peptide.

Hypomagnesemia. Caused by the massive secretion of water and electrolytes

from the stimulation of adenosine 3’,5’-cyclic phosphate (cAMP) production by

VIP.

Tetany. A manifestation of hypomagnesemia.

Severe hypotension. VIP causes vasodilatory effects throughout the body. In

the cardiovascular system, it causes dilation of blood vessels thereby leading to

vasodilatory hypotenstion. Excessive amounts of VIP causes further vasodilatory

hypotension which results to severe hypotension.

Hyperglycemia and signs and symptoms of DM. Excessive amounts of VIP

causes profound glycogenolytic effect of high portal vein VIP on the liver causing

hyperglycemia, increasing glucose tolerance and the development of signs and

symptoms of Diabetes Mellitus.

Hypochlorhydria/ achlorhydria. Hypochlorhydria results from the direct gastric

acid inhibitory effect of VIP. VIP inhibits histamine release and pentagastrin-

stimulated acid secretion. Also, hypochlorhydria results from excessive secretion

of water and electrolytes due to stimulation of adenosine 3’,5’-cyclic phosphate

(cAMP) production by VIP.

Colonic dilatation. The vasodilatory effect of VIP causes dilation of intestinal

smooth muscle and peripheral blood vessel thus causing colonic dilatation.

Abdominal distention, bloating, abdominal pain. Because of dilation of

intestinal smooth muscle , colonic dilatation occurs which causes abdominal

distention, bloating, and abdominal pain.

Secretroy, non-fasting, large volume diarrhea (dilute tea in appearance).

VIP causes dilation of intestinal smooth muscle, inhibits smooth muscle

contraction of the gallbladder and intestine, inhibits secretion by exocrine

pancreas and biliary system, ihnhibits histamine release and pentagastrin-

stimulated acid secretion, and stimulate alkaline pancreatic juice secretion to

increase intestinal motility. Increase in intestinal motility and excessive

stimulation of cAMP which causes massive secretion of water and electrolytes.

Both intestinal motility and massive secretion of water and electrolytes cause the

secretory diarrhea in VIPoma.

Dehydration & weight loss; poor skin turgor. Due to secretory large volume

diarrhea brought by the effects of excessive amouts of VIP, the body losses body

fluids and leads to volume depletion.

Thirst. Excess fluid loss triggers ADH and aldosterone secretion to reabsorb

water and sodium in the kidney. Thereby increasing sodium levels in the blood

and in turn trigger the osmoreceptors to stimulate thirst.

Tachycardia. The baroreceptors sense low blood pressure, and the smypahtetic

nervous system is stimulated to increase peripheral vasoconstriction and heart

rate.

Fatigue, paresthesia, hyporeflexia, irritability. Increased conduction of nerve

impulses secondary to an increase in the transmembrane potential leads to

neurologic manifestations of fatigue, paresthesias, hyporeflexia, and irritability.

Dysphasia, confusion, depression, convulsions, areflexia, coma. The

progressive neurologic consequences of altered nerve conduction are

manifested as dysphasia, confusion, depression, convulsion, areflexia, and

coma.

Muscle weakness & leg cramps, nephrosis. Slowed skeletal muscle contract

results in muscle weakness and leg cramps.

Paralysis. Skeletal muscle weakness worsens resulting to paralysis.

Anorexia, abdominal distention, constipation. Hypokalemia causes slowed

muscular contraction among the smooth muscles of the gastrointestinal tract.

Vomiting, ileus, urinary retention. Due to progression of hypokalemia, there is

an extreme muscle slowing of the smooth muscle contraction.

Polyuria, nocturia, ↓ plasma osmolality. Hypokalemia also inhibits the ability of

the kidney to concentrate urine, which leads to polyuria, nocturia, and a

decreased plasma osmolality.

Shallow respirations, shortness of breath, apnea. Pulmonary manifestations

of shallow respirations, shortness of breath, and apnea, culminating in respiratory

arrest, are also from progressive deterioration of respiratory muscular

contraction.

Depressed & prolonged ST segment, depressed & inverted T wave,

prominent U wave. Due to the prolongation of myocardial repolarization.

Hypotension & slow peak pulse. Hypokalemia also leads to a decrease in

myocardial contraction, which is manifested as hypotension and a slow,

weakened pulse.

Dysrythmia & Ventricular fibrillation. Dysrhythmias are common because of

increased cellular excitability. Potassium levels of less than 2.5 mEq/L increase

the risk of ventricular fibrillation and cardiac arrest.

Large distended gallbladder. Develop from the vasodilatory effects of

vasoactive intestinal peptide in the gallbladder.

Steatorrhea. It is caused by lipolysis effect of vasoactive intestinal peptide.

Chest radiography may reveal a paravertebral mass (Ferry, 2008).

Hepatomegaly may be detected if liver metastasis has occurred (Tung, 2008).

B. Pathophysiology (Client-Centered)

Produce excessive amounts of VIP: ↑ serum

VIP

Schematic Diagram

GIT

VIPoma

Mass like opacity with lobulated margins in left retrocardiac area on CXR

(03.26.10).

Benign

Ganglioneuroma on biopsy (02.04.10)

Primordial neural crest cells

Non-modifiable Risk Factors Gender: Female Idiopathic

Abdominal enlargement (01.21.10).

Abdominal pain (03.26 - 27.10).

Slightly tympanic abdomen upon

percussion (03.24.10).Massive secretion

of water and electrolytes (Na, K,

Mg, Cl)

Stimulation of cAMP

Watery diarrhea: 3-4x/ day (03.24

to 28. 10); Watery consistency on

stool examination (03.27.10)

Bronchial smooth muscle contraction

Dilation of intestinal smooth

muscle & peripheral blood

vessel

Stimulate bicarbonate

secretionGallbladder relaxation

Gallbladder Intestine

↑ Intestinal motility

A

Relaxation of lower esophageal sphincter,

gastric fundus, anal sphicter

Stimulate alkaline pancreatic juice

secretion

GIT

Inhibits secretion by exocrine

pancreas and biliary system

Inhibits smooth muscle contraction

Inhibits histamine release &

pentagastrin-stimulated acid

secretion

Vasodilatory effect

Decreased bicarbonate (16.4) in ABG (01.30.10).

Bicarbonate wasting

Hyponatremia: 133.7 (02.03.07).

Electrolyte imbalance

Hypokalemia (03.24 to 28. 10). Decreased urine

potassium: 21.9 mmol/L (02.05.10).

Hydrops of gallbladder on abdominal UTZ

(01.20.10).

Dilation of gallbladder

Large distended

gallbladderModerate gaseous

distention of intestine on CT

scan of the chest (02.01.10).

Colonic dilatation

Hyperthermia (03.26.10).

Weight loss (03.24.10).

Hypokalemia

↑ Resting membrane potential

↓ K gradient b/w ICF & plasma

Reabsorb water and Na in kidney; K is

eliminated

↑ Excitability

Loss of appetite

(03.24.10).

Slowed smooth muscle contraction

Slowed skeletal muscle

contraction

A

Presence of T-wave flattening on lead 2, U wave on Leads V4, V5, V6 on ECG ((03.25.10).

Prolonged myocardial

repolarization function

Severe hypokalemia

Appears weak (03.24.10).

Pale palpebral conjunctiva, lips,

nail beds (03.24.10).

Mild adynamic ileus from abdominal x-

ray (01.25.10).

Extreme smooth muscle slowing

Baroreceptors stimulate SNS

ADH & aldosterone secretion

↑ Na levels in blood

Increase peripheral vasoconstriction

Osmoreceptors triggers thirst

(03.24.10).mechanism


Movement of fluid from the periphery to

the circulation

Excess fluid loss & volume depletion

Synthesis of the Disease (Client-centered)

1. General Description of Vipoma

Vipomas are endocrine tumors that secrete excessive amounts of VIP, which causes a

distinct syndrome characterized by large-volume of watery diarrhea, hypokalemia, and

dehydration. The etiology of VIPoma is not known. Male-to-female ratio in children is

approximately 1:1. This ration gives equal incidence of VIPoma in males and females.

In the case of Vipsy, VIP is produced mainly by the ganglioneuroma present in

the left paravertebral area behind the posterior lips of the diaphragm. Ganglioneuroma is

a neuroblastic tumor derived from primordial neural crest cells.

The presence of ganglioneuroma causes secretion of excessive amounts of VIP

which causes the WDHA syndrome. The main system affected by VIPoma is the

digestive system. With an increased serum levels of vasoactive intestinal polypeptide,

it’s normal action is exaggerated. Vasointestinal polypeptide increases the intestinal

motility of the digestive system by (1) vasodilation of intestinal smooth muscle,

gallbladder and peripheral blood vessel, (2) inhibiting the smooth muscle contraction of

gallbladder and intesitines, (3) inhibits secretion by exocrine pancreas and biliary

system, (4) inhibits histamine release and pentagastrin acid stimulated acid secretion,

and (5) stimulates alkaline pancreatic juice secretion. VIP also causes excessive

stimulation of of adenosine 3',5'-cyclic phosphate (cAMP) production which causes

massive secretion of water and electrolytes. Both an increase in intestinal motility and

massive secretion of water and electrolytes cause the watery diarrhea of the client.

There is excess fluid and volume depletion causing stimulation of barorecptors to

increase peripheral circulation by moving fluid from the periphery to the circulation.

Volume depletion also caused dehydration and weight loss. With volume depletion,

antidiuretic hormone and aldosterone secretion is secreted to reabsorb water and

sodium in the kidney to compensate to the excess fluid loss causing increase in sodium

levels in the blood which causes the osmoreceptors to trigger thirst. Aldosterone also

contributes to elimination of potassium in the body.

Due to excessive secretion of electrolytes, hyponatremia and hypokalemia

developed. Hypokalemia causes a decrease in potassium gradient occurs between ICF

and the plasma. The decreased gradient causes the resting membrane potential to

increase, thus increasing excitability. Therefore, cell membranes are more responsive to

stimuli. In hypokalemia, muscle contraction is slowed. Slowed smooth muscle

contraction leads loss of appetite. Progression of hypokalemia causes extreme muscle

slowing leading to ileus. Slowed skeletal muscle contract results in muscle weakness.

With severe hypokalemia (2.04), ECG changes occurred. Prolongation of myocardial

repolarization caused a presence of T-wave and U-wave on the ECG.

2. Non-modifiable/ Modifiable Factors (Client-centered)

Non-modifiable Factors

Idiopathic. The exact cause is not known. There is no family health history of

malignancy which cannot be attributed to a possible occurrence of MEN among the

family members.

Gender: Vipsy is a female and she has an equal chance with a male to develop the

sporadic endocrine tumor.

3. Signs and Symptoms (Client-centered)

Increase in serum VIP >400. Increase in serum VIP is due to the presence of

ganglioneuroma, a tumor that secretes excessive amounts of vasoactive

intestinal polypeptide in the blood, located on the left paravertebral area behind

the posterior lips of the diaphragm. The serum VIP levels of Vipsy was >400 pg/

mL.

