Title Page d Avao m Edical s

8/14/2019 Title Page d Avao m Edical s

1/98

TITLE PAGED AVAO M EDICAL S CHOOL F OUNDATIONMEDICAL DRIVE, BAJADA DAVAO CITY

IN PARTIAL FULFILLMENT OF THE REQUIREMENTS NCM 101-RLESUBMITTED TO: ROXANNE ACERO, RN SUBMITTED BY: ABRACIA, JAMES ARANDIA, ALESSA ANQUE, JOANNA GRACE RUBY ALCAZARIN, IRENE LOU BELARMINO, ANGELINE BENDULO, VANESSA

BUTT, KANVAL CAPILITAN, CYRIL CASTILLO, JIRO DELFINADO, REGINE DE LEON, ANGELICA

IN


2/98

TABLE

OF

CONTENTS

Title Page......................................................................

..........................................................1 Acknowledgement.....

................................................................................

..............................4 Introduction....................................

................................................................................

.........5 Objectives...........................................................

....................................................................6 General Objective: ..............................................................................................................6 Specific Objectives:..............................................................................................................6 Patients Profile.......................................................................................................................7 PERSONALDATA............................................................................

.........................................8 MEDICAL DATA.........................................................................................................

............8 Genogram..........................................................

.....................................................................9 Health History.......................................................................................................................12 Past Health History.............................................................................................................13 History of Present Illness....................................................................................................13 Complete Definition of Final Diagnosis.................................................................................14 Developmental Data..............................................................................................................15Erickson........................................................................

.....................................................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 Symptomatology...............................................................................................32 SYMPTOMATOLOGY.........................................................................................................33 Pathophysiology...................................................................................................................34 ..........................................................................................................................

..............34 Medical, Pharmacologic and Diagnostic Exams....................

.................................................41 Hematology..................

................................................................................


3/98

...................42


4/98

Hematology.....................................................................................................................52 Coagulation Result Form.................................................................................................55 X-Ray Result....................................................................................................................56 Urinalysis........................................................................................................................57 Possible Management/Lab Tests..............

..........................................................................90 Drug Studies..........................................................................................................................95 Management.......................................................................................................................106 ............................................................................................................................................110 Nursing Care Plans..............................................................................................................110 Discharge Planning..............................................................................................................114 Prognosis.............................................................................................................................117 Bibliography:......................................................

.................................................................119


5/98

ACKNOWLEDGEMENT

We, the members of the Group 1 section A of the 3rd year nursing students of theDavao Medical School Foundation would like to extend our acknowledgement to thefollowing persons: first is for our clinical instructor, Maam Roxanne G. Acerofor continuously guiding us in all our efforts and tirelessly committing her time 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 inall medical and nursing interventions done to them and all health teachings wehave rendered.


6/98

INTRODUCTIONDengue fever is an acute febrile infectious disease, caused by all four serotypes (1, 2, 3 or 4) of a virus from genus Flavivirus, called dengue virus. Its themost prevalent flavivirus infection of humans, with a worldwide distribution inthe tropics and warm areas of the temperate zone corresponding to that of the principal vector, Aedes aegypti. When simultaneous or sequential introduction oftwo 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 is not the presence of hemorrhagic manifestations, but the abrupt increase of capillary permeability, with diffuse capillary leakage of plasma, hemoconcentrationand, in some cases, with non-hemorrhagic hypovolemic shock (dengue shock syndrome).


7/98

OBJECTIVESGENERAL OBJECTIVE: To present a case of Dengue Hemorrhagic Fever

SPECIFIC OBJECTIVES: 1) To discuss the family profile of Canas 2.) To present the index case with Dengue Hemorrhagic Fever 3) To discuss briefly DHF 4) To establish the family diagnosis, intervention and recommendation using family assessment tools


8/98

PATIENTS PROFILE


9/98

PERSONAL DATAName: Richielou Dave Canas Address: Block 45 Fatima Village Bajada Davao City Sex: Male Age: 7 yrs. old Birth Date: February 21, 2002 Birth Place: Davao City Religion: Roman Catholic Nationality: Filipino Ordinal Status: Eldest Occupation:Student Year level: Grade 1 in Holy Cross of Bajada Types of Community: Urban Civil Status: Single Fathers Name: Romulus Canas Occupation: Chief in Insular Hotel Mothers Name: Michelle Canas Occupation: Housewife Income: 10, 000 pesos S

ocioeconomic: Middle Class

MEDICAL DATADate of Admission: July 30, 2009 Time of Admission: 1:05 pm How Admitted: Wheelchair Ward: St. Anthony Ward Room and Bed #: 426-bed 3 Chief Complain: AbdominalPain Attending Physician: Dr. Ong Impression /Tentative Diagnosis: Suggestive minimal pleural effusion, right Final Diagnosis: Dengue Hemorrhagic Fever Date andTime of Discharge: August 04, 2009 @ 3:00 pm


10/98

GENOGRAM


11/98


12/98

Narrative Genogram On the paternal side of our client, his Grandfather Mr. Ricardo Destajo due to heart disease at the age of 35 years old, his wife Maricel Destajo is 56 yrs old and known to have hypertension. Mr. Ricardo and Mrs. MaricelDestajo had three children namely: Mrs. Michelle our clients mother, Ms. Rochelle, and Ms. Princess. Mrs. Michelle


13/98

HEALTH HISTORY


14/98

PAST HEALTH HISTORYRichielous Dave Canas was delivered via NSVD without any complications. He was able to experience common illness like mumps at the age of 7. He was being breastfed by his mother for only 2 days. According to the doctors record there was immunization taken; 1 BCG done; 3 doses for DPT; 3 doses for OPV; 3 doses for Hepaand 1 dose for measles. There is no prenatal infection and no exposures any drugs/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 interminent fever. Condition temporarily relieved by intake of Paracetamol 5mkd. Problem 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 admission, persistence of abdominal pain prompted consult.


15/98

COMPLETE DEFINITION OF FINAL DIAGNOSIS


16/98

DEVELOPMENTAL

DATA


17/98

ERICKSON Erik Ericksons Stages of Psychosocial TheoryEricksons theory of psychosocial development is one of the best-known theoriesof personality. Similar to Freud, Erickson believed that personality develops ina series of stages. Unlike Freuds theory of psychosocial stages, Ericksons theory describes the impact of social experience across the whole lifespan. The Eriksons 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. Guilt (purpose) Industry vs. Inferiority (competence) Identity vs. Role Confusion (fidelity) Intimacy vs. Isolation (love) Generativity vs. Stagnation (caring) EgoIntegrity 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). Hecan recognize major disparities in personal abilities relative to other children. He also feels a sense of shame if his parents unthinkingly share his failureswith others. Children who cannot master their school work may consider themselves a failure and feelings of inferiority may arise.

HAVIGURSTRobert Havighursts developmental Physiological theory Robert Havighurst believed that learning is basic to life and that people continue to learn throughout life. He described growth and development as occurring during stages, each associated 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 latertasks, while failure leads to unhappiness in the individual. Havighurst identified Six Major Stages in human life covering birth to old age. Infancy & early childhood (Birth till 6 years old) Middle childhood (6-12 years 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 expectedtasks 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 andphysical activities that are highly valued in childhood such skills as throwingand catching, kicking, tumbling, swimming, and handling simple tools.


