I. Introduction

Background & History

The origins of the word are not clear, but one theory is that it is derived from the Swahili phrase "Ka-dinga pepo", which describes the disease as being caused by an evil spirit.The Swahili word "dinga" may possibly have its origin in the Spanish word "dengue" (fastidious or careful), describing the gait of a person suffering dengue fever, or, alternatively, the Spanish word may derive from the Swahili.

Dengue, the most common arboviral illness transmitted worldwide, is caused by infection with 1 of the 4 serotypes of dengue virus. Dengue is transmitted by mosquitoes of the genus Aedes, which are widely distributed in subtropical and tropical areas of the world, and is classified as a major global health threat by the World Health Organization (WHO).

Initial dengue infection may be asymptomatic, may result in a nonspecific febrile illness, or may produce the symptom complex of classic dengue fever (DF). A small percentage of persons who have previously been infected by one dengue serotype develop bleeding and endothelial leak upon infection with another dengue serotype. This syndrome is termed dengue hemorrhagic fever (DHF). Some patients with dengue hemorrhagic fever develop shock (dengue shock syndrome [DSS]), which may cause death.

Dengue virus transmission follows two general patterns—epidemic dengue and hyperendemic dengue. Epidemic dengue transmission occurs when dengue virus is introduced into a region as an isolated event that involves a single viral strain. If the number of vectors and susceptible pediatric and adult hosts is sufficient, explosive transmission can occur, with an infection incidence of 25-50%. Mosquito-control efforts, changes in weather, and herd immunity contribute to the control of these epidemics. This is the current pattern of transmission in parts of Africa and South America, areas of Asia where the virus has reemerged, and small island nations. Travelers to these areas are at increased risk of acquiring dengue during these periods of epidemic transmission.

Hyperendemic dengue transmission is characterized by the continuous circulation of multiple viral serotypes in an area where a large pool of susceptible hosts and a competent vector (with or without seasonal variation) are constantly present. This is the predominant pattern of global transmission. In these populations, antibody prevalence increases with age and most adults are immune. Hyperendemic transmission appears to be a major risk for dengue hemorrhagic fever. Travelers to these areas are more likely to be infected than are travelers to areas that experience only epidemic transmission.

Dengue fever–like illnesses were described in Chinese medical writings dating back to 265 AD. Outbreaks of febrile illnesses compatible with dengue fever have been recorded throughout history. In 1789, Benjamin Rush, MD, published an account of a probable dengue fever epidemic that had occurred in Philadelphia in 1780. Rush coined the term breakbone fever to describe the intense symptoms reported by one of his patients.

Probable outbreaks of dengue fever occurred sporadically every 10-30 years until after World War II. The socioeconomic disruptions caused by World War II resulted in increased worldwide spread of dengue viruses.

The first epidemic of dengue hemorrhagic fever was described in Manila in 1953. After that, outbreaks of dengue fever became more common. A pattern developed in which dengue fever epidemics occurred with increasing frequency and were associated with occasional dengue hemorrhagic fever cases. Subsequently, dengue hemorrhagic fever epidemics occurred every few years. Eventually, dengue hemorrhagic fever epidemics occurred yearly, with major outbreaks occurring approximately every 3 years. This pattern has repeated itself as dengue fever has spread to new regions.

Although initial epidemics were located in urban areas, increased dengue spread has involved suburban and rural locales in Asia and Latin America. The only continents that do not experience dengue transmission include Europe and Antarctica. In the 1950s, 9 countries reported dengue outbreaks; today, the geographic distribution includes more than 100 countries worldwide. Several of these countries had not previously reported dengue, and many had not reported dengue in 20 years.

Dengue transmission spread from Southeast Asia into surrounding subtropical and tropical Asian countries, southern China and southern Taiwan, the Indian subcontinent and Sri Lanka, and down the island nations of Malaysia, the Philippines, New Guinea, northeastern Australia, and several Pacific islands, including Tahiti, Palau, Tonga, and the Cook Islands. Nepal has not reported dengue transmission. Hyperendemic transmission is reported in Vietnam, Thailand, Indonesia, Pakistan, India, Malaysia, and the Philippines.