Hydrops of gallbladder on abdominal UTZ (01.20.10). Excessive amounts of

vasoactive intestinal polypeptide causes excessive action of VIP. A known action

of VIP is its vasodilatory effect which causes over distention of the gallbladder.

Also, VIP inhibits smooth muscle contraction of the gallbladder leading to

galldbladder relaxation. Both over distention and relaxation of gallbladder caused

Hydrops of the gallbladder.

Abdominal enlargement (01.21.10); Abdominal pain (03.26 - 27.10). Because

of the vasodilatory effect of VIP, there is too much dilation of the intestinal

smooth muscle causing distention of the intestine. Also, development of hydrops

of the gallbladder caused the abdominal enlargement.

Mild adynamic ileus from abdominal x-ray (01.25.10). Excessive amounts of

VIP lead to the watery diarrhea of the client and massive loss of electrolytes

specifically potassium. Hypokalemia causes a slowed smooth muscle contraction

in the gastrointestinal wall causing a decrease in peristalsis.

Decreased bicarbonate (16.4) in ABG (01.30.10). Increase in VIP causes

excessive stimulation of the alkaline pancreatic juice secretion. This causes

stimulation of bicarbonate secretion causing bicarbonate wasting. Bicarbonate

wasting also is due to massive secretion of electrolytes through the stool which

causes a decreased in bicarbonate levels.

Moderate gaseous distention of intestine on CT scan of the chest

(02.01.10). This is due to the dilation of the intestinal smooth muscle by the

vasoactive intestinal polypeptide.

Hyponatremia: 133.7 (02.03.07). The stimulation of cAMP by VIP results in

massive secretion of water and electrolytes through the gastrointestinal system.

Ganglioneuroma on biopsy: benign (02.04.10). The cause of the development

of ganglioneuroma is idiopathic.

Decreased urine potassium: 21.9 mmol/L (02.05.10). Excessive amounts of

circulating VIP results to massive secretion of electrolytes specifically potassium.

Hypokalemia develops due to excessive secretion of potassium and no

replacement is done which also cause a decrease in urine potassium level.

Watery diarrhea: 3-4x/ day (03.24 to 28. 10); Watery consistency on stool

examination (03.27.10). This is due to the increase in intestinal motility and

stimulation of cAMP by the vasoactive intestinal polypeptide.

Weight loss (03.24.10). Because of frequent loss of fluids through the stools,

there is decrease in circulating blood volume which can be easily measured by

the weight of the client. A decrease in weight indicates excess fluid loss.

Thirst (03.24.10). Excess fluid loss triggers ADH and aldosterone secretion to

reabsorb water and sodium in the kidney. Thereby increasing sodium levels in

the blood and in turn trigger the osmoreceptors to stimulate thirst.

Pale palpebral conjunctiva, lips, nail beds (03.24.10). Decrease in circulating

blood volume causes an increase in peripheral vasoconstriction. This effect

moves fluid from the periphery into the circulation.

Loss of appetite (03.24.10). Hypokalemia causes slowed muscular contraction

among the smooth muscles of the gastrointestinal tract.

Slightly tympanic abdomen upon percussion (03.24.10). Due to the

vasodilatory effects of vipoma which causes the intestinal walls to dilate.

Appears weak (03.24.10). Hypokalemia causes a slowed skeletal smooth

muscle contraction. Hypokalemia is due to the secretory watery diarrhea effect of

excessive amounts of vasoactive intestinal peptide in the serum.

Hypokalemia (03.24 to 28. 10). VIP is a potent stimulator of adenosine 3’,5’-

cyclic phosphate (cAMP) production by the gut. Thus, overproduction leads to

massive excretion of water and electrolytes, mainly potassium. The client had

three to four watery stools per day causing an excessive loss of potassium in the

stool.

Presence of T-wave flattening on lead 2, U wave on Leads V4, V5, V6 on

ECG ((03.25.10). Due to the prolongation of myocardial repolarization caused by

decreased in potassium levels of the client.

Hyperthermia (03.26.10). Frequent watery diarrhea from the effect of excessive

vasoactive intestinal peptide causes depletion in the fluid volume which causes

dehydration.

Mass like opacity with lobulated margins in left retrocardiac area on Chest

x-ray (03.26.10). Indicates the presence of a tumor which is in congruence with

the previous chest x-ray done on her first hospitalization.

V. THE PATIENT AND HER CARE

A. MEDICAL MANAGEMENT

a. IVFs, BT, NGT Feeding, Nebulization, TPN, Oxygen Therapy, etc.

Medical Management

Treatment

Date Ordered

Date (s) Performed

Date changed/ D/C

General DescriptionIndication (s) or Purpose

(s)

Client’s response to

treatment

D5 0.33 NaCl 500 cc x 44-

45 µgtts/min for 8 hours

DO: 03/ 24/10

DP: 03/ 24/ 10

DC: 03/ 24/ 10

D5 is a nutrient solution,

which contains some form

of carbohydrate (dextrose)

and water. 0.3 NaCl is a

hypotonic solution used to

provide free water and

treat cellular dehydration.

Water from D5 is supplied

for fluid requirements and

carbohydrate for calories

and energy. It also

prevents dehydration and

ketosis. 0.3 NaCl promotes

diuresis. Promotes waste

elimination by the kidneys.

The client had good

hydration status. The client

has normal urine output.D5 0.33 NaCl 500 cc x 69

µgtts/min for 6 hours

DO: 03/ 24/10

DP: 03/ 24/ 10

DC: 03/ 24/ 10

D5 IMB 500 cc x 36-37

µgtts/min

DO: 03/ 24/10

DP: 03/ 25/ 10

DC: 03/ 25/ 10

It is a hypertonic solution.

Hypertonic solutions draw

fluid out of the intracellular

and interstitial

To expand vascular

volume lost from diarrhea.

The client maintained a

good hydration status,

however, potassium levels

did not increase.

compartments into the

vascular compartment

expanding vascular

volumes.

D5 0.33 NaCl 71.2 cc

+ KCl 2.3 cc = 74 cc to run

for 2 hours

DO: 03/ 25/10

DP: 03/ 25/ 10 (8 AM)

DC: 03/ 25/ 10

D5 is a nutrient solution,

which contains some form

of carbohydrate (dextrose)

and water. 0.3 NaCl is a

hypotonic solution used to

provide free water and

treat cellular dehydration.

To prevent dehydration

and to increase potassium

levels.

The client’s hydration

status was maintained.

The client’s potassium

level increased.

DO: 03/ 25/10

DP: 03/ 25/ 10 (5:05 PM)

DC: 03/ 25/ 10

D5 0.33 NaCl 72.5 cc

+ KCl 1.5 cc = 74 cc to run

every 2 hours

DO: 03/ 25/10

DP: 03/ 25/ 10 (8 AM)

DC: 03/ 25/ 10

DO: 03/ 25/10

DP: 03/ 25/ 10 (7:30 PM)

DC: 03/ 25/ 10

Nursing Considerations:

Prior to:

1. Prepare the equipment

6. Check Doctor’s order

7. Acquaint the patient with the requirement and need of

IV transfusion

8. Select a suitable vein to permit easier access to a

vessel

9. Select a appropriate needle suitable for type and

location of infusion

10. Clean the area of insertion

11. Use strict aseptic technique

12. Identify the client

13. Assess vital signs for baseline data

14. Assess skin turgor, allergy to tape

15. Check the status or veins to determine appropriate

venipuncture site

During:

1. Use the smallest gauge needle possible.

2. Check for patency of the tubing

3. Spike the solution container

4. Cleanse the fluid to be given, make sure it is the same

with the prescribed fluid.

5. Partially fill the drip chamber gently with solution.

6. Select a suitable vein for venipuncture

7. Dilate the vein

8. Put on clean gloves and clean the venipuncture site.

9. Check for line and infusion integrity

After:

1. Label the IVF (name, date started, number)

2. Ensure appropriate infusion flow.

3. Regulate flow rate as ordered

4. Adjust the rate of fluids appropriate to the needs f the

patient as ordered. If there is any question with the flow

rate ordered, check with the physician who gave the

order.

5. Monitor IV flow and patient’s response

6. Monitor patient for evidence of IV infiltrations

7. Check for presence of air in the tubing, if air is present,

remove immediately

8. Check for the patency of the line always.

9. Check for IV insertion for phlebitis frequently

10. Document relevant data.

b. Drugs

Name of Drug

Date

Ordered

Date Taken/

Given

Date

Changed/

D/C

Route of

Administration

Dosage and

Frequency of

administration

General Action

Functional

Classification

Mechanism of Action

Indication(s)

Client’s

response to

the

medication

with actual

side effect

Nursing responsibilities

Generic Name:

Racecadotril

Brand Name:

Hidrasec

DO: 03/ 24/

10

DG: 03/ 24/

10

DC: 03/ 26/

10

Hidrasec 10 mg/

sachet, 2 sachet

three times a

day

General Action:

Antidiarrheal

Functional Classification:

Antidiarrheal

Mechanism of Action:

Racecadotril is an

inhibitor of

enkephalinase, the

Adjunct to oral

or parenteral

rehydration in

treatment of

acute watery

diarrhea in

infants and

children

The client’s

stool was still

watery until

discharge

however, it

contains small

amounts of soft

stool and the

amount was

decreased. The

1.May be taken with or without

food.

2.Monitor for signs and symptoms

of side effects.

3.Store below 30oC.

enzyme responsible for

breaking down

enkephalins. It is a

selective but reversible

inhibitor and protects

endogenous enkephalins

which are physiologically

active in the digestive

tract.

frequency of

stool fluctuates

since Vipsy

does not like

the taste of

Hidrasec.

Generic Name:

Ampicillin

Brand Name:

Ampicin

DO: 03/ 24/

10

DG: 03/ 24/

10

IV, 500 mg/ vial,

300 mg SIVP

every 6 hours

ANST

General Action:

Anti-infective


Penicillin


Inhibits cell-wall synthesis

during bacterial

For treatment of

infection.

Infection was

treated.

Assessment:

1. Assess client’s condition before

starting therapy and regularly

thereafter to monitor drug’s

effectiveness.

2. Be alert for advers reactions

and drug interactions.

multiplication.

Evaluation:

1. Evaluate the effectiveness of

drug and client’s respond to

therapy.

Generic Name:

Carbocisteine

Brand Name:

Solmux Syrup

DO: 03/ 25/

10

DG: 03/ 25/

10

½ tsp PO three

times a day

General Action:

Cough and cold

Preparations


Mucolytic


Carbocisteine, a

derivative of

acetylcysteine, is a

mucoregulating agent.

Its major action is

thought to be on the

metabolism of mucus-

Relief of cough

associated with

excessive and

tenacious

sputum or

phlegm

The client was

relieved from

cough.

