Dengue Hemorrhagic Fever case book

2012

College of Nursing and Allied Health Sciences Silliman University 6200 Dumaguete City

M August 2012 Mrs. Emilia M. Ragay MAN, RM, RN. Clinical Instructor Level III Dear Mrs. Ragay: We, the level III section C2 is seeking for your permission to present the case of our client, on August 2012 at Silliman University College of Nursing. We have kept all data files in the strictest confidentially in which all the things that will be discuss will be for academic purposes only as stated in the patients bill of rights. The case presentation will serve as a partial fulfillment in the requirements for NCM 103. The knowledge, skill and attitude will be enhanced, as we present, the various cases of our Pediatric patients, will be invaluable. We are hoping for your kind approval. Respectfully Yours, Danah Shareen Candelario Marianne Daphne Guevarra Diana Jane Torres Deefy Rose Patun-og

Silliman University College of Nursing

Vision:

As a leading Christian Institution, Silliman University is committed to total development for the well-being of society and environment

Mission: Infuse into the academic learning the Christian faith anchored on the gospel of Jesus Christ, provide an environment where Christian fellowship and relationship can be nurtured and promoted Provide opportunities for growth and excellence in every dimension of the University life in order to strengthen character, competence, and faith Instills in all members of the university community an enlightened social consciousness and a deep sense of justice and compassion Promoted unity among people and contribute to national development

ACKNOWLEDGEMENT

Time has come for us to present what we have learned not only in the four corners of our classroom but from our actual 2 day duty in Negros Oriental Provincial Hospital- Pediatrics Department. Being a student nurse is not an easy job, how much more being a registered nurse someday. However, before fast-forwarding the event. Let us focus on what lies here in front of us now. It is very tiresome indeed to take care of patients, do all morning care, and administer medications and monitoring their status from time to time. Nevertheless, a feeling of success after you have done your task makes you forget all the sleepless nights and tiring day. This would not be possible without the guidance and protection of our Almighty God, the giver of life and our savior. We would like also to show gratitude to the following people who have helped us in finishing our case presentation papers: Our Almighty God who has guided us all throughout the day and weeks in preparing and in making this paper To our beloved instructor who has been so generous in sharing to us all knowledge and skills she has learned in her college years and for being so supportive in every step that we take. To our very supportive classmates, who helped and shared unto us the things they have learned To the staff nurses, doctors and personnel of NOPH who welcomed and helped us acquire more knowledge and skills that we cannot learn by just reading the book. Most especially to our parents, who have provided us financially in making this paper and for providing resources to complete this paper And to all those who silently guided us on our side as we took this phase of our lifes journey Thank you for all your support!

Table of contents

I. II. III. IV. V. VI. VII. VIII.

Cover page . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cover Letter/Application Letter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vision-Mission Statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Table of Contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Objectives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Psychosocial Profile: Demographic Data. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Genogram . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ecomap . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Growth & Development. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Physical Assessment Findings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy & Physiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Overview of the Disease Condition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pathophysiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Medical Management Laboratory Results. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pharmacologic Management. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Diagnostic Procedures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XIV. Functional Health Pattern. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XV. Summary of Nursing Diagnoses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XVI. Nursing Care Plan. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XVII. Journal Articles. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XVIII. Synthesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XIX. Bibliography. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . IX. X. XI. XII. XIII.

introduction
The body is one of the most amazing things that ever existed in this world. Every living creature, and even to some that are not breathing, almost everything that is seen by our naked eyes has a body. It is composed of very minute cells which make up most of it even cells have parts of their own. It has different defense mechanisms that protect it from harvesting the pathogens and succumbing to the diseases that it causes. It also has the other mechanisms that sustain its life, and excrete microorganisms and other toxins that crossed the primary defenses and entered the body. With the knowledge that we have regarding how our body responses to the different pathogens, we somehow have the responsibility of educating our patients with the factors that could lead them to possibly acquiring different diseases brought about by infectious agents. This presentation is based on our client who has been diagnosed with Dengue Hemorrhagic Fever Grade III. It will tackle on the pathophysiology of the disease condition and how it had affected the patients physiological functioning. It will also cover on the anatomy and physiology of the organs affected, the medications taken by the patient, and P. A. results of our patient. patient with dengue fever. This presentation also discusses the nursing process in the care of the

This topic deal with the care done to the toddler client having dengue hemorrhagic fever .It discusses the concepts used in the care, anatomy and physiology of the systems involved in the disease condition, its pathophysiology, and the growth and development of adolescents. It also involves carefully planned interventions and its expected outcomes, collaborative medical management and its nursing implications, and the presentation of the nursing plan of care prepared for the patient.

GENERAL OBJECTIVE:
At the end of the case presentation, our classmates shall gain/ broaden knowledge, develop basic skills, and manifest positive attitude in caring for a toddler with DENGUE HEMORRHAGIC FEVER.

SPECIFIC OBJECTIVES:

At the end of our case presentation, the learners shall: Integrate the concepts of growth and development in the care of the toddler with dengue hemorrhagic fever Identify the different system affected by the disease condition Identify the different manifestations of dengue as shown by the client Explain the pathophysiology of dengue fever as manifested by the client. Identify the actual and potential nursing diagnosis and responsibilities during the actual care of the patient Discuss the collaborative care : medical and nursing responsibilities during the actual care of the patient Relate the prescribed medications for the patient, its mechanism of action, side effects, contraindications and nursing responsibilities with the total plan of care Relate the nursing care plans to similar conditions Evaluate the rendered care Evaluate the case presentation

Nursing History
I. Demographic data Name: Emerson Dorimon Jr. Age: 2 years old Sex: Male Address: Bio-os, Amlan Negros Oriental Civil Status: Single Religion: Roman Catholic Nationality: Filipino Doctor in charge: Dr. Renacia Date and time of admission: July 9, 2012, 2:49 pm Chief Complaint: Fever and chills History of Present Illness: 2 days PTA, patient had onset of moderate grade fever associated with productive cough. No abdominal pain, (-) LBM, (-) vomiting, (-) epistaxis. Took paracetamol to lower fever. These symptoms persisted until 1 day PTA, patient loss apetite. Morning PTA, patient was crying more than usual, weak, the sought consultation at OPD where CBC was taken. General Impression: Received client lying in bed, awake, alert and coherent. Skin warm to touch and good mobility and turgor. With ongoing D5 0.3% NaCl 1 L running @ 15gtts/ hr inserted @ left metacarpal vein with 750mL left. IV site not infiltrated, no redness noted. Well- groomed, dress is appropriate to situation and environment.

GENOGRAM

Nicol asa 79 y.o

Roel 80 y.o

Mind a 60 y.o

Juan 68 y.o

Emerson 31 y.o

Mari a 28 y.o

Nicanor 25 y.o

Mari stel 28 y.o

Jose 35 y.o

John 25 y.o.

Neil 23 y.o

Chris 20 y.o

Jenn y 18

Josh 16

Jane t 15

Mike 12

Lora 10

Jess 8

Jake 5

Mary 20

ECOMAP

LEGEND:

Weak connection, Draining Energy/resources, not stressful Strong connection, Providing Energy/resources, not stressful Weak connection, No impact on Energy/resources, stressful Tenuous/uncertain connection, Providing Energy/resources, not stressful

Baranga y Service Silliman medical centre

Narcisso 30 y.o

Jess a 40 y.o

John 25

Neil 23

Chris 20

Jen ny 18

Josh 16

Jan et 15

Mike 12

Lor a 10

Jess 8

Jake 5

Ma ry 2

Church catholic

Neigh bours
High school Friends / Classm ates

Relativ es

Elemen tary school Rural health unit

Growth and development Emersons height is 82 cm (32 inches) and weighs 10.9 kilograms which appropriate for a normal toddler. Chest circumference is biger than head circumference, chest circimeference is

The term terrible twos has often been used to describe the toddler years, the period from 1 to 3 years old (12-36 mos.). It is a time of intense exploration of the environment as children attempt to find out how things work and how to control others through temper tantrums, negativism, and obstinacy. Although this can be a challenging time for parents and child as each learns to know the other better, it is an extremely important period for developmental achievement and intellectual growth. PHYSICAL GROWTH Growth slows considerably during toddlerhood. The average weight gain is 1.8 2.7 kgs (4-6 lbs.) per year. The average weight for 2 years is 12 kgs (27 lbs). The birth weight is quadrupled by 2.5 years of age. The rate of increase in height also slows. The usual increment is an addition of 7.5 cms (3 inches) per year and occurs mainly in the elongation of the legs rather than the trunk. The average height of a 2 year old is 86.6 cm (34 inches). In general adult height is about twice the 2-year old childs height. The head circumference slows somewhat by the end of infancy and

is usually equal to chest circumference by 1-2 years of age. The usual total increase in head circumference during the second year is 2.5cm (1 inch). Chest circumference continues to increase in size and exceeds head circumference during the toddler years. After the second year the chest circumference exceeds the abdominal measurement, which, in addition to the growth of the lower extremities, gives the child a taller, leaner appearance. Visual acuity of 20/40 is considered acceptable during the toddler years. The senses of hearing, smell, taste and touch become increasingly well developed, coordinated with each other, and associated with other experiences. Most of the physiologic systems are relatively mature by the end of toddlerhood. Respirations are slightly slow but still mainly abdominal. They are prone to develop otitis media, tonsillitis, and upper respiratory tract infection due to short and straight internal structures of ears and throat hence, threat of lower respiratory tract infection are less due to progressively enlarged lumens and vessels. Heart rate slows from 110 90 bpm. Blood pressure increases to about 99/64 mmHg. Brain develops at about 90% of its adult size. Stomach capacity increases, secretions become more acidic thus, gastrointestinal infections become less common. Complete myelination of the spinal cord makes the control of the urinary and anal sphincters, lets the child retain urine for up to 2 hours or longer. They have a more developed immune system. IgG and IgM antibody production becomes mature at 2 years. Toddler has difficulty of the young infant in maintaining body temperature under conditions of moderate variation in temperatue. DEVELOPMENTAL MILESTONE The major gross motor skill during the toddler years is the development of locomotion. At age 2 years, toddlers can walk up and downstairs using both feet and same step at the same time and by age 2.5 years they can jump, using both feet, stand on one foot for a second or two and manage a few steps on tiptoe. Fine motor development is demonstrated in increasingly skillful manual dexterity. By 2 years of age toddlers use their hands to build towers and can open doors by turning door knobs, and unscrew lids. Mastery of gross and fine motor skill is evident in all phases of the childs activity such as play, dressing, language, and comprehension, response to discipline, social interaction and propensity to injuries. EMOTIONAL DEVELOPMENT: Developmental Task: Autonomy versus Shame and Doubt According to Erick Erickson (1993), the developmental task of toddlerhood is acquiring a sense of autonomy while overcoming a sense of doubt and shame. Several characteristics, especially negativism and ritualism, are typical of toddlers in their quest for autonomy. As toddlers attempt to express their will they often act with negativism. The words No or Me Do! can be sole vocabulary. Emotions become very strongly expressed, usually in rapid mood swings. One minute, toddlers can be engrossed in an activity and the next minute they might be violently angered. If scolded for doing something wrong, they can have a temper tantrum and almost instantaneously pull at the parents legs to be picked up and comforted. In contrast to negativism, which frequently disrupts the environment, ritualism, the need to maintain sameness and reliability provides a sense of comfort. Toddlers can venture out with security when they know that familiar people, places, and routines still exist.

COGNITIVE DEVELOPMENT The period from 12 -24 months of age is a continuation of the final two stages of the sensory motor phase. During this time the cognitive processes develop rapidly and at times seem similar to those of mature thinking. However, reasoning skills are still quite primitive and nedd to be understood to effectively deal with the typical behaviors of a child of this age. In stage 5 Tertiary circular reaction (12-18 mos.), a toddler is described as a little scientist. In stage 6 Invention of New Means through Mental Combination (18 24 mos.) where toddlers are able to try out various actions mentally rather than having to actually perform them. One of the most dramatic achievements is in the area of complete object permanence. There is a greater symbolization of imitation. The child is acutely aware of others actions and attempts to copy them in gestures and in words which can be classified to as Domestic mimicry which is imitating household activities. Preconceptual Phase At 2 years of age, the toddler enters the preconceptual phase which lasts until 4 years old. This is primarily one of the transition, that bridges the purely self-satisfying behavior of infancy and the rudimentary socialized behavior of latency. Preoperational thought implies that children cannot think in terms of operations rather toddlers think primarily on the basis of their perception of an event. SPIRITUAL DEVELOPMENT Toddlers learn about God through the words and the actions of those closest to them. They have vague idea of God and religious teachings because of their immature cognitive processes; however, if God is spoken about with reverence, young children associate God with something special.

DEVELOPMENT OF BODY IMAGE With the increasing motor skills, toddlers recognize the usefulness of the body parts and gradually learn their respective names. At 2 years old the toddler recognizes sexual differences and reference to self by name. DEVELOPMENT OF SEXUALITY Just as toddlers explore their environment, they also explore their bodies and find that touching certain body parts is pleasurable. Genital fondling (masturbation) can occur and involves manual stimulation as well as posturing movements against objects, and sucking on fingers and toes. Other demonstration on sexual activities includes rocking, swinging, and hugging people and toys. Sex role differences become obvious to children and are evident in much of their imitative play. SOCIAL DEVELOPMENT

A major task of the toddler period is differentiation of self from significant others, usually the mother. Differentiation consists two phases. The separations emerge from symbolic fusion with the mother. Individuation marks the childrens assumption of their individual characteristics in the environment. Toddlers show less fear of stranger when parents are present but when left alone with the stranger they become very fearful and acutely anxious. Language Toddlerhood is a critical time for language development. More striking characteristic is the increasing level of comprehension. At 2 years approximately 300 words can be spoken and uses multiword sentences by stringing together two or three words. They have the ability to comprehend and understand speech is much greater than the number of words the child can say. Personal-social Behavior Personal social interaction is one of the dramatic aspects of development. It is evident in areas such as dressing, feeding, playing, and establishing self control. Play This magnifies the toddlers physical and psychosocial development. Interaction with people becomes increasingly important. The solitary play of infancy progresses to parallel play where the toddler plays alongside, not with, other children.

Physical Assessment Results

Integumentary System:

1. Skin
Skin color is brown, non-palpable lesions on the anterior and posterior side of patients right arm, no presence of edema. Her skin is dry, with excessive perspiration and oiliness. The left and right upper extremities have the same temperature, warm. Has good mobility and turgor because her skin can be lifted easily and snaps back immediately to its resting position.

2. Nails
The nail beds are pinkish in color, thick and the angle is 160 degrees, well rounded and convex. No inflammation noted.

3. Head and scalp

Her head is held upright and still, normocephalic, smooth, round, and symmetrical. The color of the scalp is lighter than the face, it is inelastic and no, scaliness and lice noted but there were dandruffs. Upon palpation there were no presence of lesions, deformities and lumps. Tenderness and masses were also not noted. Hair is color black, thick and equally distributed. Dandruffs were visible all over the hair.

4. Face
The shape of her face is round, it is symmetrical and no edema noted. The color of her face is even with the rest of the body, brown. No involuntary movements. No tenderness and masses upon palpation.

5. Eyebrows
Her eyebrows are symmetrical in appearance and movements, thick and no presence of scaliness. No lesions and tenderness.

6. Eyes

The conjunctiva is transparent, moist, pinkish in color and no swelling or lesions noted. The color of the sclera is china white. The cornea has no opacities or cloudiness, transparent, shiny and smooth and convex in shape. The lens has no presence of cloudiness as well. Pupil size is estimated to be 5mm, black in color, round and equal in both eyes. Eye lids are intact with no discharges and discoloration, it closes symmetrically. Lids do not cover the pupil but partially covers the iris when open. No presence of edema and no masses upon palpation.

7. Ears
The auricles of both ears are level with each other whose upright point of attachment is in straight line with the lateral canthus of the eye. Position is almost vertical and the color is the same as that of the face. No moles, cyst, deformities or nodules noted. Upon palpation there were no tenderness noted. The color of the auditory canal is uniformly pink with tiny hair in its outer third and with little cerumen.

8. Nose
Her nose is smooth and located in the midline. It is symmetrical and the color is the same with the other facial featured. No tenderness upon palpation and the nasal bone is firm and stable. Nasal mucosa is pinkish and moist, no swelling, exudates and bleeding. Inferior and middle turbinates are pinkish in color, no swelling, exudates and polyps.

9. Sinuses There is no presence of tenderness both in the frontal and maxillary sinuses.

10.

Mouth

The lips are pale and dry, no ulcers and lesions. The mucosa is dry and pale and no bleeding noted. The gums are pale with a tight margin at each tooth. No edema, bleeding and lesions. Her teeth are smooth, yellowish with shiny tooth enamel. No presence of caries, plaque and tartar. No loose teeth and extractions No abnormalities in shape and position. The hard palate is whitish in color and dome-shape, no deformities. The dorsum part of the tongue is dry, regular in size and pale, with raised papillae and symmetrical. The hypoglossal nerve is intact. The ventral surface of the tongue is pinkish in color and smooth with prominent vein between frenulum folds. The soft palate of the pharynx and the uvula rises symmetrically. The pharynx is pinkish in color, smooth and symmetrical, no discharges and ulcerations. Tonsils are grade 1 because the tonsils are located behind the tonsilar pillar. Uvula rises centrally.

11.

Neck

The neck is symmetrical, without scars, growth and enlargement of parotid glands, color is the same with the other body parts. Lymph nodes are non-palpable. The trachea is located at the midline of the neck, above the suprasternal notch. The thyroid gland is small, smooth and free of nodules, it ascends during swallowing but is not visible.

12. Peripheral vascular system

The size of her extremities are proportional, it is symmetrical, with insignificant lesions noted no edema and ulcers. The popliteal pulse is strong and regular. The dorsalis pedis pulse is strong and regular while the posterior tibialis is moderately strong and regular.