Currently, dengue hemorrhagic fever is one of the leading causes of hospitalization and death in children in many Southeast Asian countries, with Indonesia reporting the majority of dengue hemorrhagic fever cases. Of interest and significance in prevention and control, 3 surveillance studies in Asia report an increasing age among infected patients and increasing mortality rate. Since 1982 in Singapore, more than 50% of deaths have occurred in individuals older than 15 years. In Indonesia, young adults in Jakarta and provincial areas make up a larger percentage of infected patients. During the 2000 epidemic in Bangladesh, up to 82% of hospitalized patients were adults, and all deaths occurred in patients older than 5 years.

The epidemiology of dengue fever in Africa is more poorly characterized. Aedes aegypti is present in a large portion of the Middle East and sub-Saharan Africa. Dengue fever is present in 19 countries on the African continent. In a 1993 epidemic in the Comoros, an estimated 60,000 persons were infected with dengue. Of note, no major dengue hemorrhagic fever epidemics have occurred in Africa, despite the fact that all 4 dengue serotypes circulate in the continent. This may be explained by a genetic factor in these populations.

In the Americas, dengue epidemics were rare postwar because Aedes mosquitoes had been eradicated from most of the region through coordinated vector-control efforts. Systematic spraying was halted in the early 1970s because of environmental concerns. By the 1990s, A aegypti mosquitoes repopulated most of the countries in which they had been eliminated.

The first dengue hemorrhagic fever epidemic in the Americas occurred in Cuba in 1981, with 24,000 cases of dengue hemorrhagic fever, 10,000 cases of dengue shock syndrome, and 158 reported deaths. Since then, dengue fever and dengue hemorrhagic fever cases have progressively increased. A aegypti is abundant year-round in most countries in the Caribbean basin. Significant outbreaks of dengue have been reported in 2005 and 2006 in Puerto Rico, the US Virgin Islands, the Dominican Republic, Barbados, Curacao, Cuba, Guadeloupe, and Martinique.

Aedes albopictus, originally from Asia, is now found in limited areas of Brazil, Bolivia, Colombia, the Dominican Republic, El Salvador, Guatemala, Honduras, Mexico, Cuba, and the Cayman Islands. A aegypti is present in all countries in South America except Chile. Hyperendemic circulation of all 4 dengue serotypes is present in the northern countries of South America. Brazil (700,000 cases in 2002), Colombia, and Venezuela report the most cases of dengue and dengue hemorrhagic fever, with low-level transmission occurring year-round but with most occurring during periods of epidemic transmission.

In 1986, the first clearly identified local transmission of dengue in the United States occurred in Texas. Carriers of the virus were believed to have crossed the border from Mexico; the local vector population was then infected. Since then, seasonal autochthonous infection has been reported in both Texas and Hawaii.

Two competent vectors, A aegypti and A albopictus, are currently seasonally abundant in some areas of the southwestern and southeastern United States, including Texas, Arizona, New Mexico, Louisiana, Mississippi, Alabama, Georgia, and mid to south Florida. A aegypti has also been reported sporadically in portions of North Carolina, South Carolina, Tennessee, Arkansas, Maryland, and New Jersey. The range of A albopictus extends almost as far north as the Great Lakes. Since many cases of dengue in US citizens occur as a result of endemic transmission in some US territories, the Centers for Disease Control and Prevention (CDC) currently conducts laboratory-based surveillance in Puerto Rico.

Dengue fever does not naturally occur in the European Union and in continental Europe because these areas do not have an appropriate vector population  to allow further spread of dengue from viremic patients returning from other countries. As such, the disease is not statutorily notifiable in most member states. However, dengue does occur in several overseas territories of European Union members. In recent decades, reports of dengue infections in long-term expatriates, aid workers, military personnel, immigrants, and travelers returning from the tropics and subtropics have been increasing.

Factors believed to be responsible for dengue's spread include explosive population growth, unplanned urban overpopulation with inadequate public health systems, poor standing water and vector control, climate change (increased virus transmission has been associated with El Niño conditions), and increased international recreational, business, and military travel to endemic areas. All of these factors must be addressed to control the spread of dengue and other mosquito-borne infections.