1. Store at temperature not

exceeding 30oC.

2. Should be administered with

food.

producting cells. The

mucus produced under

the influence of

carbocisteine has an

increased content of

the less viscous

sialomucin and a

reduced content of the

highly viscious

fucomucin. Sialomucins

influence the

rheological properties

of mucus and may also,

through the inhibition

of kinins reduce or

prevent bronchial

inflammation and

bronchospasm.

Generic Name: DO: 03/ 26/ PO, 1.2 ml every General Action: Relief of fever Vipsy’s fever 1. Take and record temperature

Paracetamol

Brand Name:

Tempra drops

10

DG: 03/ 26/

10

4 hours as

needed for fever

Analgesics (Non-opioid)

and Antipyretics


Tempra is

acetaminophen

(paracetamol), a safe and

effective analgesic-

antipyretic. It is a not

salicylate. It contains no

phenacetin or caffeine. It

has no effect on

prothrombin

time. Tempra is

particularly valuable for

use in patients who do

not tolerate aspirin well

because it is less likely to

was decreased

from 37.7 to

36.3.

2. Administer with food or full

glass of water

3. Can be taken with food or an

empty stomach

4. Monitor for patient’s

temperature

5. Advise patient to increase oral

fluid intake

cause GI distress.

Generic Name:

Dicycloverine

Hydrochloride

Brand Name:

Relestal

DO: 03/ 27/

10

DG: 03/ 27/

10

PO, 2.5 ml every

8 hours

General Action:

Antispasmodic


Anticholinergic


Dicycloverine HCl acts

as a nonselective

smooth muscle relaxant

by: 1) A specific

anticholinergic effect at

the acetylcholine-

receptor sites; and 2)

Acting directly on the

bradykini- and

For the

treatment of

functional

disturbances of

gastrointestinal

motility

eg, irritable

bowel

syndrome and

renal and

biliary colic

The client did

not complain of

stomach pain

after the

administration

of Relestal.

1. May be taken with or without

food.

2. Keep patient in a cool

environment. Fever and heat

stroke due to decreased sweating

may be experienced in the

presence of high environmental

temperature.

histamine- induced

spasm. Dicycloverine

has little or no effect on

gastric secretion.

Generic Name:

Potassium Chloride

Brand Name:

Kalium Durule

DO: 03/ 25/

10

DG: 03/ 25/

10

DC: 03/ 28/

10

Incorporation of

potassium

chloride in IVF

to run in infusion

General Action:

Potassium


Electrolyte, mineral

replacement


Needed for adequate

transmission of nerve

impulses and cardiac

contraction, renal

function, intracellular ion

For hypokalemia The client’s

potassium level

decreased from

3.47 to 3.18

indicating that

the dosage is

not enough.

The client’s

potassium level

increased from

3.18 to 3.49.

Assess:

1. ECG for peaking T waves,

lowered R, depressed RST,

prolonged P-R interval, widening

QRS complex, hyperkalemia; drug

should be reduced or discontinued.

2. I&O ration; watch for decreased

urinary output; notify prescriber

immediately.

3. Cardiac status: rate, rhythm.

Administer:

PO route

1. Do not break, crush, or chew

enteric products.

DO: 03/ 27/

10

DG: 03/ 27/

10

DC: 03/ 28/

10

PO, 750 mg/

tab, 1 tab once a

day

DO: 03/ 28/

10

PO, 750 mg/

tab, 1 tab BID

DG: 03/ 28/

10maintenance. 2. With or after meals.

IV route

1. Through large-bore needle to

decrease vein inflammation; check

for extravasation

2. In large vein, avoiding scalp Nursing Responsibilities:

Prior to:

1. Check the written medication order for completeness. It should include the drug name, dosage, frequency, and duration of the

therapy.

2. Check if IV in.

3. Check to see if there are any special circumstances surrounding administration of the dose to the patient.

4. Be certain that you know the expected action, safe dosage range, special instructions for administration and adverse effects

associated with drug orders.

5. Prepare the necessary equipment.

6. Wash your hands.

7. Check the label on the medications three times before administering any drug.

8. Prepare the dosage as ordered.

9. Explain the procedure to the patient. The action of the drug and its side effects.

During:

10. Identify the patient.

11. Identify if the patient expresses any doubt about the medication; always recheck the order, drug label and dosage on the

medication card.

12. For oral meds do special regulation and precaution to avoid or prevent aspiration.

After:

13. Following administration, be certain that the patient is comfortable, then immediately record the procedure.

14. Instruct the patient to report signs of superinfection and allergy.

15. Inspect IV insertion sites for sign of phlebitis.

16. Document and assess the patient's reaction to the given drug.

c. Diet

Type of Diet

Date ordered

Date started

Date Changed

General Description Indication(s) or Purpose(s)Specific foods

taken

Client’s

Response &/ or

reaction to the

diet

Pediasure and

include two

bananas daily

DO: 03/ 24/ 10

DS: 03/ 24/ 10 Pediasure is a

Fat/carbohydrates/proteins/miner

als/vitamins combination used a

general nutrient.

Bananas have very benefitial

nutritional properties. They are

a good source of vitamin C, B6

and A. Bananas have a high

content of carbohydrates and

fiber, while they are low in

protein levels and fat free.

For childn 1-10 yr who could

physically & mentally benefit from

improved nutrition including picky

eaters, catch-up growth,

prematurity, malnutrition,

hypermetabolism, growth failure,

GI disorders, neurologic disorder

& congenital abnormalities. As a

nutritional supplement for childn

w/ failure to thrive, pre/post

surgery, severe injury, cancer,

recovery from illness or when a

lactose-free nutritional supplement

Banana,

cerelac,

pediasure,

rice

The client

tolerate the diet

well and her

potassium

increased.

They are also rich in

potassium.

is needed.

The client has an illness that

causes hypokalemia and she is

still recuperating from her previous

surgery.

Nursing Responsibilities:

Prior to:

1. Check the doctor’s order for the type of diet prescribed

2. Explain the importance of the diet given.

3. Explain the importance of compliance to the diet given.

4. Inform dietary department on the patient’s diet

5. Identify the right client

6. Update patient significant others of the patient diet change

During:

1. Give appropriate foods to the patient.

2. Enumerate the foods that the patient may or may not take.

3. Emphasize strict compliance to diet

4. Reiterate diet frequently

5. Monitor intake and output

After:

1. Document the patient’s tolerance to the diet given.

B. NURSING MANAGEMENT

1. Nursing Care Plans

Problem # 1: Fluid Volume Deficit Related To Active Fluid Losses As Evidenced By Diarrhea Secondary To Vipoma

AssessmentNursing

Diagnosis

Scientific

ExplanationObjectives Interventions Rationale

Expected

Outcome

S: Ø

O:

Patient

manifested:

Weight loss

from 12 kg to

11.8 kg

3-4 watery

stools per day

Pale

palpebral

conjunctive,

Fluid

Volume

Deficit

Related To

Active Fluid

Losses As

Evidenced

By Diarrhea

Secondary

To Vipoma

Presence of the

ganglioneuroma

produces excessive

amounts of

vasoactive intestinal

polypeptide in the

body. Excessive

amounts of VIP

causes a profound

action of VIP

causing an increase

in intestinal motility

and massive

Short term:

After 8 hours

of nursing

interventions,

the patient

will be able to

have a

decrease in

stool

episode.

Long term:

After days of

1.Established rapport

2.Monitor v/s especially

blood pressure and pulse

3.Monitor and document

vital signs.

1.To gain trust and

cooperation of so and

patient

2.Variations help identify

fluctuating intravascular

volumes.

3.Sinus tachycardia may

occur with hypovolemia to

maintain an effective

cardiac output. Usually

the pulse is weak, and

may be irregular if

electrolyte imbalance also

Short term:

The patient shall

have a decrease

in stool episode.

Long term:

The patient shall

have improved

fluid volume at a

functional level

as evidenced by

an increase in

weight.

lips and nail

beds

Increased

thirst

Hyperthermi

a

Appears

weak

The patient

may manifest:

Tachycardia

Elevated

hematocrit

levels

Decreased

skin turgor

Decreased

secretion of fluids

and electrolytes in

the gastrointestinal

tract causing fluid

losses which can

lead to dehydration

and hypokalemia.

nursing

interventions,

the patient

will improve

fluid volume

at a

functional

level as

evidenced by

an increase

in weight.

4.Monitor temperature.

5.Obtain patient history to

ascertain the probable

cause of the fluid

disturbance.

6.Assess or instruct patient

to monitor weight daily and

consistently, with same

scale, and preferably at the

same time of day.

occurs. Hypotension is

evident in hypovolemia.

4.Febrile states decrease

body fluids through

perspiration and

increased respiration.

5.This can help to guide

interventions. Causes

may include acute trauma

and bleeding, reduced

fluid intake from changes

in cognition, large amount

of drainage post-surgery,

or persistent diarrhea.

6.This facilitates accurate

measurement and follows

trends.

urine output

Increased

urine

concentration

7.Assess fluid losses,

sources, amounts and

effects, urinary output,

vomiting, diarrhea.

8.Increase fluid intake

9.Encourage patient to

drink prescribed fluid

amounts. If oral fluids are

tolerated, provide oral fluids

patient prefers. Place at

bedside within easy reach.

Provide fresh water and a

straw. Be creative in

selecting fluid sources (e.g.,

flavored gelatin, frozen

juice bars, sports drink).

7.Provides information

about body fluid losses

and depletion which can

lead to serious

consequences in the

child.

8.To replace the fluid

losses

9.Oral fluid replacement

is indicated for mild fluid

deficit.

10. Assess intake and

output accurately compare

to losses q 2-8 for I&O

determination and balance.

11. Provide oral hygiene.

12. Teach interventions to

prevent future episodes of

inadequate intake.

13. Provide oral rehydration

therapy (i.e. Pedialyte,

rehydralyte) as ordered

14. Administer parenteral

fluids as ordered. Anticipate

10. Determines loses

related to fluid deficit and

potential for dehydration.

11. This promotes

interest in drinking.

12. Patients need to

understand the

importance of drinking

extra fluid during bouts of

diarrhea, fever, and other

conditions causing fluid

deficits.

13. Promotes fluid and

electrolyte replacement

and prevent dehydration

the need for an IV fluid

challenge with immediate

infusion of fluids for patients

with abnormal vital signs.