18/98

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. toward social

He learned the give-and-take of social life among peers. He learned to make friends and to get along with enemies And developed a "social personality." He developed habits of care of the body, of cleanliness and safety, consistent with a wholesome, realistic attitude which includes a sense of physical normality and adequacy, the ability to enjoy using the body, He learned to be a boy, to act the role that is expected and rewarded. The sex role is taught so vigorously by so many agencies that the school probably has little more than a remedial function, which is to assist boys and girls who are having difficulty with the task. A concept 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 developed an inner moral control, respect for moral rules, and the beginning of a rational scale of values. Morality, or respect for rules of behavior, is imposed onthe child first by the parents. He become physically independent of his parents

but remains emotionally dependent on them. He developed social attitudes that are basically democratic by imitation of people with prestige in the eyes of thelearner.


19/98

PHYSICAL ASSESSMENT


20/98

Our client is Mr. Richellou Dave Canas, 7 years old male, admitted last July 30,2009 @ Davao Medical School Foundation Hospital, St. Anthonys ward, room 426 bed 3, under the care of Dr. Ong in due to abdominal pain, and diagnosed to have Dengue Hemorrhagic Fever type 3. I. GENERAL SURVEY Mr. Canas weights 20 Kg. Uponreceiving, 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 according 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 appears to be relaxed and is wearing a clean patients gown. He is cooperative allthroughout the interaction.

Physical Assessment

II. VITAL SIGNS At around 8:00 oclock in the morning we assessed his vital signs, the axillary temperature obtained is 36.8 C. He has radial pulse rate of 78bpm and a cardiac rate of 80 bpm respectively. He has a normal respiratory rateof 26 cpm and a normal blood pressure of 100/60 mmHg. III. SKIN Skin is dark brown in color and uniform throughout the body, with poor skin turgor. Nails are convex 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 enlargement or any masses noted. The facial structure and movement are symmetrical. Hair is fine, evenly distributed; scalp is clean and is also free from dandruff, lice, wounds, scars and other lesions. V. EYES His eyelids were proportioned withno swelling noted. His eyelashes are long and directed outward. Fine eyebrows are evenly distributed. His conjunctiva is pinkish in color and her pupils size are 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. Pinna is mobile and firm with no tenderness, swelling and lesions noted. There is no presence of discharges. Patient is able to hear normal voice tones audibly. VII.NOSE


21/98

External nose are symmetrical. No discharges, flaring, tenderness and lesions noted. Nares are patent. Frontal and maxillary sinuses are not tender. VIII. MOUTHHis lips are pale in color and slightly dry. Gums and mucosa are light pink incolor. Tongue is located at midline. Teeth are not complete; he has 12 teeth onthe lower portion and 13 teeth in the upper portion. His speech is intact; he can speak clearly and fluently using his own dialect. IX. NECK Sternocleidomastoidand trapezius muscle were equal in size. Head movements are coordinated with no

discomfort. No presence of masses, unusual swelling and enlargement noted. X. HEART His heart sounds are distinct and regular. Point of maximum impulse is located between the 5th and 6th intercostals spaces. XI. BREAST AND AXILLAE Nipplesare dark brown in color, no discharges, swelling, tenderness, masses and lesionsnoted. Axilla was light brown in color with no amount of axillary hair. No masses and swelling noted. CHEST AND LUNGS He has normal respiratory rate of 26 cpm.Has a regular breathing pattern. Lung expansion was symmetrical, abnormal sounds during auscultation is not noted. No tenderness or masses in the chest is noted. ABDOMEN The general contour of his abdomen is round without folds observed. Abdominal skin is fair. Masses are not observed. EXTREMITIES With grossly normalextremities. Nail beds are pinkish in color with a capillary refill of 2-3 seconds. Peripheral pulse is symmetrical and strong. Gait is coordinated. No inflamma

tion, lesions, tenderness, pain and deformity noted on any part of the extremities. NVS He is conscious and oriented to time and place and person. He answers toour questions appropriately. His pupils are equally round and reactive to lightand accommodation with diameter of 3 mm. Both

XII.

XIII.

XIV.

XV.


22/98

his left and right, upper and lower extremities are strong. He obeys simple instructions during the assessment.


23/98

COMPLETE DEFINITION OF FINAL DIAGNOSIS


24/98

ANATOMY AND PHYSIOLOGY


25/98

ANATOMY & PHYSIOLOGY The Circulatory System

The circulatory system is an organ system that passes nutrients (such as amino acids and electrolytes), gases, hormones, blood cells, nitrogen waste products, etc. to and from cells in the body to help fight diseases and help stabilize bodytemperature and pH to maintain homeostasis. This system may be seen strictly asa blood distribution network, but some consider the circulatory system as compo

sed of the cardiovascular system, which distributes blood, and the lymphatic system, which distributes lymph. While humans, as well as other vertebrates, have aclosed cardiovascular system (meaning that the blood never leaves the network of arteries, veins and capillaries), some invertebrate groups have an open cardiovascular system. The most primitive animal phyla lack circulatory system. The lymphatic system, on the other hand, is an open system.


26/98

The main components of the human circulatory system are the heart, the blood, and the blood vessels. The circulatory system includes: the pulmonary circulation,a "loop" through the lungs where blood is oxygenated; and the systemic circulation, a "loop" through the rest of the body to provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7 liters) of blood, whichconsists of plasma, red blood cells, white blood cells, and platelets. Also, the 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 circulatory system: blood and lymph. The blood, heart, and blood vessels form thecardiovascular system. The lymph, lymph nodes, and lymph vessels form the lymphatic system. The cardiovascular system and the lymphatic system collectively make up the circulatory system. http://en.wikipedia.org/wiki/Circulatory_system Pulmonary Circulation

Pulmonary circulation is the portion of the cardiovascular system which carriesoxygendepleted blood away from the heart, to the lungs, and returns oxygenated blood 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 comes through the pulmonary veins. The blood then moves to the left atrium of the heart then to the left ventricle where the blood is pumped through the semilunarvalve into the aorta. RIGHT HEART Oxygen-depleted blood from the body leaves thesystemic circulation when it enters the right heart, more specifically the right atrium through the Superior (upper) vena cava and Inferior (lower) vena cava.The blood is then pumped through the tricuspid valve (or right atrioventricularvalve), into the right


27/98

ventricle. Blood is then pumped through the semilunar valve and into the pulmonary artery. Arteries From the right ventricle, blood is pumped through the pulmonary semilunar valve into the pulmonary artery. This blood enters the two pulmonary arteries (one for each lung) and travels through the lungs. Lungs The pulmonary arteries carry deoxygenated blood to the lungs, while the pulmonary veins carry oxygenated blood to the red blood cells where they release carbon dioxide andpick up oxygen during respiration. Veins The oxygenated blood then leaves the l

ungs through pulmonary veins, which return it to the left heart, completing thepulmonary cycle. This blood then enters the left atrium, which pumps it throughthe bicuspid valve, also called the mitral or left atrioventricular valve, intothe left ventricle. The blood is then distributed to the body through the systemic circulation before returning again to the pulmonary circulation. http://en.wikipedia.org/wiki/Pulmonary_circulationSystemic Circulation

Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated bloodback to the heart. The term is contrasted with pulmonary circulation