II. Frequency

International

An estimated 2.5-3 billion people in approximately 110 countries worldwide are at risk for dengue infection. Yearly, approximately 100 million people are infected with dengue, and 250,000 individuals develop dengue hemorrhagic fever. Annually, approximately 24,000 deaths are attributed to dengue worldwide. The Pan American Health Organization (PAHO) member states reported twice as many cases of dengue fever and dengue hemorrhagic fever in 1998 as they did in 1997.

A recent 5-year prospective study in Thai children examined the relative economic burden of dengue infection in children on the local population.4 Most disability-adjusted life years (DALYs) lost to dengue resulted from long-duration illness in children who had not been hospitalized. The infecting serotype appeared to be a determining factor of DALYs lost, with DENV-2 and DENV-3 responsible for 30% and 29%, respectively. The mean cost of illness from dengue was significantly higher than that from other febrile illnesses.

Mortality/Morbidity

Recovery from dengue infection is usually complete. Even patients who meet strict criteria for dengue hemorrhagic fever or dengue shock syndrome usually recover without sequelae.

The fatality rate associated with dengue shock syndrome varies by country from 12-44%. In a 1997 Cuban epidemic, the fatality rate in patients who met criteria for dengue hemorrhagic fever or dengue shock syndrome was approximately 6%. The mortality rate associated with dengue fever is less than 1%.

Data from the 1997 Cuban epidemic suggests that, for every clinically apparent case of dengue fever, 13.9 cases of dengue infection went unrecognized because of absent or minimal symptoms.

Factors that affect disease severity include patient age, nutritional status, ethnicity, the sequence of infection with different dengue serotypes, virus genotype, and the quality and extent of available medical care.

Race

Dengue affects all races. Some African and Haitian data demonstrate a relative dearth of dengue hemorrhagic fever and dengue shock syndrome during dengue

fever epidemics, suggesting that these populations may share a genetic advantage to the virus. This merits further study.

Sex

Dengue viruses affect both sexes.Age

Dengue affects people of all ages. In Southeast Asia, where dengue is hyperendemic, dengue hemorrhagic fever usually affects children younger than 15 years. However, in the Americas, where dengue is becoming progressively hyperendemic, dengue hemorrhagic fever shows no age predilection.

III. ANATOMY AND PHYSIOLOGY

Functions of Blood:

1 - Transportation: o oxygen & carbon dioxideo nutrientso waste products (metabolic wastes, excessive water, & ions)

2 - Regulation - hormones & heat (to regulate body temperature)

3 - Protection - clotting mechanism protects against blood loss & leucocytes provide immunity against many disease-causing agents

Components of Blood - average adult has about 5 liters:

1. Formed elements :

o Red blood cells (or erythrocytes)o White blood cells (or leucocytes)o Platelets (or thrombocytes)

2. Plasma = water + dissolved solutes

Red Blood Cells (or erythrocytes):

1 - biconcave discs

2 - lack a nucleus & cannot reproduce (average lifespan = about 120 days)

3 - transport hemoglobin (each RBC has about 280 million hemoglobin molecules)

4 - Typical concentration is 4-6 million per cubic mm (or hematocrit [packed cell volume] of about 42% for females & 45% for males)

5 - contain carbonic anhydrase (critical for transport of carbon dioxide)

Determining the hematocrit

Erythropoiesis = formation of erythrocytes

the body must produce about 2.5 million new RBCs every second in adults, erythropoiesis occurs mainly in the marrow of the sternum, ribs,

vertebral processes, and skull bones begins with a cell called a hemocytoblast or stem cell (below) rate is regulated by oxygen levels:

o hypoxia (lower than normal oxygen levels) is detected by cells in the kidneys

o kidney cells release the hormone erythropoietin into the bloodo erythropoietin stimulates erythropoiesis by the bone marrow