15. Administer antidiarrheal

medications

and electrolyte deficits

14. Provide fluid

replacement and maintain

hydration

15. Decreases the

diarrheal episode of the

client

Problem # 2: Diarrhea related to Increase Intestinal Motility Secondary to VIPoma

AssessmentNursing

Diagnosis

Scientific

ExplanationObjectives Nursing Interventions Rationale

Expected

Outcome

S: Ø

O:

Patient

manifested:

Passage of

three to four

watery, loose

stools per day

Weakness

Pale

palpebral

conjunctiva

Pale lips and

nail beds

Watery

consistency of

Diarrhea

related to

Increase

Intestinal

Motility

Secondary

To

VIPoma

The presence of

excessive amounts

of VIP produced by

the

ganglioneuroma

exaggerates the

physiology of VIP

in the

gastrointestinal

tract causing a

further increase in

intestinal motility

and secretion of

fluids and

electrolytes

through the GIT

causing watery

Short-term:

After 5 hours

nursing

interventions,

client’s stool

consistency

will change

from loose to

semi-solid

state.

Long-Term:

After 2 days

nursing

interventions,

1. Establish rapport

2. Assess normal pattern

of bowel elimination and

characteristics of stool

3. Assess abdominal

distention, palpation and

bowel sounds for

increases in auscultation

4. Assess for temperature

elevation, irritability,

lethargy, anorexia

5. Assess for fluid loss

with a light weight loss, dry

1. To gain trust and

promote participation

2. Provides information

about baseline parameters

for comparison and reason

for changes

3. Indicates a distended

bowel with fluid for hyper

motility of bowel which

reduces the amount of

material that is absorbed by

the bowel mucosa

4. To provide information

about signs and symptoms

associated with diarrhea

5. Indicates possible

dehydration associated with

ST:

The client shall

have a change

in stool

consistency

from loose to

semi-solid

state.

LT:

The client shall

have

reestablished

and maintained

a normal

stool on

fecalysis

diarrhea. client’s bowel

functioning

will

reestablish

and maintain

a normal

pattern.

skin and mucous

membranes, poor skin

turgor

6. Evaluate diet history

7. Review food

preparation and discuss

proper food refrigeration

and handling of foods to

SO

8. Check for history of the

following:

GI diseases

9. Encourage continuation

or reinforce the child’s

regular diet as soon as

possible

10. Change diaper

fluid loss

6. To assess the cause

related to environmental

factors

7. To promote wellness

and prevent contamination

and spoiling

8. To detect cause of

diarrhea

9. Regular diet provides

adequate nutrients

10. To prevent skin

pattern of

bowel

functioning.

frequently as needed

11. Wash the perineal

area with warm water after

each diarrhea episode

12. Encourage increase

oral fluid intake

13. Encourage boiling of

drinking water

14. Expose buttocks to air

and apply skin protective

ointment to buttocks

15. Instruct parents for

signs and symptoms of

dehydration or changes in

characteristics of diarrhea

to report them to physician

breakdown and lessen

discomfort

11. To protect skin from

excretions and secretions

that are irritating and cause

excoriation and skin

breakdown

12. To replace fluid losses

and electrolytes

13. To kill microbes present

in water

14. To keep area dry and to

prevent irritation or skin

breakdown

15. To provide immediate

prevention of sever

complication of acidosis

16. Teach caregiver the

importance of fluid

replacement during

diarrheal episodes.

17. Administer

antidiarrheal medications

as ordered

18. Give medications as

ordered

16. Fluids prevent

dehydration.

17. To decrease GI motility

and minimize fluid losses

18. To treat infectious

process

Problem # 3: Hyperthermia related to dehydration

AssessmentNursing

Diagnosis

Scientific


Expected

Outcome

S: Ø

O:

Patient

manifested:

Warm to

touch skin

Weakness

Pallor

Temperature

of 37.7 oC

3-4 watery

stools per day

Patient may

manifest:

Exhibits

chills

Exhibits

Hyperthermia

related to

dehydration

Because of

excessive fluid

losses from the

inflated effects of

VIP, the body’s

fluid is not

adequate enough

to hydrate the

body causing an

increase in

temperature.

Short-term:

After 5 hours

of nursing

interventions,

the client’s

temperature

will lower of

decrease

from 37.7 oC

to a normal

range of 36.5

oC to 37.4 oC.

Long-Term:

After 2 days

nursing

interventions,

1. Establish rapport

2. Monitor vital signs

especially temperature

3. Provide tepid sponge

bath

4. Provide loose slight

fitting clothes

5. Assess for fluid loss

with a light weight loss,

dry skin and mucous

membranes, poor skin

turgor

6. Keep back dry

7. Promote adequate rest

8. Increase caloric intake

1. To gain trust and


2. Used as a baseline data

3. To lower body

temperature

4. To provide conduction

of heat and comfort

5. Indicates possible

dehydration associated

with fluid loss

6. To provide comfort and

alleviate the condition

7. To reduce metabolic

demands and consumption

8. To meet body’s

Short-term:

The client shall

have lowered

or decreased in

temperature

from 37.7 oC to

a normal range

of 36.5 oC to

37.4 oC.

Long-Term:

The client shall

be free from

signs of

hyperthermia

or will not have

increase body

diaphoresis

Tachypnea

Tachycardia

the client will

be free from

signs of

hyperthermia

or will not

have increase

body

temperature.

9. Administer

replacement fluids and

electrolytes

10. Administer

antipyretics as ordered

metabolic needs

9. Serves as a support to

the client’s circulating

volume and tissue

perfusion

10. To decrease

tempereature

temperature.

Problem # 4: Acute Pain related to Colonic Dilatation

AssessmentNursing

Diagnosis

Scientific


Expected

Outcome

S: “Tiyan, Acute With the intense Short-term: 1. Establish rapport 1. To gain trust and Short-term:

tiyan”, patient

verbalized.

O:

Patient

manifested:

Protective

behavior on

the abdominal

area

Tympanic

abdomen upon

percussion

Facial mask

Crying

The patient

may manifest:

Sleep

Pain

related to

Colonic

Dilatation

action of VIP in the

gastrointestinal

tract, it causes

overdistention of

the smooth

muscles in the

intestines. This

leads to colonic

dilatation. With

colonic dilatation,

the nerve endings

are irritated

causing abdominal

pain.

After 5 hours

nursing

interventions,

the patient’s

pain will be

relieved as

evidence by

absence of

crying and

guarding

behavior.

Long-Term:

After 2 days

nursing

interventions,

2. Assess pain

characteristics:

a. Quality (e.g.,

sharp, burning,

shooting)

b. Severity (scale of 1

to 10, with 10 being

the most severe).

Other methods such

as a visual analog

scale or descriptive

scales can be used

to identify extent of

pain.

c. Location

(anatomical


2. Serves as baseline

data

The patient’s

pain shall be

relieved as

evidence by

absence of

crying and

guarding

behavior.

Long-Term:

The patient

shall not

experience

pain.

disturbance

Autonomic

responses

the patient

will not

experience

pain.

description)

d. Onset (gradual or

sudden)

e. Duration (how

long; intermittent or

continuous)

f. Precipitating or

relieving factors

3. Observe or monitor

signs and symptoms

associated with pain,

such as BP, heart rate,

temperature, color and

moisture of skin,

restlessness, and ability

to focus.

4. Assess for probable

3. Nonverbal cues may

determine severity of

pain. Attention to

associated signs may

help the nurse in

evaluating pain.

4. Different etiological

cause of pain.

5. Assess caregiver’s

knowledge of or

preference for the array

of pain-relief strategies

available.

6. Evaluate patient’s

factors respond better to

different therapies.

5. Some caregiver may

be unaware of the

effectiveness of

nonpharmacological

methods and may be

willing to try them, either

with or instead of

traditional analgesic

medications. Often a

combination of therapies

(e.g., mild analgesics

with distraction or heat)

may prove most

effective.

6. It is important to help

response to pain and

medications or

therapeutics aimed at

abolishing or relieving

pain.

7. Respond immediately

to complaint of pain.

8. Eliminate additional

stressors or sources of

patients express as

factually as possible (i.e.,

without the effect of

mood, emotion, or

anxiety) the effect of pain

relief measures.

7. Prompt responses to

complaints may result in

decreased anxiety in the

patient. Demonstrated

concern for patient’s

welfare and comfort

fosters the development

of a trusting relationship.

8. Patients may

experience an

exaggeration in pain or a

discomfort whenever

possible.

9. Provide rest periods

to facilitate comfort,

sleep, and relaxation.

10. Give analgesics as

decreased ability to

tolerate painful stimuli if

environmental,

intrapersonal, or

intrapsychic factors are

further stressing them.

9. The patient’s

experiences of pain may

become exaggerated as

the result of fatigue A

quiet environment, a

darkened room, and a

disconnected phone are

all measures geared

toward facilitating rest.

10. Pain medications are

absorbed and

ordered, evaluating

effectiveness and

observing for any signs

and symptoms of

untoward effects.

metabolized differently

by patients, so their

effectiveness must be

evaluated from patient to

patient. Analgesics may

cause side effects that

range from mild to life-

threatening.

Problem # 5: Risk for Injury Related To Muscle Weakness Secondary To Hypokalemia

AssessmentNursing

Diagnosis

Scientific


Expected

Outcome

S: Ø

O:

Patient

manifested:

Weight loss

from 12 kg to

11.8 kg

3-4 watery

stools per day

Pale

palpebral

conjunctive, lips

and nail beds

Appears weak

Hypokalemia

Loss of

appetite

Risk For

Injury

Related To

Muscle

Weakness

Secondary

To

Hypokalemia

Excessive

secretion of VIP

from the

ganglioneuroma

causes an

increase in

intestinal motility

and massive

secretion of fluids

and electrolytes

due to the

stimulation of

cAMP. With the

increase in

intestinal motility

and massive

secretion of

electrolytes, loose

watery diarrhea

Short term:

After four

hours of

nursing

interventions,

the patient

will be at

reduced risk

of injury.

Long term:

>After three

days of

nursing

interventions,

the patient

will be free

from injury.


2.Monitor and record vital

signs

3.Increased fluid intake

4.Employ safety and

seizure precautions such

as raising side rails and

keeping the bed in a low

position with padded side

rails.

5.Place nonslippery shoes

on the client and assist her

when walking.

6.Discuss to the relatives

the need for assistance of

the patient with her

1.To gain relative and

patient’s trust and

cooperation

2.For baseline

measurement

3.To minimize

dehydration

4.To reduce the risk of

injury.

5.This prevents slipping

of the client and prevent

fall.

6.The relatives must

understand the disease

process and they should

Short term:

The patient shall

have a reduced

risk of injury.

Long term:

The patient shall

be free from

injury.

The patient may

manifest:

Falls

Seizure

results and

potassium is lost

through the feces.

Excessive

amounts of loose

watery stools

cause severe

hypokalemia

which can cause

seizure to the

client.

activities of daily living.

7.Administer medications

to increase potassium

levels.

be knowledgeable of the

effect it has on the

patient’s activities of daily

living.

7.To prevent the

progression of

hypokalemia; this can

cause further injury to the

patient.

