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TITLE PAGE

D AVAO M EDICAL S CHOOL F OUNDATION


MEDICAL DRIVE, BAJADA DAVAO CITY
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS NCM 101-RLE
SUBMITTED TO: ROXANNE ACERO, RN SUBMITTED BY: ABRACIA, JAMES ARANDIA, ALESSA ANQ
UE, JOANNA GRACE RUBY ALCAZARIN, IRENE LOU BELARMINO, ANGELINE BENDULO, VANESSA
BUTT, KANVAL CAPILITAN, CYRIL CASTILLO, JIRO DELFINADO, REGINE DE LEON, ANGELICA
IN
TABLE
OF
CONTENTS
Title Page......................................................................
..........................................................1 Acknowledgement.....
................................................................................
..............................4 Introduction....................................
................................................................................
.........5 Objectives...........................................................
....................................................................6 General Ob
jective: .......................................................................
.......................................6 Specific Objectives:...................
................................................................................
...........6 Patient’s Profile..................................................
.....................................................................7 PERSONAL
DATA............................................................................
.........................................8 MEDICAL DATA.........................
................................................................................
............8 Genogram..........................................................
.....................................................................9 Health Hi
story...........................................................................
............................................12 Past Health History..............
................................................................................
...............13 History of Present Illness....................................
................................................................13 Complete Defi
nition of Final Diagnosis.......................................................
..........................14 Developmental Data.................................
.............................................................................15
Erickson........................................................................
.....................................................16 Havigurst...............
................................................................................
.............................16 Physical Assessment.............................
................................................................................
18 Complete Definition of Final Diagnosis.......................................
...........................................22 Anatomy and Physiology............
................................................................................
...........23 Right heart.......................................................
...............................................................25 Arteries......
................................................................................
.....................................27 Capillaries.............................
................................................................................
.......27 Venules...............................................................
............................................................27 Veins............
................................................................................
...................................27 Cranial arteries..........................
................................................................................
.........29 Cerebral venous drainage............................................
......................................................29 Etiology and Symptomato
logy............................................................................
...................32 SYMPTOMATOLOGY............................................
.............................................................33 Pathophysiology
................................................................................
...................................34 ..........................................
................................................................................
..............34 Medical, Pharmacologic and Diagnostic Exams....................
.................................................41 Hematology..................
................................................................................
...................42
Hematology......................................................................
...............................................52 Coagulation Result Form.......
................................................................................
..........55 X-Ray Result.......................................................
.............................................................56 Urinalysis......
................................................................................
..................................57 Possible Management/Lab Tests..............
..........................................................................90 Dru
g Studies.......................................................................
...................................................95 Management................
................................................................................
.......................106 .....................................................
................................................................................
.......110 Nursing Care Plans...................................................
...........................................................110 Discharge Plannin
g...............................................................................
...............................114 Prognosis....................................
................................................................................
.........117 Bibliography:......................................................
.................................................................119
ACKNOWLEDGEMENT
We, the members of the Group 1 section A of the 3rd year nursing students of the
Davao Medical School Foundation would like to extend our acknowledgement to the
following persons: first is for our clinical instructor, Ma’am Roxanne G. Acero
for continuously guiding us in all our efforts and tirelessly committing her ti
me in providing us with essential knowledge for making this case study a reality
. And also for the Canias Family and their son who cooperatively participates in
all medical and nursing interventions done to them and all health teachings we
have rendered.
INTRODUCTION
Dengue fever is an acute febrile infectious disease, caused by all four serotype
s (1, 2, 3 or 4) of a virus from genus Flavivirus, called dengue virus. It’s the
most prevalent flavivirus infection of humans, with a worldwide distribution in
the tropics and warm areas of the temperate zone corresponding to that of the p
rincipal vector, Aedes aegypti. When simultaneous or sequential introduction of
two or more serotypes occurs in the same area, there may be an increased number
of cases with worse clinical presentation (dengue hemorrhagic fever). The term ‘
hemorrhagic’ is imprecise, because what characterizes this form of the disease i
s not the presence of hemorrhagic manifestations, but the abrupt increase of cap
illary permeability, with diffuse capillary leakage of plasma, hemoconcentration
and, in some cases, with non-hemorrhagic hypovolemic shock (dengue shock syndro
me).
OBJECTIVES
GENERAL OBJECTIVE: • To present a case of Dengue Hemorrhagic Fever
SPECIFIC OBJECTIVES: 1) To discuss the family profile of Canas 2.) To present th
e index case with Dengue Hemorrhagic Fever 3) To discuss briefly DHF 4) To estab
lish the family diagnosis, intervention and recommendation using family assessme
nt tools
PATIENT’S PROFILE
PERSONAL DATA
Name: Richielou Dave Canas Address: Block 45 Fatima Village Bajada Davao City Se
x: Male Age: 7 yrs. old Birth Date: February 21, 2002 Birth Place: Davao City Re
ligion: Roman Catholic Nationality: Filipino Ordinal Status: Eldest Occupation:
Student Year level: Grade 1 in Holy Cross of Bajada Types of Community: Urban Ci
vil Status: Single Father’s Name: Romulus Canas Occupation: Chief in Insular Hot
el Mother’s Name: Michelle Canas Occupation: Housewife Income: ≤ 10, 000 pesos S
ocioeconomic: Middle Class
MEDICAL DATA
Date of Admission: July 30, 2009 Time of Admission: 1:05 pm How Admitted: Wheelc
hair Ward: St. Anthony Ward Room and Bed #: 426-bed 3 Chief Complain: Abdominal
Pain Attending Physician: Dr. Ong Impression /Tentative Diagnosis: Suggestive mi
nimal pleural effusion, right Final Diagnosis: Dengue Hemorrhagic Fever Date and
Time of Discharge: August 04, 2009 @ 3:00 pm
GENOGRAM
Narrative Genogram On the paternal side of our client, his Grandfather Mr. Ricar
do Destajo due to heart disease at the age of 35 years old, his wife Maricel Des
tajo is 56 yrs old and known to have hypertension. Mr. Ricardo and Mrs. Maricel
Destajo had three children namely: Mrs. Michelle our client’s mother, Ms. Rochel
le, and Ms. Princess. Mrs. Michelle
HEALTH HISTORY
PAST HEALTH HISTORY
Richielous Dave Canas was delivered via NSVD without any complications. He was a
ble to experience common illness like mumps at the age of 7. He was being breast
fed by his mother for only 2 days. According to the doctor’s record there was im
munization taken; 1 BCG done; 3 doses for DPT; 3 doses for OPV; 3 doses for Hepa
and 1 dose for measles. There is no prenatal infection and no exposures any dru
gs/radiation and no smoking/ alcohol history. He was taking cherifer 5 ml a day.
HISTORY
OF
PRESENT ILLNESS
Problem 1: 5 days prior to admission, pt had sudden onset of undocumented interm
inent fever. Condition temporarily relieved by intake of Paracetamol 5mkd. Probl
em 2: 4 days prior to admission, still with fever. Pt had onset of LBM, watery,
non-mucoid , non-foul smelling, 2 episodes. Problem 3: 3 days prior to admission
, onset of abdominal pain located at the RUQ and epigastric area, associated wit
h 1 episode of vomiting, post-prandial. No meds given. An hour prior to admissio
n, persistence of abdominal pain prompted consult.
COMPLETE DEFINITION OF FINAL DIAGNOSIS
DEVELOPMENTAL
DATA
ERICKSON Erik Erickson’s Stages of Psychosocial Theory
Erickson’s theory of psychosocial development is one of the best-known theories
of personality. Similar to Freud, Erickson believed that personality develops in
a series of stages. Unlike Freud’s theory of psychosocial stages, Erickson’s th
eory describes the impact of social experience across the whole lifespan. The Er
ikson’s eight stages of developmental are:
1. 2. 3. 4. 5. 6. 7. 8.
Trust vs. Mistrust (hope) Autonomy vs. Shame and Doubt (will) Initiative vs. Gui
lt (purpose) Industry vs. Inferiority (competence) Identity vs. Role Confusion (
fidelity) Intimacy vs. Isolation (love) Generativity vs. Stagnation (caring) Ego
Integrity vs. Despair (wisdom)
Industry vs. Inferiority (competence) - is the central task of our patient. Mr.
Dave is comparing self worth to others (such as in a classroom environment). He
can recognize major disparities in personal abilities relative to other children
. He also feels a sense of shame if his parents unthinkingly share his failures
with others. Children who cannot master their school work may consider themselve
s a failure and feelings of inferiority may arise.
HAVIGURST
Robert Havighurst’s developmental Physiological theory Robert Havighurst believe
d that learning is basic to life and that people continue to learn throughout li
fe. He described growth and development as occurring during stages, each associa
ted with 6-20 tasks to be learned.
Developmental task which arises at a certain period in the life of an individual
, successful achievement of which leads to his happiness and success with later
tasks, while failure leads to unhappiness in the individual. Havighurst identifi
ed Six Major Stages in human life covering birth to old age.
• Infancy & early childhood (Birth till 6 years old) • Middle childhood (6-12 ye
ars old) • Adolescence (13-18 years old) • Early Adulthood (19-30 years old) • M
iddle Age (30-60years old) • Later maturity (60 years old and over) The expected
tasks for Middle childhood(6-12 years old)
Justification
Learning physical skills necessary for ordinary games.
Our patient was learned the physical skills that are necessary for the games and
physical activities that are highly valued in childhood such skills as throwing
and catching, kicking, tumbling, swimming, and handling simple tools.
Learning to get along with age mates.
Building wholesome attitudes oneself as a growing organism.
toward
Learning on appropriate masculine or feminine social role.
Developing concepts everyday living.
necessary
for
Developing conscience, morality and a scale of values.
Achieving personal independence. Developing attitudes groups and institutions. t
oward social
He learned the give-and-take of social life among peers. He learned to make frie
nds and to get along with enemies And developed a "social personality." He devel
oped habits of care of the body, of cleanliness and safety, consistent with a wh