Hemoglobin

composed of globin (made up of 4 highly folded polypeptide chains) + 4 heme groups (with iron)

each molecule can carry 4 molecules of oxygen called oxyhemoglobin when carrying oxygen & called reduced hemoglobin when

not carrying oxygen can also combine with carbon dioxide & helps transport carbon dioxide from the

tissues to the lungs

White blood cells (or leucocytes or leukocytes):

have nuclei & do not contain hemoglobin typical concentration is 5,000 - 9,000 per cubic millimeter types of WBCs:

o granular white blood cells include: neutrophils (50 - 70% of WBCs) eosinophils (1 - 4%) basophils (less than 1%)

o agranular (or non-granular) white blood cells include: lymphocytes (25 - 40%) monocytes (2 - 8%)

Granular white blood cells contains numerous granules in the cytoplasm, & their nuclei are lobed. Agranular white blood cells have few or no granules in the cytoplasm & have a large spherical nucleus. Granular white blood cells are produced in the bone marrow, while agranular white blood cells are produced in lymph tissue, e.g., Lymph nodes (specialized dilations of lymphatic tissue which are supported within by a meshwork of connective tissue called reticulin fibers and are populated by dense aggregates of lymphocytes and macrophages).

The primary functions of the various white blood cells are:

Neutrophils - phagocytosis (bacteria & cellular debris); very important in inflammation

Eosinophils - help break down blood clots & kill parasites Basophils - synthesize & store histamine (a substance released during

inflammation) & heparin (an anticoagulant); functions(s) remain unclear Monocytes - phagocytosis (typically as macrophages in tissues of the liver,

spleen, lungs, & lymph nodes) Lymphocytes - immune response (including production of antibodies)

Some important characteristics of White Blood Cells (particularly neutrophils):

1 - phagocytic

2 - capable of diapedesis (also called extravasation)

3 - capable of ameboid movement

4 - exhibit chemotaxis (attracted to certain chemicals, such as those released by damaged cells)

Platelets (or thrombocytes)

1 - formed in the bone marrow from cells called megakaryocytes

2 - have no nucleus, but can secrete a variety of substances & can also contract (because they contain actin & myosin)

3 - normal concentration in the blood is about 250,000 per cubic millimeter

4 - remain functional for about 7 - 10 days (after which they are removed from the blood by macrophages in the spleen & liver)

5- play an important role in hemostasis (preventing blood loss)

Plasma:

1 - Water - serves as transport medium; carries heat

2 - Proteins

Albuminso 60-80% of plasma proteinso most important in maintenance of osmotic balanceo produced by liver

Globulinso alpha & beta

some are important for transport of materials through the blood (e.g., thyroid hormone & iron)

some are clotting factors produced by liver

o gamma globulins are immunoglobulins (antibodies) produced by lymphocytes

Fibrinogeno important in clottingo produced by liver

3 - Inorganic constituents (1% of plasma) - e.g., sodium, chloride, potassium, & calcium

4 - Nutrients - glucose, amino acids, lipids & vitamins

5 - Waste products - e.g., nitrogenous wastes like urea

6 - Dissolved gases - oxygen & carbon dioxide

7 - Hormones

Hemostasis - prevention of blood loss from broken vessel:

1 - Vascular spasm - vasoconstriction of injured vessel due to contraction of smooth muscle in the wall of the vessel. This 'spasm' may reduce blood flow & blood loss but will not stop blood loss.

2 - Formation of a platelet plug - platelets aggregate at the point where a vessel ruptures. This occurs because platelets are exposed to collagen (a protein found in the connective tissure located just outside the blood vessel). Upon exposure to collagen, platelets release ADP (adenosine diphosphate) & thromboxane. These substances cause the surfaces of nearby platelets to become sticky and, as 'sticky' platelets accumulate, a 'plug' forms.

3 - Blood coagulation (clotting):

The result of all of this is a clot - formed primarily of fibrin threads (or polymers), but also including blood cells & platelets.

Blood clots in the right places prevent the loss of blood from ruptured vessels, but in the wrong place can cause problems such as a stroke (see below under inappropriate clotting).

Clot retraction:

"tightening" of clot contraction of platelets trapped within clot shrinks fibrin meshwork, pulling edges

of damaged vessel closer together. Over time (with the amount of time depending on the amount of damage), the clot is dissolved and replaced with normal tissue.