Problem # 6: Risk for impaired skin integrity related to moisture from frequent stool excessive

AssessmentNursing

Diagnosis

Scientific


Expected

Outcome

S: Ø

O:

Patient manifested:

3-4 watery stools

per day

The patient may

manifest:

Rashes or

redness on the

perineal area

Risk for

impaired skin

integrity

related to

moisture from

frequent stool

Increase in VIP in

the blood causes

and increase in its

actions. One of

the main actions

of VIP is to

increase intestinal

motility. Due to

extreme amounts

of VIP, intestinal

motility is also

affected causing

frequent passing

of loose watery

stools. Since the

client is on her

toilet training

stage, she is does

not know how to

Short term:

After 4 hours

of nursing

interventions,

the patient’s

skin will

remain intact.

Long term:

> after three

days of

nursing

interventions,

the patient will

not manifest

any signs of

skin integrity

such as

redness on


2.Monitor and record v/s

3.Assess skin and mucous

membranes for color

changes, warmth, dryness,

swelling or edema

4.Assess for any skin

rashes, dermatitis, and

scratching

5.Instruct relative to air dry

the buttocks after washing

the perineal area.

6.Advise to change diaper

immediately once the

1.To gain SO and

patients trust and

cooperation

2.For baseline

measurement

3.To ensure

identification and

intervention before

impairment becomes too

severe or extensive

4.Reveals skin

condition that lead to

impairment

5.This prevents moisture

build up that could lead

to irritation of the skin.

6.To prevent irritation of

the skin by the urine or

Short term:

> The patient’s

skin shall have

remained intact.

Long term:

The patient shall

not have

manifested any

signs of skin

integrity such as

redness on the

perineal area.

defecate on her

own. With the use

of diapers, loose

stools come in

contact with skin

and prolonged

contact causes

irritation and

breakdown of the

skin in the

perineal area.

the perineal

area.

diaper is soiled.

7.Place antiseptics creams

as prescribed.

feces.

7.To treat and prevent

diaper rashes or

redness.

2. ACTUAL SOAPIERs

March 24, 2010

S: Ө

O: Received patient from ER cuddled by mother on a wheelchair awake, cyring and

irritable with an ongoing IVF of #1 D5 0.3 NaCl 500 cc x 44-45 ugtts/ min at 400

cc level infusing well on the left hand, with pale nail beds, pale palpebral

conjunctiva, pale lips, appears weak, (-) vomiting, with good skin turgor, (+) loss

of appetite, with 3 episodes of watery loose stools. With vital signs as follows: T:

37.2 oC, PR: 112 bpm, RR: 26 cpm.

A: Fluid Volume Deficit Related To Active Fluid Losses As Evidenced By Diarrhea

Secondary To Vipoma

A2: Diarrhea related to Increase Intestinal Motility Secondary to VIPoma

P: After 3° of nursing intervention the client will not pass loose watery stool within

the shift.

I: > Established rapport

> Monitored and recorded VS q 4

> Needs attended

>Recorded I&O

> Assessed condition and watch out for signs and symptoms dehydration

> Fixed bed linens

> Assisted client with activities

> Encouraged frequent rest periods

> Changed position gradually every 2 hours

> Provided client safety such as raising side rails

> Maintained a restful environment

> Regulated IVF as ordered

> Instructed relative that the client is for urinalysis and fecalysis and provided

specimen cup and weebag

> Instructed relative regarding client’s diet: May give Pediasure and include two

bananas daily

>Provided adequate hydration

> Advised proper perineal hygeine

>Kept patient’s back dry

>Informed Pedia resident of admission

>Due medications given

>Endorsed

E: Goal not met as evidenced by passage of another episode of watery stool.

R: Reinforce previous plan of care.

March 25, 2010

S: Ө

O: Received patient on bed awake on a sitting position, with an ongoing IVF of #4

D5 0.3 NaCl 72.5 cc + KCl 1.5 cc = 74 cc every 2 hours at 50 cc level via soluset

infusing well on the left hand, with pale nail beds, pale palpebral conjunctiva, pale

lips, (-) weakness, (-) vomiting, with good skin turgor, with fair appetite, with 3

episodes of scanty loose stools, (+) productive cough. With vital signs as follows:

T: 37.6 oC, PR: 12 bpm, RR: 28 cpm.


Secondary To Vipoma



the shift.



> Needs attended

>Recorded I&O


> Fixed bed linens






>Still for Fecalysis, with specimen cup


> Reinforced relative regarding client’s diet: May give Pediasure and include two

bananas daily




>Seen on rounds by the attending physician with orders made and carried out:

continue medication


>Endorsed

E: Goal met as evidenced by negative bowel movement during the shift.

March 27, 2010 (Final Nurse-client interaction)

S: Ө

O: Received patient on bed asleep on a supine position, with an ongoing IVF of # 38

D5 0.3 NaCl 72.5 cc + KCl 1.5 cc = 74 cc every 2 hours at 70 cc level via soluset

infusing well on the left hand, with pinkish nail beds, pinkish palpebral

conjunctiva, pinkish lips, (-) weakness, (-) vomiting, with good skin turgor, with

fair appetite, with 2 episodes of scanty loose stools. With vital signs as follows: T:

36.6 oC, PR: 110 bpm, RR: 30 cpm.


Secondary To Vipoma



the shift.



> Needs attended

>Recorded I&O


> Fixed bed linens







> Reinforced relative regarding client’s diet: May give Pediasure and include two

bananas daily




>For potassium extraction at 6 AM


>Endorsed

E: Goal not met as evidenced by client had one loose bowel movement.

R: Reinforce previous plan of care.

VI. PATIENT’S DAILY PROGRESS IN THE HOSPITAL

A. Client’s Daily Progress Chart

DAYSADMISSION

(03/24/10)

2

(03/25/10)

3

(03/26/10)

4

(03/27/10)

DISCHARGE

(03/28/10)

Nursing Problems

Problem # 1: Fluid Volume Deficit Related To

Active Fluid Losses As Evidenced By Diarrhea

Secondary To Vipoma

Problem # 2: Diarrhea related to Increase

Intestinal Motility Secondary to VIPoma

Problem # 3: Hyperthermia related to dehydration

Problem # 4: Acute Pain related to Colonic

Dilatation

Problem # 5: Risk For Injury Related To Muscle

Weakness Secondary To Hypokalemia

Problem # 6: Risk for impaired skin integrity

related to moisture from frequent stool

Vital Signs T: 37.2 oC T: 37.6oC T: 37.7oC T: 36.5 oC T: 36.5 oC

PR: 112 bpm

RR: 26 cpm

PR: 124 bpm

RR: 28 cpm

PR: 124 bpm

RR: 28 cpm

PR: 110 bpm

RR: 26 cpm

PR: 108 bpm

RR: 25 cpm

Diagnostic and Laboratory Procedures

CBC

Hct: 0.40

Hgb: 128

Leukocytes: 4.2

Neutorphils:

0.36

Lymphocytes:

0.55

Monocytes: 0.07

Eosinophils:

0.02

Platelet count:

285

Blood Chemistry K: 2.68 6 AM

K: 2.04

2 PM

6 AM

K: 2.89

2 PM

6 AM

K: 3.47

6 AM

K: 3.18

2 PM

K: 2.34

Cl: 106.1

Na: 136.3

K: 3.49 K: 3.49

Urinalysis

Color: Light

yellow

Appearance:

Clear

pH: 6.5

Sp. Gr: 1.010

Sugar: (-)

Albumin: (-)

Pus cells:

1-3/HPF

Red cells:

1-3/HPF

Epithelial cells:

Rare

Bacteria: Few

Stool Examination

Color: Brown

Consistency:

Watery

Result: No

intestinal

parasites seen

Chest X-ray PAL view Shows

unchanged

status of mass-

like opacity

Rule out

posterior

meidastinal

mass.

The rest of the

visualized lung

fields are clear.

15 Lead ECG

T wave

flattening on

Lead II;

Presence of U

wave on Leads

V4, V5, V6

Medical Management

IVF

1. D50.3 NaCl 500 x 44-45 ugtts/min to run for 8

hours

2. D50.3 NaCl 500 x 69 ugtts/min

3. D5IMB 500 cc x 36-37 ugtts/min

4. D50.3 NaCl 71.7 cc + KCl 2.3 cc = 74 cc to run

for 2 hours

5. D50.3 NaCl 72.5 cc + KCl 1.5 cc = 74 cc to run

every 2 hours

DRUGS

1. Hidrasec 10 mg 2 sachet TID

2.Ampicillin 300 mg SIVP Q 6

3.Solmux syrup ½ tsp TID

4.Paracetamol drops1.2 ml Q4 prn x fever

5.Dicycloverine (Relestal) 2.5 ml PO Q8

6.Kalium durule 1 tab OD

7.Kalium durule 1 tab BID

DIET

1.Pediasure include Bananas Daily

VII. DISCHARGE PLANNING

A. General condition about the client upon discharge.

The client was seen by the nurse researcher 8 hours before being discharged. Vipsy

was chewing gum and was very lively. She was talkative and plays with her mother. She

has a good hygiene. Vipsy was not irritable and does not appear weak. She has a scar

on her umbilical area.

B. METHOD

M: Instructed relative that Vipsy will take the following medications:

Kalium durule 1 tablet twice a day. Kalium durule is taken to replace potassium

losses. Side effects include nausea and vomiting, bradycardia, decreased in

urine output.

Chloramphenicol suspension 5 mL every six hours for five days.

Chloramphenicol is indicated to treat infection. Adverse reactions to monitor are

nausea and vomiting, stomatitis, glossitis and rectal irritation.

E: May resume activities as tolerated

T: Home maintenance and management; Instructed to take medications as

prescribed and to watch out for worsening of signs and symptoms

H: Instructed regarding the complications that warrants medical attention

Describe prescribed drugs, including their names, dosages, actions, adverse

effects

Provided health teachings on how to prevent injury

Instructed proper hygiene

Advised to increase fluid intake and intake of high potassium diet

Instructed to provide healthy meals to the client

O: Instructed relative to come back for a follow-up check up on Wednesday (March

31, 2010) 10 AM at the physician’s clinic.

D: Advised to provide a high potassium diet to the client

SAMPLE MENU

Breakfast: Anytime Smoothie or - a bran cereal without sugar, use Sucanat for

sweetening, and 1/4 cup milk and one egg and 1 cup orange juice or other fresh or

canned unsweetened juice, high potassium, or fresh fruit or- cooked oatmeal and raisins

or blueberries or other fruit with milk or rice milk or no milk with added protein powder or

added cottage cheese, Sucanat sweetener or maple syrup or honey.

Lunch: Large salad with turkey or tuna 1-3 oz. and carrots, cucumber, sprouts, kidney

or garbanzo beans, sweet red pepper, red cabbage, lettuce or mixed greens, onions and

S&W non-fat dressing or equivalent; or- 2 cups brown rice and 1-3 oz. fish or poultry or

lean red meat and 2 cups vegetable such as asparagus or green beans and 2 fruits or 2

cups mixed fruit for dessert. To add carbohydrates add 1-2 slices of whole grain fat free

bread or add rice noodles to the salad or- soup or stew with lots of veggies and a small

amount of protein such as beans or chicken or beef or tofu and fruit for desert.