olesome, realistic attitude which includes a sense of physical normality and ade
quacy, the ability to enjoy using the body, He learned to be a boy, to act the r
ole that is expected and rewarded. The sex role is taught so vigorously by so ma
ny agencies that the school probably has little more than a remedial function, w
hich is to assist boys and girls who are having difficulty with the task. A conc
ept is an idea which stands for a large number of particular sense perceptions,
or which stands for a number of ideas of lesser degrees of abstraction. He devel
oped an inner moral control, respect for moral rules, and the beginning of a rat
ional scale of values. Morality, or respect for rules of behavior, is imposed on
the child first by the parents. He become physically independent of his parents
but remains emotionally dependent on them. He developed social attitudes that a
re basically democratic by imitation of people with prestige in the eyes of the
learner.
PHYSICAL ASSESSMENT
Our client is Mr. Richellou Dave Canas, 7 years old male, admitted last July 30,
2009 @ Davao Medical School Foundation Hospital, St. Anthony’s ward, room 426 be
d 3, under the care of Dr. Ong in due to abdominal pain, and diagnosed to have D
engue Hemorrhagic Fever type 3. I. GENERAL SURVEY Mr. Canas weights 20 Kg. Upon
receiving, he was placed in flat back rest; not in respiratory distress, awake,
responsive and coherent. He is oriented to time and place. The client looks acco
rding to his age and his nutritional state was well maintained. With an IVF of D
5IMB 500cc regulated @ 30 cc /hour infusing well at right metacarpal vein. He ap
pears to be relaxed and is wearing a clean patient’s gown. He is cooperative all
throughout the interaction.
Physical Assessment
II. VITAL SIGNS At around 8:00 o’clock in the morning we assessed his vital sign
s, the axillary temperature obtained is 36.8 °C. He has radial pulse rate of 78
bpm and a cardiac rate of 80 bpm respectively. He has a normal respiratory rate
of 26 cpm and a normal blood pressure of 100/60 mmHg. III. SKIN Skin is dark bro
wn in color and uniform throughout the body, with poor skin turgor. Nails are co
nvex in shape with capillary refill of 2-3 seconds. Nail beds are pink in color.
IV. HEAD Head configuration is normocephalic and there were no signs of enlarge
ment or any masses noted. The facial structure and movement are symmetrical. Hai
r is fine, evenly distributed; scalp is clean and is also free from dandruff, li
ce, wounds, scars and other lesions. V. EYES His eyelids were proportioned with
no swelling noted. His eyelashes are long and directed outward. Fine eyebrows ar
e evenly distributed. His conjunctiva is pinkish in color and her pupil’s size a
re equally round and reactive to light and accommodation with a diameter of 3 mm
. VI. EARS Ears are symmetrically aligned with the outer canthus of the eye. Pin
na is mobile and firm with no tenderness, swelling and lesions noted. There is n
o presence of discharges. Patient is able to hear normal voice tones audibly. VI
I.NOSE
External nose are symmetrical. No discharges, flaring, tenderness and lesions no
ted. Nares are patent. Frontal and maxillary sinuses are not tender. VIII. MOUTH
His lips are pale in color and slightly dry. Gums and mucosa are light pink in
color. Tongue is located at midline. Teeth are not complete; he has 12 teeth on
the lower portion and 13 teeth in the upper portion. His speech is intact; he ca
n speak clearly and fluently using his own dialect. IX. NECK Sternocleidomastoid
and trapezius muscle were equal in size. Head movements are coordinated with no
discomfort. No presence of masses, unusual swelling and enlargement noted. X. H
EART His heart sounds are distinct and regular. Point of maximum impulse is loca
ted between the 5th and 6th intercostals spaces. XI. BREAST AND AXILLAE Nipples
are dark brown in color, no discharges, swelling, tenderness, masses and lesions
noted. Axilla was light brown in color with no amount of axillary hair. No mass
es and swelling noted. CHEST AND LUNGS He has normal respiratory rate of 26 cpm.
Has a regular breathing pattern. Lung expansion was symmetrical, abnormal sound
s during auscultation is not noted. No tenderness or masses in the chest is note
d. ABDOMEN The general contour of his abdomen is round without folds observed. A
bdominal skin is fair. Masses are not observed. EXTREMITIES With grossly normal
extremities. Nail beds are pinkish in color with a capillary refill of 2-3 secon
ds. Peripheral pulse is symmetrical and strong. Gait is coordinated. No inflamma
tion, lesions, tenderness, pain and deformity noted on any part of the extremiti
es. NVS He is conscious and oriented to time and place and person. He answers to
our questions appropriately. His pupils are equally round and reactive to light
and accommodation with diameter of 3 mm. Both
XII.
XIII.
XIV.
XV.
his left and right, upper and lower extremities are strong. He obeys simple inst
ructions during the assessment.
COMPLETE DEFINITION OF FINAL DIAGNOSIS
ANATOMY AND PHYSIOLOGY
ANATOMY & PHYSIOLOGY The Circulatory System
The circulatory system is an organ system that passes nutrients (such as amino a
cids and electrolytes), gases, hormones, blood cells, nitrogen waste products, e
tc. to and from cells in the body to help fight diseases and help stabilize body
temperature and pH to maintain homeostasis. This system may be seen strictly as
a blood distribution network, but some consider the circulatory system as compo
sed of the cardiovascular system, which distributes blood, and the lymphatic sys
tem, which distributes lymph. While humans, as well as other vertebrates, have a
closed cardiovascular system (meaning that the blood never leaves the network o
f arteries, veins and capillaries), some invertebrate groups have an open cardio
vascular system. The most primitive animal phyla lack circulatory system. The ly
mphatic system, on the other hand, is an open system.
The main components of the human circulatory system are the heart, the blood, an
d the blood vessels. The circulatory system includes: the pulmonary circulation,
a "loop" through the lungs where blood is oxygenated; and the systemic circulat
ion, a "loop" through the rest of the body to provide oxygenated blood. An avera
ge adult contains five to six quarts (roughly 4.7 to 5.7 liters) of blood, which
consists of plasma, red blood cells, white blood cells, and platelets. Also, th
e digestive system works with the circulatory system to provide the nutrients th
e system needs to keep the heart pumping. Two types of fluids move through the c
irculatory system: blood and lymph. The blood, heart, and blood vessels form the
cardiovascular system. The lymph, lymph nodes, and lymph vessels form the lymph
atic system. The cardiovascular system and the lymphatic system collectively mak
e up the circulatory system. http://en.wikipedia.org/wiki/Circulatory_system Pul
monary Circulation
Pulmonary circulation is the portion of the cardiovascular system which carries
oxygendepleted blood away from the heart, to the lungs, and returns oxygenated b
lood back to the heart. The term is contrasted with systemic circulation.
In the pulmonary circulation, deoxygenated blood enters the right section of the
heart through the pulmonary arteries, enters the lungs and oxygenated blood com
es through the pulmonary veins. The blood then moves to the left atrium of the h
eart then to the left ventricle where the blood is pumped through the semilunar
valve into the aorta. RIGHT HEART Oxygen-depleted blood from the body leaves the
systemic circulation when it enters the right heart, more specifically the righ
t atrium through the Superior (upper) vena cava and Inferior (lower) vena cava.
The blood is then pumped through the tricuspid valve (or right atrioventricular
valve), into the right
ventricle. Blood is then pumped through the semilunar valve and into the pulmona
ry artery. Arteries From the right ventricle, blood is pumped through the pulmon
ary semilunar valve into the pulmonary artery. This blood enters the two pulmona
ry arteries (one for each lung) and travels through the lungs. Lungs The pulmona
ry arteries carry deoxygenated blood to the lungs, while the pulmonary veins car
ry oxygenated blood to the red blood cells where they release carbon dioxide and
pick up oxygen during respiration. Veins The oxygenated blood then leaves the l
ungs through pulmonary veins, which return it to the left heart, completing the
pulmonary cycle. This blood then enters the left atrium, which pumps it through
the bicuspid valve, also called the mitral or left atrioventricular valve, into
the left ventricle. The blood is then distributed to the body through the system
ic circulation before returning again to the pulmonary circulation. http://en.wi
kipedia.org/wiki/Pulmonary_circulation
Systemic Circulation
Systemic circulation is the portion of the cardiovascular system which carries o
xygenated blood away from the heart, to the body, and returns deoxygenated blood
back to the heart. The term is contrasted with pulmonary circulation
In the systemic circulation, arteries bring oxygenated blood to the tissues. As
blood circulates through the body, oxygen diffuses from the blood into cells
surrounding the capillaries, and carbon dioxide diffuses into the blood from the
capillary cells. Veins bring deoxygenated blood back to the heart. ARTERIES Oxy
genated blood enters the systemic circulation when leaving the left ventricle, t
hrough the aortic semi-lunar valve. The first part of the systemic circulation i
s the artery aorta, a massive and thick-walled artery. The aorta arches and give
s off major arteries to the upper body before piercing the diaphragm in order to
supply the lower parts of the body with its various branches. C APILLARIES Bloo
d passes from arteries to arterioles and finally to capillaries, which are the t
hinnest and most numerous of the blood vessels. These capillaries help to join t
issue with arterioles for transportation of nutrition to the cells, which absorb
oxygen and nutrients in the blood. Peripheral tissues do not fully deoxygenate
the blood, so venous blood does have oxygen, but in a lower concentration than i
n arterial blood. In addition, carbon dioxide and wastes are added. The capillar
ies can only fit one cell at a time. VENULES The deoxygenated blood is then coll
ected by venules, from where it flows first into veins, and then into the inferi
or and superior venae cavae, which return it to the right heart, completing the
systemic cycle. The blood is then re-oxygenated through the pulmonary circulatio
n before returning again to the systemic circulation. VEINS The relatively deoxy
genated blood collects in the venous system which coalesces into two major veins
: the superior vena cava (roughly speaking from areas above the heart) and the i
nferior vena cava (roughly speaking from areas below the heart). These two great
vessels exit the systemic circulation by emptying into the right atrium of the
heart. The coronary sinus empties the heart s veins themselves into the right at
rium. http://en.wikipedia.org/wiki/Systemic_circulation
Portal Circulation
The gastric, splenic and mesenteric veins, which collect the venous blood from a
ll the digestive organs, unite to form the portal vein, which carries to the liv
er this blood which has circulated through the capillaries of the stomach, splee
n, pancreas and intestines, and though dark in colour, is laden with nutriment,
the products of digestion. This important vein breaks up into capillaries (after
the manner of an artery), and distributes this blood by means of them throughou
t the liver ; it there mingles with blood supplied by the hepatic artery, and is
collected again by small veins which unite to form the hepatic vein, by which i
t is carried to the inferior vena cava, and by it is poured into the right auric
le.
http://chestofbooks.com/health/body/massage/Margaret-D-Palmer/Lessons-onMassage/
The-Portal-Circulation.html
The Cerebral Circulation Cerebral circulation refers to the movement of blood th
rough the network of blood vessels supplying the brain. The arteries deliver oxy
genated blood, glucose and other nutrients to the brain and the veins carry deox
ygenated blood back to the heart, removing carbon dioxide, lactic acid, and othe
r metabolic products. Since the brain is very vulnerable to compromises in its b
lood supply, the cerebral circulatory system has many safeguards. Failure of the
se safeguards results in cerebrovascular accidents, commonly known as strokes. T
he amount of blood that the cerebral circulation carries is known as cerebral bl
ood flow. The presence of gravitational fields or accelerations also determine v
ariations in the movement and distribution of blood in the brain, such as when s
uspended upside-down.
CRANIAL ARTERIES There are two main pairs of arteries that supply the cerebral a
rteries and the cerebellum:
• Internal carotid arteries: These large arteries are the left and right branche
s of the common carotid arteries in the neck which enter the skull, as opposed t
o the external carotid branches which supply the facial tissues. The internal ca
rotid artery branches into the anterior cerebral artery and continues to form th
e middle cerebral artery Vertebral arteries. These smaller arteries branch from
the subclavian arteries which primarily supply the shoulders, lateral chest and
arms. Within the cranium the two vertebral arteries fuse into the basilar artery
, which supplies the midbrain, cerebellum, and usually branches into the posteri
or cerebral artery.