In the systemic circulation, arteries bring oxygenated blood to the tissues. Asblood circulates through the body, oxygen diffuses from the blood into cells


28/98

surrounding the capillaries, and carbon dioxide diffuses into the blood from thecapillary cells. Veins bring deoxygenated blood back to the heart. ARTERIES Oxygenated blood enters the systemic circulation when leaving the left ventricle, through the aortic semi-lunar valve. The first part of the systemic circulation is the artery aorta, a massive and thick-walled artery. The aorta arches and gives off major arteries to the upper body before piercing the diaphragm in order tosupply 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 thinnest and most numerous of the blood vessels. These capillaries help to join tissue with arterioles for transportation of nutrition to the cells, which absorboxygen and nutrients in the blood. Peripheral tissues do not fully deoxygenatethe blood, so venous blood does have oxygen, but in a lower concentration than in arterial blood. In addition, carbon dioxide and wastes are added. The capillaries can only fit one cell at a time. VENULES The deoxygenated blood is then collected by venules, from where it flows first into veins, and then into the inferior and superior venae cavae, which return it to the right heart, completing thesystemic cycle. The blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation. VEINS The relatively deoxygenated 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 inferior vena cava (roughly speaking from areas below the heart). These two greatvessels exit the systemic circulation by emptying into the right atrium of theheart. The coronary sinus empties the heart

s veins themselves into the right atrium. http://en.wikipedia.org/wiki/Systemic_circulationPortal Circulation


29/98

The gastric, splenic and mesenteric veins, which collect the venous blood from all the digestive organs, unite to form the portal vein, which carries to the liver this blood which has circulated through the capillaries of the stomach, spleen, pancreas and intestines, and though dark in colour, is laden with nutriment,the products of digestion. This important vein breaks up into capillaries (afterthe manner of an artery), and distributes this blood by means of them throughout 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 it is carried to the inferior vena cava, and by it is poured into the right auricle.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 through the network of blood vessels supplying the brain. The arteries deliver oxygenated blood, glucose and other nutrients to the brain and the veins carry deoxygenated blood back to the heart, removing carbon dioxide, lactic acid, and other metabolic products. Since the brain is very vulnerable to compromises in its blood supply, the cerebral circulatory system has many safeguards. Failure of the

se safeguards results in cerebrovascular accidents, commonly known as strokes. The amount of blood that the cerebral circulation carries is known as cerebral blood flow. The presence of gravitational fields or accelerations also determine variations in the movement and distribution of blood in the brain, such as when suspended upside-down.


30/98

CRANIAL ARTERIES There are two main pairs of arteries that supply the cerebral arteries and the cerebellum: Internal carotid arteries: These large arteries are the left and right branches of the common carotid arteries in the neck which enter the skull, as opposed to the external carotid branches which supply the facial tissues. The internal carotid artery branches into the anterior cerebral artery and continues to form the middle cerebral artery Vertebral arteries. These smaller arteries branch from

the subclavian arteries which primarily supply the shoulders, lateral chest andarms. Within the cranium the two vertebral arteries fuse into the basilar artery, which supplies the midbrain, cerebellum, and usually branches into the posterior cerebral artery.

Both internal carotid arteries, within and along the floor of the cerebral vault, are interconnected via the anterior communicating artery. Additionally, both internal carotid arteries are interconnected with the basilar artery via bilateral posterior communicating arteries. The Circle of Willis, long considered to bean important anatomic vascular formation, provides backup circulation to the bra

in. In case one of the supply arteries is occluded, the Circle of Willis provides interconnections between the internal carotid arteries and basilar artery along the floor of the cerebral vault, providing blood to tissues that would otherwise become ischemic. CEREBRAL VENOUS DRAINAGE The venous drainage of the cerebrumcan be separated into two subdivisions: superficial and deep. The superficial system is composed of dural venous sinuses, which have wall composed of dura mater as opposed to a traditional vein. The dural sinuses are, therefore located onthe surface of the cerebrum. The most prominent of these sinuses is the Superiorsagittal sinus which flows in the sagittal plane under the midline of the cerebral vault, posteriorly and inferiorly to the torcula, forming the Confluence ofsinuses, where the superficial drainage joins with the sinus the primarily drains the deep venous system. From here, two transverse sinuses bifurcate and travellaterally 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 parallelthe upward course of the carotid arteries and drain blood into


31/98

the vena cava. The deep venous drainage is primarily composed of traditional veins inside the deep structures of the brain, which join behind the midbrain to form the Vein of Galen. This vein merges with the Inferior sagittal sinus to formthe Straight sinus which then joins the superficial venous system mentioned above at the Confluence of sinuses.

Lymphatic System

The lymphatic system and the cardiovascular system are closely related structures that are joined by a capillary system. The is important to the body

s defensemechanisms. It filters out organisms that cause disease, produces certain whiteblood cells and generates antibodies. It is also important for the distributionof fluids and nutrients in the body, because it drains excess fluids and proteinso that tissues do not swell up. "Lymph" is a milky body fluid that contains atype of white blood cells, called "lymphocytes," along with proteins and fats. Lymph seeps outside the blood vessels in spaces of body tissues and is stored inthe "lymphatic" system to flow back into the bloodstream. Through the flow of blood in and out of arteries, and into the veins, and through the lymph nodes andinto 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 quarter of the body above the diaphragm and down the midline, and the thoracic duct, astructure roughly sixteen inches long located in the mediastinum of the pleuralcavity which drains the rest of the body. It is through the actions of this system including the spleen, the thymus, lymph nodes and lymph ducts that our bodyis able to fight infection and to ward off invasion from foreign invaders. Lymphplays an important role in the immune system and in absorbing fats from the intestines. The


32/98

lymphatic vessels are present wherever there are blood vessels and transport excess fluid to the end vessels without the assistance of any "pumping" action. There are more than 100 tiny, oval structures (called lymph nodes). These are mainly 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 germs. The largest body of lymphoid tissue in the human body is the spleen. http://www.innerbody.com/image/lympov.html


33/98

ETIOLOGY

AND

SYMPTOMATOLOGY


34/98

SYMPTOMATOLOGY Signs & Symptoms Actual High Fever, Body weakness, headache, nausea, vomiting and sometimes abdominal pain Rationale In acute DHF, the patients initially develop an abrupt onset of high fever (3940C) with malaise, headache,nausea, vomiting, myalgia and, sometimes, abdominal pain due to bodys innate immune 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 fulminant hepatic failure. Most patients had extremely elevated serum levels of AST and ALT, and exhibited alteration of consciousness, seizure or neurological deficit during the febrile stage. In addition, very rare cases of encephalitis, encephalomyelitis and transverse myelities with positive dengue virus and/or IgM in the cerebrospinal fluid were reported. The overall casefatality rate was 5%. A positive tourniquet test indicating the increased capillary fragility is found inthe early febrile stage. It may be a direct effect of dengue virus as it appearsin 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


35/98

PATHOPHYSIOLOGY


36/98

Figure Precipitating Factors: Aedes aegypti mosquito Predisposing Factors: Age Heredity Sex Race

Bite of a viruscarrying mosquito

Mosquito injects fluid into victims 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 neutralize 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 pain