Anatomy and Physiology

The Cardiovascular System The cardiovascular or circulatory system is responsible primarily with the movement of blood in the body. It also plays an important role in the maintenance of homeostasis, immune response and the transport of fluids. It is composed of tubes that serve as passage of fluids to and away from the heart and the different components of blood. Arteries are the vessels that transport fluids away from the heart. Arteries carry oxygenated blood. In the past they were found to be empty on dead people thus give the name. From the words Aer= hollow Tereo= to carry. The hollow center is called the lumen. It is made up of three main layers. The tunica externa as the outermost layer, tunica media as the middle layer and tunica intima as the inner layer. The structure of the arteries gives them two special properties----- elasticity and contractility. As the ventricles of the heart start to eject blood, the arteries expand to accommodate the extra blood. Then as the ventricles start to relax, the elastic recoil of the arteries forces blood onward. The contractility of the artery comes from the smooth muscles arranged longitudinally and the rings around the lumen. These muscles are stimulated by the sympathetic nervous system to cause vasoconstriction and vasodilation.

The microscopic capillaries are the smallest blood vessels. Their exceedingly thin walls consist of a thin tunica intima. They are found near everybody cell and are distributed according to oxygen demands. The primary function of the capillary is to permit nutrient, waste, and gas exchange between the blood and the tissue cells. This exchange occurs only in capillary wall since the other blood vessels have thick walls presenting a great barrier for exchange. Veins are composed essentially of the same three coats as arteries, but they have variations in thickness. Despite the difference the vein is still able adapt to the changes volume. By the time blood leaves the capillaries and flows into the vein, its pressure I s greatly decreased. This decrease in pressure is what caused its difference from the artery. Some veins have valves to prevent backflow of unoxygenated blood due to the decrease in pressure. The blood is a connective tissue suspended in a liquid matrix called plasma. Suspended also in this matrix are formed elements------ cells and cell fragments. Plasma is a straw colored liquid that consists of mostly water (91.5%) and a variety of dissolved substances (nutrients, wastes, enzymes, hormones, respiratory gases, and ions). Formed elements are red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes). Plasma consists about 55% of whole blood and 45 % formed elements. Seven % of the dissolved components in blood plasma are proteins. Some proteins in plasma are also found elsewhere in the body. However, those confined in blood are called blood proteins. These proteins are important in the maintenance of osmotic pressure, which is important in total body fluid balance.

The liver, including albumins (54% of plasma proteins), globulins 38% and fibrinogen 7%, synthesizes most plasma proteins. Other solutes in plasma include waste products such as urea, uric acid, creatinine, ammonia, and bilirubin; nutrients; vitamins; regulatory substances such as enzymes, hormones and electrolytes. Formation of Blood Cells The process by which blood cells are formed is called hemapoiesis or hematopoiesis. During the embryonic stage of life there are several centers for production. The yolk sac, liver, spleen, thymus gland, lymph nodes, and bone marrow will all participate at various times in producing formed elements. After birth however, hematopoiesis occurs only in the red marrow (myeloid tissue). Red bone marrow is found in the proximal epiphysis on the humerus and femur,; flat bones such as the sternum, ribs and cranial bones; and the pelvis. Stem cells which give rise to differentiated blood cells and also replenish themselves reside mainly in the red marrow, Although few circulate in the blood. Five types of cells develop from pluripotent hematopoietic stem cells (hemocytoblasts), which are derived from the mesenchyme. 1. Proerythroblasts ( rubiblasts) form erythrocytes 2. Myeloblasts- form mature neutrophils, eosinophils, and basophils. 3. Monoblasts- form mature monocytes 4. lyphoblasts form mature lymphocytes 5. Megakaryoblasts- form platelets or thrombocytes Several hematopoietic factors stimulate differentiation along particular paths and promote proliferation of certain proginator cells. Erythropoietin or EPO a hormone mainly by the kidneys and also in small amounts produced by the liver stimulates the formation of erythrocyte precursors and thrombopoietin stimulate the formation of thrombocytes. In addition there are several cytokines that regulate hematopoiesis of different blood cell types. Cytokines are small glycoproteins produced by the red bone marrow cells, leukocytes, macrophages and fibroblasts. They act locally as autocrines and paracrines that stimulate normal cell function and stimulate proliferation. Two important families of cytokines that stimulate blood cell formation are called colony stimulating factors (CSFs) and interleukins.

The causes of hematopoietic growth will be later shown in the table.

Most growth factors are available through recombinant DNA technology. They hold tremendous potential for medical uses in situations where a persons ability to produce blood cells are diminished or ineffective. Recombinant erythropoietin is very effective in diminished erythrocyte production. Red Blood Cells: More than 99% of the formed elements in blood are erythrocytes. They contain the oxygen-carrying pigment hemoglobin, which is responsible for the red color of whole blood. Red Blood Cell Anatomy: Under a microscope, RBCs appear as biconcave discs averaging about 8m in diameter. The flexible biconcave shape allows the RBC to squeeze through the narrow capillaries, which may only be 3m wide. Mature red blood cells are simple in structure. They lack nucleus and other organelles and can neither reproduce nor carry extensive metabolic activities. The plasma membrane encloses the hemoglobin, which was synthesized before the loss of the nucleus and which constitutes about 33% cells weight. Hemoglobin is then dissolved in the cytosol. Anatomy and Physiology of Platelets Like red blood cells, platelets are anuclear and discoid; they measure 1.53.0 m in diameter. The body has a very limited reserve of platelets and so they can be rapidly depleted. They contain RNA, a canalicular system, and several different types of granules; lysosomes (containing acid hydrolases), dense bodies (containing ADP, ATP serotonin and calcium) and alpha granules (containing fibrinogen, factor V, vitronectin, thrombospondin and von Willebrand factor), the contents of which are released upon activation of the platelet. These granule contents play an important role in both hemostasis and in the inflammatory response.

Production

Platelets are produced in the bone marrow; the progenitor cell for platelets is the megakaryocyte. This large, multinucleated cell sheds platelets into the circulation. Thrombopoietin (c-mpl ligand) is a hormone, mainly produced by the liver, that stimulates platelet production. It is bound to circulating platelets; if platelet levels are adequate, serum levels remain low. If the platelet count is decreased, more thrombopoeitin circulates freely and increases marrow production. Circulation The circulating life of a platelet is 910 days. After this it is sequestered in the spleen. Decreased function (or absence) of the spleen may increase platelet counts, while hypersplenism (overactivity of the spleen, e.g. in Gaucher's disease, leukemia and cirrhosis) may lead to increased elimination and hence low platelet counts. Function Platelets are activated when brought into contact with collagen (which is exposed when the endothelial blood vessel lining is damaged), thrombin (primarily through PAR-1), ADP, with receptors expressed on white blood cells or the endothelial cells of the blood vessels, among other activators. Once activated, they release a number of different coagulation factors and platelet activating factors. Platelet activation further results in the scramblase mediated transport of negatively charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by phosphatidylserine and phosphatidylethanolamine) for the tenase and prothrombinase complexes. The platelets adhere to each other via adhesion receptors or integrins, and to the endothelial cells in the wall of the blood vessel forming a haemostatic plug in conjunction with fibrin. The high concentration of myosin and actin filaments

in platelets are stimulated to contract during aggregation, further reinforcing the plug. The most common platelet adhesion receptor is glycoprotein (GP) IIb/IIIa; this is a calcium-dependent receptor for fibrinogen, fibronectin, vitronectin, thrombospondin and von Willebrand factor (vWF). Other receptors include GPIb-V-IX complex (vWF) and GPVI (collagen) Activators There are many known platelet activators. They include

Collagen, especially with von Willebrand factor which is exposed when endothelial blood vessel lining is damaged and binds to GPVI on the platelet; Thrombin, primarily through cleavage of the extracellular domain of PAR1 and PAR4; Thromboxane A2 (TxA2), which binds to TP; ADP through creation of TxA2, which can be blocked by conversion of ADP to cAMP; Human neutrophil elastase (HNE) cleaves the IIb3 integrin on the platelet surface; P-selectin, which binds to PSGL-1 on endothelial cells and white blood cells; and Convulxin, (a purified protein from snake venom) which binds to GPVI.

Inhibitors

Prostacyclin opposes the actions of Thromboxane A2 Nitric oxide Clotting factors II, IX, X, XI, XII Nucleotidases by breaking down ADP

Role in disease High and low counts A normal platelet count in a healthy person is between 150,000 and 400,000 per mm3 of blood. 95% of healthy people will have platelet counts in this range. Some will have statistically abnormal platelet counts while having no abnormality, although the likelihood increases if the platelet count is either very low or very high. Both thrombocytopenia (or thrombopenia) and thrombocytosis may present with coagulation problems. Generally, low platelet counts increase bleeding risks (although there are exceptions, e.g. immune heparin-induced thrombocytopenia) and thrombocytosis (high counts) may lead to thrombosis (although this is mainly when the elevated count is due to myeloproliferative disorder). Low platelet counts are generally not corrected by transfusion unless the patient is bleeding or the count has fallen below 5 (x 109/L); it is contraindicated in thrombotic thrombocopenic purpura (TTP) as it fuels the coagulopathy. In patients having surgery, a level below 50 (x 109/L) is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as epidurals are avoided for levels below 80-100. Normal platelet counts are not a guarantee of adequate function. In some states the platelets, while being adequate in number, are dysfunctional. For instance, aspirin irreversibly disrupts platelet function and hence normal hemostasis; normal platelet function may not return until the aspirin is ceased and new ones, which may take over a week, have replaced the affected platelets. Similarly, uremia (a consequence of renal failure) leads to platelet dysfunction that may be ameliorated by the administration of desmopressin.

Diseases

Disorders leading to a reduced platelet count:

Thrombocytopenia
o o o

Idiopathic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Drug-induced thrombocytopenia, e.g. heparin-induced thrombocytopenia (HIT)

Gaucher's disease Aplastic anemia

Disorders leading to platelet dysfunction or reduced count:

HELLP syndrome Hemolytic-uremic syndrome Chemotherapy

Disorders featuring an elevated count:

Thrombocytosis, including benign essential thrombocytosis (elevated counts, either reactive or as an expression of myeloproliferative disease); may feature dysfunctional platelets

Disorders of platelet adhesion or aggregation:

Bernard-Soulier syndrome

Glanzmann's thrombasthenia Scott's syndrome von Willebrand disease

Disorders of platelet metabolism

Decreased cyclooxygenase activity, induced or congenital Storage pool defects, acquired or congenital

Anatomy and Physiology of the liver The liver is the largest internal organ in the body, and weighs about 3 pounds in an adult. The liver is located in the right upper quadrant of the abdomen, just below the diaphragm. A thick capsule of connective tissue called Glisson's capsule covers the entire surface of the liver. The liver is divided into a large right lobe and a smaller left lobe. The falciform ligament divides the two lobes of the liver. Each lobe is further divided into lobules that are approximately 2 mm high and 1 mm in circumference.

These hepatic lobules are the functioning units of the liver. Each of the approximately 1 million lobules consists of a hexagonal row of hepatic cells called hepatocytes. The hepatocytes secrete bile into the bile channels and perform a variety of metabolic functions. Between each row of hepatocytes are small cavities called sinusoids. Each sinusoid is lined with Kupffer cells, phagocytic cells that remove amino acids, nutrients, sugar, old red blood cells, bacteria and debris from the blood that flows through the sinusoids. The main functions of the sinusoids are to destroy old or defective red blood cells, to remove bacteria and foreign particles from the blood, and to detoxify toxins and other harmful substances. Approximately 1500 ml of blood enters the liver each minute, making it one of the vascular organs in the body. Seventy-five percent, of the blood flowing to the liver comes through the portal vein; the remaining 25% is oxygenated blood that is carried by the hepatic artery The liver is responsible for important functions, including:

Bile production and excretion Excretion of bilirubin, cholesterol, hormones, and drugs Metabolism of fats, proteins, and carbohydrates Enzyme activation Storage of glycogen, vitamins, and minerals Synthesis of plasma proteins, such as albumin and globulin, and clotting factors Blood detoxification and purification The liver synthesizes and transports bile pigments and bile salts that are needed for fat digestion. Bile is a combination of water, bile acids, bile

pigments, cholesterol, bilirubin, phospholipids, potassium, sodium, and chloride. Primary bile acids are produced from cholesterol. When bile acids are converted or "conjugated" in the liver, they become bile salts.

Bilirubin is the main bile pigment that is formed from the breakdown of heme in red blood cells. The broken-down heme travels to the liver, where it is secreted into the bile by the liver. Bilirubin production and excretion follow a specific pathway. When the reticuloendothelial system breaks down old red blood cells, bilirubin is one of the waste products. This "free bilirubin" is a lipid soluble form that must be made water-soluble to be excreted. The conjugation process in the liver converts the bilirubin from a fat-soluble to a water-soluble form. The liver also plays a major role in excreting cholesterol, hormones, and drugs from the body. The liver plays an important role in metabolizing nutrients such as carbohydrates, proteins, and fats. The liver helps metabolize carbohydrates in three ways:

Through the process of glycogenesis, glucose, fructose, and galactose are converted to glycogen and stored in the liver. Through the process of glycogenolysis, the liver breaks down stored glycogen to maintain blood glucose levels when there is a decrease in carbohydrate intake. Through the process of gluconeogenesis, the liver synthesizes glucose from proteins or fats to maintain blood glucose levels. The liver synthesizes about 50 grams of protein each day, primarily in the form of albumin. Liver cells also chemically convert amino acids to

produce ketoacids and ammonia, from which urea is formed and excreted in the urine. Digested fat is converted in the intestine to triglycerides, cholesterol, phospholipids, and lipoproteins. These substances are converted in the liver into glycerol and fatty acids, through a process known as ketogenesis. The liver produces both prothrombin and fibrinogen, substances needed to help blood coagulate. The liver also produces the anticoagulant heparin and releases vasopressor substances after hemorrhage.

Liver cells protect the body from toxic injury by detoxifying potentially harmful substances. By making toxic substances more water soluble, they can be excreted from the body in the urine. The liver also has an important role in vitamin storage. High concentrations of riboflavin or Vitamin B1 are found in the liver. 95% of the body's vitamin A stores are concentrated in the liver. The liver also contains small amounts of Vitamin C, most of the body's Vitamin D stores, and Vitamins E and K.

Anatomy and physiology of the Skin

The skin is the body's largest organ, covering the entire outside of the body and weighing approximately six pounds. In addition to serving as a protective shield against heat, light, injury, and infection, the skin also regulates body temperature, stores water, fat, and vitamin D and can sense painful and pleasant stimulation. Throughout the body, the skin's characteristics vary (i.e., thickness, color, texture). For instance, the head contains more hair follicles than anywhere else, while the soles of the feet contain none. In addition, the soles of the feet and the palms of the hands have much thicker layers. The skin is made up of the following layers, with each layer performing specific functions: epidermis, dermis, and fat layer.

The epidermis is the thin outer layer of the skin. The epidermis itself is made up of three sub-layers:

Stratum corneum (horny layer) This layer contains continually shedding, dead keratinocytes (the primary cell type of the epidermis). The keratin, a protein formed from the dead cells, protects the skin from harmful substances.

keratinocytes (squamous cells) This layer contains living keratinocytes (squamous cells), which help provide the skin with what it needs to protect the rest of the body.

Basal layer The basal layer is the inner layer of the epidermis, containing basal cells. Basal cells continually divide, forming new keratinocytes and replacing the old ones that are shed from the skin's surface.

The epidermis also contains melanocytes, which are cells that produce melanin (skin pigment). The dermis is the middle layer of the skin. The dermis is made up of the following:

blood vessels lymph vessels hair follicles sweat glands

A protein called collagen, made by fibroblasts (skin cells that give the skin its strength and resilience), holds the dermis together. This layer also contains pain and touch receptors.

The sub cutis is the deepest layer of skin and is also known as the subcutaneous layer. The sub cutis, consisting of a network of collagen and fat cells, helps conserve the body's heat while protecting other organs from injury by acting as a "shock absorber."