Dinner: Soup or stew or casserole with some protein from poultry or fish or legumes; or

tofu and lots of vegetables, served with whole grain fat free bread (optional); or- 1-3 oz.

of protein as above (more if beans are your source) and rice or pasta (use tomato based

sauce to replace the missing potassium in pasta); or a large baked potato with the skin

and 2-3 oz. protein and 2 cups of vegetables or salad with lots of veggies in it plus 2

more servings of fruit.

Condiments: Salsa adds C, bioflavonoids and potassium. Low salt, low sugar (or home-

made) ketchup. Tomato sauces. Parmesan cheese. All spices and herbs. Wysong mixed

salt or VegeSalt. Soy sauce without preservatives. Butter. Cream cheese. Sour cream.

Most non-fat dressings but look for the most natural without artificial flavorings and

preservatives. Our favorite is S&W. Small amounts of olive oil or peanut oil. Lots of garlic

and onion. Yeast flakes to flavor popcorn.

(http://www.krispin.com/potassm.html#SAMPLE).

VIII. SUMMARY OF FINDINGS

VIPoma is a very rare type of pancreatic endocrine tumor. It affects hormone-

producing cells in the pancreas, known as islet cells. The disease causes these cells to

produce extremely high levels of vasoactive intestinal peptide (VIP), a hormone that

regulates water transport in the intestines. It is also called Verner-Morrison syndrome or

pancreatic cholera. Excessive amounts of VIP causes a distince syndrome characterized

by large-volume watery diarrhea, hypokalemia, and dehydration. The syndrome is also

called WDHA syndrome of watery diarrhea, hypokalemia, and achlorhydria. The exact

cause of Vipoma is not known, although genetics are believed to be a factor. A family

history of MEN and similar syndromes can also increase one’s risk. Most patients are

adults between 40s to 50s, and women are more likely to develop it than men. Children

are rarely affected having a ratio of 1:1 in both males and females. When it occurs in

children, it is usually caused by a ganglioneuroma or ganglioneuroblastoma. VIPomas

are usually malignant when diagnosed in adults, however, in children, they are benign.

The principal symptoms are large-volume diarrhea which is secretory in nature that is

severe enough to cause hypokalemia, dehydration, hypochlorhydria, and flushing. The

diarrhea is secretory in nature, persists during fasting, and is almost always > 3 L/d.

Most patients do not have accompanying steatorrhea, and the increased stool volume is

due to increased excretion of sodium and potassium, which, with the anion, account for

the osmolality of the stool. Clients frequently have hyperglycemia due to the

glycogenolytic effect of the VIP.

VIP is a 28-amino-acid peptide that is an important neurotransmitter ubiquitously

present in the central nervous system and GI tract. Its known action include stimulation

of small-intestinal chloride secretion and effects on smooth muscle contractility, inhibition

of acid secretion, and vasodilatory effects which explains most features of the clinical

syndrome. The most significant effect of VIP is in the gastrointestinal system wherein it

continuously secretes fluids and electrolytes specifically potassium which causes

profound hypokalemia.

The goal of treatment for clients with VIPoma is to replace fluids and electrolytes

loss and maintain a good hydration status. Surgery can be performed to remove the

tumor secreting VIP. For clients with malignancy, chemotherapy is advised. With

metastasis, multiply organ resections are done to decrease the symptoms of the patient.

A somatostatin drug called Octreotide blocks the action of vasoactive intestinal

polypeptide and can reduce the diarrheal episodes of clients.

IX. CONCLUSION

Based on the summary of findings, VIPoma is a rare disease that has little

definition in literature. Little medical management is known to prevent the complications

of the disease and mostly it is done by surgery. Unlike other diseases that have many

alternatives in managing the disease, VIPoma only is usually managed by hydration,

surgery and with the use of a somatostatin drug.

The main affectation of VIPoma is in the gastrointestinal system wherein it

causes secretory watery diarrhea in large-volume enough to cause dehydration and

electrolyte imbalances. The chief electrolyte affected in these clients is potassium.

Potassium is easily replaced by diet and intravenous infusion of potassium chloride;

however, if the secretory diarrhea is not controlled or the tumor is not eliminated, signs

and symptoms of the disease will recur back.

X. RECOMMENDATIONS

In light of the foregoing findings and conclusions drawn, the following

recommendations are hereby offered:

1. Since VIPoma affects both adults and children, frequent medical

screening should be stressed by the nurses to their clients because

tumors can occur sporadically in one individual.

2. Since the cause of VIPoma is not known, it is important to have further

studies on this illness since it has detrimental effects to the clients

afflicted with this disease.

3. The physicians should discover more medical treatment for VIPoma

even though it is a very rare disease. They should not always result to

surgery or multiple resections of vital organs especially when dealing with

pediatric clients.

4. Clients experiencing signs and symptoms of illness unfamiliar with their

medical history should promptly seek medical attention to prevent

complications.

XI. LEARNING DERIVED

Life indeed is precious especially to clients with this rare disease. In the case of Vipsy,

her life is only starting and it is saddening to know that she is already facing trials at this

point in her life. People should be thankful with the advancement of medical treatment

nowadays. Rare diseases are diagnosed and treated with the prescribed medical

management. However, since these diseases are rare, only little is known about them.

What the researcher learned in her study is to appreciate what she has in her life

right now as compared to her client. It is a blessing that the researcher is healthy and is

not facing medical obstacles in her life. Also, it is important to always maintain a positive

attitude in life, whether you are afflicted with an illness or other problems in life. It is very

crucial to always have faith and to remember that God will not give you problems you do

not know how to handle.

XII. BIBLIOGRAPHY

BOOKS

Bare, Brenda. Brunner and Sudddarths Textbook of Medical-Surgical Nursing . 11th ed.

Vol. 1 & 2. Pennsylvania: Lippincott Williams and Wilkins, 2004.

Black, Joyce M. and Hawks, Jane Jokanson. Medical-Surigcal Nursing: Clinical

Management for Positive Outcomes. 7th ed. Volume 1. Singapore: Elsevier Inc.,

2005.

Comer, Sheree. Delmar’s Critical Care Nursing Care Plans. 2nd ed. Asia: Delmar

Learning, 2005.

Flethcer, Christopher. Diagnostic Histopathology of Tumors. 3rd ed. Vol. 2. USA: Elsevier

Limited, 2007.

Goldman, Lee and Dennis Ausiello. Cecil Medicine. 23rd ed. USA: Elsevier, Inc., 2008.

Greenspan, Francis and David Gardner. Basic and Clinical Endocrinolog. 6th ed. USA:

McGraw-Hill Companies, Inc., 2001.

Greenspan, Francis and John Baxter. Basic and Clinical Endocrinolog. 4th ed. USA:

Appleton & Lange, 1994.

Kasper, Dennis, et. al. Harrison’s Principles of Internal Medicine. 16 d. USA: McGraw-

Hill Companies, Inc., 2005.

Kozier, Barbara, et. al. Fundamentals of Nursing: Concepts, Process and Practice. 7th

ed. Phil: Pearson Education South Asia Pte Ltd., 2004.

Rubin, Emmanuel. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 4th ed.

USA: Lippincott Williams & Wilkins, 2005.

Seeley, Rod R. et. al. Essentials of Anatomy and Physiology. 5th ed. New York:

McGraw-Hill Companies, Inc., 2005.

Skidmore-Roth, Linda. Mosby’s Nursing Drug Reference. USA: Mosby, Inc., 2008.

INTERNET SOURCES

Ferry, Robert Jr. VIPoma. <http://emedicine.medscape.com/article/925341-followup> Jul

8, 2008.

Vinik, Aaron. Vasoactive Intestinal Peptide Tumor (VIPoma)

<http://www.endotext.org/guthormones/guthormone6/guthormone6.htm> August

2, 2004 .

Ong, Evan. Neoplasms of the Endocrine Pancreas.

<http://emedicine.medscape.com/article/276943-diagnosis> Dec 23, 2009.

Tung, Daniel. VIPomas. <http://emedicine.medscape.com/article/125910-overview>

Dec 18, 2008.

http://www.knowcancer.com/oncology/vipoma/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2517072/


www.mimsonline.com



XIII. APPENDICES

World J Surg Oncol. 2008; 6: 80.

Published online 2008 July 28. doi: 10.1186/1477-7819-6-80.

PMCID: PMC2517072

Copyright © 2008 Joyce et al; licensee BioMed Central Ltd.

Multi-visceral resection of pancreatic VIPoma in a

patient with sinistral portal hypertension

David L Joyce,1 Kelvin Hong,2 Elliot K Fishman,3 Joshua Wisell,4 and Timothy M Pawlik 1

Background

VIPomas are rare neuroendocrine tumors with an annual incidence of about 1 per

10,000,000 individuals.[1] The majority of VIPomas in adults (> 90%) are primary tumors

of the pancreas.[2] As with other neuroendocrine tumors of the pancreas, on occasion

these lesions can be exceptionally large with invasion of adjacent visceral and vascular

structures. As such, accurate preoperative imaging is critical. In particular, assessment

of the relationship between the tumor and adjacent vascular structures, such as the

portal and superior mesenteric vein (SMV) as well as the celiac and superior mesenteric

artery (SMA), is critical in determining preoperative resectability. On occasion, invasion

of the tumor into the adjacent splenic-portal venous system can lead to sinistral, or left-

sided, portal hypertension.

Surgical resection of pancreatic VIPoma provides the only chance at long-term cure, as

systemic chemotherapeutic agents are associated with poor response rates.[3]

Nevertheless, aggressive resection in patients with advanced VIPoma neuroendocrine

tumors has rarely been reported. While part of the reason for this undoubtedly is due to

the rarity of VIPomas, another factor may be related to the reluctance to perform

http://www.ncbi.nlm.nih.gov/pubmed/7904550



http://www.ncbi.nlm.nih.gov/pmc/about/copyright.html

aggressive resection due to possible increased morbidity and mortality.[4] With careful

attention to pre- and intra-operative details, aggressive resection of VIPomas can be

accomplished safely, thereby providing the patient with an opportunity for extended long-

term survival. We herein report a case of multi-visceral resection of pancreatic VIPoma

in a patient with sinistral portal hypertension. Furthermore, we provide a brief review of

the role of aggressive resection of pancreatic neuroendocrine tumors and highlight

several key technical points that allowed for successful resection.