37/98

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 (


38/98

Severe hemorrhage

Bloody vomitus, Hematuria, Bloody stool

Intractable shock

Multi organ failure

Death Death


39/98

Narrative Pathophysiology of Dengue Hemorrhagic FeverThe dengue viruses, the cause of dengue illness, are members of the Flaviviridaefamily. Four genetically related but distinct serotypes, designated DENV-1, DENV-2, DENV-3, DENV-4, are circulating worldwide. The main vector for dengue virustransmission is the Aedes aegypti species of mosquitos. Dengue viruses, similarto other flaviviruses, have a positive single-stranded RNA genome packaged inside 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 RNAencoding 3 structural proteins and 7 non-structural proteins. Viral protein andRNA synthesis occur predominantly in the cytoplasm of host cells. Replication isslow and begins within 15 hours after infection. Low amounts of dengue virus are released into the supernatant fluid. Dengue virus replication does not significantly affect the metabolic function of the host cell as exemplified by normal levels of protein synthesis by the infected cells. Dengue fever, caused by an infection with dengue virus, is not a new disease, but recently because of its serious emerging health treats, coupled with possible dire consequences including death, it has aroused considerable medical and public health concerns worldwide. Today, dengue is considered one of the most important arthropod-borne viral diseases 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 these, there are 200,000 to 500,000 cases of potential life-threatening dengue hemorrhagic fever (DHF)/ dengue shock syndrome (DSS), characterized by thrombocytopenia and increased vascular permeability. Risk factors of DHF are the following: Age (DHF/ DSS is more predominantly in children


40/98

Humoral immunity is mainly mediated by B cells, which is produce different classes of antibodies, both natural and pathogen induced. Natural IgM antibodies areproduced mainly by CD5+ B cells (B1 cells) and are component of innate immunity.These nonspecific circulating natural antibodies can bind to pathogens, providing early host protection. Natural antibodies may facilitate antigen uptake, processing, and presentation by B lymphocytes via complement and Fc receptors. Interestingly, 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 circulating antibodies are pentameric IgM molecules, a small amount of hexameric IgM, IgG, and IgA natural antibodies circulate as well. The physiologic roles of the natural IgM antibodies are not known. The multimeric structures makes IgM a strong complement activator; a single-bound IgM pentamer can trigger the classical pathway of complement activation and can lyse a red blood cell, while approximately a thousand IgG molecules are required to accomplish the same. Furthermorethe hexamer IgM, even though it circulates in smaller amounts, is 15 -20 times more efficient in activating complement system. Unfortunately a deep role of circulating IgM-immune complex in DHF/DSS is unknown. Platelets One of the clinicalmanifestations in dengue diseases is thrombocytopenia, otherwise known as low platelet count. This arises from both decreased production and increase destructio

n of platelets. During dengue virus infection, platelets may provide a wonderfulshield for the virus from exposure and binding to neutralizing preexisting antibody. Interestingly, there are few reports that dengue virus may associate withplatelets, directly or indirectly through antibody. Now we can envision that thevirus-plateletsantibody complexes may enhanced phagocytosis or be engulfed by macrophages or monocytes. This can lead to vasculopathy (plasma leakage), thrombocytopenia (


41/98

If the patient is not cured immediately, fluid shift due to prolonged plasma leakage can lead to increased hematocrit leading to hypovolemia the later, tissue acidosis. Tissue acidosis, thrombocytopenia and coagulopathy may lead to disseminated intravascular coagulation (DIC) which can lead to severe hemorrhage. The patient will experience an intractable shock leading to multi-organ failure then death.


42/98

MEDICAL, PHARMACOLOGIC AND DIAGNOSTIC

EXAMS


43/98

D AVAO M EDICAL S CHOOL F OUNDATION H OSPITAL M EDICAL DRIVE , B AJADA D AVAO CITY

HEMATOLOGYName: Mr. Canas Date: August 3, 2009 Age: 7 years old Room: Sex: Male Physician:Dr. Ong


44/98


45/98

TestHEMOGLOBIN

Resul t155

Unit

g/dL

ReferenceM:140-170 F:120-150

Clinical Significance = anemia, liver or kidney disease =primary and secondary polycythemia, COPD, CHF, burns

FunctionsHemoglobin is responsible for binding oxygen in the lungs and in transporting the bound oxygen throughout the body where it is used in aerobic metabolic pathways. RBCs transport oxygen bound to hemoglobin; also transports small amount of c

arbon dioxide.

ERYTHROCYTES

5.91

1012/ L

4.0-6.0

=anemia, acute

LEUKOCYTE

L 3.0

109/L

5.0-10.0

Segmenters (eg.neutroph ils)

0.50

%

0.45-0.65

and chronic hemorrhage, leukemia, and chronic infection =primary and secondarypolycythemia, erythropoietinsecreting tumors, and renal disorders =leukopeniaviral infections, bone marrow depression due to drugs, radiation and primary bone


46/98

marrow disorders. =leukocytosisacute infection (degree depends on the severityof infection, age, resistance, and presence of trauma, tissue necrosis or inflammation and hemorrhage). =neutropeniain acute bacterial infection, viral infection, some parasitic infection, aplastic and pernicious anemia, anaphylactic shock, and renal disease. =neutrophila-in acute localized and general bacterial infection, gout and uremia,

Leukocytes functions as phagocytes of bacteria, fungi and viruses, detoxification 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 oracute infection.


47/98

Date: July 30, 2009; 6 pm

TestHEMATOCRIT

Resu lt0.48

Unit%

ReferenceM: 0.400.60 F: 0.8-0.4

Clinical Significance=anemia or

FunctionsHematocrit is a measure of the proportion of blood volume that is occupied by RB

Cs. Thrombocytes are needed for normal blood clotting; initiate clotting cascade by clinging to broken area; help control blood loss from broken blood vessels.

THROMBOCYTES

L 15

109/ L

140-450

hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage

, inflammatory disease, hemolytic anemia, etc.

Date: July 30, 2009; 6 pm

TestHEMATOCRIT

Resu lt0.48

Unit%

ReferenceM: 0.400.60 F: 0.8-0.4


FunctionsHematocrit is a measure of the proportion of blood volume that is occupied by RBCs. Thrombocytes are needed for normal blood clotting; initiate clotting cascade by clinging to broken area; help control blood loss from broken blood vessels.

hemodilution

=dehydration,

THROMBOCYTES


48/98

L 15

109/ L

140-450

polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemolytic anemia, etc.

Date: July 31, 2009; 2 am


49/98

TestHEMATOCRIT

Resu lt0.45

Unit

%

ReferenceM: 0.400.60 F: 0.8-0.4



THROMBOCYTES

L 30

109/ L

140-450

hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemolytic anemia, etc.

Date: July 31, 2009; 8 am

TestHEMATOCRIT

Resu lt0.44

Unit%

ReferenceM: 0.400.60 F: 0.8-0.4



hemodilution=dehydration,

THROMBOCYTES

L 32


50/98

109/ L

140-450

polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly

tic anemia, etc.

Date: July 31, 2009


51/98


52/98

109/ L

140-450

polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage, inflammatory disease, hemoly

tic anemia, etc.