Both internal carotid arteries, within and along the floor of the cerebral vault
, are interconnected via the anterior communicating artery. Additionally, both i
nternal carotid arteries are interconnected with the basilar artery via bilatera
l posterior communicating arteries. The Circle of Willis, long considered to be
an important anatomic vascular formation, provides backup circulation to the bra
in. In case one of the supply arteries is occluded, the Circle of Willis provide
s interconnections between the internal carotid arteries and basilar artery alon
g the floor of the cerebral vault, providing blood to tissues that would otherwi
se become ischemic. CEREBRAL VENOUS DRAINAGE The venous drainage of the cerebrum
can be separated into two subdivisions: superficial and deep. The superficial s
ystem is composed of dural venous sinuses, which have wall composed of dura mate
r as opposed to a traditional vein. The dural sinuses are, therefore located on
the surface of the cerebrum. The most prominent of these sinuses is the Superior
sagittal sinus which flows in the sagittal plane under the midline of the cereb
ral vault, posteriorly and inferiorly to the torcula, forming the Confluence of
sinuses, where the superficial drainage joins with the sinus the primarily drain
s the deep venous system. From here, two transverse sinuses bifurcate and travel
laterally and inferiorly in an S-shaped curve that form the sigmoid sinuses whi
ch go on to form the two jugular veins. In the neck, the jugular veins parallel
the upward course of the carotid arteries and drain blood into
the vena cava. The deep venous drainage is primarily composed of traditional vei
ns inside the deep structures of the brain, which join behind the midbrain to fo
rm the Vein of Galen. This vein merges with the Inferior sagittal sinus to form
the Straight sinus which then joins the superficial venous system mentioned abov
e at the Confluence of sinuses.
Lymphatic System
The lymphatic system and the cardiovascular system are closely related structure
s that are joined by a capillary system. The is important to the body s defense
mechanisms. It filters out organisms that cause disease, produces certain white
blood cells and generates antibodies. It is also important for the distribution
of fluids and nutrients in the body, because it drains excess fluids and protein
so that tissues do not swell up. "Lymph" is a milky body fluid that contains a
type of white blood cells, called "lymphocytes," along with proteins and fats. L
ymph seeps outside the blood vessels in spaces of body tissues and is stored in
the "lymphatic" system to flow back into the bloodstream. Through the flow of bl
ood in and out of arteries, and into the veins, and through the lymph nodes and
into the lymph, the body is able to eliminate the products of cellular breakdown
and bacterial invasion. Two very large areas are of significance in this system
- the right lymphatic duct which drains lymph fluid from the upper right quarte
r of the body above the diaphragm and down the midline, and the thoracic duct, a
structure roughly sixteen inches long located in the mediastinum of the pleural
cavity which drains the rest of the body. It is through the actions of this sys
tem including the spleen, the thymus, lymph nodes and lymph ducts that our body
is able to fight infection and to ward off invasion from foreign invaders. Lymph
plays an important role in the immune system and in absorbing fats from the int
estines. The
lymphatic vessels are present wherever there are blood vessels and transport exc
ess fluid to the end vessels without the assistance of any "pumping" action. The
re are more than 100 tiny, oval structures (called lymph nodes). These are mainl
y in the neck, groin and armpits, but are scattered all along the lymph vessels.
They act as barriers to infection by filtering out and destroying toxins and ge
rms. The largest body of lymphoid tissue in the human body is the spleen. http:/
/www.innerbody.com/image/lympov.html
ETIOLOGY
AND
SYMPTOMATOLOGY
SYMPTOMATOLOGY Signs & Symptoms Actual High Fever, Body weakness, headache, naus
ea, vomiting and sometimes abdominal pain Rationale In acute DHF, the patients i
nitially develop an abrupt onset of high fever (39–40°C) with malaise, headache,
nausea, vomiting, myalgia and, sometimes, abdominal pain due to body’s innate i
mmune response from the virus. In DHF, abnormal hemostasis due to vasculopathy,
thrombocytopenia and coagulopathy may lead to various hemorrhagic manifestations
. The unusual manifestation of hepatic encephalopathy is possibly due to hypoten
sion, cerebral edema, microvascular or frank hemorrhage, hyponatremia and fulmin
ant hepatic failure. Most patients had extremely elevated serum levels of AST an
d ALT, and exhibited alteration of consciousness, seizure or neurological defici
t during the febrile stage. In addition, very rare cases of encephalitis, enceph
alomyelitis and transverse myelities with positive dengue virus and/or IgM in th
e cerebrospinal fluid were reported. The overall case–fatality rate was 5%. A po
sitive tourniquet test indicating the increased capillary fragility is found in
the early febrile stage. It may be a direct effect of dengue virus as it appears
in the first few days of illness during the viremic phase.
Hemorrhagic Phenomena such as easy bruising, bleeding at the venipuncture site,
gum bleeding. Hepatomegaly
(+) Tourniquet test
PATHOPHYSIOLOGY
Figure Precipitating Factors: Aedes aegypti mosquito Predisposing Factors: Age H
eredity Sex Race
Bite of a viruscarrying mosquito
Mosquito injects fluid into victim’s skin
Virus enters in the host blood stream
Infects cells and replicate in sufficient amount
Platelet will provide a shield for the virus from exposure and binding to neutra
lize pre-existing antibody
Initiates an immune response
Macrophages or monocytes engulfed the virus having a platelet (phagocytosis)
Activation of memory T-cell response during reexposure
Stimulates release of cytokines
High Fever, Body weakness, headache, nausea, vomiting and sometimes abdominal pa
in
Virus – complex
antibody
(binding of ab-virus)
Cytokines destroy cell membrane and cell wall(viral antigens found in monocytes)
Abuptake
enhanced Complement system activation
Cytolysis Vascular endothelial cell activation
Coagulopathy (PT/APTT)
Thrombocytopenia (<100 x 109/L)
Vasculopathy (plasma leakage)
Fluid shifting ICF to ECF
Petechial rashes in several areas of the body
Management: If not managed: *Promote rest *Medication Hypovolemia *Rapid replace
ment of body fluids *Blood transfusion *Precautions Tissue acidosis
Patient recovers Disseminated Intravascular Coagulation
Severe hemorrhage
Bloody vomitus, Hematuria, Bloody stool
Intractable shock
Multi organ failure
Death Death
Narrative Pathophysiology of Dengue Hemorrhagic Fever
The dengue viruses, the cause of dengue illness, are members of the Flaviviridae
family. Four genetically related but distinct serotypes, designated DENV-1, DEN
V-2, DENV-3, DENV-4, are circulating worldwide. The main vector for dengue virus
transmission is the Aedes aegypti species of mosquitos. Dengue viruses, similar
to other flaviviruses, have a positive single-stranded RNA genome packaged insi
de a core protein, which is surrounded by an icosahedral scaffold and covered by
a lipid envelope. The genome of the dengue virus contains 11-kb plussensed RNA
encoding 3 structural proteins and 7 non-structural proteins. Viral protein and
RNA synthesis occur predominantly in the cytoplasm of host cells. Replication is
slow and begins within 15 hours after infection. Low amounts of dengue virus ar
e released into the supernatant fluid. Dengue virus replication does not signifi
cantly affect the metabolic function of the host cell as exemplified by normal l
evels of protein synthesis by the infected cells. Dengue fever, caused by an inf
ection with dengue virus, is not a new disease, but recently because of its seri
ous emerging health treats, coupled with possible dire consequences including de
ath, it has aroused considerable medical and public health concerns worldwide. T
oday, dengue is considered one of the most important arthropod-borne viral disea
ses in humans in terms of morbidity and mortality. Globally, it is estimated tha
t approximate 50-100 million new dengue virus infections occur annually. Among t
hese, there are 200,000 to 500,000 cases of potential life-threatening dengue he
morrhagic fever (DHF)/ dengue shock syndrome (DSS), characterized by thrombocyto
penia and increased vascular permeability. Risk factors of DHF are the following
: Age (DHF/ DSS is more predominantly in children <15years of age), Heredity (in
fants in mother having an antibodies to dengue serotype, immunity to one dengue
virus serotype may enhance response to the secondary infection), Sex (common in
females than males), Race (common in Caucasian, dengue virus generally cause a b
enign syndrome, DF. And severe syndrome DHF/DSS in Southeast Asia). Dengue infec
tion starts in a bite of virus-carrying mosquito (aedes aegypti). The mosquito i
njects fluid into the host skin then the virus can freely enter in the bloodstre
am. In the bloodstream, the virus will infect cells (mononuclear phagocyte linea
ge) and will replicate in sufficient amount. And will initiate an immune respons
e. Normally all humans have their own innate immune system which is inborn in na
ture. This immune system is a universal and ancient form of host defense against
infection. The innate immune system has been shown to consist of several compon
ents broadly ranging from skin barriers to cellular effector mechanisms and geno
me-encoded molecules, which act in concert to provide the host with an initial b
arrier against foreign organism. The innate immune system thus includes natural
antibody and factors involved in the maintenance of the homeostasis. Key feature
s of innate immunity are that it is not antigen specific, and can respond immedi
ately or within a few hours after encountering a novel intruder and thereby to p
revent or reduce infection. The innate immune response to dengue infection, I is
basically a subject that is too a large extent underexplored. There are two imp
ortant components of the innate immune system, the natural IgM antibody and plat
elets, are likely to play a critical role in the period of dengue virus infectio
n. Natural IgM Antibody:
Humoral immunity is mainly mediated by B cells, which is produce different class
es of antibodies, both natural and pathogen induced. Natural IgM antibodies are
produced mainly by CD5+ B cells (B1 cells) and are component of innate immunity.
These nonspecific circulating natural antibodies can bind to pathogens, providi
ng early host protection. Natural antibodies may facilitate antigen uptake, proc
essing, and presentation by B lymphocytes via complement and Fc – receptors. Int
erestingly, it has been suggested that B cells are the principal circulating mon
onuclear cells infected by dengue virus. Although in humans about 30% of the cir
culating antibodies are pentameric IgM molecules, a small amount of hexameric Ig
M, IgG, and IgA natural antibodies circulate as well. The physiologic roles of t
he natural IgM antibodies are not known. The multimeric structures makes IgM a s
trong complement activator; a single-bound IgM pentamer can trigger the classica
l pathway of complement activation and can lyse a red blood cell, while approxim
ately a thousand IgG molecules are required to accomplish the same. Furthermore
the hexamer IgM, even though it circulates in smaller amounts, is 15 -20 times m
ore efficient in activating complement system. Unfortunately a deep role of circ
ulating IgM-immune complex in DHF/DSS is unknown. Platelets One of the clinical
manifestations in dengue diseases is thrombocytopenia, otherwise known as low pl
atelet count. This arises from both decreased production and increase destructio
n of platelets. During dengue virus infection, platelets may provide a wonderful
shield for the virus from exposure and binding to neutralizing preexisting anti
body. Interestingly, there are few reports that dengue virus may associate with
platelets, directly or indirectly through antibody. Now we can envision that the
virus-plateletsantibody complexes may enhanced phagocytosis or be engulfed by m
acrophages or monocytes. This can lead to vasculopathy (plasma leakage), thrombo
cytopenia (<100) and coagulopathy (prolonged PT/ APTT). It is also possible that
platelets can serve as the reservoir for dengue virus replication; however this
issue is a subject of further investigation. Hyper-thermal Factors Dengue fever
is one of the hallmarks of dengue virus infection. Fever is the normal physiolo
gic response of the body to mediators that are generated during the acute phase
of dengue virus infection. In fact, fever is a condition induced by the host to
subdue and contain the adverse effects of the infection, making it unfavorable f
or the infecting agent, and is designed to promote body health. Heat inducible f
actors from host cells are expressed and released into the circulation. Most pro
minent among this heat inducible factors are the cytokines the trigger fever (fe
ver inducers) such as TNF-alpha, IL-1, and IL-6. On the other hand, activation o
f memory T-cell response during re-exposure to second infection stimulates the r
elease of a massive amount of proinflammatory cytokines, which induces vascular
cell activation and is likely cause of the capillary leak syndrome. This respons
e also can enhance virus-antibody complex leading to cytolysis. Treatment can be
supportive, administration of anti-pyretic (avoid NSAID and aspirin), ORS in ca
se of N/V. Normal saline is indicated but over hydration can lead to pulmonary e
dema. Blood, platelets is indicated in significant hemorrhage. There is no need
of IV immunoglobulins and steroids.
If the patient is not cured immediately, fluid shift due to prolonged plasma lea
kage can lead to increased hematocrit leading to hypovolemia the later, tissue a
cidosis. Tissue acidosis, thrombocytopenia and coagulopathy may lead to dissemin
ated intravascular coagulation (DIC) which can lead to severe hemorrhage. The pa
tient will experience an intractable shock leading to multi-organ failure then d
eath.
MEDICAL, PHARMACOLOGIC AND DIAGNOSTIC
EXAMS
D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO C
ITY
HEMATOLOGY
Name: Mr. Canas Date: August 3, 2009 Age: 7 years old Room: Sex: Male Physician:
Dr. Ong
Test
HEMOGLOBIN
Resul t
155
Unit
g/dL
Reference
M:140-170 F:120-150
Clinical Significance = anemia, liver or kidney disease =primary and secon
dary polycythemia, COPD, CHF, burns
Functions
Hemoglobin is responsible for binding oxygen in the lungs and in transporting th
e bound oxygen throughout the body where it is used in aerobic metabolic pathway
s. RBC’s transport oxygen bound to hemoglobin; also transports small amount of c
arbon dioxide.
ERYTHROCYTES
5.91
10ˆ12/ L
4.0-6.0
=anemia, acute

