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.

Arkansas. Hyperendemic circulation of all 4 dengue serotypes is present in the northern countries of South America. reports of dengue infections in long-term expatriates. with 24. dengue does occur in several overseas territories of European Union members. Mississippi. Louisiana. 10. By the 1990s. the Dominican Republic. Systematic spraying was halted in the early 1970s because of environmental concerns. Colombia. Cuba. Significant outbreaks of dengue have been reported in 2005 and 2006 in Puerto Rico. Guatemala. New Mexico. including Texas. Carriers of the virus were believed to have crossed the border from Mexico. Cuba. the first clearly identified local transmission of dengue in the United States occurred in Texas. Alabama. In recent decades. A aegypti has also been reported sporadically in portions of North Carolina. Curacao. with low-level transmission occurring year-round but with most occurring during periods of epidemic transmission. aid workers.000 cases of dengue hemorrhagic fever. Two competent vectors.000 cases of dengue shock syndrome. Mexico. Since then. seasonal autochthonous infection has been reported in both Texas and Hawaii. A aegypti mosquitoes repopulated most of the countries in which they had been eliminated. and Venezuela report the most cases of dengue and dengue hemorrhagic fever. and 158 reported deaths. immigrants. Arizona. Maryland. military personnel. and Martinique. Guadeloupe. the Dominican Republic. As such. dengue epidemics were rare postwar because Aedes mosquitoes had been eradicated from most of the region through coordinated vector-control efforts. and the Cayman Islands. the Centers for Disease Control and Prevention (CDC) currently conducts laboratory-based surveillance in Puerto Rico. Bolivia. A aegypti is abundant year-round in most countries in the Caribbean basin. the disease is not statutorily notifiable in most member states. the US Virgin Islands. Tennessee. Honduras. is now found in limited areas of Brazil. and travelers returning from the tropics and subtropics have been increasing. The first dengue hemorrhagic fever epidemic in the Americas occurred in Cuba in 1981. . dengue fever and dengue hemorrhagic fever cases have progressively increased. the local vector population was then infected. Since many cases of dengue in US citizens occur as a result of endemic transmission in some US territories. Brazil (700. A aegypti and A albopictus. Barbados. Colombia. Georgia. are currently seasonally abundant in some areas of the southwestern and southeastern United States. 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. Aedes albopictus. and New Jersey.000 cases in 2002). In 1986. South Carolina.In the Americas. originally from Asia. However. and mid to south Florida. Since then. The range of A albopictus extends almost as far north as the Great Lakes. El Salvador. A aegypti is present in all countries in South America except Chile.

All of these factors must be addressed to control the spread of dengue and other mosquito-borne infections. Factors that affect disease severity include patient age. Data from the 1997 Cuban epidemic suggests that. In a 1997 Cuban epidemic. and military travel to endemic areas. poor standing water and vector control. 13. for every clinically apparent case of dengue fever.5-3 billion people in approximately 110 countries worldwide are at risk for dengue infection. ethnicity. and 250. Annually. with DENV-2 and DENV-3 responsible for 30% and 29%. Race • Dengue affects all races.000 individuals develop dengue hemorrhagic fever. Mortality/Morbidity • • • • Recovery from dengue infection is usually complete. Frequency International An estimated 2. unplanned urban overpopulation with inadequate public health systems. A recent 5-year prospective study in Thai children examined the relative economic burden of dengue infection in children on the local population. and the quality and extent of available medical care. The mean cost of illness from dengue was significantly higher than that from other febrile illnesses.4 Most disability-adjusted life years (DALYs) lost to dengue resulted from long-duration illness in children who had not been hospitalized. 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. respectively. nutritional status. the sequence of infection with different dengue serotypes. Yearly. and increased international recreational. Even patients who meet strict criteria for dengue hemorrhagic fever or dengue shock syndrome usually recover without sequelae. approximately 24. the fatality rate in patients who met criteria for dengue hemorrhagic fever or dengue shock syndrome was approximately 6%.9 cases of dengue infection went unrecognized because of absent or minimal symptoms. climate change (increased virus transmission has been associated with El Niño conditions).Factors believed to be responsible for dengue's spread include explosive population growth. II. virus genotype. approximately 100 million people are infected with dengue. business.000 deaths are attributed to dengue worldwide. The infecting serotype appeared to be a determining factor of DALYs lost. The mortality rate associated with dengue fever is less than 1%. Some African and Haitian data demonstrate a relative dearth of dengue hemorrhagic fever and dengue shock syndrome during dengue . The fatality rate associated with dengue shock syndrome varies by country from 12-44%.