Date: August 1, 2009; 8 pm


53/98

TestHEMATOCRIT

Resu ltL 0.37

Unit

%

ReferenceM: 0.400.60 F: 0.8-0.4



THROMBOCYTES

L 40

109/ L

140-450


Date: August 1, 2009; 2 am

Test

Resu lt

Unit

Reference



HEMATOCRIT

0.41

%

M: 0.400.60 F: 0.8-0.4



54/98

polycythemia or hemoconcentratio n=thrombocytop

THROMBOCYTES

L 23

109/ L

140-450

enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage,inflammatory disease, hemolytic anemia, etc.



55/98

TestHEMATOCRIT

Resu ltL 0.31

Unit

%

ReferenceM: 0.400.60 F: 0.8-0.4



THROMBOCYTES

L 17

109/ L

140-450



56/98


TestHEMATOCRIT

Resu lt0.42

Unit%

ReferenceM: 0.400.60 F: 0.8-0.4


FunctionsHematocrit is a measure of the proportion of blood volume that is occupied by RB

Cs. Thrombocytes are needed for normal blood clotting; initiate clotting cascade by clinging to broken area; help control blood loss from broken blood vessels.

THROMBOCYTES

L 30

109/ L

140-450

hemodilution =dehydration, polycythemia or hemoconcentratio n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occurs after hemorrhage

, inflammatory disease, hemolytic anemia, etc.


Test

Resu ltL 0.37

Unit

Reference



HEMATOCRIT

%

M: 0.400.60 F: 0.8-0.4

hemodilution


57/98

=dehydration,

THROMBOCYTES

L 40

109/ L

140-450




58/98

Test

Resul tL 0.37

Unit

Reference



HEMATOCRIT

%

M: 0.400.60 F: 0.8-0.4

hemodilution =dehydration, polycythemia or hemoconcentration=thrombocytopeni

THROMBOCYT ES

L 49

109/L

140-450

a, cause of bleeding disorders =thrombocytosis, occurs after hemorrhage, inflammatory disease, hemolytic anemia, etc.

Date: August 2, 2009

Test

Resu ltL 0.38

Unit

Reference



HEMATOCRIT

%


59/98

M: 0.400.60 F: 0.8-0.4


THROMBOCYTES

L 64

109/ L

140-450


Date: August 2, 2009;6 pm

TestHEMATOCRIT

Resu ltL 0.35

Unit%

ReferenceM: 0.400.60 F: 0.8-0.4

Clinical Significance

=anemia or

FunctionsHematocrit is a measure of the proportion of blood volume that is occupied


polycythemia or hemoconcentratio


60/98

THROMBOCYTES

L 70

109/ L

140-450

n =thrombocytop enia, cause of bleeding disorders =thrombocytosi s, occursafter hemorrhage, inflammatory disease, hemolytic anemia, etc.

by RBCs. Thrombocytes are needed for normal blood clotting; initiate clotting cascade by clinging to broken area; help control blood loss from broken blood vessels.

L EGEND :H-High N-Normal; results within normal values are not necessarily marked with anindicator L-Low SH-Slightly High


61/98


HEMATOLOGYName: Mr. Canas Date: August 3, 2009 Age: 7 years old Room: Sex: Male Physician:Dr. Ong


62/98


63/98

Test

Resul t

Unit

Reference

Clinical Significance= anemia, liver

FunctionsHemoglobin is responsible for binding oxygen in the lungs and in transporting the bound oxygen throughout the body where it is used in aerobic metabolic pathways.

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

1012/ L

4.0-6.0

LEUKOCYTE

N 5.0

109/L

5.0-10.0

Segmenters (eg.neutroph ils)

L 0.27

%

0.45-0.65


64/98

and chronic hemorrhage, leukemia, and chronic infection =primary and secondarypolycythemia, erythropoietinsecreting tumors, and renal disorders =leukopeniaviral infections, bone marrow depression due to drugs, radiation and primary bonemarrow disorders. =leukocytosisacute infection (degree depends on the severityof infection, age, resistance, and presence of trauma, tissue necrosis or inflammation 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 infection, gout and uremia,

RBCs transport oxygen bound to hemoglobin; also transports small amount of carbon dioxide.

Leukocytes functions as phagocytes of bacteria, fungi and viruses, detoxification 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.


65/98


COAGULATION RESULT FORMName: Mr. Canas Date: August 3, 2009 Protime 11.1 Patient sec INR 0.85 Control 13.9 APTT Patient 47.7 sec Control 30.2 sec Normal: 1.0-1.2 Therapeutic: 2.0-3.0Normal: 25-36 sec

Age: 7 years old Room:

Sex: Male Physician: Dr. Ong


66/98


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 is clear. A small meniscoid density is appreciated within the right costophrenicsulcus. Diaphragmatic outline are otherwise unremarkable. The heart is normal insize. The rest of the included soft tissue shadows and osseous structures are unremarkable. Impression: Suggestive Minimal Pleural Effusion, Right


67/98


68/98


69/98

POSSIBLE MANAGEMENT/LAB TESTS Virus Isolation Viruses are obligate intracellular parasites that require living cells in order to replicate. Cultured cells, eggs and laboratory animals maybe used for virus isolation. Although embroyonated eggs and laboratory animals are very useful for the isolation of certain viruses, cell cultures are the solesystem for virus isolation in most laboratories. The development of methods forcultivating animal cells has been essential to the progress of animal virology.

To prepare cell cultures, tissue fragments are first dissociated, usually with the aid of trypsin or collagenase. The cell suspension is then placed in a flatbottomed glass or plastic container (petri dish, a flask, a bottle, test tube) together with a suitable liquid medium. e.g. Eagle

s, and an animal serum. After avariable lag, the cells will attach and spread on the bottom of the container and then start dividing, giving rise to a primary culture. Attachment to a solid support is essential for the growth of normal cells. Primary and Secondary Cultures Primary cultures are maintained by changing the fluid 2 or 3 times a week. When the cultures become too crowded, the cells are detached from the vessel wallby either trypsin or EDTA, and portions are used to initiate secondary cultures.In both primary and secondary cultures, the cells retain some of the characteristics 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. The cells may then continue to multiply at a constant rate over many successive transfers. Eventually, after a number of transfers, the cells undergo culture senescence and cannot be transferred any longer. For human diploid cell cultures, the growth rate declines after about 50 duplications. During the multiplication ofthe cell strain, some cells become altered in that they acquire a different morphology, grow faster, and become able to start a cell culture from a smaller number of cells. These cells are immortalized and have an unlimited life-span. However, they retain contact inhibition. Cell Cultures Cell cultures are separated into 3 types:1. Primary cells - prepared directly from animal or human tissues and 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 can 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, Hep2 Cell cultures vary greatly in their susceptibility to different viruses. It isof utmost importance that the most sensitive cell cultures are used for a particular suspected virus. Specimens for cell culture should be transported to the laboratory as soon as possible upon being taken. Swabs should be put in a vial containing virus transport medium. Bodily fluids and tissues should be placed in asterile container. Upon receipt, the specimen is inoculated into several different types of cell culture depending on the nature of the specimen and the clinical90 P a g e