Anatomy and Physiology of the Respiratory System It is the function of the respiratory system to transport gases to and from the circulatory system. The respiratory system involves both External and Internal respiration. External Respiration is the exchange of gases between the atmosphere and the blood. Internal Respiration is the exchange of gases between the blood and the cells of the body. Cellular Respiration or Aerobic Respiration involves the use of oxygen to break down glucose in the cell. We will examine the structures and mechanisms that carry oxygen to the cells for use in aerobic respiration and that eliminate the carbon dioxide that is produced by the same process. Respiration is a vital function of all living organisms. Respiration occurs at two different levels. The level of the cell, in the mitochondria of eukaryotic cells, aerobic respiration requires oxygen to break down glucose, releases carbon dioxide, and produces large amounts of ATP. This level of respiration is called internal respiration or cellular respiration. An organism must get oxygen into its cells and carbon dioxide back out. This level of respiration is called external respiration because the exchange of gases. The exchange of gases, oxygen and carbon dioxide between the air and blood. A respiratory system is a group of organs working together of bring about the exchange of oxygen and carbon dioxide in the environment. Each cell consumes oxygen and produces

carbon dioxide. Large multicellular organism must have a respiratory system to ensure the effective exchange of gasses with the atmosphere quickly and efficiently to survive. The human respiratory system consists of the nose, nasal cavity, pharynx, larynx, trachea, smaller conducting passages (bronchi and bronchioles) and lungs. The respiratory system may be divided into the upper respiratory tract (consist of parts outside the chest cavity) composed of the nose, nasal cavities, pharynx, larynx, and the upper trachea. The lower respiratory tract consists of the trachea and the lungs themselves. Air enters the respiratory system through the mouth or nose. Air entering the nose passes into the nasal cavity. The Nasal Cavity is richly supplied with arteries, veins, and capillaries, which bring nutrients and water to its cells. As air pushes back from the nasal cavity, it enters the pharynx. The Pharynx is located in the back of the mouth and serves as a passageway for both air and food. When food is swallowed, a flap of cartilage, called the epiglottis, presses down and covers the opening to the air passage. From the pharynx, the air moves through the larynx, the upper end of the trachea, and into the trachea that leads directly to the lungs. These passageways provide a direct connection between the outside air and some of the most delicate tissue in the body. These passageways must filter out dust, dirt, smoke, bacteria, and a variety of other contaminants found in air. The first filtering is done in the nose. The nose will do three things as we breathe in: 1.filter the air 2.warm the air 3.provide moisture. As air passes through the nasal cavities it is warmed and humidified, so that air that reaches the lungs is warmed and moist. The Nasal Airways are lined with Cilia and kept moist by mucous secretions. The combination of cilia and mucous helps to filter out solid particles from the air warm and moisten the air, which prevents damage to the respiratory tissues. The moisture in the nose helps to heat and humidify the air, increasing the amount of water vapor the air entering the lungs contains. This helps to keep the air entering the nose from drying out the lungs and other parts of the respiratory system. At the top of the Trachea is the larynx (Voice Box or Adam's apple). Inside and stretched across the larynx are two highly elastic folds of tissue (Ligaments) called the vocal cords. Air rushing through the voice box causes the vocal cords to vibrate producing sound waves. At the top of the trachea is the larynx (Voice Box or Adam's apple). Inside and stretched across the Larynx are two highly elastic folds of tissue (Ligaments) called the

vocal. Air rushing through the voice box causes the vocal cords to vibrate producing sound waves. The walls of the trachea are made up of C-Shaped rings of tough flexible cartilage. These rings of cartilage protect the trachea, make it flexible, and keep it from collapsing or over expanding. The cells that line the trachea produce mucus; the mucus helps to capture things still in the air (dust and microorganisms), and is swept out of the air passageway by tiny cilia. Within the thoracic cavity, the trachea divides into two branches, the right and left bronchi. Each bronchus enters the lung on its respective side. The lungs are the site of gas exchange between the atmosphere and the blood. The right lung has three. Divisions or lobes, and is slightly larger than the two lobed left lung. The lungs are inside the thoracic cavity, bounded by the rib cage and diaphragm. Lining the entire cavity and encasing the lungs are pleural membranes that secrete a fluid that decreases friction from the movement of the lungs during breathing. The further branching of the bronchial tubes is often called the bronchial tree. Both bronchi and bronchioles contain smooth muscle tissue in their walls. This muscle tissue controls the size of the air passage. The bronchioles continue to subdivide until they finally end in clusters of tiny hallow air sacs called alveoli. All exchange of gasses take place in the alveoli. The Alveoli consist of thin, flexible membranes that contain an extensive network of capillaries. The Membranes separate a gas from liquid. The gas is the air we take in through our respiratory system, and the liquid is blood

Overview of the disease condition

Dengue and dengue hemorrhagic fever (DHF) result from infection by any of four serotypes of dengue viruses. Transmission occurs through the bite of infected Aedes mosquitoes, principally Aedes aegypti, which is also the principal urban vector of yellow fever. Hundreds of thousands of cases of dengue and DHF are reported each year in tropical regions of the Americas, Africa, Asia and Oceania. From 1980 through 1987, 879 632 cases of

dengue were reported to the Pan American Health Organization from countries in the American region. Outbreaks of the more severe form of dengue, DHF, occurred in Cuba in 1981 and in Venezuela in 1989. The majority of DHF cases, however, occur in Southeast Asia. From 1981 through 1986, 796 386 cases of DHF and 9774 deaths caused by dengue were reported to the World Health Organization (WHO) from countries in Southeast Asia. History The early history of dengue is clouded by the similarity of its clinical picture to that of other febrile illnesses. Dengue-like epidemics occurred in Egypt and on Java in 1779, but these may actually have been caused by chikungunya virus. Dengue or dengue-like epidemics were reported throughout the 19th and early 20th centuries in the Americas, southern Europe, North Africa, the Middle East, Asia and Australia and on various islands in the Indian Ocean, South and Central Pacific and the Caribbean. Generally these epidemics consisted of nonfatal febrile illnesses, often associated with rash and either muscle or joint pains. Deaths occurred during dengue epidemics in Australia in 1897 and in Greece in 1928, when over 1000 deaths were reported. Hemorrhagic manifestations, including gastrointestinal hemorrhage, were described during dengue epidemics in Texas and Louisiana in 1922. Nevertheless through the first half of the 20th century, dengue was generally described as a self-limited, nonfatal febrile illness, with occasional hemorrhagic manifestations such as petechiae, epistaxis, gingival bleeding and menorrhagia, that only rarely resulted in more severe or fatal outcomes. In 1944 two immunologically distinct but related viruses, now referred to as dengue 1 (DEN-I) and DEN-2, were isolated by Sabin from patients with clinically diagnosed dengue. In 1956 Hammon et al. and coworkers isolated two new serotypes of dengue viruses, designated DEN-3 and DEN-4, as well as the previously recognized DEN-I and DEN-2, during epidemics of severe hemorrhagic illness among children in the Philippines. Outbreaks of what came to be known as DHF24 occurred throughout Southeast Asia during succeeding years. The term dengue shock syndrome was coined to describe the cases of DHF with shock, which clinical studies indicated was caused by increased vascular permeability and resultant intravascular hypovolemia.Eventually the WHO case definition of DHF was modified to make increased vascular permeability the hallmark of the disease.Cases of severe hemorrhage or even deaths caused by dengue infection that do not show evidence of increased capillary permeability are not currently classified as DHF according to WHO criteria. The emergence of DHF in the Americas is believed by some researchers to be following a similar pattern to that seen

in Southeast Asia more than 30 years ago. With the reinfestation of many countries in the American region by A. aegypti, dengue epidemics have recently struck cities and countries in the Americas that had been free of this disease for many years. Epidemiology Female A. aegypti mosquitoes acquire the dengue virus by biting an infected human during the viremic phase, which usually lasts for 4 to 5 days but may last up to 12 days. An extrinsic incubation period in the mosquito of 8 to 10 days must pass before the virus can be transmitted. The extrinsic incubation period is lengthened by cooler ambient temperatures. After this extrinsic incubation period the mosquito may transmit the virus during every subsequent feeding of its life. In most disease-endemic areas dengue transmission has a definite seasonality, but the reasons for the seasonal patterns are not fully understood. In some areas increases in dengue transmission coincide with periods of increased rainfall. The interactions between temperature and rainfall or variations in daily microclimates may be important determinants of dengue transmission. Cooler temperatures may affect adult mosquito survival, which may also influence transmission rates. Rainfall and temperature may affect patterns of mosquito feeding and reproduction. Human behavior, such as the changes in patterns of water storage in containers, which serve as breeding sites for the mosquitoes, may also affect disease transmission patterns.

The mechanism by which dengue virus circulation is maintained between epidemics is not fully understood. Forest cycles of dengue between monkeys and mosquitoes have been described, but recent techniques of studying molecular evolution in dengue viruses indicate that viruses from forest cycles in Africa do not represent a natural maintenance reservoir for epidemic dengue in humans. Both dengue and DHF affect persons of all ages, but whereas dengue attack rates are either uniform across age groups or in some studies increase with age, most DHF cases occur among children younger than 15 years of age. Some studies have found higher dengue attack rates among women than among men and early work suggested that DHF was more common in girls than in boys, but recent surveillance data from Thailand showed almost even proportions of boys and girls among the reported DHF cases. Similar proportions have been found among DHF cases in Puerto Rico and Indonesia. Several authors have indicated that race may be a risk factor for DHF, but interpretation of the data presented thus far is confused by possible interaction of other risk factors and by the lack of clear selection criteria for the study groups used to compare rates between races. A genetic risk for DHF was suggested by one study finding a possible relation- ship between histocompatibility antigens and DHF.

The rate of DHF among dengue-infected individuals is difficult to determine but would be expected to vary with underlying risk factors and perhaps with the infecting virus strain estimates of this rate have ranged from 1 to 7 DHF cases per 100 dengue infections Initially DHF case fatality rates, when the disease was not treated, were as high as 50%, but with appropriate recognition and treatment the reported case fatality rate in Thailand has dropped to less than 1%. Infection with a particular dengue serotype is believed to provoke long lasting homotypic immunity. In one study of experimental infection, heterotypic immunity lasted for 2 months, after which patients were susceptible to infection with another serotype. Another study presented epidemiologic data that suggested that heterotypic immunity might last for up to 1 year.

CLINICAL MANIFESTATION Since the recognition of DHF in the 1950s investigators have sought to define the clinical differences between severe and mild forms of dengue. Mild hemorrhagic manifestations, such as epistaxis, petechiae, gingival bleeding and menorrhagia, are accepted as part of the clinical picture of classic dengue. Manifestations of severe dengue include severe hemorrhage leading to shock through blood loss, sudden increased vascular permeability leading to shock with or without hemorrhage and severe encephalopathy with hepatitis. The classification of severe dengue has been complicated by the variety of these clinical pictures, for which the underlying pathophysiology may be different. The following description of the clinical course of classic dengue infection is based on the work of Riley and Sabin, who observed and described adults with naturally acquired or experimentally induced infections. Two to 15 days after the bite of an infective mosquito, the patient typically suffers sudden onset of headache, fever, retroorbital pain, backache, bone and joint pain, weakness, depression and malaise. Some patients have an evanescent rash over the thorax and joint flexures. There may be flushing of

the face and conjunctivitis as well as taste aberrations, anorexia, nausea, vomiting and abdominal pain. Lymphadenopathy and hepatomegaly may occur but splenomegaly is infrequent. Patients may complain of sore throat, cough, groin pain, hyperesthesia, dizziness, photophobia, eye pain and, rarely, a "yellow flamelike" color to objects. Fever and associated symptoms may subside after 3 or 4 days and the patient may recover completely. Alternatively the decline in fever may be followed 1 to 3 days later by a resurgence of fever and symptoms, giving a "saddleback" appearance to the temperature curve. A second rash, varying in form from scarlatiniform and maculopapular to petechial and occasionally purpuric, may appear with the initial decline of the fever. Severe itching, especially of the hands and feet, may accompany this rash, which is sometimes followed by desquamation. The symptoms persist for 1 to 3 days more and then subside with the fever. During the course of the illness there is often a relative or paradoxical bradycardia in the face of increased temperature. Patients may have hemorrhagic manifestations such as epistaxis or menorrhagia. Jaundice is rare. Convulsions may occur with the onset of fever. The spinal fluid is almost always clear with no elevation of cell count but the pressure may be increased. Depression, weakness and blurred vision may resolve slowly during convalescence. Patients may take several weeks to recover completely. Although these symptoms characterize "classical" dengue fever, dengue virus infection may also manifest as a nonspecific febrile illness which can be confused with influenza, measles or any nonspecific vital syndrome. The lack of a clear clinical pattern for dengue makes laboratory diagnosis a necessary part of any definitive evaluation of the disease. Patients who develop DHF or other severe manifestations of dengue generally have an onset of illness similar to that seen in "classical" or nonhemorrhagic dengue. The course usually begins with the sudden onset of fever, headache, nausea, vomiting, abdominal pain, pharyngitis, lymphadenopathy and sometimes a rash, which may be petechial or even ecchymotic early in the course.

The liver may become enlarged and pleural effusions may develop, usually beginning on the right side. As the fever begins to drop around Day 3 to 5, circulatory instability may develop with signs of decreased peripheral perfusion. Profound shock may follow. Disseminated intravascular coagulation and severe gastrointestinal hemorrhage have been described. The descriptions of such patients led to the following WHO case definitions for DHF: fever; hemorrhagic manifestations, including at least a positive tourniquet test (except in shock cases), and either major or minor bleeding phenomena; thrombocytopenia (platelet count less than or equal to 100 000/ mm3); and hemoconcentration (hematocrit increased by 20% or more relative to baseline values, or objective evidence of increased capillary permeability). In addition to this pattern of DHF, cases of severe dengue with massive gastrointestinal hemorrhage preceding the onset of shock, and without evidence of increased vascular permeability, have been described. Many of these fatal hemorrhagic cases did not meet the WHO case definition for DHF. Severe encephalopathy with convulsions and/or coma has also been described with dengue infection. Increased spinal fluid white blood cell counts (up to 27/ mm) were found in one series and normal spinal fluid was seen in another. Significant thrombocytopenia may occur in both DHF and "classical" dengue. A fall in platelet count associated with a rising hematocrit may suggest the development of DHF. Results of coagulation tests may be abnormal; prolonged partial thromboplastin and thrombin times are noted more frequently than prolonged prothrombin times. Elevated concentrations of serum aspartate amino- transferase have been noted in several studies. Hyponatremia is commonly found in DHF patients with shock and may be a cause of convulsions. Results of urinalysis are usually normal, but hematuria, trace amounts of albumin and urinary casts have been reported. DIAGNOSIS

Classical dengue fever may be confused with a variety of febrile ill- nesses, including influenza, measles, typhoid fever and malaria. DHF may be confused with sepsis, toxic shock and any of the viral hemorrhagic fevers including yellow fever. Diseases with specific treatments, such as bacterial meningitis, sepsis, malaria and Lassa fever, should be ruled out. Specific diagnosis of dengue infection is made by isolating the virus from the patient's blood. Acute serum samples are inoculated into tissue cultures of mosquito cells or directly into live Toxorhynchites or Aedes mosquitoes. Isolates can be identified from 2 to 7 days after inoculation depending on the actual technique used. Viruses are most likely to be isolated from acute serum samples obtained within 5 days after the onset of illness. Specific dengue serotypes can be identified by the indirect fluorescent antibody test, with the use of type-specific monoclonal antibodies on the isolated virus. Immunodiagnostic methods for determining dengue infection include detection of anti-dengue IgM and IgG by enzyme-linked immunosorbent assay (ELISA) and detection of hemagglutination inhibition antibody. Dengue-induced hemagglutination inhibition antibody cross-reacts broadly with other flaviviruses such as yellow fever and St. Louis encephalitis viruses. Complement fixation and neutralization antibody tests are more specific than hemagglutination inhibition. Most serologic screening for dengue infection is now done with an IgM ELISA. With appropriately timed samples, the sensitivity and specificity of this test in diagnosing dengue infection appear to be high. In a review of 131 patients from whom dengue virus was isolated at the Centers for Disease Control, Dengue Branch, 96% of the 76 samples drawn between 7 and 20 days after the onset of illness were positive by IgM capture ELISA (DJ Gubler, G Kuno, I Gomez, et al. unpublished data). A study of the performance of IgM ELISA in Thailand showed the sensitivity of this test in convalescent samples to be 97%, and none of the samples from the 2 groups of noninfected controls (98 soldiers and 39 schoolchildren) were positive. The pattern of HI response has been used to classify dengue infections as primary or secondary, based on the concept that initial, or primary dengue infections tend to elicit lower HI titers than do secondary infections (subsequent infections with a different dengue serotype or antigenically related

flavivirus). IgM:IgG ratios as determined by ELISA may be an alternative method of distinguishing primary from secondary infections. The rise in neutralizing antibody in primary infection is believed to be relatively type-specific and can be used to determine the infecting serotype. In secondary infections, because the immunologic cross- reactivity to different flaviviruses and anamnestic responses may result in heterologous titer elevations, the only reliable method for determining the infecting serotype is virus isolation. In summary diagnosis of dengue infection is best accomplished by obtaining an acute serum sample within 5 days after the onset of illness for virus isolation and antibody testing and a convalescent serum sample 14 to 21 days after illness onset for detecting IgG antibody titer rise and/or the presence of antidengue IgM. TREATMENT Treatment for classic dengue fever is supportive. Patients should be encouraged to drink plenty of fluids. Acetaminophen may be taken to control fever and aching if necessary. Aspirin is contraindicated both because of its anticoagulant effects and the increased risk of developing Reye syndrome. Patients or parents should be carefully instructed of the need to seek medical attention immediately if major or ongoing hemorrhage, signs of impending shock or any change in mental status should occur. The onset of cardiovascular collapse in patients who develop DHF may be sudden. Patients with significant hemorrhage or signs of increased capillary permeability such as hemoconcentration, effusions, edema or low serum albumin, as well as patients with mental status changes or with abnormal fluid and electrolyte balance, should be hospitalized and may require admission to an intensive care unit. Isolation is not necessary in mosquito- free environments. Usual precautions handling blood specimens should be observed. Intravenous fluid therapy is the mainstay of treatment for patients with DHF. Patients with dehydration and hemoconcentration may require intravenous fluids similar in volume and composition to regimens used to treat dehydration due to diarrheal illness. Patients in shock should be given fluids and other therapy according to accepted regimens for shock. The administration of heparin may need to be considered in patients who develop DIC.

There is some controversy over the role of steroids in treatment of severe dengue. Studies by Sumarmo et al. showed no benefit, over fluid therapy alone, of hydrocortisone injection given 30 mg/kg/day or 50 mg/kg in a single dose. The potential effect of high dose methylprednisolone in certain severe cases may need further evaluation.