Case presentation

A 46-year-old obese woman presented to an outside hospital in August of 2005 with

significant abdominal pain and diarrhea. Computed tomography (CT) revealed a 17 × 13

cm mass in the left upper quadrant that appeared to arise from the body and tail of the

pancreas. The patient was taken to the operating room at an outside institution, but the

mass was deemed unresectable due to reported involvement of the SMA, stomach, and

colon. Wedge biopsy of the mass was consistent with pancreatic VIPoma. Over the next

2 years, the patient was treated with long-acting somatostatin with some improvement in

her symptoms. The patient, however, developed repeat episodes of upper and lower

gastrointestinal bleeding with associated anemia and ongoing transfusion requirements.

Repeat CT scan revealed thrombosis of the splenic vein with numerous large splenic

and gastric varices consistent with sinistral portal hypertension. In the summer of 2007,

the patient underwent a failed transjugular intrahepatic portosystemic shunt (TIPS)

procedure at an outside institution. The patient was therefore referred to the Johns

Hopkins Department of Interventional Radiology for variceal embolization.

The patient's case was reviewed at the Johns Hopkins multi-disciplinary pancreas tumor

board. A repeat three-dimensional (3-D) pancreas protocol CT scan revealed an 18 × 12

cm mass abutting the liver, stomach, spleen, left adrenal, colon and invading the distal

duodenum – proximal jejunum at the ligament of Treitz. The splenic vein was occluded.


Large collateral vessels surrounded the mass and were associated with extensive

gastric collaterals (Figure (Figure1). 1 ). The mass displaced the SMA and SMV, but

these vessels were patent and uninvolved (Figure (Figure2). 2 ). As such, there were no

obvious contraindications to resection and surgery was recommended.

Given the size of the mass and the associated extensive varices, the patient underwent

preoperative proximal splenic artery embolization (Figure (Figure3). 3 ). Twenty-four

hours following this, the patient was taken to surgery where she was found to have a

very large mass arising from the body and tail of the pancreas that invaded the left

diaphragm, stomach, left adrenal, fourth portion of the duodenum – first portion of the

jejunum, transverse colon, and spleen. In order to better expose the SMV at the inferior

border of the pancreatic neck, the right colon and root of the small bowel mesentery

were mobilized in the fashion of Cattell and Braasch. The SMA medial to the SMV was

exposed as it coursed into the small bowel mesentery. The tumor was noted to closely

abut and displace both the SMV and SMA, but the vessels were not encased. After

developing the retro-pancreatic plane over the SMV – portal vein, the pancreatic neck

was transected. The mass was subsequently resected en bloc with a portion of the left

diaphragm, entire stomach, spleen, left adrenalectomy, fourth portion of the duodenum –

proximal jejunum and transverse colon. Gastrointestinal continuity was restored using a

Roux-en-Y method with a hand sewn end-to-side esophago-jejunostomy, a duodeno-

jejuneal anastomsis (50 cm distally), and a stapled colo-colonic anastomosis. The

pancreatic remnant was closed with pledgeted sutures. Estimated blood loss was 500

ml. Final pathology confirmed a VIPoma originating from the pancreatic body with

invasion of the stomach, spleen, small bowel, and colon (Figure (Figure4). 4 ). All margins

were uninvolved by tumor. The patient is alive and disease-free.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2517072/figure/F4/




The patient tolerated the procedure well. On post-operative day four, a swallow study

demonstrated a normal post-surgical esophago-jejunal anastomosis with no evidence of

leak. The patient was discharged home on post-operative day ten tolerating a post-

gastrectomy diet. She received no adjuvant therapy and is currently alive and disease-

free at 6 months of follow-up.

Discussion

VIPomas are rare tumors that have been infrequently reported in the literature.[5] These

pancreatic tumors secrete excessive amounts of VIP (Vasoactive Intestinal Peptide), a

structural homologue of secretin. Elevated serum VIP levels cause increased intestinal

secretion of Na+, K+, HCO3-, and Cl-, as well as bone resorption, vasodilation, and

inhibition of gastric acid section. These effects lead to a well-defined clinical syndrome,

characterized by watery diarrhea, hypokalemia, and hypochlorhydria. Despite this, the

VIPoma syndrome can be difficult to diagnosis and these tumors can elude prompt

diagnosis.[5] As such, similar to other neuroendocrine tumors, VIPomas can be quite

large at the time of presentation and involve adjacent structures. As in the current case,

locoregional extension can include invasion into visceral structures. However, with an

aggressive surgical approach that allows for complete tumor extirpation, extended,

meaningful survival can be achieved for VIPoma patients.[5]

Norton et al.,[4] have reported that aggressive surgery can be done with acceptable

morbidity and low mortality rates for patients with advanced neuroendocrine tumors. In a

series of 20 patients with advanced tumors, Norton et al.,[4] reported a post-operative

complication rate of 30% and no operative deaths. In that study, surgery variably

included pancreatectomy, splenectomy, superior vein reconstruction, and liver resection.

In the current case, the patient underwent an extensive procedure that included



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pancreatectomy, splenectomy, total gastrectomy, left adrenalectomy, diaphragmatic

resection, as well as small and large bowel resection. An R0 resection (microscopically

negative margins) was achieved and the patient did well post-operatively. Patients with

locally advanced neuroendocrine tumors that can be technically resected with an R0

margin should therefore be offered surgical resection even when a multi-visceral

resection is necessary. In high-volume institutions, these procedures can be

accomplished with acceptable morbidity and near-zero mortality.[4,6,7]

Accurate CT imaging is critical in assessing locoregional resectability.[8,9] Recently, 3-D

CT scan has been reported to enhance the assessment of the tumor-vascular interface,

[10] as the 3-D format allows for better viewing of oblique orientations.[11] Accurate

information concerning the relation of the tumor with the SMA is particularly critical as

major arterial encasement may preclude an R0 resection. It is important to note,

however, that intraoperative assessment of the tumor-SMA relationship can be very

limited – especially in patients with large tumors.[12] This is evidenced in the current

case in which the initial surgeon deemed the lesion to be unresectable based on an

intraoperative assessment that the SMA was encased. High-quality cross-sectional

imaging clearly demonstrated, however, that the SMA was indeed not involved (Figure

(Figure3). 3 ). This case highlights how intraoperative assessment of the tumor-SMA

interface may be both limited and misleading. Rather, thin-section contrast-enhanced CT

should be utilized as the modality of choice in assessing the relationship of the primary

tumor to major vascular structures such as the SMV, PV, SMA, and celiac axis. Such

determinations have important clinical implications in deciding which patients are

candidates for aggressive resection of advanced pancreatic tumors.

For tumors such as the one presented here, the surgeon should still evaluate the SMV

and SMA early in the course of surgery. Full exposure of the SMV is mandatory and

requires mobilization of the colon and root of the small bowel mesentery to expose the










SMV where it lies anterior to the third portion of the duodenum. This mobilization should

be carried to the left by incising the omental attachment to the mesocolon. After

performing a wide Kocher maneuver, the SMA should similarly be identified at the

junction of the third and fourth portions of the duodenum as it courses distally. The

connective tissue attachments between the portal vein/SMV and SMA can then be

divided, thereby isolating the vessels. This "medial" approach allows for early dissection

and evaluation of the critical vascular structures. Once the relation of the tumor to these

structures has been established, more lateral dissection along the spleen and tail of the

pancreas can be accomplishing with little difficulty. This method of dissecting the SMA

and SMV first allows the surgeon to avoid committing to an extensive resection prior to

determining whether or not an R0 resection is feasible.[13]

Sinistral, or left-sided, portal hypertension rarely causes gastrointestinal hemorrhage.

Although there are many causes of sinistral hypertension, it is usually due to pancreatic

pathology that compresses/invades the left portal – splenic venous system.[14,15]

Splenic vein occlusion results in back pressure which is transmitted to the short gastric

and gastroepiploic veins with subsequent formation of varices. Our patient had extensive

gastric and peri-tumoral varices that were associated with ongoing bleeding and

transfusion requirements. Management of sinistral hypertension traditionally involves

surgical removal of the primary tumor if possible. In the current case, although resection

was deemed to be feasible, the risk of intra-operative massive hemorrhage was felt to be

considerable given the extent of the varices, as well as the size and location of the

primary pancreatic mass. Preoperative proximal splenic artery embolization has

previously been shown to be a safe and efficacious portal decompression technique.

[16,17] Umeda et al., [17] have shown that proximal splenic artery embolization

shortened operative time, reduced blood loss, and led to less need for transfusion in

living donor liver transplantation recipients. In a separate study, Adams and







colleagues[16] assessed the benefit of preoperative control of splenic arterial inflow on

intraoperative blood loss in a cohort of patients with splenic venous occlusion and

sinistral hypertension secondary to chronic pancreatitis. In this study, the mean

reduction in blood loss associated with embolization was 1560 ml. The employment of

preoperative proximal splenic artery embolization in the present case undoubtedly

contributed to our relatively modest blood loss (~500 ml). In complex cases

characterized by large tumors, splenic vein occlusion, and significant left-side portal

hypertension with associated varices, preoperative embolization of the proximal splenic

artery should be considered to allow for portal decompression as a means to reduce

intraoperative blood loss. Preoperative splenic artery embolization should be used

selectively, however, as it may have associated risks.[18]

Conclusion

The current case is a unique example of a rare pancreatic tumor (VIPoma) that

highlights several important peri- and intra-operative concepts. Aggressive resection of

VIPomas is warranted and may provide the only chance at long-term survival. When

done at large volume, experienced centers even complex multi-visceral resections can

be done with low morbidity and near zero morality. In the subset of patients with

associated severe sinistral hypertension, proximal splenic artery embolization should be

considered as a preoperative means to decrease blood loss and improve outcome. Only

by utilizing a multi-modality approach that incorporates state-of-art cross-sectional

imaging, interventional radiology, and surgery can these complex patients be managed

successfully.





Yale J Biol Med. 2010 March; 83(1): 27–33.

Published online 2010 March.

PMCID: PMC2844690

Copyright ©2010, Yale Journal of Biology and Medicine

Amelioration of Symptoms and Reduction of VIP Levels after

Hepatic Artery Chemoembolization in a Patient with Sandostatin

Resistant VIPoma

Walid Shaib,a Kisha Mitchell,b and M. Wasif Saifb*

aHospital of Saint Raphael, New Haven, Connecticut

bYale University School of Medicine, New Haven, Connecticut

INTRODUCTION

We would like to report a case in which hepatic chemoembolization of a metastatic

hepatic lesion of VIPoma (Vasoactive Intestinal Polypeptide secreting islet cell tumor)

leads to a reduction of VIP (Vasoactive Intestinal Polypeptide) levels and resolution of

symptoms in a patient with pancreatic VIPoma unresponsive to increased doses of an

octreotide analog.