where dengue is hyperendemic. where dengue is becoming progressively hyperendemic. dengue hemorrhagic fever usually affects children younger than 15 years.fever epidemics. However.Age Dengue affects people of all ages. . Sex • • Dengue viruses affect both sexes. dengue hemorrhagic fever shows no age predilection. in the Americas. suggesting that these populations may share a genetic advantage to the virus. This merits further study. In Southeast Asia.

excessive water.Protection .lack a nucleus & cannot reproduce (average lifespan = about 120 days) 3 .ANATOMY AND PHYSIOLOGY Functions of Blood: 1 . Formed elements: o o o Red blood cells (or erythrocytes) White blood cells (or leucocytes) Platelets (or thrombocytes) 2.average adult has about 5 liters: 1. Plasma = water + dissolved solutes Red Blood Cells (or erythrocytes): 1 . & ions) 2 .Typical concentration is 4-6 million per cubic mm (or hematocrit [packed cell volume] of about 42% for females & 45% for males) 5 .Transportation: o o o oxygen & carbon dioxide nutrients waste products (metabolic wastes.clotting mechanism protects against blood loss & leucocytes provide immunity against many disease-causing agents Components of Blood .biconcave discs 2 .transport hemoglobin (each RBC has about 280 million hemoglobin molecules) 4 .contain carbonic anhydrase (critical for transport of carbon dioxide) .hormones & heat (to regulate body temperature) 3 .Regulation .III.

vertebral processes. ribs.5 million new RBCs every second in adults. erythropoiesis occurs mainly in the marrow of the sternum. and skull bones begins with a cell called a hemocytoblast or stem cell (below) rate is regulated by oxygen levels: o o o hypoxia (lower than normal oxygen levels) is detected by cells in the kidneys kidney cells release the hormone erythropoietin into the blood erythropoietin stimulates erythropoiesis by the bone marrow .Determining the hematocrit Erythropoiesis = formation of erythrocytes • • • • the body must produce about 2.

immune response (including production of antibodies) .9.8%) Granular white blood cells contains numerous granules in the cytoplasm. lungs. Granular white blood cells are produced in the bone marrow. & lymph nodes) Lymphocytes . e. The primary functions of the various white blood cells are: • • • • • Neutrophils .4%)  basophils (less than 1%) o agranular (or non-granular) white blood cells include:  lymphocytes (25 .phagocytosis (bacteria & cellular debris). Agranular white blood cells have few or no granules in the cytoplasm & have a large spherical nucleus.. functions(s) remain unclear Monocytes . very important in inflammation Eosinophils .phagocytosis (typically as macrophages in tissues of the liver.g. while agranular white blood cells are produced in lymph tissue. & their nuclei are lobed.70% of WBCs)  eosinophils (1 .synthesize & store histamine (a substance released during inflammation) & heparin (an anticoagulant). 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).40%)  monocytes (2 . spleen.help break down blood clots & kill parasites Basophils .000 per cubic millimeter types of WBCs: o granular white blood cells include:  neutrophils (50 .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 .

Some important characteristics of White Blood Cells (particularly neutrophils): 1 .Water .exhibit chemotaxis (attracted to certain chemicals. such as those released by damaged cells) Platelets (or thrombocytes) 1 . carries heat 2 .capable of diapedesis (also called extravasation) 3 .formed in the bone marrow from cells called megakaryocytes 2 .g.normal concentration in the blood is about 250.phagocytic 2 .play an important role in hemostasis (preventing blood loss) Plasma: 1 .serves as transport medium. but can secrete a variety of substances & can also contract (because they contain actin & myosin) 3 .capable of ameboid movement 4 .have no nucleus.remain functional for about 7 . thyroid hormone & iron)  some are clotting factors  produced by liver o gamma globulins are immunoglobulins (antibodies) produced by lymphocytes Fibrinogen o important in clotting o produced by liver ..10 days (after which they are removed from the blood by macrophages in the spleen & liver) 5.Proteins • • • Albumins o 60-80% of plasma proteins o most important in maintenance of osmotic balance o produced by liver Globulins o alpha & beta  some are important for transport of materials through the blood (e.000 per cubic millimeter 4 .