Pathophysiology

Medical management

Lab results and correlation

HEMATOCRIT 7/15/09 44.4 44.5 46.2 46.9 7/16/09 47.7 47.2 43.2 43.7 7/17/09 47.1 42.2 41.5 40.6 40.7 7/16/09 39.5 39.7 PLATELET COUNT 7/15/09 22 20 17 7/16/09 14 15 10 7/17/09 35 14 20 12 7/16/09 17 19 44 7/19/09 33 10 Since the patient is experiencing dengue hemorrhagic fever it is expected for the platelet to decrease since there is damage to the megakaryocytes---- the mother cells of platelets. Platelets, which play an essential role in blood coagulation, are very small fragments of the cytoplasm from large precursor cells in the bone marrow called megakaryocytes. Platelets have an average survival in the circulation of about 10 days, and when they wear out, they are removed by macrophages in the spleen. While there is a slight increase in the hematocrit as a sign of bleeding since the hematocrit increases in cases of hemoconcentration due to loss of blood. CORRELATION

39.5 7/19/09 39.2 37.9 7/20/09 39.1 7/21/09 40.0

45 7/20/09 82

Urine and stool 8 hour urine July 15 July 16 3-11=2x 11-7=3x 7-3=2x 3-11=2x 11-7=3x 7-3=x 3-11=2x 11-7=4x 7-3=3x 3-11=2x 11-7=x 3-11=0 11-7=0 7-3=0 3-11=0 11-7=0 7-3=0 3-11=0 11-7=0 7-3=0 3-11=0 11-7=0 8 hour stool

July 17

July 18

July 19

July 20

7-3=2x 3-11=2x 11-7=2x 7-3=3x 3-11=2x 11-7=2x (PATIENT DISCHARGED) (PATIENT DISCHARGED)

7-3=0 3-11=0 11-7=0 7-3=0 3-11=0 11-7=0

July 21

The patients urine color is yellow (straw to dark amber).Transparency is turbid (clear). Specific gravity= 1.010 (1.010-1.025). Has no presence of glucose or sugar, Bilirubin, Ketone. Has large volume of blood and pH= 6.5 (4.6-8). Has no presence of potein. Its Urobilinogen is normal. Absence of nitrite and Leukocytes noted. Has no presence of pus in the urine. Has numerous red cells and abundance of Epithelial cells and Bacteria. And has few Mucus threads. Complete Blood Count

The primary goal of laboratory examination of specimen obtained from the patient is to yield accurate and precise information to aid in patients diagnosis. It aids in establishing facts together with diagnostic examination and physical examination to confirm a specific disease condition and identify occurrence of exacerbation. It helps the doctor execute medical managements that will be necessary for the wellness of the patient. Laboratory exam Normal value Result Implication Correlation Red blood cells make up about 45% of HCT the volume of whole blood. This Male: 42-50 % 44.4% Increased percentage is called the hematocrit. If 7/15/09 Female: 37-44% 39.2% the number of red cells is low the 7/19/09 hematocrit decreases. Men have somewhat higher hematocrits than do women. Low hematocrit indicates anemia. Haemoglobin value is obtained to

HGB

Male: 13-16 g% Female:12-14%

15.30 %

Increased

measure the amount of haemoglobin in the whole blood. The amount of haemoglobin determines the oxygen carrying capacity of the blood A WBC is obtained to determine the presence of infection.

WBC

4.5 11 T/cumm

4990T/cumm

Increased

Differential cont: Eosinophil Monocyte 1 - 4% 1 6% 0% 2% Decreased Normal Increased in specific infections. Increased in viral infections; low numbers leave person dangerously susceptible to infection Indicative of a possible viral infection Blood platelets are even smaller than red cells. Their function is to stop bleeding from injured small blood vessels as in cuts or abrasions by sticking together and forming plugs. A variety of disease conditions can cause low numbers of platelets. Such patients may bleed more

Lymphocyte Platelet
7/15/09 7/19/09

20 35% 150 400 T/cumm

22% 22T/cumm 33T/cumm

Normal Decreased Decreased

easily and excessively. Higher than normal platelet counts occur in pregnancy or after strenuous exercise. Increased platelets are noted in more serious conditions such as diseases of the bone marrow. Platelets do contribute to coronary heart disease and blood clot formation

Pharmacologic management study

Paracetamol
Generic Name: Acetaminophen Brand Name: Paracetamol Classification: Analgesics (Non-Opioid) & Antipyretics Indications: Mild pain, fever Mechanism of Action: Paracetamol exhibits analgesic action by peripheral blockage of pain impulse generation. It produces antipyresis by inhibiting the hypothalamic heat-regulating centre. Its weak anti-inflammatory activity is related to inhibition of prostaglandin synthesis in the CNS. Indication: Mild pain or fever Route and Dosage: Children <12 yr should not receive >5 doses/24 hr without notifying physician or other health care professional PO (Adults and Children > 12 yr): 325-650 mg q 4-6 hr or 1 g 3-4 times daily or 1300 mg q 8 hr (not to exceed 4 g or 2.5 g/24 hr in patients with hepatic/renal impairment) PO (Children 1-12 yr): 10-15 mg/kg/dose q 4-6 hr as needed (not to exceed 5 doses/24 hr) PO (Infants ): 10-15 mg/kg/dose q 4-6 hr as needed (not to exceed 5 doses/24 hr) PO (Neonates ): 10-15 mg/kg/dose q 6-8 hr as needed Rect (Adults and Children > 12 yr): 325-650 mg q 4-6 hr as needed or 1 g 3-4 times/day (not to exceed 4 g/24 hr) Rect (Children 1-12 yr): 10-20 mg/kg/dose q 4-6 hr as

needed Rect (Infants ): 10-20 mg/kg/dose q 4-6 hr as needed Rect (Neonates ): 10-15 mg/kg/dose q 6-8 hr as needed Contraindication: Contraindicated to patients hypersensitive to drug; use cautiously in patients with long-term alcohol use because therapeutic doses cause hepatotoxicity in these. Side/Adverse Effects: Nausea, allergic reactions, skin rashes, acute renal tubular necrosis Interactions: Drug-Drug: Chronic high-dose acetaminophen (>2 g/day) may increase the risk of bleeding with warfarin (PT should be monitored regularly and INR should not exceed 4) Hepatotoxicity is additive with other hepatotoxic substances , including alcohol Concurrent use of sulfinpyrazone , isoniazid , rifampin , rifabutin , phenytoin , barbiturates , and carbamazepine may the risk of acetaminophen-induced liver damage (limit self-medication); these agents will also therapeutic effects of acetaminophen Concurrent NSAIDs the risk of adverse renal effects (avoid chronic concurrent use) Propranolol metabolism and may effects May effects of lamotrigine and zidovudine Pharmacokinetics: Absorption: Well absorbed following oral administration. Rectal absorption is variable Distribution: Widely distributed. Crosses the placenta; enters breast milk in low concentrations Metabolism and Excretion: 85-95% metabolized by the liver. Metabolites may be toxic in overdose situation. Metabolites excreted by the kidneys Half-life: Neonates: 2-5 hr. Adults: 1-3 hr TIME OF ACTION: PO: onset: 0.5-1 hour, peak: 1-3 hour, duration: 3-8 hour. Rect: onset:0.5-1 hour, peak 1-3 hour, duration: 3-4 hour. Nursing responsibilities:

Warn patient that high doses and unsupervised long term use can cause liver damage

Excessive alcohol use may increase the risk for liver damage Tell patient not to use if fever is persisting longer than 3 days unless directed by physician Use liquid for children and for patients who have difficulty in swallowing In children, do not exceed 5 doses in 24 hours Tell parents to consult prescriber before giving medications to children below 2 years old

Tranexamic acid
Generic name: Tranexamic acid Brand name: Cyklokapron Classification:Therapeutic: hemostatic agents, Pharmacologic: antifibrinolytics , plasminogen inactivators Indications: Prevention or reduction of hemorrhage following dental surgery in hemophiliacs Mechanism of Action: Inhibits activation of plasminogen, thereby preventing Route and dosage: the conversion of plasminogen to plasmin PO (Adults and Children ): 25 mg/kg 3-4 times daily beginning the day before surgery, then 3-4 times daily for 2-8 days postop IV (Adults and Children ): 10 mg/kg just prior to surgery with appropriate replacement therapy, then 3-4 times daily for 2-8 days Renal Impairment PO (Adults and Children ): Serum creatinine 1.36-2.83 mg/dl--15 mg/kg twice daily; serum creatinine 2.83-5.66 mg/dl-- 15 mg/kg daily; serum creatinine >5.66 mg/dl-- 15 mg/kg every 48 hr or 7.5 mg/kg once daily Renal Impairment IV (Adults and Children ): Serum creatinine 1.36-2.83 mg/dl--10 mg/kg twice daily; serum creatinine 2.83-5.66 mg/dl-- 10 mg/kg daily; serum creatinine >5.66 mg/dl-- 10 mg/kg every 48 hr or 5 mg/kg once daily

Contraindications/precautions Hypersensitivit y Active intravascular clotting Acquired defective color vision Subarachnoid hemorrhage Use Cautiously in: Renal impairment (increased dosing interval is recommended if serum creatinine >1.36 mg/dl) Hematuria originating in the upper urinary tract Conditions associated with increased thrombus formation Pregnancy or lactation (safety not established) Adverse reactions/side effects: CNS: dizziness, EENT: visual abnormalities, CV: hypotension, thromboembolism, thrombosis, GI: diarrhea, nausea, vomiting Interactions: Drug-Drug: Concurrent use of clotting factor complexes may increase the risk of thrombotic complications (give tranexamic acid 8 hr following clotting factor replacement therapy) Pharmacokinetics: PO: onset: unknown, peak: 3 hour, duration: 7-8 hour. IV: onset: unknown, peak: unknown, duration: 7-8 hours. Antifibrinolytic concentration in plasma. Tissue levels persists for 17 hours.

Nursing responsibilities: Instruct patient to take tranexamic acid as directed. Do not take more or less than directed. If a dose is missed, take as soon as possible unless almost time for next dose; do not double doses Advise patient to inform health care professional of any changes in vision. Inform patients on prolonged therapy of the importance of regular ophthalmologic follow-up Caution patient to avoid products containing aspirin or NSAIDs without consulting health care professional Instruct patient to notify health care professional if signs and symptoms of thrombosis (severe, sudden headache; pains in chest, groin, or legs, especially calves; sudden loss of coordination; sudden and unexplained shortness of breath; slurred speech; visual changes; weakness or numbness in arm or leg) occur.

Salbutamol
Generic name: Albuterol Sulfate Classification: Bronchodilators, Adrenergic Indications: Used as a bronchodilator to control and prevent reversible airway obstruction caused by asthma or COPD Inhaln: Used as a quick-relief agent for acute bronchospasm and for prevention of exercise-induced bronchospasm PO: Used as a long-term control agent in patients with chronic/persistent bronchospasm Mechanism of Action: Binds to beta2-adrenergic receptors in airway smooth muscle, leading to activation of adenyl cyclase and increased levels of cyclic-3', 5'-adenosine monophosphate (cAMP). Increases in cAMP activate kinases, which inhibit the phosphorylation of myosin and decrease intracellular calcium. Decreased intracellular calcium relaxes smooth muscle airways Relaxation of airway smooth muscle with subsequent bronchodilation Relatively selective for beta2 (pulmonary)

receptors Route and Dosage: PO (Adults and Children >12 yr): 2-4 mg 3-4 times daily (not to exceed 32 mg/day) or 4-8 mg of extended-release tablets twice daily PO (Geriatric Patients ): Initial dose should not exceed 2 mg 3-4 times daily, may be increased carefully (up to 32 mg/day) PO (Children 6-12 yr): 2 mg 3-4 times daily or 0.3-0.6 mg/kg/day as extended-release tablets divided twice daily; may be carefully increased as needed (not to exceed 8 mg/day) PO (Children 2-6 yr): 0.1 mg/kg 3 times daily (not to exceed 2 mg 3 times daily initially); may be carefully increased to 0.2 mg/kg 3 times daily (not to exceed 4 mg 3 times daily) Inhaln (Adults and Children >4 yr): Via metered-dose inhaler--2 inhalations q 4-6 hr or 2 inhalations 15 min before exercise (90 mcg/spray); some patients may respond to 1 inhalation. NIH Guidelines for acute asthma exacerbation: Children--4-8 puffs q 20 min for 3 doses then q 1-4 hr; Adults-4-8 puffs q 20 min for up to 4 hr then q 1-4 hr prn Inhaln (Adults and Children >12 yr): NIH Guidelines for acute asthma exacerbation via nebulization or IPPB--2.5-5 mg q 20 min for 3 doses then 2.5-10 mg q 1-4 hr prn; Continuous nebulization-10-15 mg/hr Inhaln (Children 2-12 yr): NIH Guidelines for acute asthma exacerbation via nebulization or IPPB--0.15 mg/kg/dose (minimum dose 2.5 mg) q 20 min for 3 doses then 0.15-0.3 mg/kg (not to exceed 10 mg) q 1-4 hr prn or 1.25 mg 3-4 times daily for children 10-15 kgor 2.5 mg 3-4 times daily for children >15 kg; Continuous nebulization-0.5-3 mg/kg/hr Inhaln (Adults and Children >4 yr): Via Rotahaler inhalation device--200 mcg (as Ventolin Rotacaps) q 4-6 hr (up to 400 mcg q 4-6 hr). May also be given 15 min before exercise Contraindications: Hypersensitivity to adrenergic amines Hypersensitivity to fluorocarbons (some inhalers) Use Cautiously in: Cardiac disease Hypertension Hyperthyroidis m Diabetes Glaucom a Seizure disorders

 Geriatric patients ( risk adverse reactions; may require dosage reduction) Pregnancy (near term), lactation, and children <2 yr (safety not established) Excess inhaler use may lead to tolerance and paradoxical bronchospasm Adverse Reactions: CNS: nervousness, restlessness, tremor, headache, insomnia (occurs more frequently in young children than adults), hyperactivity in children, CV: chest pain, palpitations, angina, arrhythmias, hypertension, GI: nausea, vomiting, Endo: hyperglycemia, F and E: hypokalemia, Neuro: tremor Interactions:
Drug-Drug:

Concurrent use with other adrenergic agents will have adrenergic side effects Use with MAO inhibitors may lead to hypertensive crisis Beta blockers may negate therapeutic effect May decrease serum digoxin levels Cardiovascular effects are potentiated in patients receiving tricyclic antidepressants Risk of hypokalemia concurrent use of potassium-losing diuretics Hypokalemia the risk of digoxin toxicity Drug-Natural: Use with caffeine-containing herbs (cola nut, guarana, tea , coffee ) stimulant effect Pharmacokinetics: Absorption: Well absorbed after oral administration but rapidly undergoes extensive metabolism Distribution: Small amounts appear in breast milk Metabolism and Excretion: Extensively metabolized by the liver and other tissues

Half-life: Oral 2.7-5 hr; Inhalation: 3.8 hr Time of action: PO: onset 15-30 mins, peak: 2-3 hour, duration: 4-6 hour or more. PO-ER: onset: 30 min, peak: 2-3 hour, duration: 4-6 hour. Inhalation: onset: 5-15 mins, peak: 60-90 mins, duration: 3-6 hour. Nursing Responsibilities: Instruct patient to take albuterol exactly as directed. If on a scheduled dosing regimen, take missed dose as soon as remembered, spacing remaining doses at regular intervals. Do not double doses or increase the dose or frequency of doses. Caution patient not to exceed recommended dose; may cause adverse effects, paradoxical bronchospasm (more likely with first dose from new cannister), or loss of effectiveness of medication Instruct patient to contact health care professional immediately if shortness of breath is not relieved by medication or is accompanied by diaphoresis, dizziness, palpitations, or chest pain Instruct patient to prime unit with 4 sprays before using and to discard cannister after 200 sprays. Actuators should not be changed among products Inform patient that these products contain hydrofluoralkane (HFA) and the propellant and are described as non-CFC or CFC-free (contain no chlorofluorocarbons) Advise patient to consult health care professional before taking any OTC medications , natural/herbal products, or alcohol concurrently with this therapy. Caution patient also to avoid smoking and other respiratory irritants Inform patient that albuterol may cause an unusual or bad taste Inhaln: Instruct patient in the proper use of the metered-dose inhaler, Rotahaler, or nebulizer (see Appendix B ) Advise patients to use albuterol first if using other inhalation medications and allow 5 min to elapse before administering other inhalant medications unless otherwise directed Advise patient to rinse mouth with water after each inhalation dose to minimize dry mouth Instruct patient to notify health care professional if no response to the usual dose of albuterol or if contents of one canister are used in less than 2 wk Pedi: Caution adolescents and their parents about overuse of inhalers, which can cause heart damage and life-threatening arrhythmias

Ceftriaxone
Generic name: Ceftriaxone Brand name: Rocephin Classification: Therapeutic: anti-infectives, Pharmacologic: third-generation cephalosporins Indications:

Treatment of: Skin and skin structure infections Bone and joint infections Complicated and uncomplicated urinary tract infections Uncomplicated gynecological infections including gonorrhea Lower respiratory tract infections Intra-abdominal infections Septicemia Meningitis Otitis media Perioperative prophylaxis Mechanism of Action: Binds to the bacterial cell wall membrane, causing cell death Therapeutic Effects: Bactericidal action against susceptible bacteria Spectrum: Similar to that of second-generation cephalosporins, but activity against staphylococci is less, while activity against gram-negative pathogens is greater, even for organisms resistant to first- and second-generation agents. Route and Dosage: IM, IV (Adults ): Most infections--1-2 g every 12-24 hr Gonorrhea--250 mg IM (single dose). Meningitis--2 g every 12 hr.Perioperative prophylaxis-1 g 0.5-2 hr before surgery (single dose) IM, IV (Children ): Most infections--50-75 mg/kg/day (not to exceed 2 g/day) divided every 12-24 hr. Meningitis--100 mg/kg/day (not to exceed 4 g/day) divided every 12-24 hr or Uncomplicated gonorrhea--125 mg IM (single dose).Acute otitis media--50 mg/kg (not to exceed 1 g) IM single dose Contraindications:

 Hypersensitivity to cephalosporins Serious hypersensitivity to penicillins Hyperbilirubinemic neonates (may lead to kernicterus)
Use Cautiously in:

Combined severe hepatic and renal impairment (dosage reduction/increased dosing interval recommended) History of GI disease, especially colitis Pregnancy and lactation Adverse Reactions: CNS: SEIZURES (HIGH DOSES), GI: PSEUDOMEMBRANOUS COLITIS, diarrhea, cholelithiasis, sludging in the gallbladder, Derm: rashes, urticaria, Hemat: bleeding, eosinophilia, hemolytic anemia, leukopenia, thrombocytosis, Local: pain at IM site, phlebitis at IV site, Misc: ALLERGIC REACTIONS INCLUDING ANAPHYLAXIS, superinfection, Interactions: Drug-Drug: Probenecid decreases excretion and increases levels Pharmacokinetics: Absorption: Well absorbed following IM administration; IV administration results in complete bioavailability Distribution: Widely distributed. CSF penetration better than with first- and second-generation agents.Crosses the placenta; enters breast milk in low concentrations Protein Binding: >90% Metabolism and Excretion: 33-67% excreted in urine as unchanged drug; remainder excreted in feces Half-life: 6-9 hr Time of action: IM: onset: rapid, peak: 1-2 hour, duration: 12-24 hour. IV onset: rapid, peak: end of infusion, duration: 12-24 hour.