LEUKOCYTE
L 3.0
10ˆ9/L
5.0-10.0

Segmenters (eg.neutroph ils)


0.50
%
0.45-0.65

and chronic hemorrhage, leukemia, and chronic infection =primary and secondary
polycythemia, erythropoietinsecreting tumors, and renal disorders =leukopeniavi
ral infections, bone marrow depression due to drugs, radiation and primary bone
marrow disorders. =leukocytosisacute infection (degree depends on the severity
of infection, age, resistance, and presence of trauma, tissue necrosis or inflam
mation and hemorrhage). =neutropeniain acute bacterial infection, viral infecti
on, some parasitic infection, aplastic and pernicious anemia, anaphylactic shock
, and renal disease. =neutrophila-in acute localized and general bacterial infe
ction, gout and uremia,
Leukocytes functions as phagocytes of bacteria, fungi and viruses, detoxificatio
n of toxic proteins that may results from allergic reactions and cellular injury
, and immune systems.
Neutrophils are active phagocytes; number increases rapidly during short-term or
acute infection.
Date: July 30, 2009; 6 pm
Test
HEMATOCRIT
Resu lt
0.48
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
L 15
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: July 30, 2009; 6 pm
Test
HEMATOCRIT
Resu lt
0.48
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
hemodilution
=dehydration,
THROMBOCYTES
L 15
10ˆ9/ L
140-450
polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding diso
rders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly
tic anemia, etc.
Date: July 31, 2009; 2 am
Test
HEMATOCRIT
Resu lt
0.45
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
L 30
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: July 31, 2009; 8 am
Test
HEMATOCRIT
Resu lt
0.44
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
hemodilution
=dehydration,
THROMBOCYTES
L 32
10ˆ9/ L
140-450
polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding diso
rders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly
tic anemia, etc.
Date: July 31, 2009
Test
HEMATOCRIT
Resu lt
0.43
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
31
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: July 31, 2009; 8 pm
Test
HEMATOCRIT
Resu lt
0.40
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
hemodilution
=dehydration,
THROMBOCYTES
L 25
10ˆ9/ L
140-450
polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding diso
rders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly
tic anemia, etc.
Date: August 1, 2009; 8 pm
Test
HEMATOCRIT
Resu lt
L 0.37
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
L 40
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: August 1, 2009; 2 am
Test
Resu lt
Unit
Reference
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
HEMATOCRIT
0.41
%
M: 0.400.60 F: 0.8-0.4
hemodilution
=dehydration,
polycythemia or hemoconcentratio n
=thrombocytop
THROMBOCYTES
L 23
10ˆ9/ L
140-450
enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage,
inflammatory disease, hemolytic anemia, etc.
Date: August 1, 2009; 8 am
Test
HEMATOCRIT
Resu lt
L 0.31
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
L 17
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: August 1, 2009; 2 pm
Test
HEMATOCRIT
Resu lt
0.42
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
THROMBOCYTES
L 30
10ˆ9/ L
140-450
hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocyto
p enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage
, inflammatory disease, hemolytic anemia, etc.
Date: August 1, 2009; 8 pm
Test
Resu lt
L 0.37
Unit
Reference
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
HEMATOCRIT
%
M: 0.400.60 F: 0.8-0.4
hemodilution
=dehydration,
THROMBOCYTES
L 40
10ˆ9/ L
140-450
polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding diso
rders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly
tic anemia, etc.
Date: August 2, 2009; 2 am
Test
Resul t
L 0.37
Unit
Reference
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
HEMATOCRIT
%
M: 0.400.60 F: 0.8-0.4
hemodilution =dehydration, polycythemia or hemoconcentration
=thrombocytopeni
THROMBOCYT ES
L 49
10ˆ9/L
140-450
a, cause of bleeding disorders =thrombocytosis, occurs after hemorrhage, infl
ammatory disease, hemolytic anemia, etc.
Date: August 2, 2009
Test
Resu lt
L 0.38
Unit
Reference
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied by RB
C’s. Thrombocytes are needed for normal blood clotting; initiate clotting cascad
e by clinging to broken area; help control blood loss from broken blood vessels.
HEMATOCRIT
%
M: 0.400.60 F: 0.8-0.4
hemodilution
=dehydration,
THROMBOCYTES
L 64
10ˆ9/ L
140-450
polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding diso
rders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly
tic anemia, etc.
Date: August 2, 2009;6 pm
Test
HEMATOCRIT
Resu lt
L 0.35
Unit
%
Reference
M: 0.400.60 F: 0.8-0.4
Clinical Significance
=anemia or
Functions
Hematocrit is a measure of the proportion of blood volume that is occupied
hemodilution
=dehydration,
polycythemia or hemoconcentratio
THROMBOCYTES
L 70
10ˆ9/ L
140-450
n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs
after hemorrhage, inflammatory disease, hemolytic anemia, etc.
by RBC’s. Thrombocytes are needed for normal blood clotting; initiate clotting c
ascade by clinging to broken area; help control blood loss from broken blood ves
sels.
L EGEND :
H-High N-Normal; results within normal values are not necessarily marked with an
indicator L-Low SH-Slightly High
D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO C
ITY
HEMATOLOGY
Name: Mr. Canas Date: August 3, 2009 Age: 7 years old Room: Sex: Male Physician:
Dr. Ong
Test
Resul t
Unit
Reference
Clinical Significance
= anemia, liver
Functions
Hemoglobin is responsible for binding oxygen in the lungs and in transporting th
e bound oxygen throughout the body where it is used in aerobic metabolic pathway
s.
HEMOGLOBIN
L 107
g/dL
M:140-170 F:120-150
or kidney disease =primary and secondary polycythemia, COPD, CHF, burns
=anemia, acute
ERYTHROCYTES
N 4.11
10ˆ12/ L
4.0-6.0

LEUKOCYTE
N 5.0
10ˆ9/L
5.0-10.0

Segmenters (eg.neutroph ils)