glucose. sodium.Inorganic constituents (1% of plasma) . Upon exposure to collagen.Hormones Hemostasis . & calcium 4 .Vascular spasm .platelets aggregate at the point where a vessel ruptures.formed primarily of fibrin threads (or polymers).e..Blood coagulation (clotting): The result of all of this is a clot .g. a 'plug' forms. but in the wrong place can cause problems such as a stroke (see below under inappropriate clotting).prevention of blood loss from broken vessel: 1 . Fibrinolysis: • • dissolution of clot mechanism = plasminogen (a plasma protein) is activated by many factors & becomes PLASMIN. Blood clots in the right places prevent the loss of blood from ruptured vessels. the clot is dissolved and replaced with normal tissue.Formation of a platelet plug . pulling edges of damaged vessel closer together. 2 . Over time (with the amount of time depending on the amount of damage).. platelets release ADP (adenosine diphosphate) & thromboxane. chloride.3 . but also including blood cells & platelets. lipids & vitamins 5 .g.oxygen & carbon dioxide 7 . This occurs because platelets are exposed to collagen (a protein found in the connective tissure located just outside the blood vessel). 3 . nitrogenous wastes like urea 6 .Nutrients . This 'spasm' may reduce blood flow & blood loss but will not stop blood loss.e. Plasmin then breaks down fibrin meshwork & phagocytic WBCs remove products of clot dissolution • Human Habitation . amino acids. These substances cause the surfaces of nearby platelets to become sticky and. potassium. Clot retraction: • • "tightening" of clot contraction of platelets trapped within clot shrinks fibrin meshwork. as 'sticky' platelets accumulate.Waste products .Dissolved gases .vasoconstriction of injured vessel due to contraction of smooth muscle in the wall of the vessel.

Pathophysiology Environmental Factor Human Habitation Bite of female Aedes 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 Increase Capillary Permeability Capillary fragility Plasma Leakag e Hemoconcentrationn Petichial rash Skin hemorrhage Bleeding .IV.

A Age: 21 years old Sex: Female Marital Status: Married Religion: Catholic Address: Phase1 blk. Fever Injuries or accidents: None Hospitalizations and operations: None Obstetric History (for female clients only): G1P1 Menarche at 13 years old Immunization BCG: /√/ at birth /√/ School Entrance DPT: /x/ 1st dose /x/2nd dose /x/3rd dose OPV: /x/ 1st dose /x/ 2nd dose /x/ 3rd dose AMV: /x/ TT: /√/ 1st dose /√/ 2nd dose /√/ 3rd dose /√/ 4th dose /√/ 5th dose Hepatitis B Vaccine: /x/ 1st dose /x/ 2nd dose /x/ 3rd dose /x/ 4th dose . Manila Race/Nationality: Filipino Usual Source of Medical Care: Health Center Source and Reliability of Information: Patient Reason for Seeking Care 1. 1987. Fever Headache Severe Vomiting Body Rashes Past Medical History i. ii. iii. Colds. iv. 4. 3.V. Patient’s Profile Client’s Name or Initial: Mrs.9 lot3 Francisco Homes San Jose Del Monte Bulacan Birth Date and place of birth: April 27. v. 2. Pediatric/Childhood/Adult Illness: Cough.

Allergies Food (specify): none Drugs (specify): none Chemicals (specify): none Environmental Allergens (specify): none Data Base Two days prior to admission fever is on & off. internal medicine. Laboratory Hematology Hematology (American English) or haematology (British English) is the branch of biology (physiology). A few hours prior to admission patient develops vomiting 6x accompanied by poor appetite and body weakness.vi. prognosis. the blood-forming organs. and pediatrics that is concerned with the study of blood. diagnosis. Haematology includes the study of etiology. flat. treatment. She’s usual elimination pattern is U=5x/day S=1x/day. ambulatory HEENT: dry lips Lungs: clear breath sounds Abdomen: soft. pathology. and prevention of blood diseases. . slight epigastric Extremities: body rashes are present Course in the Ward The patient usually play with her cellphone & talks to her mother frequently. The lab work that goes into the study of blood is performed by a Medical Technologist. Physical Assessment V/S BP: 90/60 Temp: 38.5 degree Celsius RR: 23cpm tenderness PR: 100bpm Gen. She is ambulatory and can use the bathroom independently. VI.Survey : weak looking. clinical laboratory. She does not sleep often. and blood diseases.

40 0.09 10^12/uL Hemoglobin 122 g/l Hematocrit 0.47 Segmenters 0.37-0.70 10/6 6:20am 103 0.4 120-160 0.31 118x100 .20-0.37 Platelet 198x100 162x100 Lymphocyte Segmenters WBC.36 0.50-0. (10/5 6pm) Decrease indicates hemorrhage Platelet.37 Platelet 210x100 /mm3 Lymphocyte 0.6 10/4 6pm 10/5 6am WBC RBC Hemoglobin 121 123 Hematocrit 0.2-5.Laboratory Result Prior to Admission (Oct.47 140-340x100 0. 4.33 124x100 NORMAL VALUE 5-10 4.53 Laboratory Result from Oct.(10/5 6pm) Decrease indicates DIC.(10/5) Decrease indicates hemorrhage Hematocrit-(10/4 6pm). 08) VALUE UNITS WBC 6. hemorrhage Lymphocytes-(10/4 upon admission) Increase indicates infection 10/5 6pm 110 0.Normal RBC-Normal Hemoglobin.4 to Oct.20 10^g/l RBC 4.