Nursing Responsibilities: PATIENT/FAMILY TEACHING Advise patient to report signs of superinfection (furry overgrowth on the tongue, vaginal itching or discharge, loose or foul-smelling stools) and allergy Instruct patient to notify health care professional if fever and diarrhea develop, especially if stool contains blood, pus, or mucus. Advise patient not to treat diarrhea without consulting health care professional

Doctors Order

7/15/09 (8:50 am)

(9:30 pm)

(11:00 pm) (12:50 pm)

Vital Signs Sheet

Time/Date 7/15/09 0800H 0900H 1000H 1100H 1200H 1300H 1400H BP 110/80mmHg 90/60 mmHg 100/70 mmHg 90/60 mmHg 90/60 mmHg 92/58 mmHg 90/60 mmHg 95/59 mmHg 7/16/09 HR 88bpm 96 bpm 88 bpmpm) (10:45 100 bpm 96 bpm 85 bpm 75 bpm (1:00 76 bpmam) (3:30 pm) (8:00 pm)

Doctors order -admitted under the service of Dr. AES -secure consent to care -TPR every 4 H, to prioritize room please (include BP monitoring -diet: DAT, exclude choco colored food -labs: CBC, platelet, U/A stat -IVF: PNSS 1 Liter run 400 cc as fast drip then regulate at 40-41 gtts/min - meds: Ranitidine (Zantac) 35 mg slow IVTT every 2H Paracetamol (Tempra) 250 mg/ 5ml 7.5 ml every 4H for T> 38C -refer persisitent vomiting -note character of stool and vomitus -MIO every shift -secure 4 bags of patients blood type B+ and process with 3 components of RBC, concentrate, FFP - Hematocrit at 12 noon -IVF # PNSS 1 L @ 40-41 gtts/min -repeat HCT and platelet at 6 pm -start another IV @ right arm with PNSS 1 liter @ 24-25 gtts/min -regulate IVF @ left arm @ 24-25 gtts/min -Dopamine (premixed) @ 6 cc/hr -vit. K 2mg IVTT - IVF as follows: RR T Right arm Dioluven 500cc @ 32-33 O2SAT 25gtts/min 37.9C Left arm PNSS 1 L @ 24-25 gtts/min 26cpm 38.9C PB= Dopamine @ 9 cc/hr 25 cpm -repeat HCT and pH38.7C pm @ 10 26 cpm -transfuse 4 units of 38.7C concentration of platelet patients blood type.38.3C Transfuse as fast drip one 29 cpm after the other. 26 cpm 37.8C 98% - Hydroluocontrite (38.1Ccorisef) 35 g slow 99% solu28 cpm IVTT 27 cpm now. 37.8C 98% -repeat HCT at 2 am - HCT and pH at 6 am - please secure additune 4 units platelet concentrate - repeat HCT and platelet at 12 noon -Dopamine @ 60 cc/hr, to consume

REMARKS Strong peripheral pulses

1500H 1600H 1700H 1800H 1900H 2000H 2100H 2200H 2300H 2400H 0100H 7/16/09 0800H 0900H 1000H 1100H 1200H 1300H 1400H 1500H 1600H 1700H 1800H 1900H 2000H 2100H 2200H 2300H 2400H 0100H 0200H

92/60 mmHg 94/60 mmHg 80/50 mmHg 70/50 mmHg 70/110 mmHg 70/50 mmHg 80/50 mmHg 90/50 mmHg 80/40 mmHg 90/70 mmHg 90/110 mmHg 90/60 90/60 90/60 90/60 90/60 90/60 90/60 mmHg mmHg mmHg mmHg mmHg mmHg mmHg

86 bpm 78 bpm 92 bpm 92 bpm 74 bpm 72 bpm 78 bpm 63 bpm 65 bpm 65 bpm 85 bpm 70bpm 66 bpm 63 bpm 69 bpm 71 bpm 70 bpm 67 bpm 65 bpm 73 bpm 69 bpm 73 bpm 75 bpm 77 bpm 76 bpm 70 bpm 69 bpm 73 bpm 61 bpm 66 bpm

32 cpm 28 cpm 25 cpm 25 cpm 25 cpm 28 cpm 26 cpm 22 cpm 23 cpm 26 cpm 24 cpm 28cpm 25 cpm 22 cpm 27 cpm 31 cpm 26 cpm 32 cpm 30 cpm 31 cpm 28 cpm 36 cpm 28 cpm 35 cpm 31 cpm 32 cpm 32 cpm 27 cpm 28 cpm 32 cpm

37.1C 37.2C 36.8C 36.8C 36.5C 36.2C 36.2C 36.0C 36.5C 36.5C 36.5C 36.4C 37.3C 37C 37.4C 37.3C 37.1C 37.3C 37.2C 37.2C 37.6C 37.7C 37.4C 37.3C 37.1C 37C 32C 32C 27C 28C

100% 100% 99% 99% 99% 99% 99% 98% 98% 99% 99% 98% 99% 99% 99% 99% 97% 99% 100% 97% 99% 98% 98% 97% 98%

100/80 mmHg 95/60 mmHg 100/70 mmHg 100/70 mmHg 90/60 mmHg 80/60 mmHg 90/60 mmHg 70/50-80/50 mmHg 80/50 mmHg 90/60 mmHg 90/60 mmHg

0300H 0400H 0500H 0600H 0700H 7/17/09 0800H 0900H 1000H 1100H 1200H 1300H 1400H 1500H 1600H 1700H 1800H 1900H 2000H 2100H 2200H 2300H 2400H 0100H 0200H 0300H 0400H 0500H 0600H 0700H

80/50 mmHg 90/60 90/60-100/70 mmHg 90/60 mmHg 90/60 mmHg 100/70 mmHg 110/80 mmHg 100/70 mmHg 100/60 mmHg 110/80 mmHg 110/70 mmHg 110/70 mmHg 100/70 mmHg 90/60 mmHg 90/60 mmHg 90/60 mmHg 100/60 mmHg 100/60 mmHg 90/60 mmHg 90/60 mmHg 90/60 mmHg 90/60 mmHg 100/60 mmHg 100/60 mmHg 90/60 mmHg 95/60 mmHg 100/70 mmHg 90/60 mmHg 100/60 mmHg

63 bpm 66 bpm 66 bpm 81 bpm 60 bpm 61bpm 66 bpm 73 bpm 85 bpm 64 bpm 65 bpm 75 bpm 76 bpm 79 bpm 68 bpm 65 bpm 75 bpm 68 bpm 77 bpm 67 bpm 69 bpm 70 bpm 61 bpm 70 bpm 67 bpm 65 bpm 62 bpm 77 bpm 67 bpm

31 cpm 30 cpm 24 cpm 24cpm 21 cpm 20 cpm 23 cpm 25 cpm 26 cpm 27 cpm 26 cpm 22 cpm 25 cpm 24 cpm 26 cpm 28 cpm 32 cpm 29 cpm 29 cpm 25 cpm 26 cpm 24 cpm 22 cpm 23 cpm 22 cpm 29 cpm 28 cpm

32C 31C 30C 24C 36.8C 36.6C 37C 37C 36.5C 36.6C 36C 36.4C 36.5C 36.3C 36.4C 36.6C 36.7C 36.4C 36.6C 36.6C 36C 36C 36C 36C 36C 36.2C 36.4C 36C

98% 98% 97% 98%

97% 98% 98% 99% 98% 100% 100% 99% 98% 99% 96%

97% 97% 95% 96% 95-96% 96% 97% 96% 97% 96%

7/18/09 0800H 0900H 1000H 1100H 1200H 1300H 1400H 7/19/09 2400H 0100H 0200H 0300H 0400H 0500H

117/80 mmHg 110/80 mmHg 110/90 mmHg 110/80 mmHg 100/80 mmHg 90/60 mmHg 90/60 mmHg 90/60mmHg 90/60mmHg 100/70mmHg 100/70mmHg 110/70mmHg 110/70mmHg

90 bpm 66 bpm 64 bpm 68 bpm 60 bpm 83 bpm 80 bpm 68bpm 72bpm 72bpm 74bpm 85bpm 80bpm

33 cpm 32 cpm 30 cpm 32 cpm 28 cpm 24 cpm 24cpm 24cpm 23cpm 22cpm 32cpm 24cpm

36.3C 36.4C 36.6C 36C 36.2C 36.6C 36.1C 36C 36.6C 36.4C

Functional Health Patterns Usual Functional Patterns Initial Appraisal Ongoing Appraisal (7/20/09) Ongoing Appraisal(7/21/09)

I. Health Perception-Health management Pattern Sought consultation @ NOPH and was prescribed with penl and co-amoxiclav 625 mg. Patients bantay is not aware whether the patient was born in a normal delivery or CS Usually experiences cough and colds Doesnt take vitamin supplements Patient doesnt know if she is complete with immunizations. No previous hospitalizations Been easy to follow doctors orders Her father smokes but not in front of them If symptoms of cough and colds persists usually patient doesnt mind it. The brother of the patient perceived him self as strong, as verbalized, kaya man nako mu tabang ug trabaho para sa ako pamilya. -

Client compliant of treatment - Client compliant of regimen treatment regimen Sought admission on July 15, - Described health as better, 2009 at around 8: 27 am due as verbalized, nakatulog ko to fever and vomiting. maau, dili na kayo kapoy Described health as poor, as akong lawas - With # 14 D5 0.3 NaCl 1 L verbalized, kapoy ko @ 16 gtts/min Skin is dry with flakes and - With SD # 2 Dopamine 250 warm to touch mL @ 2 cc/hr via infusion Complained of nausea and pump had episodes of vomiting - CBR without bathroom during the past days privileges as ordered by Dr. Cross matching slip AE Sison B Rh+ - Skin is dry and still warm to With # 13 D5 0.3 NacL 1 L @ touch 16 gtts/min - Excessive perspiration noted With SD #2 Dopamine 250 mL - Scheduled for another @ 2cc/hr via infusion pump Brother of the patient hematocrit and platelet count verbalized, kapoy na pod, dili - Father of patient verbalized, kaau ko katulog Vital signs: (8:00 am) kapoy na day nya dako na kaau amu balayran diri sa T= 36.0 hospital P=74 bpm - Vital signs: ( 8 am) R= 22 cpm T= 36.3 C BP= P= 75 bpm, regular, moderately 12 noon strong T= 37.1 C

Client complaint of treatment regimen Described health as well, as verbalized, okay na ko IVF terminated as well as infusion pump Skin is dry and warm to touch

- Vital signs: (8 am) T= 36 C P= 92 bpm, regular, strong R= 25 cpm, regular, effortless BP= 100/80 mmHg with strong peripheral pulses ( 12 noon) T= 36.6C P= 85 bpm, regualar, strong R= 22 cpm, regular, effortless BP= 120/70 mmHg with strong peripheral pulses Latest hematocrit and platelet count Hematocrit= 40.0% Platelet= 218 T/cumm

No allergies

P= 128 bpm R= 22 cpm BP= 80/60 mmHg - Medications: Dopamine 250 mL SD Ranitidine (Zantac) 35 mg IVTT every 2H Paracetamol (Tempra) 250 mg/ 5 mg 7.5 mL every 4H for T> 38C Laboratory Results: (07/15/09) Complete Blood Count Hgb= 15.30 % (12-14%) Hematocrit= 44.4% (37-44%) WBC= 4990 T/cumm (4500-11000) Segmenters= 76% (55-70%) Lymphocytes= 22% (20-35%) Eosinophils= 0 % (1-4% Monocytes= 2% (1-6%) Basophils= 0% (0-0.5%) Platelet count = 22 T/cumm (150400 T/cumm) RBC= 5.2 M/cumm (42-5.4 M/cumm) Mean Corpuscular Volume = 85.4 Fl (80-96) Mean corpuscular Volume= 29.4 pg (27-31) Mean Corps. Hgb Concentration= 34.5% (33-36%) Latest Hematocrit and Platelet count (7/19/09) Hematocrit= 39.2 % (37-44%)

R= 22 cpm, regular, effortless BP= 100/70 mmHg with strong peripheral pulses (12 noon) T= 36.6 C P= 76 bpm, regular, moderately strong R= 24 cpm, regular, effortless BP=90/70 mmHg with strong peripheral pulses Latest hematocrit and platelet count Hematocrit= 39.1 % Platelet= 82 T/cumm

Platelet= 33 T/cumm (150-400 T/cumm) Urinalysis Color= yellow (straw to dark amber) Transparency= turbid (clear) Specific gravity= 1.010 (1.010-1.025) Glucose= negative (none) Bilirubin= negative (none) Ketone= negative ( none) Blood= large pH= 6.5 (4.6-8) protein= + (none) Urobilinogen= normal (normal) Nitrite= negative Leukocytes= negative Pus cells= 0-1 Red cells= TNTC Epithelial cells= ABUNCH Bacteria = Abundt Mucus threads= few II. Nutritional Metabolic Pattern Daily food intake: Breakfast: I cup of rice Fish (1 piece) Soup Lunch: 1 cup of rice Fish/ meat Breakfast: cup of rice Meat of vegetables Lunch: cup of rice Meat Dinner:

Breakfast: cup of rice Meat 1 cup vegetables Lunch: cup of rice

Breakfast: 1 cup of rice Fish 1 cup of vegetable Lunch: 1 cup of rice Meat

banana Dinner: 1 cup of rice Fish Soup Banana No food allergies Appetite is good No supplements taken Able to feed herself Patients brother doesnt know the birth weight of her sister No skin rashes noted Favorite food is chicken joy No difficulty in eating

cup of rice Meat Soup Appetite is poor Able to feed herself no difficulty in eating diet: DAT, exclude chococolored food - consumed half of share - complained of bitter taste - there is decreased salivation as verbalized, mala akung baba Intake: 07/19 7-3= 400mL 3-11=756 mL 11-7=736mL 7-3

Fish Dinner: cup 1 cup vegetable -appetite is poor - able to feed herself -diet: DAT, exclude choco-colored food - consumed half of share Intake: 7-3=790mL Dinner: 1 cup of rice Meat -appetite is good - able to feed herself - consumed all share Intake: ( no MIO done)

III. Elimination Pattern - Urinates 4-6x a day, yellowish in color, 350-450 mL, no discomforts - Defecates once a day, soft, semi formed, brown in color with no discomforts - No excessive perspiration

3-11 11-7 -

urinated 2x, dark yellow in color, no discomforts, 400 mL have not defecated the whole day urinated 2x, dark yellow in color, no discomforts, 500mL have not defecated urinated 2x, dark yellow in

Urinated 3x, dark yellow in color, no discomforts, 400 mL Have not defecated Excessive perspiration noted

-(no MIO done) -no excessive perspiration noted

color, no discomforts, 500 mL have not defecated excessive perspiration noted

IV. Activity exercise pattern - Takes a bath once a day - Dresses by herself - Not so active in play because she is busy in her work - Perceived herself as strong - At Tayasan, her mother is a full time house wife, and so she maintains the cleanliness of their home to protect them from illness. - Enjoys having a conversation with her friends or siblings. - No musculoskeletal impairement - Movement not limited.

bed bath done by the nurses aid dressing up needs assistance very silent in the hospital ,doesnt talk with other patients no musculoskeletal impairment movement not limited breathing pattern is normal Vital signs: (8:00 am) T= 36.0 P=74 bpm R= 22 cpm BP= 12 noon T= 37.1 C P= 128 bpm R= 22 cpm BP= 80/60 mmHg

Bed bath done Dressing up needs assistance - Still doesnt interact with other patients in the hospital - No musculoskeletal impairment - Movement not limited but she is on CBR as ordered. - Vital signs: ( 8 am) T= 36.3 C P= 75 bpm, regular, moderately strong R= 22 cpm, regular, effortless BP= 100/70 mmHg with strong peripheral pulses (12 noon) T= 36.6 C P= 76 bpm, regular, moderately strong

Have not taken a bath because she refused. - She changed by herself into her clothes - Still shy - No musculoskeletal impairment - Movement not limited - Vital signs: (8 am) T= 36 C P= 92 bpm, regular, strong R= 25 cpm, regular, effortless BP= 100/80 mmHg with strong peripheral pulses ( 12 noon) T= 36.6C P= 85 bpm, regualar, strong R= 22 cpm, regular, effortless BP= 120/70 mmHg with strong peripheral pulses -

R= 24 cpm, regular, effortless BP=90/70 mmHg with strong peripheral pulses V. Sleep Rest pattern Sleeps 6-7 hours a day No nightmares The brother sleeps 4-5 hours VI. Cognitive perceptual pattern -verbally responsive - no problem in hearing and visual senses - she is able to state her name, her address and the time of the day - - The final stage of cognitive development is the formal operation; the ability to think in abstract terms and use scientific method to arrive at a conclusion. VII. Self Perception - Sometimes moody - Perceived herself as good girl, as verbalized buutan ra Slept 4-5 hours No nightmares Sleep disruptions: Hospital procedures Platelet and hematocrit test The brother wasnt able to sleep well Slept 4-5 hours No nightmares Wasnt able to sleep well because of the platelet and hematocrit test The brother also wasnt able to sleep well Slept 6 hours but woke up at 4 am because of the platelet and hematocrit test No nightmares The father wasnt able to sleep well, experienced headache

Verbally responsive, speech is coherent no problem in hearing and vision the formal operation stage was not manifested during her hospitalization

Verbally responsive, speech is coherent Np problem in hearing and vision

verbally responsive and speech is coherent

no eye contact when having a

No eye contact when she

sometimes she would

man dgwy. Her brother perceived the patient to be a good girl as verbalized, buutan ug pabuyag pod Never felt the feeling of being lonely Patients brother verbalized, kapoy na pero kayanun ra Afraid of ghosts

conversation verbalized, gi kapoy nko posture is good brother verbalized, kapoy nako diri sa hospital feels lonely sometimes because her brother often stays outside of the room

talks to me because she is too shy Posture is good patient verbalized, kapoy kaau they dont communicate that much her brother is taking care of her.