70/98

presentation. The maintenance media should be changed after 1 hour or if that isnot practicable, the next morning. The inoculated tubes should be incubated at35-37oC in a rotating drum. Rotation is optimal for the isolation of respiratoryviruses and result in an earlier appearance of the CPE for many viruses. If stationary tubes are used, it is critical that the culture tubes be positioned so that the cell monolayer is bathed in nutrient medium. The inoculated tubes shouldbe 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 produce a CPE-like effect. If toxic effects are extensive, it may be necessary to passage the inoculated cells. Cell cultures that are contaminated by bacteria should either be put up again or passed through a bacterial filter. Cell cultures should be kept for at least one to two weeks (longer in the case of CMV). Cell cultures should be refed with fresh maintenance medium at regular intervals or ifrequired should the culture medium become too acidic or alkaline. When CPE is seen, it may be advisable to passage infected culture fluid into a fresh culture of the same cell type. For cell-associated viruses such as CMV and VZV, it is necessary to trypsinize and passage intact infected cells. Other viruses such as adenovirus 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 responseto treatment. c. Inform the patient that the test requires a blood sample. d. Inform 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 intravenousline. Hemodilution with intravenous fluids causes a false decrease in the values of some test. Post test: a) Apply pressure to the venipuncture site. b) Afterapplying 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 inspecific IgM antibody levels 3 to 5 days after the onset of symptoms; this generally persists for 30 to 60 days. IgG levels also become elevated after 10 to 14days and remain detectable for life. During secondary infection, IgM levels gene

rally rise more slowly and reach lower levels than in primary infection, while IgG levels rise rapidly from 1 to 2 days after the onset of symptoms. Diluted patient serum (serum diluent contains sorbent to remove rheumatoid factor and humanIgG interference) is added to wells coated with purified antigen. IgM specificantibody, if present, binds to the antigen. All unbound materials are washed away and the enzyme conjugate is added to bind to the antibody-antigen complex, ifpresent. Excess enzyme conjugate is washed off and substrate is added. The plateis incubated to allow the hydrolysis of the substrate by the enzyme. The intensity of the color generated is proportional to the amount of IgM specific antibody in the sample. STORAGE AND STABILITY91 P a g e


71/98

1. 2. 3. 4.

Store the kit at 2-8 C. Keep microwells sealed in a dry bag with desiccants. The reagents are stable until expiration of the kit. Do not expose test reagents to 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 licensed reagents. However, as there is no test method that can offer complete assurance that HIV, Hepatitis B virus or other infectious agents are absent, these reagents should be handled at the Biosafety Level 2, as recommended in the Centers for Disease Control/National Institutes of Health manual, "Biosafety in Microbiological and Biomedical Laboratories." 1984. 2. Optimal results will be obtained by strict adherence to the test protocol. Precise pipetting as well as followingthe exact time and temperature requirements is essential. 3. Do not pipette by mouth. Do not smoke, eat, or drink in the areas in which specimens or kit reagents are handled. 4. The components in this kit are intended for use as an integralunit. The components of different lots should not be mixed. 5. Control sera and

sample diluent contain preserved with sodium azide. Sodium azide may react withlead and copper plumbing to form explosive metal azide. On disposal, flush witha large volume of water. SPECIMEN COLLECTION AND HANDLING 1. Collect blood specimens and separate the serum. 2. Specimens may be refrigerated at 28 C for upto seven days or frozen for up to six months. Avoid repetitive freezing and thawing. REAGENT PREPARATION Prepare 1X Wash buffer by adding the contents of the bottle (25 mL, 20X) to 475 mL of distilled or deionized water. Store at RT. PREPARATION FOR ASSAY Bring all specimens and kit reagents to room temperature (20-25C) and gently mix. ASSAY PROCEDURE 1. Place the desired number of coated stripsinto the holder. 2. Negative control, positive control, and calibrator are ready to use. Prepare 1:21 dilution of test samples, by adding 10 L of the sample to 200 L of sample diluent. Mix well. 3. Dispense 100 L of diluted sera, calibrator and controls into the appropriate wells. For the reagent blank, dispense 10

0L sample diluent in92 P a g e


72/98

1A well position. Tap the holder to remove air bubbles from the liquid and mix well. Incubate for 20 minutes at room temperature. 4. Remove liquid from all wells. Wash wells three times with 300-350 L of 1X wash buffer. Blot on absorbancepaper or paper towel. 5. Dispense 100 L of enzyme conjugate to each well and incubate for 20 minutes at room temperature. 6. Remove enzyme conjugate from all wells. Wash wells three times with 300350 L of 1X wash buffer. Blot on absorbance 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 450nm using ELISA reader within 15 min. A dual CALCULATION OF RESULTS 1. Check Calibrator Factor (CF) value on the calibrator bottle. This value might vary from lot to lot. Make sure you check the value on every kit. 2. Calculate the cut-off value: Calibrator OD x Calibrator Factor (CF). 3. Calculate the Ab (Antibody) Index of each determination by dividing the O.D. value of each sample by cut-off value. QUALITY CONTROL The test run may be considered valid provided the followingcriteria 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 forPositive control should be greater than 1.2. INTERPRETATION The following is intended as a guide to interpretation of Dengue virus IgM test results; each laboratory is encouraged to establish its own criteria for test interpretation based

on sample populations encountered. Antibody Index Interpretation 1.1 Detectable antibody to Dengue virus IgM by ELISA. LIMITATIONS OF THE TEST 1. To enhance sensitivity and specificity of this IgM test provided sample diluent has been formulated to block IgG and Rheumatoid Factor (RF) interferences. Turbidity could be seen after diluting serum with sample diluent. This turbidity is due to the blocking of serum IgG and has shown no interference with test results. It can be removed by centrifugation. 2. In specimens with high RF and high autoimmune antibodies, the possibility of eliminating the interferences cannot be ruled out entirely. 3. The testresults obtained using this kit serve only as an aid to diagnosis and should beinterpreted in relation to the patients history, physical findings and other diagnostic procedures. 4. Lipemic or hemolyzed samples may cause erroneous results

93 P a g e


73/98

DRUG STUDIES


74/98

Generic name: Paracetamol (Acetaminophen) Brand name: Tempra Date ordered: July30, 2009 Ordered dose: 250mg/5ml, 5ml q4 hrs, p.r.n for fever Classification: Central Nervous System Agent; Narcotic Analgesic; Antipyretic Suggested dose: For mild to moderate pain, fever o Children ages 6-8 yrs old: 320 mg P.O. q 4-6 hrs, p.r.n Therapeutic actions: Thought to produce analgesia by blocking pain impulses of prostaglandin in the CNS or of other substances that sensitize pain receptors to stimulation. The drug may relieve fever through central action in the

hypothalamic heat-regulating center. Indications: Fever reduction Temporaryrelief of mild to moderate pain Generally as substitute for aspirin when thelater is no tolerated or is contraindicated. Contraindications and cautions: Hypersensitivity to acetaminophen or phenacin Long term alcohol use (may causehepatotoxicity) Children < 3 years old unless directed by a physician Malnutrition Thrombocytopenia Arthritic or rheumatoid conditions affecting children < 12 years old Safety during pregnancy (category B) or lactation is not established. Adverse effects: Hematologic: hemolytic anemia, leukopenia, pancytopenia, neutropenia Hepatic: jaundice Metabolic: hypoglycemia Skin: rash, urticaria Interactions: Nursing considerations: Monitor for s/s of: o hepatotoxicity, even with moderate acetaminophen doses, especially in individuals with poornutrition or who have ingested alcohol over prolonged periods o poisoning, usua

lly from accidental ingestion or suicide attempts o Potential abuse from psychological dependence (withdrawal has been associated with restless and excited responses). The drug should not be taken with other medication (e.g. cold preparations) containing acetaminophen without medical advice; overdosing and chronic use can cause liver damage without consulting a physician Advise client not to self medicate for pain more than 10 days (5 days in children) without consultinga physician. This medication should not be used without medical direction for:fever persisting longer than 3 days, fever over 39.5 C (103F), or recurrent fever.