Half-Life: Neonates: 25hr. rash. pancytopen Products ia.51hr pea k 13hr 13hr dur atio n 38hr 34hr Nursing considertion Assess overall health status and alcohol usage before administration. urticuria saccharin sugar. Distribution: widely distributed. Advise patient to consult physician if discomfort or fever is not relieved of routine doses or if fever is greater than 39. Metabolites excreted by the kidneys. Advise patient to avoid alcohol if taking this drug Avoid taking concurrently with salicylates or NSAIDs for more than a few days. Metabolites may be toxic in overdose situation. alcohol. Hepatic failure. Drug Study Paracetamol (500mg/tab q 4 hours for fever) Name of Drug Paracetamol Action Inhibits the synhesis of prostagl andin that may serve as mediator s of pain and fever.5C or lasts longer than 3 days. Metabolism and excretion: 85%-95% metabolized by the liver. . Previous neutropenia hypersensiti . vity. Crosses the placenta. hepatotoxic Contraindic ity. aspartame. renal ation failure.51hr 0. Side effect Pharmacokinetics Absorption: Well absorbed following oral administration. containing leucopenia. primaril y in the CNS. unless directed. enters breast milk in low concentrations. Adults: 1-3hr Pharmacodynamics rout ons e et PO Rec t 0. ot tartrazine should be avoided. Has no significa nt antiinflamm atory properti es or GI toxicity Indication Mild Pain. Fever.VII. Rectal absorption is variable. Administer with food or an empty stomach.

Our Lady of Fatima University Quezon City A Case Study About DENGUE Prepared By: Mariano. Kleir Ann Ravancho. John Leomar Mostoles. Efren (Leader) Tano. Moonyeen October 2008 .

Table of Contents I. IX. III. IV. V. VI. VII. VIII. Introduction Frequency Anatomy and Physiology Pathophysiology Patients Profile Laboratory Drug Study NCP Discharge Plan . II.

.

. of 38. back into normal >To decrease temp >To promote wellness >To reduce anxiety >To decrease temp Evaluation After 1 hour of nursing intervention the patient temperature had been decreased. NCP Subjective >”dalawang araw na akong nilalagnat at itoy pabalikbalik” as verbalize. r/t inflammatory process Analysis Hypothalamus which controls the bodys thermoregulation releases heat due to the presence of infection Planning After 1 hour of nursing intervention the patient temp will decrease.RR >Thermoregulation >Render TSB/ warm bath >Promote bedrest >Provide comfort >Administer medication as prescribe Rationale >For temperature assessment if change >To assess client stability >To regulate body temp. Objective: >dry lips >pale color >weak looking >temp.5 degree celcius Nursing Dx Increased body temp. Implementation >Monitor core temp.PR.VIII. >Monitor BP.

I. of nursing intervention the filling of vomiting of the patient >Water therapy will decrease & the patient will be at >promote clean comfort environment .NCP Subjective >”Anim na beses na akong nagsusuka” as verbalize. Objective: >Weak looking >Dry lips >Pale color Nursing Dx >Vomiting r/t gastric distention Analysis >G.I irritation in response to the presence of blood in the G.T Planning Implementatio n >Encourage reverse T-position >Bed rest Rationale >To back flow the vomitous >To promote comfort >To minimize the risk of dehydration >for relaxation Evalution >After 1hr.of nursing intervention the feeling of the patient had been decreased & patient had been at comfort >After 1hr.

the patient the patient is advised to: 1. 4. . .IX. its risk factors. Clean environment: .may drink fruit juices such as calamansi juices for Vitamin C supplementation 6.elimination of stagnant water . As part of the plan. Eat foods rich in vitamins and minerals.early detection of signs and symptoms of the disease may decrease risk of DHF’s complications 2. and methods of prevention and control. 8. Report reoccurrence of fever and signs of bleeding to physician immediately. Used insect propellant. 7. management and some complications of the condition if not managed or not treated well.proper disposal of garbage 3. Drink adequate fluids at least eight glasses a day. 5. Report any signs and symptoms of DHF such as high fever. Discharge Planning The discharge plan includes health teaching about Dengue Hemorrhagic Fever. abdominal pain and headache.dispose old used tires .clean water drainage .cover water containers . Avoid too many hanging clothes inside the house. . Use soft bristle toothbrush.

. .

Sign up to vote on this title
UsefulNot useful