VIII. Role Relationship Pattern - Her father works a care taker and her mother is a full time housewife - Her older siblings work to help the family - She also works as a housekeeper at Dauin, Negros Oriental - Hot tempered when she has her period - Patients brother is satisfied with their life except with their financial needs. - Financial problems and sibling rivalry are the usual problems that the family experience - She has no problem adjusting to school and even

already look at me when I ask her a question sometimes she would already look at me when I ask her questions Patient verbalized, dili naman kaau kapoy pero luya jpon ko Father verbalized, mau ra jud nga makagawas nami her father is the one taking care of her, her brother went home already

her brother is the one taking care of her in the hospital she and her brother dont interact much she wants to finish high school and college she wants to become a successful businesswoman someday she wants to go to school but due to financial problems she cant. no problem adjusting at the hospital.

Her brother is still the one taking care of her. No problem adjusting at the hospital. She wants to go home as soon as possible to go back to work.

-her father is the one taking care of her, her brother went home already, -she has adjusted to the hospital setting. -she wants to go home as soon as possible to go back to work.

misses to go to school She is close to her younger sister When she goes home to their house she helps her mother with the household chores and takes care of her younger siblings According to Eric Erikson the psychosocial development of early adolescents is identity vs. role confusion. They decide who they are and what kind of person they will be.

IX. Sexuality Reproductive Pattern - Patient perceived herself as a girl - Shes very active but she also loves to hang out with her friends and do chika2x before she worked as a housekeeper. - Her playmates in her hometown are all girls. - Genital stage is the psychosexual development of a teenager according to Freud. Adolescent focus on the genitals as an erogenous

-Patient prefers - she is not active in the hospital; too weak to move - shes a fan of John Lloyd Cruz and Bea Alonzo -she is shy when a male nurse would come over

Shes still not active in the hospital, especially because she is on CBR She doesnt talk to other patients She is shy when a male nurse would come over

she sits up already and smiles to other patients

zone and engage in masturbation and in sexual relation with others.

X. Coping Stress Tolerance Pattern - She cries when she experiences pain and hardships. - Doesnt usually open up to her mother when she has a problem; she opens up to her sister. - Stressors in school: Work Financial problems Family problems - Sleeps when shes tired - Collaborative play is the kind of play that adolescents usually are into. They learn how to cooperate in a group.

she is in pain all the time during hospitalization stressors in the hospital: hospital procedures noises from other patients hospital bill she sleeps when shes tired no play manifested in the hospital

She is still in pain Still the same stressors in the hospital She sleep most of the time No play manifested in the hospital

less pain felt excited about going home slept before going home no play manifested in the hospital

XI. Value belief pattern They are roman catholic She goes to church every

Sunday but not as a family, usually she goes with her sister She prays before eating and going to sleep She doesnt question the existence of God, as verbalized mutuo man ko sa Ginoo wala ko ga problema tungod ana

she prays before going to sleep wasnt able to go to church due to hospitalization she prays before and after eating

She prays before going to sleep She sometimes forget to pray before eating

she prays before sleeping and eating

Summary of Nursing Diagnosis Deficient fluid volume related to nausea and vomiting Imbalanced nutrition: less than the body requirements related to altered taste and decreases appetite secondary to dengue Risk for falls related to orthostatic hypotension Altered thermoregulation R/T excess heat production secondary to Dengue fever

 Risk for deficient fluid volume: bleeding R/T decreased platelet count secondary to Dengue Risk for ineffective tissue perfusion related to labored breathing Risk for injury related to sedative effect of drug and frequent bed movement Fatigue R/T physical weakness secondary to Dengue fever Impaired skin integrity R/T presence of petichae and itchiness

Silliman University College of Nursing Dumaguete City NURSING CARE PLAN CUES/ EVIDENCES NURSING DIAGNOSIS OBJECTIVE NURSING INTERVENTION RATIONALE EVALUATION

Subjective cues: Patient brother verbalized. ga sigi man ni siya ug suka adtong pila ka adlaw. Patient verbalized,kapoy gihapon kayo ang akong lawas. Objectives cues: Vital signs: T=37.6C HR=117bpm RR=22cpm BP=90/70mmHg Excessive sweating Dry mucus membrane Dry lips Dry skin with flakes noted Clear breath sounds Increased urine concentration Skin is warm to touch Lab exams:

Deficient fluid volume related to nausea and vomiting

At the end of our care, my patient will be able to achieve fluid balance as evidenced by: 1. Vital signs within normal range: T=36.5-37.5C HR=60-100bpm,regular and strong RR=12-20cpm, effortless, without use of accessory muscles BP=100-140/60-90mmHg 2. Absence of weakness

Independent: 1. Monitor vital signs 2. Assess breath sounds 3. Note change in usual mentation/behav ior/ functional abilities

4. Observe urinary output, color and measure amount and specific gravity 5. Encourage oral fluid intake 6. Provide at bedside oral fluids that client prefers

1. To provide baseline data 2. Clear breath sound indicates fluid volume deficit 3. These signs indicate sufficient dehydration to cause poor cerebral perfusion and/ or electrolyte imbalance 4. To more accurately determine replacement needs 5. To replenish the insensible fluid loss 6. Fluid intake may be greater when desired fluids are provided 7. To prevent

At the end my care, patient fluid volume balance will be maintained as evidenced by: 1. Vitals signs within normal range: T=36.4C HR=80bpm regular and strong RR=24cpm, effortless and without use of accessory muscles BP=110/70mmHg 2. (met) absence of weakness, child verbalized, ma gawas naman mi hospital. 3. (met) absence of vomiting 4. (met) claimed that the color of her urine is light yellow 5. (met) decreased perspiration 6. (met) child

3. Absence of vomiting 4. Decreased urine concentration 5. Decreased in perspiration 6. Moist in the mucus membranes

Color=yellow Transparency=turbid Specific gravity=1.010 7. Explains measure that can be taken to treat or prevent fluid volume loss

7. Provide oral and eye care 8. Discuss factors related occurrence of deficit

injury from dryness 8. Early identification of risk factors can decrease occurrence and severity of complications associated with hypovolemia 9. It inhibits basal and stimulated secretion of gastric acid, reducing both volume and the acid and pepsin content of the secretion 10. Produces analgesia by unknown mechanism, perhaps by action on peripheral nervous system. Reduces fever by direct action on

verbalized, dili na mala ako paminaw sa akong ilong. 7. (met) child verbalized, gidaghanan naman nako ang ako pag inom ug tubig.

Dependent: 9. Ranitidine (Zantac) 35mg IVTT every 2 hrs

10. Paracetamol (Tempra) 250mg 15mL 7.5mL q 4hrs for T>38C

hypothalamus heat-regulating center with consequent peripheral vasodilation, sweating. Unlike aspirin, acetaminophen has little effect on platelet aggregation, does not affect bleeding time, and generally produces no gastric bleeding

11. Monitor input and output

11. To determine the amount of intake and output of the body thus preventing fluid loss or excess

Silliman University College of Nursing Dumaguete City

Cues and evidences Nursing Diagnosis objectives Subjective cues: Imbalanced nutrition: At the end of my care, less than the body the child will Child verbalized, wala requirements related to demonstrate improved

Intervention Independent: 1. Identify if the patient is at risk

Rationale 1. Be able to perform proper

Evaluation At the end of my care, patient demonstrated improved nutrition as

man ko gana mukaon lain ang ako dila. Child verbalized, mura man ko kasukaon if daghan ang ako kan on. Child verbalized, pait man ang ako dila dili ko ganahan mukaon. Objectives cues: Vital signs: T=37.6C HR=117bpm RR=22cpm BP=90/70mmHg Loss of appetite Claimed bitter taste Decreased salivation Dry mucus

altered taste and decreases appetite secondary to dengue

nutrition as evidenced by: 1. Vital signs within normal range: T=36.5-37.5C HR=60100bpm,regular and strong RR=12-20cpm, effortless, without use of accessory muscles BP=100-140/6090mmHg

for malnutrition 2. Determine ability to chew , swallow and taste 3. Auscultate that significant others understands the individual nutritional need 4. Discuss the eating habits including food preferences 5. Assess weight, age, body build, strength activity or rested level 6. Note total daily intake

intervention 2. To determine what factors that affect ingestion and or digestion of nutrients 3. To determine what need of information to provide the significant others and the patient herself 4. To appeal patients likes and dislikes 5. Provides comparative baseline 6. To reveal changes that should be made in patients dietary intake 7. To stimulate appetite

evidenced by: 1. (met) vital signs within normal range: T=36.4C HR=80bpm regular and strong RR=24cpm, effortless and without use of accessory muscles BP=110/70mmHg

2. Improved weight

3. Consume

7. Encourage patient to choose foods that are appealing

2. (un met) weight not noted ,child verbalized, mura gyud ug naniwang ko agi dugay hospital. 3. (partially met)

membrane Usually or of share cosumed

hospital meal 4. More intake of foods

5. Increases fluid intake

8. Promote pleasant, relaxing environment 9. Emphasize importance of well- balanced nutritious intake Dependent: 10. Ranitidine (Zantac) 35 mg IVTT every 2H

8. To enhance intake 9. To promote wellness

slight increased intake of food

4. (met) increased

fluid intake 5. (partially met) Patient brother demonstrated stable weight promotion behavior: gave small frequent milk feedings 6. (met) Improved appetite as observed , most of the share was consumed 7. (partially met) Patient verbalized, dili naman pod kayo pait ang ako dila medyo naa nkao gamay gana.

6. Good appetite

10. It inhibits basal and stimulated secretion of gastric acid, reducing both volume and the acid and pepsin content of the secretion 11. Produces analgesia by unknown mechanism, perhaps by action on peripheral nervous system. Reduces fever by direct action on

7. Absence of bitter taste

11. Paracetamol

(Tempra) 250 mg/ 5 mg 7.5 mL every 4H for T> 38C

8. Verbalized

ganahan nako

mukaon ug lami na pagkaon.

Collaborative: 12. Collaborate with dietary department 13. Monitor weight

hypothalamus heat-regulating center with consequent peripheral vasodilation, sweating. Unlike aspirin, acetaminophen has little effect on platelet aggregation, does not affect bleeding time, and generally produces no gastric bleeding

Silliman University College of Nursing Dumaguete City

Cues and Evidences Subjective cues:

Nursing Diagnosis

Objectives At the end of my 2 day

Interventions Independent:

Rationale

Evaluation At the end of my care,

Patient Risk for falls related verbalized,kalipun to orthostatic gon man ko kung hypotention mulingkod ko. Patient verbalized,kapoy kayo ang ako lawas. Patient verbalized, malipong man ko mura ug mutuyok ang ako paminaw. Objectives cues: Vital signs: T=37.6C

care, my patient will be free from falls as evidenced by: 1. Vital signs T=36.5-37.5C HR=60100bpm,regular and strong RR=12-20cpm, effortless, without use of accessory muscles BP=100-140/6090mmHg 2. Absence of weakness 3. Absence of fatigue

1. Monitor vital signs 2. Carefully assess the clients ability to ambulate and transfer 3. Review history of prior falls associated with immobility, weakness, prolonged bed rest, and sedentary lifestyle 4. Consider environment hazards in the setting and/ or home 5. Practice client safety 6. Instruct client to rise slowly from a lying to sitting to standing position and to

1. To monitor the baseline 2. To determine the level of assistance that the nurses should provide 3. To predict current risk for falls

patient will be free from risk for falls as evidenced by: 1. vital signs within normal range: T=36.4C HR=80bpm regular and strong RR=24cpm, effortless and without use of accessory muscles BP=110/70mmHg

HR=117bpm regular and strong RR=22cpm silent ,without use of accessory muscles BP= 90/70mmHg Prolonged bed rest No physical activity

4. Provides opportunities for intervention and / or instruction 5. Demonstrates behaviors for client/ caregivers to emulate 6. To prevent client from falling

4. Absence of dizziness and lightheadedness 5. Able to change in position like sitting to

2. (met) absence of weakness 3. (Met) absence of fatigue, child verbilzed,kusga n nako ma out na gani mi hospital. 4. (met)absence of dizziness
5. (met) able to

change position like sitting to

standing without any dizziness 6. Independent in changing position like sitting to standing

stand in place for several seconds before walking 7. Place bedside tables and over bed tables near bed

standing 6. (met) independent in standing

7. To prevent client from overreaching and consequently lose their balance 8. For the client to move in and out of bed easily

8. Keep hospital beds in low position and wheels locked when not providing care 9. Evaluate clients cognitive status Dependent: 10. Dopamine 200ml SD via infusion pump

9. Affects ability to perceive non limitations or recognize danger 10. to treat shock and correct and hemodynamic imbalances, to improve perfusion to vital organs to increase cardiac output and to

correct hypotension Collaborative: 11. For hematocrit and platelet monitoring as ordered by Dr. Sison 11. to determine amount of intake and output

Actual care done Monitoring of vital signs every 4 hours To gather baseline data for comparisons as well as to monitor the patients health status so that specific nursing interventions may be given and make referrals in case problems may arise. Morning care To provide comfort, let the patient feel relaxed during her hospital stay and cleanses client to remove microorganisms preventing infection. Physical Assessment during the first day of actual care to the patient.

The major systems involved during the examination are the skin, nails, head face, eyebrows, eyes nose ears, mouth and pharynx, neck, respiratory, abdomen and musculoskeletal system. This procedure will help t gather pertinent information regarding the clients condition. IV Monitoring The patency is checked as well as the site of therapy to note any untoward findings that may be harmful to the client. There might be leaks, infiltration or other IVF complications. Moreover, it helps in monitoring the nutritional intake of the patient through IV instillation. Monitoring Intake and output per shift To detect the level of hydration/dehydration and allow making immediate actions/interventions as indicated Making referrals to the attending physician and staff nurses for any unusualities Allows immediate intervention for the unusualities that may happen (Collaborative) Monitoring diet therapy (diet as tolerated-No dark colored foods) To ensure if the patient is receiving adequate nutrition and ensure that the patient is not taking any foods contraindicated to his condition

Journals Silliman journal, 1994 Knowledge of Dengue Hemorrhagic Fever By a Parents- Teachers Group in a Filipino High School (Jeffrey L. Lennon) School-age children are particularly susceptible to Dengue Hemorrhagic Fever. During January 1993, schools of Dumaguete City, Philippines were found to have breeding sites for the Aedes Aegypti mosquito, the carrier of the dengue virus. In response to dengue outbreak, a mass media campaign followed. In addition, dengue information sheets with parental return slips were distributed among the pupils of the citys schools. Parent/teacher meetings were held as a response to the information sheet distribution. One high school parent/teacher group was evaluated on dengue knowledge by questionnaire. About 75% of the participants claimed exposure to dengue health communication other than the information sheets. The total correct response rate to the questionnaire was 64.5 %. The questionnaire topics included dengue transmission, treatment, and control. The most favorable response dealt with the knowledge of mosquito breeding sites. The least favorable response dealt with effective mosquito control.

Dengue Hemorrhagic Fever (DHF), also known as H-fever or Philippine Hemorrhagic fever, was first reported in the Philippines in 1954. (San Juan, 1960) Since then dengue has occurred around the world in the tropics in locations such as the Caribbean (Kouri et al., 1986) and South America (Figueiredo, et al. 1990; Phillips, et al., 1992). Dengue is perilous in that there are no vaccines or anti-viral available for prevention or treatment. Immunity to one of the four dengue serotypes does not lessen susceptibility to the other three serotypes. Dengue is capable of attacking infants despite the immune status of their mothers. Young children are most often the host of dengue. Individuals infected with the dengue virus can develop vascular permeability and abnormal hemostasis. (Halsted, 1988) Dengue hemorrhagic fever (DHF) begins with fever and malaise which may last two days to a week. In the absence of virological testing and diagnosis (which is the case in most community settings) the diagnosis must be based upon serological laboratory findings. The World Health Organization has set classifications based upon laboratory values of hemoconcentration and thrombocytopenia. This may necessitate up to 48 hours before confirmation of dengue. In the meantime the disease may have vascular permeability to compromise the patient before receiving further medical attention. This may present an especially critical situation in children (Sanford, 1987). The more severe form of dengue, called dengue shock syndrome (DSS), is characterized by internal bleeding and shock. The mortality associate with dengue may reach as high as 10 %. Thus according to Gubler and Casta-valdez (1991), dengue is currently the most important vector-borne viral disease afflicting humanity, in terms of both morbidity and mortality. As there are difficulties in the diagnosis and treatment of DHF, it is essential to emphasize the prevention and control the disease. It is therefore essential to control the vector of dengue, the Aedes aegypti mosquito (Brown, 1975). Weikel states, long-term control of dengue viral infections depends on health education and community projects, aimed at reducing the breeding sites of Aedes mosquitoes (Weikel, 1987).