Fibrinolysis:

dissolution of clot mechanism = plasminogen (a plasma protein) is activated by many factors &

becomes PLASMIN. Plasmin then breaks down fibrin meshwork & phagocytic WBCs remove products of clot dissolution

Human Habitation

IV. Pathophysiology

Environmental Factor

Bite of femaleAedes Aegypti

Replication of virus in the dendrite cells

Immune mediators that serve to share the quantity, type and

duration of cellular and normal immune response to

both the initial and subsequent virus infection

Thrombocytopenia Capillary fragility

Increase Capillary Permeability

Plasma Leakag

e

Petichial rash

Skin hemorrhage

Hemoconcentrationn

Bleeding

Human Habitation

V. Patient’s Profile

Client’s Name or Initial: Mrs. AAge: 21 years oldSex: FemaleMarital Status: MarriedReligion: CatholicAddress: Phase1 blk.9 lot3 Francisco Homes San Jose Del Monte BulacanBirth Date and place of birth: April 27, 1987, ManilaRace/Nationality: FilipinoUsual Source of Medical Care: Health CenterSource and Reliability of Information: Patient

Reason for Seeking Care

1. Fever2. Headache3. Severe Vomiting4. Body Rashes

Past Medical History

i. Pediatric/Childhood/Adult Illness:Cough, Colds, Fever

ii. Injuries or accidents:None

iii. Hospitalizations and operations:None

iv. Obstetric History (for female clients only):G1P1 Menarche at 13 years old

v. Immunization

BCG: /√/ at birth /√/ School EntranceDPT: /x/ 1st dose /x/2nd dose /x/3rd doseOPV: /x/ 1st dose /x/ 2nd dose /x/ 3rd doseAMV: /x/TT: /√/ 1st dose /√/ 2nd dose /√/ 3rd dose /√/ 4th dose /√/ 5th doseHepatitis B Vaccine: /x/ 1st dose /x/ 2nd dose /x/ 3rd dose /x/ 4th dose

vi. Allergies

Food (specify): noneDrugs (specify): noneChemicals (specify): noneEnvironmental Allergens (specify): none

Data BaseTwo days prior to admission fever is on & off. A few hours prior to admission

patient develops vomiting 6x accompanied by poor appetite and body weakness.

Physical Assessment

V/S Gen.Survey : weak looking, ambulatoryBP: 90/60 HEENT: dry lipsTemp: 38.5 degree Celsius Lungs: clear breath sounds RR: 23cpm Abdomen: soft, flat, slight epigastric tendernessPR: 100bpm Extremities: body rashes are present

Course in the Ward

The patient usually play with her cellphone & talks to her mother frequently. She does not sleep often. She is ambulatory and can use the bathroom independently. She’s usual elimination pattern is U=5x/day S=1x/day.

VI. Laboratory

Hematology

Hematology (American English) or haematology (British English) is the branch of biology (physiology), pathology, clinical laboratory, internal medicine, and pediatrics that is concerned with the study of blood, the blood-forming organs, and blood diseases. Haematology includes the study of etiology, diagnosis, treatment, prognosis, and prevention of blood diseases. The lab work that goes into the study of blood is performed by a Medical Technologist.

Laboratory Result Prior to Admission (Oct. 4, 08)

VALUE UNITS NORMAL VALUEWBC 6.20 10^g/l 5-10RBC 4.09 10^12/uL 4.2-5.4Hemoglobin 122 g/l 120-160Hematocrit 0.37 0.37-0.47Platelet 210x100 /mm3 140-340x100Lymphocyte 0.47 0.20-0.40Segmenters 0.53 0.50-0.70

Laboratory Result from Oct.4 to Oct.610/4 6pm 10/5 6am 10/5 6pm 10/6 6:20am

WBCRBCHemoglobin 121 123 110 103Hematocrit 0.36 0.37 0.33 0.31Platelet 198x100 162x100 124x100 118x100LymphocyteSegmenters

WBC- Normal

RBC-Normal

Hemoglobin- (10/5)Decrease indicates hemorrhage

Hematocrit-(10/4 6pm), (10/5 6pm)Decrease indicates hemorrhage

Platelet- (10/5 6pm)Decrease indicates DIC, hemorrhage

Lymphocytes-(10/4 upon admission)Increase indicates infection

VII. Drug Study

Paracetamol (500mg/tab q 4 hours for fever)

Name of Drug

Action Indication Side effect Pharmacokinetics Nursing considertion

Paracetamol Inhibits the synhesis of prostaglandin that may serve as mediators of pain and fever, primarily in the CNS. Has no significant anti-inflammatory properties or GI toxicity

Mild Pain. Fever.