L 0.27
%
0.45-0.65
and chronic hemorrhage, leukemia, and chronic infection =primary and secondary
polycythemia, erythropoietinsecreting tumors, and renal disorders =leukopeniavi
ral infections, bone marrow depression due to drugs, radiation and primary bone
marrow disorders. =leukocytosisacute infection (degree depends on the severity
of infection, age, resistance, and presence of trauma, tissue necrosis or inflam
mation and hemorrhage). =neutropeniain acute bacterial infection, viral infecti
on, some parasitic infection, aplastic and pernicious anemia, anaphylactic shock
, and renal disease. =neutrophila-in acute localized and general bacterial infe
ction, gout and uremia,
RBC’s transport oxygen bound to hemoglobin; also transports small amount of carb
on dioxide.
Leukocytes functions as phagocytes of bacteria, fungi and viruses, detoxificatio
n of toxic proteins that may results from allergic reactions and cellular injury
, and immune systems.
Neutrophils are active phagocytes; number increases rapidly during short-term or
acute infection.
D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO C
ITY
COAGULATION RESULT FORM
Name: Mr. Canas Date: August 3, 2009 Protime 11.1 Patient sec INR 0.85 Control 1
3.9 APTT Patient 47.7 sec Control 30.2 sec Normal: 1.0-1.2 Therapeutic: 2.0-3.0
Normal: 25-36 sec
Age: 7 years old Room:
Sex: Male Physician: Dr. Ong
D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO C
ITY
X-RAY RESULT
(This report is based on radiographic finding and must be correlated clinically)
Name: Mr. Canas Date: August 3, 2009
Age: 7 years old Room: 441-1
Sex: Male Physician: Dr. Ong
OR No.: 0414335 Room No.: 441-1 Report: The right lung is hazed. The left lung i
s clear. A small meniscoid density is appreciated within the right costophrenic
sulcus. Diaphragmatic outline are otherwise unremarkable. The heart is normal in
size. The rest of the included soft tissue shadows and osseous structures are u
nremarkable. Impression: Suggestive Minimal Pleural Effusion, Right
D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO C
ITY
URINALYSIS
Name: Mr. Canas Date: August 3, 2009 P HYSICAL E XAMINATION
C OLOR : T RANSPARENCY : straw, clear amber slightly cloudy
Age: 7 years old Room: 441-1 Sex: Male
R ENAL C ELLS : G LUCOSE A LBUMIN R EACTION
Physician: Dr. Ong
C HEMICAL E XAMINATION
(-) (+)
02/np+
M ICROSCOPIC E XAMINATION
P US
CELLS :
M UCUS T HREADS :
01/hpf (+)
S PECIFIC G RAVITY
6.0 1.02 0
I NTERPRETATIONS :
B ASIC T EST W/
NORMAL VALUES
I NTERPRETATION
Abnormal colored urine may be due to the presence of red blood cells (smoky),
bilurubin (brownish-yellow to yellow-green; melatonic tumor or Addision’s (black
), alkaptonuria (black) and pophyria (port wine). Normal: Pale yellow to amber
colored urine. Cloudy urine may indicate presence of pus (WBC’s), red blood cel
ls (RBC’s) or bacteria due to urinary tract infection or shreds. Normal: Clear
to slightly hazy Presence may indicate infection Normal: Negative or traces
P HYSICAL CHARACTERISTICS : O COLOR O CHARACTER

M ICROSCOPIC FINDINGS : O PUS CELLS O MUCUS THREADS O RENAL CELLS C HEMICAL CHAR
ACTERISTICS : O GLUCOSE O ALBUMIN O SPECIFIC GRAVITY

Increased amounts (glycosuria) in patients with diabetes mellitus, myocardial in


farction. Normal: Negative Large number indicates renal disease. Normal: Neg
ative or traces High specific gravity (above 1.025) can occur in diabetes mellit
us, increased secretion of ADH, nephrosis, CHF. Low specific gravity may occur i
n patient with diabetes insipidus, glomerulonephritis with pyelonephritis and se
vere renal damage. Normal: 1.015-1.025 with normal fluid intake
POSSIBLE MANAGEMENT/LAB TESTS
• Virus Isolation Viruses are obligate intracellular parasites that require livi
ng cells in order to replicate. Cultured cells, eggs and laboratory animals may
be used for virus isolation. Although embroyonated eggs and laboratory animals a
re very useful for the isolation of certain viruses, cell cultures are the sole
system for virus isolation in most laboratories. The development of methods for
cultivating animal cells has been essential to the progress of animal virology.
To prepare cell cultures, tissue fragments are first dissociated, usually with t
he aid of trypsin or collagenase. The cell suspension is then placed in a flatbo
ttomed glass or plastic container (petri dish, a flask, a bottle, test tube) tog
ether with a suitable liquid medium. e.g. Eagle s, and an animal serum. After a
variable lag, the cells will attach and spread on the bottom of the container an
d then start dividing, giving rise to a primary culture. Attachment to a solid s
upport is essential for the growth of normal cells. Primary and Secondary Cultur
es Primary cultures are maintained by changing the fluid 2 or 3 times a week. Wh
en the cultures become too crowded, the cells are detached from the vessel wall
by either trypsin or EDTA, and portions are used to initiate secondary cultures.
In both primary and secondary cultures, the cells retain some of the characteri
stics of the tissue from which they are derived. Cell Strains and Cell Lines Cel
ls from primary cultures can often be transferred serially a number of times. Th
e cells may then continue to multiply at a constant rate over many successive tr
ansfers. Eventually, after a number of transfers, the cells undergo culture sene
scence and cannot be transferred any longer. For human diploid cell cultures, th
e growth rate declines after about 50 duplications. During the multiplication of
the cell strain, some cells become altered in that they acquire a different mor
phology, grow faster, and become able to start a cell culture from a smaller num
ber of cells. These cells are immortalized and have an unlimited life-span. Howe
ver, they retain contact inhibition. Cell Cultures Cell cultures are separated i
nto 3 types:1. Primary cells - prepared directly from animal or human tissues an
d can be subcultured only once or twice e.g. primary monkey or baboon kidney 2.
Semi-continuous diploid cells - which are derived from human fetal tissue and ca
n be subcultured 20 to 50 times e.g. human diploid fibroblasts such as MRC-5 3.
Continuous cells - derived from tumours of human or animal tissue e.g. Vero, Hep
2 Cell cultures vary greatly in their susceptibility to different viruses. It is
of utmost importance that the most sensitive cell cultures are used for a parti
cular suspected virus. Specimens for cell culture should be transported to the l
aboratory as soon as possible upon being taken. Swabs should be put in a vial co
ntaining virus transport medium. Bodily fluids and tissues should be placed in a
sterile container. Upon receipt, the specimen is inoculated into several differ
ent types of cell culture depending on the nature of the specimen and the clinic
al
90 | P a g e
presentation. The maintenance media should be changed after 1 hour or if that is
not practicable, the next morning. The inoculated tubes should be incubated at
35-37oC in a rotating drum. Rotation is optimal for the isolation of respiratory
viruses and result in an earlier appearance of the CPE for many viruses. If sta
tionary tubes are used, it is critical that the culture tubes be positioned so t
hat the cell monolayer is bathed in nutrient medium. The inoculated tubes should
be read at least every other day for the presence of cytopathic effect. Certain
specimens, such as urine and faeces, may be toxic to cell cultures that may pro
duce a CPE-like effect. If toxic effects are extensive, it may be necessary to p
assage the inoculated cells. Cell cultures that are contaminated by bacteria sho
uld either be put up again or passed through a bacterial filter. Cell cultures s
hould be kept for at least one to two weeks (longer in the case of CMV). Cell cu
ltures should be refed with fresh maintenance medium at regular intervals or if
required should the culture medium become too acidic or alkaline. When CPE is se
en, it may be advisable to passage infected culture fluid into a fresh culture o
f the same cell type. For cell-associated viruses such as CMV and VZV, it is nec
essary to trypsinize and passage intact infected cells. Other viruses such as ad
enovirus can be subcultured after freezing and thawing infected cells.
Pre-test: a. Explain the procedure to the client/watcher. b. Explain that this t
est helps determine if the patient has anemia or polycythemia or assess response
to treatment. c. Inform the patient that the test requires a blood sample. d. I
nform the patient that there is no food or fluid restriction. During the test A.
Ensure that the blood is not taken from the hand or arm that has an intravenous
line. Hemodilution with intravenous fluids causes a false decrease in the value
s of some test. Post test: a) Apply pressure to the venipuncture site. b) After
applying pressure to the puncture site, tape a gauze pad firmly over it.
c) Watch for bleeding from the puncture site.
IgM ELISA test Primary dengue virus infection is characterized by elevations in
specific IgM antibody levels 3 to 5 days after the onset of symptoms; this gener
ally persists for 30 to 60 days. IgG levels also become elevated after 10 to 14
days and remain detectable for life. During secondary infection, IgM levels gene
rally rise more slowly and reach lower levels than in primary infection, while I
gG levels rise rapidly from 1 to 2 days after the onset of symptoms. Diluted pat
ient serum (serum diluent contains sorbent to remove rheumatoid factor and human
IgG interference) is added to wells coated with purified antigen. IgM specific
antibody, if present, binds to the antigen. All unbound materials are washed awa
y and the enzyme conjugate is added to bind to the antibody-antigen complex, if
present. Excess enzyme conjugate is washed off and substrate is added. The plate
is incubated to allow the hydrolysis of the substrate by the enzyme. The intens
ity of the color generated is proportional to the amount of IgM specific antibod
y in the sample. STORAGE AND STABILITY
91 | P a g e