Dengue in the Philippines and Dumaguete City The number of cases and rate of dengue hemorrhagic fever (H fever), at its earliest listing in 1964 in the Philippines were 74 and 0.3 per 100,000 respectively. The total number of dengue cases in the Philippines for the years 1954 t 1958 was 1,579 (San Juan, 1960). In 1965, the number of dengue (H-fever) cases, mortality rate, number of deaths and mortality rate were 652; 2.0 per 100,000; 109 and 0.3 per 100,000, respectively. By 1985 the number of dengue cases, case rate, number of deaths and mortality rate had increased to 2,096, 3.8 per 100,000; 210 and 0.4 per 100,000, respectively. Over 75 % of the 1985 dengue cases occurred between 14 years age and birth. The greatest number of dengue cases listed for the 21year period from 1965 to 1986 registered was in 1966, with 9,384 cases. However the average number of dengue cases per year from 1966 to 1985 was 1,384. The number of cases and rate per 100,000 for dengue in the entire Philippines for 1985 were 2,096 and 3.8 per, respectively. (Health, 1988) In 1985 the number of dengue cases and rate in Dumaguete City, Negros Oriental were 2 and 2.8 per 100,000 cases, respectively. There were no dengue registered deaths in Dumaguete for 1985. (Health, 1988). The number of dengue cases per year in Dumaguete for year 1988, 1989, 1990,

1991 and 1992 were, respectively, 96, 15, 45, 130, and 134 cases. The five year dengue morbidity rate from 1986 to 1990 in Dumaguete was 25.05 per 100,000. The 1991 dengue rate in Dumaguete was 161.06 per 100,000. The rate of dengue cases in 1992 in Dumaguete City had risen approximately 165 per 100,000. There were two registered dengue related deaths in Dumaguete for 1992. For the year 1992 Dumaguete City registered dengue cases for every month except the dry Philippines summer month of April, December 1992 registered the greatest number of confirmed dengue cases with 37. There were a total of 96 suspected cases of dengue in December 1992. The period of January through March 1993 shows an increase unconfirmed cases from the same period for 1992. The cases of dengue in Dumaguete were distributed in all but the three of the barangays (community-level government unit). The majority of dengue cases were in barangays located within one kilometer of the Bay and north of the Banica River. The heavily populated barangays of Poblacion Taclobo and Daro lead the list with the most dengue cases. (Dumaguete, 1993; Pinero, 1992). A Response to the Dengue Situation in Dumaguete In response to the increased number of dengue cases in December 1992 Silliman University College of Education students enrolled in the Environmental Sanitation and Health course surveyed the campuses of six Dumaguete elementary schools in January 1993. Each school had multiple preventable mosquito breeding sites. Subsequently, the education students of the university began a dengue health communication campaign in cooperation with the Provincial Department of Health (Lennon, 1993). The students presented classroom talks, led assemblies, and passed out dengue information sheets (with a parental return slip acknowledging the reading of the sheet and family implementation of anti-dengue measures) in 25 of 31 Dumaguete City elementary schools and high schools. In a total city school population of over 20,000, a total of 7,822 dengue information sheets were passed out to the pupils. The pupils returned 3,961 parental acknowledgment slips with a response rate of 50.6%. The dengue information sheets were based upon a pamphlet developed by the Philippine Region 7 Department of Health entitled, What everyone should know about dengue fever (Department of Health). Radio, television, and newspapers discussed the problem of dengue in Dumaguete. These combined health communication activities generated interest among the Parent/Teacher associations of various schools to hold dengue information meetings. (Dengue, Rabies, 1993) In developing dengue prevention programs in U.S Virgin Islands and Puerto Rico, Gubler and Casta-Velez (1991) stated, one key population group is school-age children; major educational work has been directed toward the schools. However, the principal groups of people that will reinforce any health behavior or environmental clean-up changes promoted through pupils are teachers and parents- most especially parents. Therefore, this studys objective was to gain insight into the knowledge of parents and teachers about prevention and control of dengue fever. The results of this study may better define strategies and develop appropriate anti-dengue health education materials. Discussion

Nearly three-quarters of the P.T.A claimed to have received previous dengue health communication by way of mass media or meeting. There was, however, no significant differences between the responses of those who claimed to have received health communication prior to the questionnaire administration and those P.T.A participants who claimed not to have received prior dengue health communications. In the instructions preceding the questionnaire administration, it was specified that questions no. 10 did not refer to the dengue health information fact sheets, which was distributed to all of the pupils in the high school. It is possible, then, that the higher percentage score among those who claimed no previous health communication exposure versus those that claimed previous health communication might have been attributed to exposure to the dengue information sheet brought home by the pupils. The unsure group scored lower than the other two groups on all questions except no.6. Perhaps those unsure of their exposure to dengue health communication before the questionnaire administration were actually the people with no previous dengue information exposure. Questions no. 8 and 4 consistently received the lowest responses among all groups of the P.T.A. Both questions dealt with mosquito control. These responses go against the advice of the dengue information sheet and the Philippine Department of Health advice that, measures directed toward adult mosquitoes are expensive, temporary and not effective for routine mosquito control, thus measures directed towards larval mosquitoes should be utilized. (Department of Health) The P.T.A group correctly identified the breeding sites of mosquitoes in question no.6 at 98.9 % (as this was the groups overall best question response). They did not connect it with the importance of larvae control in question no.5 at 68.1%. Question no.5 implied the destruction of the vector related to dengue. The question was written to not give away the carrier species. The majority of the P.T.A. grouped scored correctly on questions 1, 2, and 3. Question no.3 has relevance to the school age population in that the Aedes aegypti mosquito may bite during the day (unlike the malaria carrying Anopheles mosquito, which bites at night). Thus, the times those children go to and from school or the period they are on the school grounds may place them at risk for dengue. Preliminary studies had already indicated the presence of Aedes aegypti on school campuses in Dumaguete. In addition, A. aegypti was identified in family living quarters about 200 meters from one school. (Lennon, 1993) In response to dengue epidemics in the 1970s to early 1980s, Cuba conducted an A. aegypti eradication program. From their Cuban experience Armanda Gessa and Figueredo Gonzales stated, The most effective way of fighting aegypti is to adopt rigorous environmental sanitation measures. In addition to insecticide spraying, the Cuban anti-mosquito campaign emphasized the stocking of larvivirous fish in ponds and lakes, the prohibition of open water containers, prohibition of car tires in yards, the prohibition of plants that accumulate water, and strict enforcement of sanitary regulations. It is possible that these measures will be applied to the Philippines as well. (Armanda Gessa and Figueredo Gonzales, 1986). Gubler further asserts that dengue fever has been on the rise because of lack of effective, long-term mosquito control in most tropical countries. therefore an anti-dengue program should be on-going, with appropriate environmental measures to control the development of mosquitoes, especially mosquito larvae. This level of control cannot be accomplished by spraying or fogging alone. (Gubler, 1989)

Question no.7 was the only question dealing with dengue treatment. This question requires technical background. About 40% scored incorrectly on this answer. Since the dengue virus attacks the blood clotting mechanisms and increases vascular permeability, is not advisable to administer aspirin. Aspirin may worsen the dengue illness by increase hemorrhaging. (Halstead, 1988, Sanford, 1983, Department of Health) A key component of their approach was to design health education materials based on the knowledge, attitudes, and behaviors of various sociocultural-economic groups within their respective communities. While recognizing the importance of government has continued material, financial, and organizational support in dengue control, the role of the people was emphasized for disease control in Puerto Rico. Gubler and Casta-Velez (1991) state: Dengue can be prevented by controlling these domestic larval habitats, but only people involved can effectively clean the areas around their own homes to prevent mosquito breeding. It might be added that people (teachers, staff, pupils, and parents) are the ones best able to clean up their school environments in order to control dengue transmission. This will only occur when participants have a clear understanding of the problem. Effective health education therefore is essential to facilitate an understanding of dengue problem (Gubler and Casta-Velez, 1991). The current study of the P.T.A. group in a Filipino high school demonstrated some of the strengths and weakness of media in health education. A high percentage of the parents and teachers had become aware of the dengue problem as a result of mass media (74.5%) and virtually 100% by the dengue information sheets brought home by the pupils. The dengue information sheets dealt with multiple behaviors or practices related to the control of DHF. However the mass media and dengue information sheets were insufficient to convince a majority of the P.T.A. that control of mosquito larvae was of pre-eminent importance, as indicated by the low scores on questions nos.4 and 8 of the questionnaire. While mass media increases knowledge (predisposing factors) it is unable to promote much health behavioral change (Green et al., 1980). With respect to health education strategies, Green et al. (1980) stated, education strategies that influence predisposing factors only will generally have short-term effects; programs that are designed to influence predisposing, reinforcing, and enabling factors will have the greatest pay offs in long-term behavioral changes. Therefore, the dengue information sheets were meant to be read not only by the pupils but also their parents. The parental return slip at the bottom of the dengue information sheet was an attempt to influence the reinforcing factors. The P.T.A. meeting (the day of the dengue questionnaire administration) which utilized lecture-discussion was a further attempt at influencing the reinforcing factors. Environmental clean up on the schools

campus was a result of the P.T.A. session. However, more strategies that are educational may be necessary to maintain a sustained dengue control program both at the pupils homes and at school. Concern about childrens exposure to dengue at school was voiced over 30 years ago in the suggestion that schools be closed during extensive outbreaks of H-fever (San Juan, 1960). That may not be feasible. The bulk of the dengue cases occur during the rainy season. The rainy season corresponds to the Philippine school year of June to March. A part of dengue control strategy in Puerto Rico, schools was particularly targeted for health education (Gubler and Casta-Velez, 1991). This health education strategy ought t apply to other countries affected by DHF, such as Philippines, as well. Recommendations 1. 2. 3. 4. 5. Encourage an anti-dengue hemorrhagic campaign through the schools, especially elementary schools Focus on the importance of control of mosquito breeding sites and larva destruction Develop health education materials related to control of mosquito breeding sites and larvae destruction for school and the community Parents should be involved in all school anti-dengue programs A distribution of responsibilities for ongoing school campus clean up for mosquito hazards by pupils, teachers, and staff with parental assistance may enable a program to be sustainable. 6. Develop and enforce legislation to restrict environmental violations related to DHF 7. Any school anti-dengue program should have a complementary counterpart in the barangays (communities) 8. Anti-dengue health information campaigns should precede the known peak denote months and continue on through the rainy season and school year.

Summary and Reaction

School-age children are particularly susceptible to dengue hemorrhagic fever. During January 1993, schools of Dumaguete City, Philippines were found to have breeding sites for the Aedes Aegypti mosquito, the carrier of the dengue virus. Dengue Hemorrhagic Fever (DHF), also known as H-fever or Philippine Hemorrhagic fever, was first reported in the Philippines in 1954. (San Juan, 1960) Since then dengue has occurred around the world in the tropics in location. Dengue is perilous in that there are no vaccines or anti-viral available for prevention or treatment. Dengue is capable of attacking infants despite the immune status of their mothers. Young children are most often the host of dengue. Dengue Hemorrhagic Fever (DHF) begins with fever and malaise which may last two days to a week. In the absence of virological testing and diagnosis (which is the case in most community setting) the diagnosis must be base upon serological laboratory findings. The World Health Organization has set classifications based upon laboratory values of hemoconcentration and thrombocytopenia.

The more severe form of dengue, called dengue shock syndrome (DSS), is characterized by internal bleeding and shock. The mortality associate with dengue may reach as high as 10 %. Thus according to Gubler and Casta-Velez (1991), dengue is currently the most important vector-borne viral disease afflicting humanity, in terms of both morbidity and mortality. The number of cases and rate of dengue hemorrhagic fever (H fever), at its earliest listing in 1964 in the Philippines were 74 and 0.3 per 100,000 respectively. The total number of dengue cases in the Philippines for the years 1954 t 1958 was 1,579 (San Juan, 1960). In 1965, the number of dengue (H-fever) cases, mortality rate, number of deaths and mortality rate were 652; 2.0 per 100,000; 109 and 0.3 per 100,000, respectively. By 1985 the number of dengue cases, case rate, number of deaths and mortality rate had increased to 2,096, 3.8 per 100,000; 210 and 0.4 per 100,000, respectively. Over 75 % of the 1985 dengue cases occurred between 14 years age and birth. The greatest number of dengue cases listed for the 21year period from 1965 to 1986 registered was in 1966, with 9,384 cases. However the average number of dengue cases per year from 1966 to 1985 was 1,384. The number of cases and rate per 100,000 for dengue in the entire Philippines for 1985 were 2,096 and 3.8 per, respectively. (Health, 1988) In 1985 the number of dengue cases and rate in Dumaguete City, Negros Oriental were 2 and 2.8 per 100,000 cases, respectively. There were no dengue registered deaths in Dumaguete for 1985. (Health, 1988). The number of dengue cases per year in Dumaguete for year 1988, 1989, 1990, 1991 and 1992 were, respectively, 96, 15, 45, 130, and 134 cases. The five year dengue morbidity rate from 1986 to 1990 in Dumaguete was 25.05 per 100,000. The 1991 dengue rate in Dumaguete was 161.06 per 100,000. The rate of dengue cases in 1992 in Dumaguete City had risen approximately 165 per 100,000. In response to the increased number of dengue cases in December 1992 Silliman University College of Education students enrolled in the Environmental Sanitation and Health course surveyed the campuses of six Dumaguete elementary schools in January 1993. Each school had multiple preventable mosquito breeding sites. Subsequently, the education students of the university began a dengue health communication campaign in cooperation with the Provincial Department of Health (Lennon, 1993). Nearly three-quarters of the P.T.A claimed to have received previous dengue health communication by way of mass media or meeting. There was, however, no significant differences between the responses of those who claimed to have received health communication prior to the questionnaire administration and those P.T.A participants who claimed not to have received prior dengue health communications. In response to dengue epidemics in the 1970s to early 1980s, Cuba conducted an A. aegypti eradication program. From their Cuban experience Armanda Gessa and Figueredo Gonzales stated, The most effective way of fighting aegypti is to adopt rigorous environmental sanitation measures. A key component of their approach was to design health education materials based on the knowledge, attitudes, and behaviors of various sociocultural-economic groups within their respective communities. While recognizing the importance of government has continued material, financial, and organizational support in dengue control, the role of the people was emphasized for disease control in Puerto Rico. Gubler and Casta-Velez (1991) state: Dengue can be prevented by controlling these domestic larval habitats, but only people involved can effectively clean the areas around their own homes to prevent mosquito breeding.

The epidemic of dengue here in Dumaguete caused chaos in every community. Several researches were done to look for a cure or treatment of this disease. Dengue is very common here in Philippines and to other tropical countries. Until now, there is no specific cure on this. Doctor is only monitoring its BP, platelet and hematocrit count to check from time to time its status, coz severe bleeding or low BP may lead death to an individual. Everyone should have a background about this disease because every individual could help or lessen the epidemic of dengue especially that we are now in rainy season wherein mosquitoes are numerous. Over the years, many researchers were studying the pathophysiology of dengue and everything about dengue in order to have a treatment. The government should focus their attention in this disease instead of the so-called swine flu now. Dengue is more death threatening than swine flu. We should encourage individuals to help themselves in lessening the reproduction of more mosquitoes. Clean up drive would do and proper health and environment sanitation would help.

Dengue Fever in America Anna Manzanarez seemed the picture of health, except for the bad case of flu that she was fighting. Then, the 28 year old waitress from the coastal community of Seaside, Calif, collapsed while getting out of the shower one morning. Her family rushed her to the hospital, where she died the next day. While the young womans sudden death understandably shocked family and friends, the discovery of what killed her was even more shocking to the public health officials. The centers for Disease Control and Prevention confirmed that Manzanarez died of Dengue Hemorrhagic fever, an illness almost unheared of in this country, which she had apparently contracted during a trip to Maxico. In January ,Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, warned that widespread appearance of dengue in the continental United States is a real possibility. Worldwide, dengue is among the most important remerging infectious deiseases. Public health officials need to take the threat seriously. Yet most health care providers in the United States are not familiar with dengue. West Nile virus was unknown in this country until 1999. Passed by the bite of infected mosquitoes, West Nile has now reached nearly every state, killed over 1,000 Americans, and sickened 27,000 more. SARS was a disease never before seen in humans until crossed the species barrier and swept around the world in 2003. West Nile and SARS were unpleasant surprises. However, dengue fever does not have to surprise us. We as nurses have the chance to prepare for its possible arrival by arming ourselves with knowledge of the diseases cause, its symptoms, diagnosis, and treatment.