75/98

Do not give children more than 5 doses in 24 hrs unless prescribed by a physician. Advise clients/patients not to breast feed while taking this drug withoutconsulting physician. Effects on Laboratory Results: May decrease glucose andhemoglobin levels and hematocrit. May decrease neutrophil, WBC, RBC, and platelet counts. May cause false-positive result for urinary 5-hydroxyindoleaceticacid. May falsely decrease glucose level in home monitoring systems. Teaching points: 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 toconsult prescriber if giving to children for more than 5 days and for adults longer than 10 days. ALERT: Advise patient or caregiver that many OTC products contain acetaminophen and should be counted when calculating total dose. Tell parent not to use for marked fever (temperature higher than 39.5C), fever persisting longer than 3 days, or recurrent fever unless directed by prescriber. ALERT: Warn patient that high doses or unsupervised long-term use can cause liver damage. 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 that drug appears in breast milk in low levels (< 1% of dose). Drug may be used safely if therapy is short-term and doesnt exceed recommended doses. Generic name: 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 Children 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 inhibits the action of antihistamine on the H2 at the receptor sites of parietal cells, decreasing gastric acid secretions. Indications: Effective treatment of GERD and Peptic Ulcers in children (FAMOTIDINE ONLY) Effective treatment of Peptic Ulcer Disease: relief of symptoms, acceleration of healing, prevention of recurrence Control of Hypersecretory Stomach Disorders Treatment of Reflux Esophagitis Treatment of Heartburn


76/98

Prevention of Heartburn Contraindications and cautions: Contraindicated in patients hypersensitive to the drug. Ulcer rebound/perforation may occur if drugs are stopped abruptly when being used to treat ulcers. Once medicines are stopped, immediate contact of the physician must be done. Use of these medicinesand symptom relief does not absolutely remove the possibility of gastric malignancy. Adverse effects: Drug-induced hepatitis Bone marrow depression (Lowered white blood cells or hemoglobin),rare Confusion (particularly in compromised

elderly with some of these drugs) Low blood platelet counts (all the above are case report to rare effects) Abnormal heart rhythm changes (slow heart beator atrioventricular block) Bronchospasm, rare Impotence Interactions: Nonesignificant. Nursing considerations: Assess patient for abdominal pain. Lookfor blood in emesis, stool or gastric aspirate. Oral suspension must be reconstituted and shaken before use. Store reconstituted oral suspension below 30C.Effects on Laboratory Results: Blood platelet counts: may be decreased by allhistamine (H2) blockers. Complete blood counts: rare with white blood cell (granulocytes) decrease. Liver enzymes (SGPT, OT, etc.): can be increased with liver damage. May increase BUN and creatinine. May cause false negative-results in skin tests using allergen extracts. May antagonize pentagastrin in gastricacid secretion tests. Teaching points: Instruct patient in proper use of OTC

product if appropriate.Warn patient with PKU that Peptic AC chewable tabletscontain phenylalanine. Tell patient to take prescription drug with a snack, if

desired. Remind patient that prescription drugs most effective is taken at bedtime. Tell patient taking 20 mg twice daily to take one dose at bedtime. Advise patient to limit use of prescription drug no longer than 8 weeks, unless ordered by the prescriber, and OTC drug no longer than 2 weeks. With prescribersknowledge. Let patient take antacids together especially at the beginning of therapy when pain is severe. Urge patient to avoid cigarette smoking because it may increase gastric acid secretion and worsen disease. Advise patient to report abdominal pain or blood in stools or vomit. Generic name: Furosemide Brand name: Furosemide Classification: Loop diuretic


77/98

Date ordered: July 31, 2009 Ordered dose: 10.0 mg slow IVTT(single order stat) Therapeutic actions: A potent drug that inhibits sodium and chloride reabsorption 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 sulfonamides. Use during pregnancy only if potential benefits to mother clearly outwe

igh risks to fetus. Adverse effects: CNS: vertigo, headache, dizziness, paresthesia, weakness, restlessness, fever. CV: orthostatic hypotension, thrombophlebitits with I.V. administration. EENT: transient deafness, blurred or yellowedvision, tinnitus. GI: abdominal discomfort and pain, diarrhea, anorexia, nausea, vomiting, constipation, pancreatitis. GU: nocturia, polyuria frequent urination, oliguria. Hematologic: agranulocytosis, aplastic anemia, leukopenia, thrombocytopenia, azotemia, anemia. Hepatic: hepatic dysfunction, jaundice. Metabolic: volume depletion and dehydration, asymptomatic hyperurecemia, impairedglucose tolerance, hypokalemia, hypochloremic alkalosis, hyperglycemia, dilutional 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 Amphotericin B, corticosteroids, corticotrophin, metolazone: may increase risk of hypokalemia. Monitor potassium level closely. o Ant diabetics: may decrease hypoglycemic effects. Monitor glucose level. o Antihypertensive: may increase risk of hypotension. Use together cautiously. Decrease antihypertensive dose if needed. o Cardiac glycosides, neuromuscular blockers: may increase toxicity of these drugsfrom furosemide induced hypokalemia. Monitor potassium level. o Chlorothiazide,chlorthalidone, hydrochlorothiazide, indapamide, metolazone: may cause excessivediuretic response, causing serious electrolyte abnormalities or dehydration. Adjust doses carefully and monitor patient for signs and symptoms of excessive diuretic response.


78/98

Ethacrynic acid: may increase risk of ototoxicity. Avoid using together. Lithium: may decrease lithium excretion resulting in lithium toxicity. Monitor lithiumlevel. o NSAIDS: may inhibit diuretic response. Use together cautiously. o Phenytoin: may inhibit diuretic effect of furosemide. Use together cautiously. o Propanolol: may increase propanolol level. Monitor patient closely. o Salicylates: may cause salicylate toxicity. Use together cautiously. o Sucralfate: may reducediuretic and hypertensive effect. Discourage use together. Separate doses by 2 h

rs. Drug-herb: o Aloe: may increase drug effect. Discourage use together. o Dandelion: may interfere with drug activity. Discourage use together. o Ginseng: may decrease drug effect. Discourage use together. o Licorice: may cause unexpected rapid potassium loss. Discourage use together. Drug-lifestyle: o Sun exposure: may increase risk for photosensitivity reactions. Advise patient to avoid excessive sunlight exposure. Nursing considerations: To prevent nocturia, give P.O. and I.M. preparations in the morning. Give second dose 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 electrolytedepletion. If oliguria or azotemia develops or increases, drug may need to bestopped. Monitor fluid intake and output and electrolyte, BUN, and carbon dioxide levels frequently. Watch for signs of hypokalemia, such as muscle weaknes

s and cramps.Consult prescriber and dietitian about a high-potassium diet orpotassium supplements. Foods rich in potassium include citrus fruits, tomatoes,

bananas, dates and apricots. Monitor glucose level in diabetic patients. Drugs may not be well absorbed orally in patient with severe heart failure. Drug may need to be given I.V. even if patient is taking other oral drugs. Teaching points: Advise patient to take drug with food to prevent GI upset, and to take drug in the morning to prevent the frequent need to urinate at night. If patient needs second dose, tell him or her to take it early in the afternoon, 6-8 hrs after morning dose. Inform patient of possible need for potassium or magnesium supplements. Instruct patient to stand slowly to prevent orthostatic dizziness,and to limit alcohol intake and stenous exercise in hot weather to avoid worsening dizziness upon standing quickly. Advise patient to immediately report ringing in the ears, severe abdominal pain, or sore throat and fever, these symptoms

may indicate toxicity. ALERT: Discourage patient from storing different typesof drugs in the same container, increasing risk of drug errors. The most popularstrengths of this drug and digoxin are white tablets about equal in size. Tell patient to check with prescriber or pharmacist before taking OTC drugs.o o