CASE REPORT

An 80-year-old Caucasian woman with a history of VIPoma diagnosed in 1997 was

treated for a 3.5 cm lesion in the head of the pancreas by Whipple procedure surgery

(Figure 1). She tolerated the surgery well, except for the development of diabetes

controlled with insulin postoperatively. In December 2004, follow-up CT imaging showed

a new 2.5 cm mass in the bed of the pancreas. She underwent another resection with

positive margins and one out of three lymph nodes positive for malignancy, for which

levels of VIP were >400 pg/ml (normal <75), chromogranin A 16.2 U/L (<31), gastrin16

pg/ml (<110) and serotonin 15 ng/ml (<71). Follow-up serial octreotide scans showed


http://www.ncbi.nlm.nih.gov/pmc/about/copyright.html

stable disease. In May 2005, a follow-up octreotide scan showed the same unresectable

retropancreatic tumor with new involvement of the right hepatic lobe (Figure 2). Due to

the long and indolent course of the disease and because the patient was asymptomatic,

she was treated with Sandostatin long acting (LAR) depot monthly. In September 2006,

the patient complained of worsening diarrhea, up to 10 bowel movements in 24 hours.

Laboratory data showed that VIP levels were still >400 pg/ml. Patient was re-started on

a loading dose of short-acting Sandostatin at 150 micrograms subcutaneously every

eight hours for two weeks, followed by LAR Sandostatin 20 mg intramuscularly every 28

days. Due to persistent diarrhea, the dose of LAR Sandostatin was escalated by

increments of 10 mg every 28 days to a maximum dose of 100 mg. The VIP levels

continued to be high (>400 pg/ml), and diarrhea transiently improved. Another flare-up

occurred in March 2008, manifested by intractable diarrhea and severe metabolic

acidosis. Because there are no guidelines in the treatment and follow-up of this disease,

we elected to initiate treatment with 5 Fluorouracil (5-FU) and streptozocin, based on

reports and success rates. No improvement of diarrhea (consistency and frequency) was

noted on this treatment. 5-FU was changed to capecetabine with the same results as 5-

FU. She underwent chemo-ablation with mitomycin c, cisplatin, and doxorubicin. Her

hospital course after the chemoablation was complicated by pulmonary embolism, atrial

fibrillation, pneumonia, and vancomycin-resistant enterococcus bacteremia. After

treatment, her diarrhea improved to less than two stools per day. In addition, the VIP

levels decreased to122 pg/ml (Figure 3). Three months later, patient was started on

temozolomide as maintenance therapy.

DISCUSSION

VIPomas are neuroendocrine tumors that secrete excessive amounts of VIP that cause

distinct syndromes characterized by large-volume diarrhea, hypokalemia, and

dehydration. The annual incidence of these tumors is estimated to be about 1 per



10,000,000 individuals in the general population [1]. The mean age of VIPoma patients

is 49 years. This syndrome is also called Verner-Morrison syndrome, pancreatic cholera,

or WDHA (watery diarrhea, hypokalemia, and achlorhydria) syndrome. In addition to the

WDHA, patients can present with flushing secondary to the vasodilatory effect of the

VIP. These tumors are usually solitary, more than 3 cm in diameter and occur in the

pancreas in 80 percent to 90 percent of cases, mainly in the pancreatic tail (50 percent

to 75 percent) with 37 percent to 68 percent hepatic metastasis at diagnosis.

Demonstration of elevated levels (>75 pg/ml) of VIP confirms diagnosis in the clinical

setting [2,3]. For localizing and staging of these tumors, somatostatin receptor

scintigraphy with octreotide scan has been recommended as the best imaging technique

[4]. Treatment preferences depend on the presence of metastasis. In metastatic tumors,

long-acting somatostatin analogs are the drugs of choice. Somatostatin analogs are

typically initiated at 20 mg daily dosage, and gradual escalation of the dose as needed,

for optimal control of symptoms, is recommended [5]. Hepatic resection is indicated for

the treatment of metastatic liver disease in the absence of diffuse bilobar involvement,

compromised liver function, or extensive extrahepatic metastases [6].

Other treatment options have been described with no set recommendations. Interferon-

alfa added to octreotide is used as one of the modalities for treatment of refractory

diarrhea in these patients [7]. Experiences with chemotherapeutic agents are limited.

Fjallskoga et al. concluded that combined streptozotocin and liposomal doxorubicin is a

safe and efficient treatment for endocrine pancreatic tumors. The efficacy seems to be

comparable to that of combined streptozotocin and doxorubicin; whereas, the cardiac

toxicity clearly favors using the liposomal drug combination [8]. Streptozotocin plus 5-

fluorouracil produced objective responses in 17 out of 31 (54 percent) patients with a

median duration of response of 23 months [9].






http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844690/#R4




Medical management with octreotide analogs has proven useful in the management of

pancreatic islet cell tumors with unresectable disease and/or metastases [10,11].

Neuroendocrine gastrointestinal tumors express somatostatin receptors (sstrs) in 80

percent to 90 percent of cases, and somatostatin analogs have become increasingly

important in the management of these patients. Most of the currently available

somatostatin analogs bind to the sstr2 and sstr5 receptor types and in higher doses to

sst3 of the ssts 1-5 described. Clinical improvement during somatostatin analog therapy

is mainly mediated via a direct inhibitory effect on hormone production from the tumors,

seen in 30 percent to 70 percent of patients. Indirect non-tumor mediated effects on

peripheral target organs contribute to the subjective improvement achieved in 30 percent

to 70 percent of patients. Significant improvement of quality of life has been

demonstrated with long-acting depot formulations. There is little or no effect on tumor

growth during octreotide therapy. Tumor shrinkage has been reported in 10 percent to

20 percent of patients, but stabilization of tumor growth can be achieved in about half of

the patients in eight to 16 months after starting treatment. Induction of apoptosis has

been reported by octreotide analogs as a possible mechanism of action on these tumors

[12]. Octreotide inhibits hormone secretion by various neuroendocrine tumors and may

occasionally reduce metastatic tumor burden [13]. Varying data exist about the

quantitative reduction of tumor size and symptomatic relief. Oberg et al. reported a

significant tumor response in <5 percent of patients but a symptomatic response in 60

percent of patients [14]. Maton et al. observed 83 percent symptomatic response but

fewer than 20 percent reduction in tumor size [15]. A case report by Kraenzlin et al.

showed that long-acting Sandostatin not only controlled the diarrhea without side effects,

but also appeared to have possibly induced a reduction in metastatic tumor size.

Conventional measures of surgery, chemotheraphy, and hepatic artery embolization

ultimately failed to control the severity of diarrhea, resulting from vasoactive intestinal







polypeptide hypersecretion [16]. Cho and Vinik evaluated tumor blood flow using

angiography in eight patients with different types of neuroendocrine tumors receiving

octreotide. They found a marked decrease in blood flow in two patients with gastrinomas

and two patients with VIPomas, with a hypothesis that octreotide either decreases blood

flow to these tumors or decreases tumor size or hormonal secretion [17].

Contrary to all these reports, VIP hypersecretion kept elevating in our patient, although

long-acting octreotide analog doses were increased. Similar to our report, Lamberts et

al. reported two patients with metastatic VIPomas developed resistance to somatostatin

analog with regard to clinical and inhibitory effect [18]. An “escape phenomenon” to

somatostatin analog was noticed for a few days with a usual response after

discontinuation of the treatment [19]. In another report, 10 patients with metastatic

pancreatic endocrine tumors were treated with the long-acting somatostatin analog

octreotide. Three patients showed no response, clinically or biochemically, and

treatment was, therefore, withdrawn. The seven remaining patients continued treatment

for a median period of 28 months (range 13-54 months). Treatment was initially

effective, symptoms improved, and the concentrations of tumor-related hormones were

reduced. Worsening of symptoms and rising levels of tumor-related hormone

concentrations occurred at a median of five months (range 1-6 months) after the start of

therapy and were initially reversed by increasing the dose of octreotide over a median of

10 months (range 6-16 months). However, after a median of 13 months (range 5-34

months) at the maximum dosage, symptoms recurred and were no longer responsive to

a further increase in dosage of octreotide or other therapeutic measures. All patients

died within five months once this “resistance phase” of their illness had been reached

[20]. However, resistance was never confirmed on histological or biochemical studies.

Arterial chemoembolization is recommended for patients with significant symptoms who






have failed to respond to more conservative therapy and are not surgical candidates

[21].

For patients with hepatic metastasis, initial expectant observation and medical

management of symptoms is appropriate in view of the long and indolent course of the

disease. As mentioned earlier, hepatic resection is indicated for the treatment of

metastatic liver disease in the absence of diffuse bilobar involvement, compromised liver

function, or extensive extrahepatic metastases. VIPomas are often large or

metastasizing, but generally require surgical debulking to alleviate hormonal symptoms

and have favorable survival outcomes [6]. In a clinical trial conducted by Eriksson et al.,

patients having midgut, foregut carcinoids and neuroendocrine pancreatic tumors,

treatment of liver metastases by surgical resection and/or radiofrequency ablation (RFA)

was successful in patients with midgut carcinoids with only less success in reducing

symptoms in patients with foregut carcinoids or neuroendocrine tumors. In addition,

patients with non-functioning neuroendocrine tumors may benefit from debulking

procedure to reduce morbidity and improve survival. Proposal of surgical debulking or

RFA as means that limit procedure-related morbidity and efficiently alleviate symptoms

has been beneficial in these patients, especially as this disease has a high incidence of

recurrence [6,22]. Azimuddin et al. reported that hepatic arterial embolization is the

preferred management in these cases [23]. Case et al. confirmed the finding that hepatic

artery embolization can be very effective and durable as a treatment modality for

patients with metastatic VIPomas (or other neuroendocrine tumors) who are clinically

symptomatic from the effects of hormone hypersecretion. It is applied as a palliative

technique in symptomatic patients with unresectable hepatic metastasis [24].

Furthermore, the study of Gupta et al. at MD Anderson has compared embolization

alone to chemoembolization of the hepatic artery and has concluded that in pancreatic

islet cell tumors (without specifying the subtype of the tumor), chemoembolization has







improved response rate by 50 percent compared to 25 percent with embolization alone.

Moreover, chemoembolization of these tumors had a survival benefit as compared to

embolization alone (31.5 months vs. 18.2 months) [25]. Yao et al. demonstrated that for

unresectable but liver dominant disease, chemoembolization was the treatment of

choice, with median survival of 32 months post chemoembolization and a five-year

survival rate of 40 percent. Chemoembolization effectively controlled tumor growth and

alleviated symptoms in 90 percent of patients [26]. This modality helped in controlling the

symptoms of our patient. Moreover; the VIP levels trended down as shown by the graph

in Figure 3. Huang et al. concluded that treatment for metastatic pancreatic islet cell

tumors require a multidisciplinary approach. Metastasis of the tumor is not a

contraindication for aggressive therapy. Combined cytoreductive surgery and TACE can

relieve symptoms and are of benefit for patients with pancreatic islet cell tumors with

liver metastases [27].

Temozolomide is another treatment option for metastatic disease. As a monotherapy, it

has acceptable toxicity and antitumoral effects in a small series of patients with

advanced malignant neuroendocrine tumors with some radiologic responses [28].








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