Contraindication

Previous hypersensitivity. Products containing alcohol, aspartame, saccharin sugar, ot tartrazine should be avoided.

Hepatic failure, hepatotoxicity, renal failure, neutropenia, pancytopenia, leucopenia, rash, urticuria

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: 2-5hr; Adults: 1-3hr

Pharmacodynamics

route

onset

peak

duration

PO

Rect

0.5-1hr

0.5-1hr

1-3hr

1-3hr

3-8hr

3-4hr

Assess overall health status and alcohol usage before administration.

Administer with food or an empty stomach.

Advise patient to avoid alcohol if taking this drug

Avoid taking concurrently with salicylates or NSAIDs for more than a few days, unless directed.

Advise patient to consult physician if discomfort or fever is not relieved of routine doses or if fever is greater than 39.5C or lasts longer than 3 days.

Our Lady of Fatima University

Quezon City

ACase Study

AboutDENGUE

Prepared By:

Mariano, Efren (Leader)Tano, John LeomarMostoles, Kleir Ann

Ravancho, Moonyeen

October 2008

Table of Contents

I. Introduction

II. Frequency

III. Anatomy and Physiology

IV. Pathophysiology

V. Patients Profile

VI. Laboratory

VII. Drug Study

VIII. NCP

IX. Discharge Plan

VIII. NCP

Subjective Nursing Dx Analysis Planning Implementation Rationale Evaluation

>”dalawang araw na akong nilalagnat at itoy pabalik-balik” as verbalize.

Objective:>dry lips>pale color>weak looking>temp. of 38.5 degree celcius

Increased body temp. r/t inflammatory process

Hypothalamus which controls the bodys thermoregulation releases heat due to the presence of infection

After 1 hour of nursing intervention the patient temp will decrease.

>Monitor core temp.>Monitor BP,PR,RR>Thermoregulation

>Render TSB/ warm bath>Promote bedrest>Provide comfort>Administer medication as prescribe

>For temperature assessment if change>To assess client stability>To regulate body temp. back into normal>To decrease temp

>To promote wellness>To reduce anxiety>To decrease temp

After 1 hour of nursing intervention the patient temperature had been decreased.

NCP

Subjective Nursing Dx

Analysis Planning Implementation

Rationale Evalution

>”Anim na beses na akong nagsusuka” as verbalize.

Objective:>Weak looking>Dry lips>Pale color

>Vomiting r/t gastric distention

>G.I irritation in response to the presence of blood in the G.I.T

>After 1hr. of nursing intervention the filling of vomiting of the patient will decrease & the patient will be at comfort

>Encourage reverseT-position>Bed rest

>Water therapy

>promote clean environment

>To back flow the vomitous

>To promote comfort>To minimize the risk of dehydration>for relaxation

>After 1hr.of nursing intervention the feeling of the patient had been decreased & patient had been at comfort

IX. Discharge Planning

The discharge plan includes health teaching about Dengue Hemorrhagic Fever, its risk factors, management and some complications of the condition if not managed or not treated well, and methods of prevention and control.

As part of the plan, the patient the patient is advised to:

1. Report any signs and symptoms of DHF such as high fever, abdominal pain and headache.

- early detection of signs and symptoms of the disease may decrease risk of DHF’s complications

2. Clean environment:- elimination of stagnant water- cover water containers- dispose old used tires- clean water drainage- proper disposal of garbage

3. Used insect propellant.

4. Avoid too many hanging clothes inside the house.

5. Drink adequate fluids at least eight glasses a day.- may drink fruit juices such as calamansi juices for Vitamin C

supplementation

6. Eat foods rich in vitamins and minerals.

7. Use soft bristle toothbrush.

8. Report reoccurrence of fever and signs of bleeding to physician immediately.

.