1. 2. 3. 4.
Store the kit at 2-8 C. Keep microwells sealed in a dry bag with desiccants. Th
e reagents are stable until expiration of the kit. Do not expose test reagents t
o heat, sun or strong light.
WARNINGS AND PRECAUTIONS 1. Potential biohazardous materials: The calibrator and
controls contain human source components, which have been tested and found non-
reactive for hepatitis B surface antigen as well as HIV antibody with FDA licens
ed reagents. However, as there is no test method that can offer complete assuran
ce that HIV, Hepatitis B virus or other infectious agents are absent, these reag
ents should be handled at the Biosafety Level 2, as recommended in the Centers f
or Disease Control/National Institutes of Health manual, "Biosafety in Microbiol
ogical and Biomedical Laboratories." 1984. 2. Optimal results will be obtained b
y strict adherence to the test protocol. Precise pipetting as well as following
the exact time and temperature requirements is essential. 3. Do not pipette by m
outh. Do not smoke, eat, or drink in the areas in which specimens or kit reagent
s are handled. 4. The components in this kit are intended for use as an integral
unit. The components of different lots should not be mixed. 5. Control sera and
sample diluent contain preserved with sodium azide. Sodium azide may react with
lead and copper plumbing to form explosive metal azide. On disposal, flush with
a large volume of water. SPECIMEN COLLECTION AND HANDLING 1. Collect blood spec
imens and separate the serum. 2. Specimens may be refrigerated at 2–8 C for up
to seven days or frozen for up to six months. Avoid repetitive freezing and thaw
ing. REAGENT PREPARATION Prepare 1X Wash buffer by adding the contents of the bo
ttle (25 mL, 20X) to 475 mL of distilled or deionized water. Store at RT. PREPAR
ATION FOR ASSAY Bring all specimens and kit reagents to room temperature (20-25
C) and gently mix. ASSAY PROCEDURE 1. Place the desired number of coated strips
into the holder. 2. Negative control, positive control, and calibrator are read
y to use. Prepare 1:21 dilution of test samples, by adding 10 L of the sample t
o 200 L of sample diluent. Mix well. 3. Dispense 100 L of diluted sera, calibr
ator and controls into the appropriate wells. For the reagent blank, dispense 10
0 L sample diluent in
92 | P a g e
1A well position. Tap the holder to remove air bubbles from the liquid and mix w
ell. Incubate for 20 minutes at room temperature. 4. Remove liquid from all well
s. Wash wells three times with 300-350 L of 1X wash buffer. Blot on absorbance
paper or paper towel. 5. Dispense 100 L of enzyme conjugate to each well and in
cubate for 20 minutes at room temperature. 6. Remove enzyme conjugate from all w
ells. Wash wells three times with 300350 L of 1X wash buffer. Blot on absorbanc
e paper or paper towel 7. Dispense 100 L of TMB substrate and incubate for 10 m
inutes at room temperature. 8. Add 100 L of stop solution. 9. Read O.D. at 450
nm using ELISA reader within 15 min. A dual CALCULATION OF RESULTS 1. Check Cali
brator Factor (CF) value on the calibrator bottle. This value might vary from lo
t to lot. Make sure you check the value on every kit. 2. Calculate the cut-off v
alue: Calibrator OD x Calibrator Factor (CF). 3. Calculate the Ab (Antibody) Ind
ex of each determination by dividing the O.D. value of each sample by cut-off va
lue. QUALITY CONTROL The test run may be considered valid provided the following
criteria are met: 1. The O.D. of the Calibrator should be greater than 0.250. 2
. The Ab index for Negative control should be less than 0.9. 3. The Ab Index for
Positive control should be greater than 1.2. INTERPRETATION The following is in
tended as a guide to interpretation of Dengue virus IgM test results; each labor
atory is encouraged to establish its own criteria for test interpretation based
on sample populations encountered. Antibody Index Interpretation <0.9 No detecta
ble antibody to Dengue virus IgM by ELISA. 0.9-1.1 Borderline positive. Follow-u
p testing is recommend if clinically indicated. >1.1 Detectable antibody to Deng
ue virus IgM by ELISA. LIMITATIONS OF THE TEST 1. To enhance sensitivity and spe
cificity of this IgM test provided sample diluent has been formulated to block I
gG and Rheumatoid Factor (RF) interferences. Turbidity could be seen after dilut
ing serum with sample diluent. This turbidity is due to the blocking of serum Ig
G and has shown no interference with test results. It can be removed by centrifu
gation. 2. In specimens with high RF and high autoimmune antibodies, the possibi
lity of eliminating the interferences cannot be ruled out entirely. 3. The test
results obtained using this kit serve only as an aid to diagnosis and should be
interpreted in relation to the patient’s history, physical findings and other di
agnostic procedures. 4. Lipemic or hemolyzed samples may cause erroneous results
93 | P a g e
DRUG STUDIES
Generic name: Paracetamol (Acetaminophen) Brand name: Tempra Date ordered: July
30, 2009 Ordered dose: 250mg/5ml, 5ml q4 hrs, p.r.n for fever Classification: Ce
ntral Nervous System Agent; Narcotic Analgesic; Antipyretic Suggested dose: Fo
r mild to moderate pain, fever o Children ages 6-8 yrs old: 320 mg P.O. q 4-6 hr
s, p.r.n Therapeutic actions: Thought to produce analgesia by blocking pain im
pulses of prostaglandin in the CNS or of other substances that sensitize pain re
ceptors to stimulation. The drug may relieve fever through central action in the
hypothalamic heat-regulating center. Indications: Fever reduction Temporary
relief of mild to moderate pain Generally as substitute for aspirin when the
later is no tolerated or is contraindicated. Contraindications and cautions: H
ypersensitivity to acetaminophen or phenacin Long term alcohol use (may cause
hepatotoxicity) Children < 3 years old unless directed by a physician Malnut
rition Thrombocytopenia Arthritic or rheumatoid conditions affecting childre
n < 12 years old Safety during pregnancy (category B) or lactation is not esta
blished. Adverse effects: Hematologic: hemolytic anemia, leukopenia, pancytope
nia, neutropenia Hepatic: jaundice Metabolic: hypoglycemia Skin: rash, urt
icaria Interactions: Nursing considerations: Monitor for s/s of: o hepatotoxic
ity, even with moderate acetaminophen doses, especially in individuals with poor
nutrition or who have ingested alcohol over prolonged periods o poisoning, usua
lly from accidental ingestion or suicide attempts o Potential abuse from psychol
ogical dependence (withdrawal has been associated with restless and excited resp
onses). The drug should not be taken with other medication (e.g. cold preparat
ions) containing acetaminophen without medical advice; overdosing and chronic us
e can cause liver damage without consulting a physician Advise client not to s
elf medicate for pain more than 10 days (5 days in children) without consulting
a physician. This medication should not be used without medical direction for:
fever persisting longer than 3 days, fever over 39.5 °C (103°F), or recurrent f
ever.
Do not give children more than 5 doses in 24 hrs unless prescribed by a physic
ian. Advise clients/patients not to breast feed while taking this drug without
consulting physician. Effects on Laboratory Results: May decrease glucose and
hemoglobin levels and hematocrit. May decrease neutrophil, WBC, RBC, and plat
elet counts. May cause false-positive result for urinary 5-hydroxyindoleacetic
acid. May falsely decrease glucose level in home monitoring systems. Teaching p
oints: Tell parents to cosult prescriber before giving drug to childen younger
than age 2. Advise parents that drug is only for short-term use; urge them to
consult prescriber if giving to children for more than 5 days and for adults lo
nger than 10 days. ALERT: Advise patient or caregiver that many OTC products c
ontain acetaminophen and should be counted when calculating total dose. Tell p
arent not to use for marked fever (temperature higher than 39.5°C), fever persis
ting longer than 3 days, or recurrent fever unless directed by prescriber. ALE
RT: Warn patient that high doses or unsupervised long-term use can cause liver d
amage. Excessive alcohol use may increase the risk of liver damage. Caution long
-term alcoholics to limit drug to 2 g/day or less. Tell breast-feeding women t
hat drug appears in breast milk in low levels (< 1% of dose). Drug may be used s
afely if therapy is short-term and doesn’t exceed recommended doses. Generic nam
e: Famotidine Brand name: Famotidine: Pepcid, Pepcid AC (nonprescription) Classi
fication: H2 receptor antagonist Date ordered: July 30, 2009 Ordered dose: 17 mg
, t.i.d Suggested dose: • Short-term treatment for benign gastric ulcer o Childr
en ages 1-16: 0.5 mg/kg/day P.O. at bedtime or divided b.i.d., up to 40 mg daily
. • Gastroesophageal reflux disease ( GERD) o Children ages 1-16: 1mg/kg/day P.O
. divided twice daily up to 40 mg b.i.d. Therapeutic action: Competitively inh
ibits the action of antihistamine on the H2 at the receptor sites of parietal ce
lls, decreasing gastric acid secretions. Indications: Effective treatment of G
ERD and Peptic Ulcers in children (FAMOTIDINE ONLY) Effective treatment of Pep
tic Ulcer Disease: relief of symptoms, acceleration of healing, prevention of re
currence Control of Hypersecretory Stomach Disorders Treatment of Reflux Eso
phagitis Treatment of Heartburn
Prevention of Heartburn Contraindications and cautions: Contraindicated in p
atients hypersensitive to the drug. Ulcer rebound/perforation may occur if dru
gs are stopped abruptly when being used to treat ulcers. Once medicines are st
opped, immediate contact of the physician must be done. Use of these medicines
and symptom relief does not absolutely remove the possibility of gastric malign
ancy. Adverse effects: Drug-induced hepatitis Bone marrow depression (Lowere
d white blood cells or hemoglobin),rare Confusion (particularly in compromised
elderly with some of these drugs) Low blood platelet counts (all the above ar
e case report to rare effects) Abnormal heart rhythm changes (slow heart beat
or atrioventricular block) Bronchospasm, rare Impotence Interactions: None
significant. Nursing considerations: Assess patient for abdominal pain. Look
for blood in emesis, stool or gastric aspirate. Oral suspension must be recons
tituted and shaken before use. Store reconstituted oral suspension below 30°C.
Effects on Laboratory Results: Blood platelet counts: may be decreased by all
histamine (H2) blockers. Complete blood counts: rare with white blood cell (g
ranulocytes) decrease. Liver enzymes (SGPT, OT, etc.): can be increased with l
iver damage. May increase BUN and creatinine. May cause false negative-resul
ts in skin tests using allergen extracts. May antagonize pentagastrin in gastric
acid secretion tests. Teaching points: Instruct patient in proper use of OTC
product if appropriate. Warn patient with PKU that Peptic AC chewable tablets
contain phenylalanine. Tell patient to take prescription drug with a snack, if
desired. Remind patient that prescription drugs most effective is taken at be
dtime. Tell patient taking 20 mg twice daily to take one dose at bedtime. Advi
se patient to limit use of prescription drug no longer than 8 weeks, unless orde
red by the prescriber, and OTC drug no longer than 2 weeks. With prescriber’s
knowledge. Let patient take antacids together especially at the beginning of the
rapy when pain is severe. Urge patient to avoid cigarette smoking because it m
ay increase gastric acid secretion and worsen disease. Advise patient to repor
t abdominal pain or blood in stools or vomit. Generic name: Furosemide Brand nam
e: Furosemide Classification: Loop diuretic
Date ordered: July 31, 2009 Ordered dose: 10.0 mg slow IVTT(single order stat) T
herapeutic actions: A potent drug that inhibits sodium and chloride reabsorpti
on at the proximal distal tubules and the ascending loop of Henle. Indication:
Acute pulmonary edema Edema Hypertension Contraindications and cautions:
Contraindicated in patients hypersensitive to the drug and those with anuria.
Use cautiously in patients with hepatic cirrhosis and those in allergic to sulfo
namides. Use during pregnancy only if potential benefits to mother clearly outwe
igh risks to fetus. Adverse effects: CNS: vertigo, headache, dizziness, parest
hesia, weakness, restlessness, fever. CV: orthostatic hypotension, thrombophle
bitits with I.V. administration. EENT: transient deafness, blurred or yellowed
vision, tinnitus. GI: abdominal discomfort and pain, diarrhea, anorexia, naus