Dengue fever is among the four dozen emerging or re-emerging infectious diseases tracked by the CDC. Dengue is considered a re-emerging diseases because its returning to locations once free of it. Dengue is also increasing in virulence. Fauci calls it one of the worlds most aggressive reemerging infections. The World Health Organization estimates there are 50 million to 100 million cases of dengue annually, with half a million hospitalizations and at least 22,000 deaths . In 2007, the Pan American Health Organization reported nearly 1 million cases of dengue fever in the Americans. More than 2 million of the 6.5 billion inhabitants are at risk of acquiring the worlds most important mosquito borne viral disease. Dengue is endemic-constantly present- in over 100 countries in Southeast Asia, Africa, the Western Pacific, the American and the Caribbean. Dengue fever is no stranger to the United States. Outbreaks occurred in Hawaii during 2001-2002 and in Texas in 2005. The primary mosquito vector for dengue fever is Ades aegypti,which is believed to have been dispersed tropical and subtropical settings from its original African home by shipping and trade over 400 years ago Aedes albopictus,also known as the Asian tiger mosquito,is becoming an ingcreasingly important alternate vector and was identified as the vector in the Hawaiian outbreak.Both species are present in the continental United States.Ae.aegypti is prevalent in over a dozen southern states while Ae.albopictus has spread to 36 states since its introduction in 1985. ALL ABOUT AEDES Aedes is an urban, day-biting mosquito that prefers to live in heavily populated areas where adequate food (human beings) and habitat (small amounts of standing water in empty food and drying containers, discarded tires, etc.)Abound. Aedes is not seasonal ,but bites year-round in areas warm enough to sustain its life cycle. Ae.aegypti is an especially efficient vector because its bite is nearly painless. These mosquitoes typically feed from several people before obtaining enough blood to promote egg maturation, thus increasing thr likelihood of spreading the virus between people. By comparison, the Anopheles mosquito that carries the malaria parasites typically obtains its full blood meal with one feeding. Aedes mosquitoes are also capable of transovarial transmission,the passage of virus from infected female to egg, meaning that a new generation of offspring may be capable of passing the virus without having bitten infected people Dengue fever is caused by a flavivirus, the family viruses that includes yellow fever and West Nile virus,as well as Japanese and St.Louis encephalitis. Its a single stranded RNA virus with four serotypes closely related groups of viruses differentiated by characteristic antigens known as DEN-1,DEN-2,DEN-3 andDEN-4.Infection with one serotype confers lifelong immunity to future infection by the same secrotype and transient protection against the other secrotypes. That protection lasts only a few months Humans are the principal reservoir for the dengue virus although Asian and African primates also may be infected. THE ORIGINAL EPIDEMICS The first reported epidemics of dengue lever occurred in 1779 and 1780 in Asia, Africa and North America. The nearly simultaneous occurrence of outbreaks on three continents suggests that the virus has had a worldwide distribution for at least 225 years. Widespread mosquito-control projects during the 20th century help to curb dengues spread in some countries. However, with a 30-fold increase in incidence over the past 50 years, dengue has expanded to almost all tropical and subtropical countries, many of which are popular tourist destinations. Dengue now appears to be moving into

temperate climes. Since the 1980s, dengue has dramatically expanded throughout its range, with regions changing from hypoendemic (areas of infection with one serotype) to hyperendemic (areas of infection with two or more serotypes). Human factors- such as uncontrolled urbanization and population growth, the deterioration of public health infrastructure, the large increase in the number of air travellers, and the lack of effective mosquito-control programs- have all contributed to the spread of dengue fever, especially over the past two decades. Dengue viruses collect within the salivary glands of infected Aedes mosquitoes. Each time a mosquito feeds , she injects saliva into the bloodstream. (only female mosquitoes take blood meals). Most cases of dengue are transmitted by the bite of infected mosquitoes; however, placental transmission is not uncommon. After an infected mosquito bite a person, the dengue virus replicates in regional lymph nodes and is disseminated through the lymphatic and blood systems to other tissues. The virus circulates for seven to ten days allowing ample time for mosquitoes to bite the viremic person and carry the virus to uninfected people. The incubation period for dengue- the time before symptoms appear- varies from three to 14 days, with four to seven days being the norm. Dengue presents with a continuum of disease that includes asymptomatic infection, mild febrile illness, dengue fever, DHF and DSS. The majority of people who become infected with dengue for the first time are asymptomatic or experience fever and symptoms similar to that founf with a mild case of flu. Yet the presence of dengue antibodies sets the stage for more serious disease should a subsequent infection with another serotype occur. A classic case of dengue fever may include sudden onset of some or all of the following Fever up to 105 F (can last five to seven days) Frontal headache , often severe Retro-orbital pain, often severe Bone, joint, and muscle pain, often severe. Dengue fever was once called break-bone fever because of the severity of the pain Maculopapular rash (a flat red rash with small raised bumps) with island sparing (areas within the rash in which skin appears normal); rash begins as fever wanes and lasts two to four days. Lymphadenopathy GI symptoms (nausea/vomiting/diarrhea) Upper respiratory infection symptoms (sore throat/nasal congestion/cough/reddened conjunctiva) Depression following recovery

As previously mentioned, infection with second dengue serotype may cause DHF or DSS. The mechanisms for this are not fully understood. But scientists believe that crossreactive antidengue antibodies from the previous infection bind to the new infecting serotype, enhancing viral uptake of monocytes and macrophages. This results in an amplified cascade of cytokines and complement activation, causing endothelial dysfunction, platelet destruction and consumption of coagulation factors. This in turn leads to plasma leakage and hemorrhagic manifestations. The severity of symptoms depends on the strain and serotype of the infecting virus, the patients age and genetic background, and the viral load. A patient with dengue hemorrhagic fever may manifest some or all of the above symptoms and the following as well: petechiae and ecchymosis, heavy meases, bleeding from the nose or gums, melena, hematuria, and hematemesis. Plasma leakage develops four to seven days after the onset of the disease and may be heralded by abdominal pain and vomiting, restlessness , a change in the level of consciousness, a sudden change from a febrile to hypothermic stage, and a marked decrease in platelet count. Worst case scenario According to the WHO classification of dengue hemorrhagic fever (available in the online version of this module, at www.nurse.com/ce), DSS is a subset of DHF, a worst-case scenario, with bleeding and substantial plasma leakage leading to hypovolemic shock and cardiovascular collapse, DSS is characterized by a rapid, weak pulse with a narrowing pulse pressure or profound hypotension. The duration of shock is short, with patients either recovering rapidly or dying within 12 to 24 hours. The mortality for DSS is as high as 40%. Shock is more common in children while hemorrhage is more common in adults. Some health authorities are calling for revision of the WHO classification, saying that often symptoms dont fit into the categories. For example, some DHF signs, such as thrombocytopenia, epistaxis, and petechiae, are present in 10% of uncomplicated dengue cases and are not necessarily predictive of disease severity or progression to shock. On the other hand, several studies showed that 18%-69% of infants and children with shock and laboratory-confirmed dengue did not meet all four WHO criteria for DHF. The WHO classification doesnt even mention some symptoms. For example, astudy in Singapore found relative bradycardia among dengue patients. Normally febrile patients experience tachycardia- heart rates above 100 beats per minute. In the study, patients with dengue fever averaged 87.6 bpm, or nearly 20 bpm less than patients with other infections and similar temperatures. This led researchers to believe that dengue fever may directly affect cardiac function, a symptom not included in the WHO system. Researchers recommended that large studies be undertaken to obtain the evidence needed to formulate a more robust dengue classification scheme that clinicians and epidemiologists can use regardless of their location. Making the diagnosis Similar to West Nile virus infections, most infections with dengue virus result in a subclinical and virtually asymptomatic illness. Clinical disease usually causes an acute febrile illness, or dengue fever. Patients typically recover completely within two weeks although they may left with fatigue or depression lasting several weeks or months. An estimated quarter-million causes of DHF occur annually. About 95% of the people who develop DHF and DSS are children under age 15 usually after having been previously infected by a different serotype.

Some researchers feel undue emphasis is placed on hemorrhage, pointing out that DSS derives not from hemorrhage, but form capillary leakage of intravascular fluids, electrolytes and small proteins into perivascular tissues. This may lead to pleural and pericardial efflasions, decreasing blood pressure, low tissue perfusion and oliguria. Shock can be predicted by a gradually increasing hematocrit over several hours despite normal hydration, encephalopathy may occur, with high mortality. As with many other viral diseases, making a definitive diagnosis of dengue fever can be a challenge that requires sophisticated laboratory capabilities. None of the available tests can easily aid the clinician in making an immediate positive diagnosis. This is in contrast to malaria, which usually can be quickly diagnosed by visualizing the parasite in blood. Tests for dengue virus include: Isolating dengue virus from serum, tissue, or cerebrospinal fluid. This test has a sensitivity of less than 30% and is not commonly available. While dengue virus may be present in blood early in the disease process, it can take days or weeks to isolate the virus and obtain results. Detecting dengue antigens in blood. Dengue antigens can be identified in serum and in peripheral blood mononuclear cells(PBMCs, or white blood cells round nuclei, such as lymphocytes and monocytes) using the ELISA test (enzyme- linked immunosorbent assay). The antigens can be found most easily on day 4 of illness in the PBMC and on the day 5 in the serum Identifying viral RNA. The genomic sequence of dengues RNA can be found by polymerase chain reaction(PCR) testing. The test has a sensitivity of 90% in the first few days of illness, but quickly declines to less than 10% a week after the onset of symptoms. Detecting dengue antibodies. Rapid diagnostic tests to detect antibodies to dengue virus have high sensitivity (71% to 100%) and high specificity( 86% to 100%). However, it takes the body several days to produce antibodies to dengue infection, so these tests are most accurate four to five days after the onset of symptoms.

DHF may be suspected when laboratory findings of thrombocytopenia and hemoconcentration are present plus pleural effusion and spontaneous bleeding most often from the nose or gums. The tourniquet test is a crude measure of hemorrhagic tenderness performed by inflating a blood pressure cuff to a point halfway between the patients systolic and diastolic blood pressure for five minutes. The test is positive if there are 20 or more petechiae per square inch on the forearm; in one study, 44% of patients were positive. No cure No acute or specific treatment exists for dengue infection. General supportive care includes treating pain and fever with acetaminophen rather than aspirin or other NSAIDs, which may aggravate the bleeding tendency associated with the disease. The patient should receive adequate fluids to prevent volume depletion, with electrolytes added as needed. Large amounts of fluids may be needed to treat capillary leakage associated with DHF and DSS. One study among Vietnamese children with DSS showed that Fungers lactate produced better outcomes than other tested fluids although its uncertain if these findings can be extrapolated to other populations. Blood and blood products may be administered if hemorrhage warrants their use.

While many nurses will never encounter patients with dengue fever, certainly some will for example, military nurses and nurses working in developing nations. Also, nurses working in EDs in the United States may encounter patients presenting with fevers of unknown origin. Such patients should be questioned about their recent travel. With 14 million Americans annually travelling to areas of endemic dengue fever, such as Asia, the Caribbean, Mexico, Central and South America and the Pacific ( Tahiti, the Philippines, Fiji), dengue patients will probably turn up in the nations EDs. Most dengue infections occur among people who have travelled to Asia and Americas. Some studies have shown that dengue infection is second only to malaria as the most frequent cause of hospitalization among travellers returning from areas of endemic dengue. Nurses can advise patients, family members, friends, and the community about the danger of travelling to tropical and subtropical regions where dengue fever is endemic. Unlike with malaria, no medications are available to prevent dengue infection. However, nurses can ensure that people know how to protect themselves from mosquito bites. This includes using mosquito repellents that contain DEET on bare skin. These products come in various formulations, such as sprays and lotions and some are safe to use on infants as young as 2 months. Wearing long-sleeved shirts and pants or clothing made of newer fabrics treated with mosquito repellent also offers protection. Travellers should stay in rooms with window and door screens, and should use insecticide screens and should use insecticide-treated bed nets while camping or sleeping in rural areas without screens. Risks in health care While dengue is largely transmitted by mosquitoes, health workers should know that dengue has been transmitted by mucocutaneous exposure to infected blood, by accidental needlestick, by bone marrow transplantation and by blood transfusion. The American Public Health Association recommends blood precautions with patients with suspected or confirmed dengue fever. A study of blood donors in Puerto Rico during a 2005 dengue epidemic found that one in every 1300 donors tested positive for the virus, leading the American Red Cross and public health officials to institute a research project to screen donated blood for dengue virus in Puerto Rico. At present, screening for dengue virus is not part of blood bank protocol in the United States. No vaccine is yet available to prevent dengue infection although several are in Phase II clinical trials. A successful vaccine must protect against all four serotypes because immunity to one serotype-whether acquired naturally or by vaccination- could lead to DHF or DSS if subsequent infection by another serotype occurs. Investigational vaccines include those made with inactivated and live attenuated viruses or viral RNA and genetically modified or chimeric formulations. One example of a chimera vaccines uses the yellow fever vaccine as its genetic backbone, replacing protein genes form the yellow fever viruss envelope with those from dengue viruses. The Walter Reed Army Institute of Research has produced a vaccine made of attenuated dengue viruses that has achieved an 80% to 90% seroconversion rate (development of antibodies in response to antigens) among a few human volunteers. A major concern of all dengue vaccine candidates is this: Will antibodties decline over time to the point that they no longer protect from infection, but in fact enhance it? One day, a vaccine will be able to prevent dengue infection plus perhaps antiviral medications to cure it . in the meantime, nurses should keep themselves and their patients informed about the potential for this dangerous and widespread disease.

Summary and Reaction

The Center of Disease Control considers dengue fever as one of the four dozen re-emerging or emerging infectious disease also it is increasing in virulence. WHO estimates that there are 50 million to 100 million cases of dengue annually with half a million hospitalizations and at least 22,000 deaths. The disease is caused by a flavivirus, the family viruses that include yellow fever and West Nile virus, as well as Japanese and St.Louis encephalitis. Human factors- such as uncontrolled urbanization and population growth, the deterioration of public health infrastructure, the large increase in the number of air travellers, and the lack of effective mosquito-control programs- have all contributed to the spread of dengue fever, especially over the past two decades. The primary mosquito vector of the disease is Aedes egypti which is an urban, day biting mosquito and bites throughout the year in areas warm enough to sustain its life cycle. The said mosquito is efficient because its bite is nearly painless. These mosquitoes typically feed from several people before obtaining enough blood to promote egg maturation, thus increasing the likelihood of spreading the virus between people. Also, the mosquitoes are capable of transovarial transmission, the passage of virus from infected female to egg which means that a new generation of offspring may be capable of passing the virus without having bitten infected people. The incubation period for dengue is from three to 14 days, with four to seven days being the norm. Dengue presents with a continuum of disease that includes asymptomatic infection, mild febrile illness, dengue fever, DHF and DSS. The majority of people who become infected with dengue for the first time are asymptomatic or experience fever and symptoms similar to that of a mild case of flu. A classic case of dengue fever may include sudden onset of some or all of the following Fever up to 105 F (can last five to seven days) Frontal headache , often severe Retro-orbital pain, often severe Bone, joint, and muscle pain, often severe. Dengue fever was once called break-bone fever because of the severity of the pain Maculopapular rash (a flat red rash with small raised bumps) with island sparing (areas within the rash in which skin appears normal); rash begins as fever wanes and lasts two to four days. Lymphadenopathy

GI symptoms (nausea/vomiting/diarrhea) Upper respiratory infection symptoms (sore throat/nasal congestion/cough/reddened conjunctiva) Depression following recovery

There is no specific treatment that exists for dengue infection. General supportive care includes treating pain and fever with acetaminophen rather than aspirin or other NSAIDs, which may aggravate the bleeding. The patient should receive adequate fluids to prevent fluid volume deficit, with electrolytes added as needed. Large amounts of fluids may be needed to treat capillary leakage associated with DHF and DSS. There are no medications available to prevent dengue. However, nurses can ensure that people know how to protect themselves from the mosquito. It includes using mosquito repellents that contain DEET on bare skin. These products come in different formulations, like sprays and lotions. Wearing long-sleeved shirts and pants or clothing made of newer fabrics treated with mosquito repellent also offers protection. Travellers should stay in rooms with windows and door with screens, and should use insecticide screens and also insecticide-treated bed nets while camping or sleeping in rural areas without screens. Health workers should be aware that mosquitoes do not only transmit dengue but it can also be transmitted by mucocutaneous exposure to infected blood by accidental needle stick, by bone marrow transplantation and blood transfusion. A study of blood donors in Puerto Rico during a 2005-dengue epidemic found that one in every 1300 donors tested positive for the virus, leading the American Red Cross and public health officials to institute a research project to screen donated blood for dengue virus in Puerto Rico. At present, screening for dengue virus is not part of blood bank protocol in the United States. As of now, there is no vaccine that can prevent dengue fever but we hope that someday doctors can produce that vaccine. Therefore, for the meantime the responsibility of the nurses is to inform clients on the widespread of this disease and teach those ways of preventing it. We definitely agree that Dengue Hemorrhagic Fever is widespread today and that no one is an exception. Even the most powerful and influential country, United States of America cannot escape from it. Millions of people die because of this emerging and re-emerging disease not just in America but also all over the world. The worst part is no one has yet to find a cure. This is disappointing to hear especially because a patient suffering from this disease could die. All health care team should take part in providing care to dengue patients, not just the doctors in giving medications but also us nurses in giving individualized care. Human factors such as uncontrolled urbanization and population growth, unsanitary environment etc. have all contributed to the widespread of Dengue fever and with this; we should do something right away so that we can minimize its occurrence. Maintaining a clean environment is very important because dengue fever is a re-emerging disease, it stops for a period of time and it re occurs after some time.

Even here in the Philippines dengue fever can kill many innocent lives, and that we, as part of the health care team cannot do anything about it. But as nurses we can minimize its widespread by keeping our patient/patients family or people in the community be informed everything about Dengue Hemorrhagic Fever.

Bibliography and Readings

Textbooks:

Atlas, R.M. (1995). Microorganisms in Our World. Mosby. St. Louis. Black, J. & Hawks J. (2004). Medical-surgical nursing. 7th ed. Vol.1 Philadelphia: WB Saunders Co. Black,J & Mathassarin-Jacobs, E. Luckman and Sorensens Medical Surgical Nursing. 3rd ed. Philadelphia: WB Saunders Co. Dettenmeier, P. (1992). Pulmonary nursing care. Mosby Yearbook. USA Marieb, E. (2002). Esentials of Human Anatomy and Physiology. Singapore: Pearson Education Asia Maebius, L. (2000). Medical Surgical Nursing. 3rd ed. Saunders. New York. Novak, T.J. & Handford, G. A. (1994). Essentials of Pathophysiology. England: WNC Publishers Potter & Perry (2001). Fundamentals of nursing. 5th ed. Missouri: Mosby Inc. Steltzer, S.C.(2000). Medical Surgical Nursing. 9th ed. Lipincott. London. Tortora & Grabowski. (1993). Principles of Anatomy and Physiology 7th ed. New York: RR Donelly & Sons Inc. Drug Handbook: Nursing Drug Handbook. Lipincott Williams & Wilkins. (2005) USA Journals: Silliman journal, 1994 Knowledge of Dengue Hemorrhagic Fever by a Parents- Teachers Group in a Filipino High School (Jeffrey L. Lennon) Nurse.com June 20, 2008 Nursing Spectrum, DC/Maryland/Virginia Edition, Time and Motion Study reveals forces that pull nurses from the bedside.

REMARKS: Pls. arrange casebook according to the following: Cover page Cover Letter/Application Letter Vision-Mission Statement Acknowledgment Table of Contents (with corresponding pages) Introduction Objectives Psychosocial Profile: Demographic Data Genogram Ecomap Growth & Development Physical Assessment Findings Anatomy & Physiology Overview of the Disease Condition Pathophysiology Medical Management XX. Laboratory Results XXI. Pharmacologic Management XXII. Diagnostic Procedures Functional Health Pattern Summary of Nursing Diagnoses (at least five) Nursing Care Plan Journal Articles (2 articles) Synthesis

Bibliography Comments: please include the DIAGNOSIS of your client in the application letter and it should be in portrait view and not landscape please proofread carefully your paper before submitting the final casebook casebook should be individualized or should be unique to your clients condition describe how G&D relates to your client indicate the significance of the laboratory findings in relation to your clients condition; do not just copy information from the book encode or include photocopy of the journal readings, make a summary in your own words and a reaction of each reading journal readings should be focused on new developments, research studies related to the condition in the case presented please improve the content of your casebook