79/98

Teach patient to avoid direct sunlight and to use protective clothing and a sun block because of risk of photosensitivity. Generic name: Diphenhydramine Hydrochloride Brand name: Benadryl Classification: Ethanolamine derivative Date ordered: August 1, 2009 Ordered dose: 17 g slow IVTT Therapeutic actions: Competeswith histamine for H1-receptor sites. Prevents but does not reverse, histamine-mediated 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 symptoms, motion sickness, Parkinson disease Sedation Nighttime sleep aid Nonproductive cough Contraindications and cautions: Contraindicated in patients hypersensitive to the drug; newborns; premature neonates; breast-feeding women; patients with angle-closure glaucoma, stenosing peptic ulcer, symptomatic prostatichypertrophy, bladder neck obstruction; and those having an acute asthmatic attack. Avoid use in patients taking MAO inhibitors. Use with caution in patientswith prostatic hyperplasia, asthma, COPD, increased intraocular pressure, hyperthyroidism, CV disease, and hypertension. Children younger than age 12 shoulduse 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: thrombocytopenia, agranulocytosis, hemolytic anemia. Respiratory: thickening of bronchial secretions. Skin: urticaria, photosensitivity, rash. Other: anaphylactic shock. Interactions: Drug-drug: o Aspirin/NSAIDs (e.g., ibuprofen), anticoagulants ("blood thinners" such as warfarin or heparin), aminocaproic acid, factor IX complex, antiinhibitor coagulant concentrates, drugs that can cause blood clots (e.g., estrogens or birth control pills). Nursing considerations: To prevent nocturia, give P.O. and I.M. preparations in the morning. Give second dose early in the afternoon.


80/98

ALERT: Monitor weight, blood pressure, and pulse rate routinely with longtermuse 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 dioxide levels frequently. Watch for signs of hypokalemia, such as muscle weakness and cramps. Consult prescriber and dietitian about a high-potassium diet or potassium supplements. Foods rich in potassium include citrus fruits, tomatoes, ban

anas, dates and apricots. Monitor glucose level in diabetic patients. Drugsmay not be well absorbed orally in patient with severe heart failure. Drug may need to be given I.V. even if patient is taking other oral drugs. IV Administration: Make sure the site is patent. Infiltration causes irritation. Dont exceed 25mg/minute. Teaching points: Warn patient no to take drug with any other products that contain diphenhydramine (including topical therapy) because of increased adverse reactions. Insturct patient to take drug 30 mins before travel to prevent motion sickness. Tell patient to take the drug with food or milk toreduce gastric distress. Warn patient to avoid alcohol and hazardous activities that require alertness until CNS effects of durg are known. Tell patients that 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 differentantihistamine may be required.


81/98

Generic name: Tranexamic Acid Brand name: Cyklokapron Date ordered: August 2, 2009 Ordered dose: 15 mg t.i.d Classification: Antifibrinolytic, antihemorrhagic Suggested dose: For mild to moderate pain, fever o Children ages 6-8 yrs old: 320 mg P.O. q 4-6 hrs, p.r.n Therapeutic actions: Tranexamic acid competitivelyinhibits activation of plasminogen, thereby reducing conversion of plasminogento plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, andother plasma proteins, including the procoagulant factors V and VIII. Tranexami

c acid also directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation. In vitro, the antifibrinolytic potency of tranexamic acid is approximately 5 to 10 times that of aminocaproic acid. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasingplasmin-induced activation of the first complement protein. Indications: Contraindications and cautions: Intravascular clotting, active (risk of serious, even fatal, thrombus formation) Defective color vision, acquired (condition precludes assessment of color vision, which may be required to determine toxicity) Hematuria of upper urinary tract origin (risk of intrarenal obstruction secondary to clot retention in the renal pelvis and ureters if hematuria is massive; also, 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 thedegree of impairment is recommended) Sensitivity to tranexamic acid, history of Thrombosis, predisposition to or history of (medication inhibits clot dissolution and may interfere with mechanisms for maintaining blood vessel patency; itis recommended that tranexamic acid be administered in conjunction with anticoagulant therapy, if at all) Adverse effects: Blurred vision or other changes invision hypotension (dizziness or lightheadedness; unusual tiredness or weakness) may be associated with too-rapid intravenous administration thrombosis orthromboembolism (pains in chest, groin, or legs [especially calves]; severe, sudden headache; sudden and unexplained shortness of breath, slurred speech, vision changes, and/or weakness or numbness in arm or leg; sudden loss of coordinatio

n)depending on site of thrombus formation or embolization Diarrhea


82/98

Nausea vomiting Incidence unknown Unusual menstrual discomfort caused by clotting of menstrual fluid Interactions: Anti-inhibitor coagulant complex or Factor IX complex (although tranexamic acid is often used in conjunction withclotting factor replacement for the perisurgical management of hemophilic patients, concurrent use may increase the risk of thrombotic complications.) Contraceptives, estrogen-containing, oral or Estrogens (concurrent use with tranexamicacid may increase the potential for thrombus formation) Thrombolytic agents (t

he actions of tranexamic acid and of thrombolytic agents [e.g., alteplase (tissue-type plasminogen activator, recombinant; tPA), anistreplase (anisoylated plasminogen-streptokinase activator complex; APSAC), streptokinase, or urokinase] aremutually antagonistic; although controlled studies to demonstrate its efficacyhave not been done in humans, tranexamic acid may be useful in treating severe hemorrhage caused by a thrombolytic agent. Nursing considerations: Antifibrinolytic agents are ineffective in bleeding caused by loss of vascular integrity; adefinite clinical diagnosis or confirmation of hyperfibrinolysis (hyperplasminemia) via laboratory studies is required before tranexamic acid is used to treat hemorrhage. Carcinogenicity/Tumorigenicity PregnancyTranexamic acid crossesthe 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, eyeground, and visual fields


83/98


84/98

Medical Management Actual Medical Management MEDICAL ORDER RATIONALE July 30, 2009; 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 condition. May take food as tolerated and to monitor blood loss through the GI tract.To monitor patients vital signs: blood pressure, temperature, cardiac rate andrespiratory rate. And to monitor if there is sign for potential shock or bleeding. Complete Blood Count - to identify persons who may have an infection and to identify acute and chronic illness, bleeding tendencies, and white blood cell disorders such as leukemia Urinalysis for routine urine analysis; to check for pr

esence

Documents

Title Page d Avao m Edical s