ea, vomiting, constipation, pancreatitis. GU: nocturia, polyuria frequent urin
ation, oliguria. Hematologic: agranulocytosis, aplastic anemia, leukopenia, th
rombocytopenia, azotemia, anemia. Hepatic: hepatic dysfunction, jaundice. Me
tabolic: volume depletion and dehydration, asymptomatic hyperurecemia, impaired
glucose tolerance, hypokalemia, hypochloremic alkalosis, hyperglycemia, dilution
al hyponatremia, hypocalcemia, hypomagnesemia. Musculoskeletal: muscle spasm.
Skin: dermatitis, purport, photosensitivity reactions, transient pain at I.M.
injection site. Other: gout. Interactions: Drug-drug: o Amino glycoside anti
biotics, cisplatin: may increase ototoxicity. Use together cautiously. o Amphote
ricin B, corticosteroids, corticotrophin, metolazone: may increase risk of hypok
alemia. Monitor potassium level closely. o Ant diabetics: may decrease hypoglyce
mic effects. Monitor glucose level. o Antihypertensive: may increase risk of hyp
otension. Use together cautiously. Decrease antihypertensive dose if needed. o C
ardiac glycosides, neuromuscular blockers: may increase toxicity of these drugs
from furosemide induced hypokalemia. Monitor potassium level. o Chlorothiazide,
chlorthalidone, hydrochlorothiazide, indapamide, metolazone: may cause excessive
diuretic response, causing serious electrolyte abnormalities or dehydration. Ad
just doses carefully and monitor patient for signs and symptoms of excessive diu
retic response.
Ethacrynic acid: may increase risk of ototoxicity. Avoid using together. Lithium
: may decrease lithium excretion resulting in lithium toxicity. Monitor lithium
level. o NSAIDS: may inhibit diuretic response. Use together cautiously. o Pheny
toin: may inhibit diuretic effect of furosemide. Use together cautiously. o Prop
anolol: may increase propanolol level. Monitor patient closely. o Salicylates: m
ay cause salicylate toxicity. Use together cautiously. o Sucralfate: may reduce
diuretic and hypertensive effect. Discourage use together. Separate doses by 2 h
rs. Drug-herb: o Aloe: may increase drug effect. Discourage use together. o Da
ndelion: may interfere with drug activity. Discourage use together. o Ginseng: m
ay decrease drug effect. Discourage use together. o Licorice: may cause unexpect
ed rapid potassium loss. Discourage use together. Drug-lifestyle: o Sun exposu
re: may increase risk for photosensitivity reactions. Advise patient to avoid ex
cessive sunlight exposure. Nursing considerations: To prevent nocturia, give P
.O. and I.M. preparations in the morning. Give second dose early in the afternoo
n. ALERT: Monitor weight, blood pressure, and pulse rate routinely with longte
rm use and during rapid dieresis. Use can lead to profound water and electrolyte
depletion. If oliguria or azotemia develops or increases, drug may need to be
stopped. Monitor fluid intake and output and electrolyte, BUN, and carbon dio
xide levels frequently. Watch for signs of hypokalemia, such as muscle weaknes
s and cramps. Consult prescriber and dietitian about a high-potassium diet or
potassium supplements. Foods rich in potassium include citrus fruits, tomatoes,
bananas, dates and apricots. Monitor glucose level in diabetic patients. Dru
gs may not be well absorbed orally in patient with severe heart failure. Drug ma
y need to be given I.V. even if patient is taking other oral drugs. Teaching poi
nts: Advise patient to take drug with food to prevent GI upset, and to take dr
ug in the morning to prevent the frequent need to urinate at night. If patient n
eeds second dose, tell him or her to take it early in the afternoon, 6-8 hrs aft
er morning dose. Inform patient of possible need for potassium or magnesium su
pplements. Instruct patient to stand slowly to prevent orthostatic dizziness,
and to limit alcohol intake and stenous exercise in hot weather to avoid worseni
ng dizziness upon standing quickly. Advise patient to immediately report ringi
ng in the ears, severe abdominal pain, or sore throat and fever, these symptoms
may indicate toxicity. ALERT: Discourage patient from storing different types
of drugs in the same container, increasing risk of drug errors. The most popular
strengths of this drug and digoxin are white tablets about equal in size. Tel
l patient to check with prescriber or pharmacist before taking OTC drugs.
o o
Teach patient to avoid direct sunlight and to use protective clothing and a su
n block because of risk of photosensitivity. Generic name: Diphenhydramine Hydro
chloride Brand name: Benadryl Classification: Ethanolamine derivative Date order
ed: August 1, 2009 Ordered dose: 17 g slow IVTT Therapeutic actions: Competes
with histamine for H1-receptor sites. Prevents but does not reverse, histamine-m
ediated responses, particularly those of the bronchial tubes, GI tract, uterus,
and blood vessels. Structurally related to local anesthetics, drug provides loca
l anesthesia and suppresses cough reflex. Indication: Rhinitis, allergy sympto
ms, motion sickness, Parkinson disease Sedation Nighttime sleep aid Nonpro
ductive cough Contraindications and cautions: Contraindicated in patients hype
rsensitive to the drug; newborns; premature neonates; breast-feeding women; pati
ents with angle-closure glaucoma, stenosing peptic ulcer, symptomatic prostatic
hypertrophy, bladder neck obstruction; and those having an acute asthmatic attac
k. Avoid use in patients taking MAO inhibitors. Use with caution in patients
with prostatic hyperplasia, asthma, COPD, increased intraocular pressure, hyper
thyroidism, CV disease, and hypertension. Children younger than age 12 should
use drug only as directed by the prescriber. Adverse effects: CNS: drowsiness,
sedation, sleepiness, incoordination, seizures, confusion, insomnia, headache,
vertigo, fatigue, restlessness, tremor, nervousness. CV: palpitations, hypoten
sion, tachycardia. EENT: diplopia, blurred vision, nasal congestion, tinnitus.
GI: dry mouth, nausea, epigastric distress, vomiting, diarrhea, constipation,
anorexia. GU: dysuria, urine retention, urinary frequency. Hematologic: thr
ombocytopenia, agranulocytosis, hemolytic anemia. Respiratory: thickening of b
ronchial secretions. Skin: urticaria, photosensitivity, rash. Other: anaphyl
actic shock. Interactions: Drug-drug: o Aspirin/NSAIDs (e.g., ibuprofen), anti
coagulants ("blood thinners" such as warfarin or heparin), aminocaproic acid, fa
ctor IX complex, antiinhibitor coagulant concentrates, drugs that can cause bloo
d clots (e.g., estrogens or birth control pills). Nursing considerations: To p
revent nocturia, give P.O. and I.M. preparations in the morning. Give second dos
e early in the afternoon.
ALERT: Monitor weight, blood pressure, and pulse rate routinely with longterm
use and during rapid dieresis. Use can lead to profound water and electrolyte de
pletion. If oliguria or azotemia develops or increases, drug may need to be st
opped. Monitor fluid intake and output and electrolyte, BUN, and carbon dioxid
e levels frequently. Watch for signs of hypokalemia, such as muscle weakness a
nd cramps. Consult prescriber and dietitian about a high-potassium diet or pot
assium supplements. Foods rich in potassium include citrus fruits, tomatoes, ban
anas, dates and apricots. Monitor glucose level in diabetic patients. Drugs
may not be well absorbed orally in patient with severe heart failure. Drug may n
eed to be given I.V. even if patient is taking other oral drugs. IV Administrati
on: Make sure the site is patent. Infiltration causes irritation. Don’t exce
ed 25mg/minute. Teaching points: Warn patient no to take drug with any other p
roducts that contain diphenhydramine (including topical therapy) because of incr
eased adverse reactions. Insturct patient to take drug 30 mins before travel t
o prevent motion sickness. Tell patient to take the drug with food or milk to
reduce gastric distress. Warn patient to avoid alcohol and hazardous activitie
s that require alertness until CNS effects of durg are known. Tell patients th
at coffee or tea may reduce drowsiness. Irge caution if palpitations develop.
Inform patient that sugarless gum, hard candy or ice chips may relieve dry mouth
. Tell patient to notify prescriber if tolerance develops because a different
antihistamine may be required.
Generic name: Tranexamic Acid Brand name: Cyklokapron Date ordered: August 2, 20
09 Ordered dose: 15 mg t.i.d Classification: Antifibrinolytic, antihemorrhagic S
uggested dose: For mild to moderate pain, fever o Children ages 6-8 yrs old: 3
20 mg P.O. q 4-6 hrs, p.r.n Therapeutic actions: Tranexamic acid competitively
inhibits activation of plasminogen, thereby reducing conversion of plasminogen
to plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and
other plasma proteins, including the procoagulant factors V and VIII. Tranexami
c acid also directly inhibits plasmin activity, but higher doses are required th
an are needed to reduce plasmin formation. In vitro, the antifibrinolytic potenc
y of tranexamic acid is approximately 5 to 10 times that of aminocaproic acid.
In patients with hereditary angioedema, inhibition of the formation and activit
y of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing
plasmin-induced activation of the first complement protein. Indications: Contr
aindications and cautions: Intravascular clotting, active (risk of serious, ev
en fatal, thrombus formation) Defective color vision, acquired (condition prec
ludes assessment of color vision, which may be required to determine toxicity)
Hematuria of upper urinary tract origin (risk of intrarenal obstruction seconda
ry to clot retention in the renal pelvis and ureters if hematuria is massive; al
so, if hematuria is associated with a disease of the renal parenchyma, intravasc
ular precipitation of fibrin may occur and exacerbate the disease) Hemorrhage,
subarachnoid (increased risk of cerebral edema and cerebral infarction) Renal
function impairment (medication may accumulate; dosage adjustment based on the
degree of impairment is recommended) Sensitivity to tranexamic acid, history o
f Thrombosis, predisposition to or history of (medication inhibits clot dissol
ution and may interfere with mechanisms for maintaining blood vessel patency; it
is recommended that tranexamic acid be administered in conjunction with anticoa
gulant therapy, if at all) Adverse effects: Blurred vision or other changes in
vision hypotension (dizziness or lightheadedness; unusual tiredness or weakne
ss)— may be associated with too-rapid intravenous administration thrombosis or
thromboembolism (pains in chest, groin, or legs [especially calves]; severe, su
dden headache; sudden and unexplained shortness of breath, slurred speech, visio
n changes, and/or weakness or numbness in arm or leg; sudden loss of coordinatio
n)—depending on site of thrombus formation or embolization Diarrhea
Nausea vomiting Incidence unknown Unusual menstrual discomfort —caused b
y clotting of menstrual fluid Interactions: Anti-inhibitor coagulant complex o
r Factor IX complex (although tranexamic acid is often used in conjunction with
clotting factor replacement for the perisurgical management of hemophilic patien
ts, concurrent use may increase the risk of thrombotic complications.) Contrac
eptives, estrogen-containing, oral or Estrogens (concurrent use with tranexamic
acid may increase the potential for thrombus formation) Thrombolytic agents (t
he actions of tranexamic acid and of thrombolytic agents [e.g., alteplase (tissu
e-type plasminogen activator, recombinant; tPA), anistreplase (anisoylated plasm
inogen-streptokinase activator complex; APSAC), streptokinase, or urokinase] are
mutually antagonistic; although controlled studies to demonstrate its efficacy
have not been done in humans, tranexamic acid may be useful in treating severe h
emorrhage caused by a thrombolytic agent. Nursing considerations: Antifibrinol
ytic agents are ineffective in bleeding caused by loss of vascular integrity; a
definite clinical diagnosis or confirmation of hyperfibrinolysis (hyperplasminem
ia) via laboratory studies is required before tranexamic acid is used to treat h
emorrhage. Carcinogenicity/Tumorigenicity Pregnancy—Tranexamic acid crosses
the placenta. Breast-feeding-tranexamic acid is distributed into breast milk;
concentrations reach approximately 1% of the maternal plasma concentration Oph
thalmological examinations, including tests for visual acuity, color vision, eye
ground, and visual fields
MANAGEMENT
Medical Management Actual Medical Management MEDICAL ORDER RATIONALE July 30, 20
09; 1:20 pm

Please admit Diet for age except dark color foods VS q hour and record

To provide good nutrition of the patient. No special diet may prevent the condit
ion. May take food as tolerated and to monitor blood loss through the GI tract.
To monitor patient’s vital signs: blood pressure, temperature, cardiac rate and
respiratory rate. And to monitor if there is sign for potential shock or bleedin
g. Complete Blood Count - to identify persons who may have an infection and to i
dentify acute and chronic illness, bleeding tendencies, and white blood cell dis
orders such as leukemia Urinalysis – for routine urine analysis; to check for pr
esence of pus, blood, sugar, albumin, and the like in the urine; to check specif
ic gravity and pH of urine. Blood typing- it is to assess the what specific anti
gen are present to the blood of the patient and if it is Rh negative or positive
. It is an efficient and effective method of supplying fluids directly into the
intravascular fluid compartment and replacing electrolyte losses. PLR is an isot
onic solution which is good for hydrating the patient.

Dx: CBC, blood typing and U/A, X-ray For repeat platelet and hematocrit on July
31, 2009 @ 2 am

Fast drip PLR 150 cc now and recheck BP = 80/50

Meds: 1. Famotidine 17 mg tid 2. Paracetamol 250mg/5ml 4.5ml q4° prn

CBR without BRP I and O q shift and record Refer for BP less than 90/60, weak pu
lse, and other unusualities.
An antacid that reduces gastric acid by binding with phosphate in the intestin
e, and then is excreted as aluminum carbonate in feces. Inhibits the synthesis
of prostaglandins that may serve as mediators of pain and fever, primarily in t
he CNS. This provides measure of safety. Accurate measurement is essential i
n detecting negative fluid balance. These unusualities are indicative of an im
pending danger on the patient’s physiological status
Stand by O2 tank @ bedside 11:45am • Followed up D5INB 1L @ 90cc/hour July 31, 2
009; 9:10 am • Repeat platelet and hematocrit at 8am • IVF to follow D5IMB 1L @
90cc/hour

In case, shock will occur, there is supplementation of oxygen. Maintaining adequ


ate circulating blood volume is a priority.

Specific deficiencies guide treatment therapy.



Decrease IV rate to 70cc/hour • Repeat platelet and hematocrit @8 pm, 4pm and at
2 am tomorrow August 1, 2009 • Furosemide (single order stat) 10.0 mg slow iVtt
-initial 7 and repeat platelet and hematocrit @ 8 am, 2pm, and 8 pm today • Ref
er for any unusualities August 2, 2009 • Decrease IVF rate to 30 cc/hour • IVF t
o follow D5IMB 500 cc @ 30 cc/hour • Repeat platelet and hematocrit @ 2 am, 8 am
and 6 pm today until stabilized • VSq4 August 3, 2009 • Decrease IVF rate to KV
O for C/D • Repeat CBC • VSq4, I/Oqshift August 4, 2009 • Home med: Zeeplus 5ml
once a day
A potent drug that inhibits sodium and chloride reabsorption at the proximal d
istal tubules and the ascending loop of Henle. Effective in treating pulmonary e
dema.

To maintain health, the balance of fluids and electrolytes in the intracellular


and extracellular spaces needs to remain relatively constant. IV therapy that pr
ovides the patient of the sustaining fluids, electrolytes and medications offers
the advantages of immediate and predictable therapeutic effects To monitor the
condition of the patient. It is also to check improvement with the client.

The patient’s condition has improved and does not need an intravenous fluid supp
lement anymore.

This formulation combines the synergistic effects of vitamin C and zinc in enhan
cing the immune function, in promoting wound healing and tissue repair and in op
timizing longitudinal growth.
To evaluate patient’s condition and check for improvement

Follow up in 7 days

Possible Medical Management Blood Transfusion


It is the introduction of whole blood or components of blood such as plasma, ser
um, erythrocytes or platelets into the venous circulation. This is to restore or
increase circulating blood volume after surgery, trauma, and child birth. It is
also to restore or increase the red blood cell after severe or chronic anemia,
maintain blood hemoglobin levels such as leukemia and to increase platelet count
for thrombocytopenia. Types of blood and blood products and indications for use
:
Type Whole blood type (type A,B,AB, O and /or Indications To treat volume defici
encies for example
RH+ or RH-)
Packed red cells (High hematocrit since approximately 80% of the plasma is remov
ed) Platelets
Albumin
Prothrombin complex contains factors VII, IX, and XI and prothrombin Factors VII
I Fibrinogen preparations
in acute hemorrhage, not indicated for chronic anemia. To expand blood volume, t
o restore circulation and renal blood flow when plasma volume is decrease when t
he red cell mass is adequate, as in acute dehydration or burns, to replace defic
ient coagulation factors in bleeding disorders. Used when the blood volume is ad
equate but the red cell mass is inadequate, as in chronic anemia. For patients w
ith severe thrombocytopenia (reduced platelets) Replaces platelets for example i
n Dengue hemorrhagic fever. To expand the blood volume rapidly when blood volume
is reduced in shock or burns; also to increase level of albumin in patients wit
h hypoalbuminemia. Used for bleeding associated with deficiencies with these fac
tors. For hemophiliacs Caution: May transmit infection, transfuse with filter. U
sed particularly for bleeding especially associated with congenital hypofibrinog
enemia.
NURSING CARE PLANS
DISCHARGE PLANNING
DISCHARGE PLAN
Medication Present to the significant other all take home medications. Give emph
asis to the brand and generic name, therapeutic and side effects as well as its
daily dose and proper route. ® This will lessen the anxiety and will encourage t
he proper compliance of the drug • Educate the significant other to avoid taking
medications that are not prescribed by the physician. Motivate the patient and
the family as well, to seek for physician’s medical advices if there are unusual
ities felt before continuing taking the medicines. ® Over the counter drugs may
interfere with the effectiveness of the prescribed drugs. It can also harm the p
atient if the drug is contraindicated • Inform the family to seek medical help i
mmediately if adverse reactions or allergies occur. ® To prevent further complic
ations and enables the physician to directly intervene untoward reactions to the
drug Exercise Instruct the client not to engage in very strenuous activities. ®
To avoid injury and to restore energy and promotes comfort and healing Treatmen
t • • • • Encourage the patient to participate diligently in the treatment modal
ities advised to him by the physician. ® To hasten the improvement of her health
status Encourage the patient to verbalize honest information to the physician a
nd other health care provider. ® To aid accurate detection of a disease and earl
y medical intervention Tell the family that they should take part on the treatme
nt of the patient. ® To strengthen the support system of the client Inform the p
atient and her family not self-medicate, especially when unusualities occur. ®Ce
rtain drugs are contraindicated to his case. • •
Hygiene • • • Instruct the patient to take a bath regularly. ® To prevent the ri
sk of infection and promote comfort Instruct the parents to close the container
when they collect water. ® Clean water is conducive for formation of eggs. Instr
uct parents to clean the surroundings and spray insecticides. ® To prevent occur
rence.
Out-patient orders • Instruct to take the medications as ordered.
• Diet • •
® Compliance would help in the recovery of the disease Follow up check up after
1 week. ® To check patient’s recovery.
Encourage to eat a well balanced diet. ® To avoid too much intake or less intake
of one or more substance Instruct to increase intake of carbohydrates and incre
ase protein intake ® To have enough energy with carbohydrates.
PROGNOSIS
PROGNOSIS
Poor Fair Good 1 2 3 Justification
The patient experienced fever and on the third day with vomiting, then the fever
subsides. After a week pain occurred.

The patient was not diagnosed at an early stage. The patient only went to the ho
spital when he experie

Predisposing factor such as the poor environmental condition is observed The pat
ient took the prescribed medicines and complied with all the necessary diagnosti
c procedures. The patient’s immune system is not that fully developed. In his ag
e, he is more prone to infection and

The patient has a poor environment because the canal is situated near their hous
e and most of the tim mosquitoes and other vectors. The patient was accompanie
d by his parents all the time and was well taken care of by his family.
4 2 6 14
12 /7=1.71
General Prognosis
The general prognosis of the patient is fair. Four out of the seven criteria und
er the specific/detailed prognosis has showed poor forecast and one is justified
as fair and two are justified as good. Based from the gathered data, the patien
t had not gone to the hospital when his fever was recurring. The patient only we
nt to the hospital when he experienced abdominal pain, thus he was not early dia
gnosed of dengue.
BIBLIOGRAPHY:
• • • •

• • •
http://www.drugs.com/mmx/tranexamic-acid.html http://www.wikipedia.com http://ww
w.ehow.com/about_4674809_pathophysiology_dengue_hemor rhagic.fever.html http://e
n.wikipedia.org/wiki/Circulatory_system http://en.wikipedia.org/wiki/Pulmonary_c
irculation http://chestofbooks.com/health/body/massage/Margaret-DPalmer/Lessons-
on-Massage/The-Portal-Circulation.html http://www.innerbody.com/image/lympov.htm
l Doenges, Moorhouse, Murr.Nurse’s Pocket Guide Diagnoses, Rationales and Interv
entions 9th Ed.