PAPER OF ENGLISH NURSING

DENGUE HAEMORRHAGIC FEVER

Created by: Group 10 AndriFibriyanto (11.11011037) BagusAdiSaputera (11.11011039) FirjonSepartagusWalHabby (11.11011047) KhoirulHidayat (11.11011050)

S1 NURSING STUDY PROGRAM FACULTY OF HEALTH SCIENCE UNIVERSITY OF MUHAMMADIYAH JEMBER 2012

PREFACE

Thanks to God that we have completed this paper entitled DENGUE HAEMORRHAGIC FEVER, to fulfill the project of English Nursing subject. We would like to express our gratitude to all those who have given us the possibility to complete this paper. We want to thank to Mr. Sigit, M.Kep the lecturer of S1 Nursing Study Faculty of Health Science University of MuhammadiyahJember. We also would like to thank to all of our friends in S1 Nursing Study Faculty of Health Science University of MuhammadiyahJember for giving us supports and encourage us to finish this paper. We realized that this paper far from perfectness, so we apologize and we really appreciate and welcome any constructive criticisms and suggestions to improve this paper.

Jember, June 2012

CONTENT

The development of aexample of assessment steps developed from the nursing process which includes: 1. Assessment - collection of patient data 2. Determining the Nursing Diagnosis with identification of nursing diagnoses, goals and outcomes 3. Planning Actually putting together and writing the care plan (include interventions) 4. Implementation - putting the Care plan into action 5. Evaluation How will you evaluate it and ensure it is periodically updated DENGUE HAEMORRHAGIC FEVER (DHF) Dengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases, that occurs in the tropics. Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. Dengue is transmitted to humans by the Aedesaegypti (rarely Aedesalbopictus) mosquito, which feeds during the day. The first epidemics occurred almost simultaneously in Asia, Africa, and North America in the 1780s. The disease was identified and named in 1779. A global pandemic began in Southeast Asia in the 1950s and by 1975 DHF had become a leading cause of death among children in many countries in that region. Epidemic dengue has become more common since the 1980s by the late 1990s, dengue was the most important mosquito-borne disease affecting humans after malaria, there being around 40 million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each year. There was a serious outbreak in Rio de Janeiro in February, 2002 affecting around one million people and killing sixteen.

Significant outbreaks of dengue fever tend to occur every five or six years. There tend to remain large numbers of susceptible people in the population despite previous outbreaks because there are four different strains of the dengue virus and because of new susceptible individuals entering the target population, either through childbirth or immigration. There is significant evidence, originally suggested by S.B. Halstead in the 1970s, that dengue hemorrhagic fever is more likely to occur in patients who have secondary infections by serotypes different from the primary infection. One model to explain this process is known as antibody-dependent enhancement (ADE), which allows for increased uptake and virion replication during a secondary infection with a different strain. Through an immunological phenomena, known as original antigenic sin, the immune system is not able to adequately respond to the stronger infection, and the secondary infection becomes far more serious. This process is also known as superinfection. 1. Signs and Symptoms This infectious disease is manifested by a sudden onset of fever, with severe headache, muscle and joint pains (myalgias and arthralgias severe pain gives it the name break-bone fever or bonecrusher disease) and rashes; the dengue rash is characteristically bright red petechia and usually appears first on the lower limbs and the chest in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting or diarrhea. Some cases develop much milder symptoms which can, when no rash is present, be misdiagnosed as influenza or other viral infection. Thus travelers from tropical areas may inadvertently pass on dengue in their home countries, having not been properly diagnosed at the height of their illness. Patients with dengue can only pass on the infection through mosquitoes or blood products while they are still febrile.

The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the fever (the so-called biphasic pattern). Clinically, the platelet count will drop until the patients temperature is normal. Cases of DHF also show higher fever, hemorrhagic phenomena, thrombocytopenia, and hemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate. Conclusion symptomsof dengue haemorrhagic fever:

Fever within 5 to 6 days after you have been bitten by an infected mosquito High fever, up to 105 degrees Fahrenheit Severe headache Retro-orbital (behind the eye) pain Severe joint and muscle pain Nausea and vomiting Rash

2. Causative Agent Arthropod-borne virus belonging to the family Flaviviridae. There are four known serotypes: DEN-1, DEN-2, DEN-3, and DEN-4. Mode of Transmission is Aedesaegypti The viruses are transmitted via the bite of various day-feeding mosquitoes of the subgenus Stegomyia. The principal vector is Aedesaegypti. Once infected, a mosquito remains infective for life. Infected humans circulate the virus in their blood, mosquitoes ingest viruses when feeding on the infective individual. Humans serve as an amplifying host, though some monkeys may also serve as a source of the virus. Female mosquitoes can also transmit the virus transovarially, passing it down to the next generation.

3. Diagnosis The diagnosis of dengue is usually made clinically. The classic picture is high fever with no localizing source of infection, a petechial rash with thrombocytopenia and relativeleukopenia. There exists a WHO definition of dengue hemorrhagic fever that has been in use since 1975; all four criteria must be fulfilled: a. Fever Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea). Thrombocytopenia (<100,000 platelets per mm or estimated as less than 3 platelets per high power field). Evidence of plasma leakage (hematocrit more than 20% higher than expected, or drop in hematocrit of 20% or more from baseline following IV fluid, pleural effusion, ascites, hypoproteinemia). b. Encephalitic occurrences Dengue shock syndrome is defined as dengue hemorrhagic fever plus: Weak rapid pulse Narrow pulse pressure (less than 20 mm Hg) Cold, clammy skin and restlessness Dependable, immediate diagnosis of dengue can be performed in rural areas by the use of Rapid Diagnostic Test kits, which also differentiate between primary and secondary dengue infections. Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated.

4. Incubation Period The incubation period of dengue fever is approximately four days. 5. Pathogenesis/Pathophysiology Dengue infection is caused by 1 of 4 related, but antigenically distinct, viral serotypes: dengue virus 1 (DENV-1), dengue virus 2 (DENV-2), dengue virus 3 (DENV-3), and dengue virus 4 (DENV-4). Albert Sabin speciated these in 1944. Each serotype is known to have several different genotypes. Dengue viruses are small, spherical, single-stranded enveloped RNA viruses of the family Flaviviridae, genus Flavivirus. Infection with one dengue serotype confers lifelong homotypic immunity and a very brief period of partial heterotypic immunity, but each individual can eventually be infected by all 4 serotypes. Several serotypes can be in circulation during an epidemic. Dengue viruses are transmitted by the bite of an infected Aedes mosquito. Globally, aaegypti is the predominant highly efficient mosquito vector for dengue infection, but Aalbopictus and other Aedes species can also transmit dengue with varying degrees of efficiency. Aedes mosquito species have adapted well to human habitation, often breeding around dwellings in small amounts of stagnant water found in old tires or other small containers discarded by humans. Female Aedes mosquitoes are daytime feeders. They inflict an innocuous bite and are easily disturbed during a blood meal, causing them to move on to finish a meal on another individual, making them efficient vectors. Entire families who develop infection within a 24- to 36-hour period, presumably from the bites of a single infected vector, is not unusual. Humans serve as the primary reservoir for dengue; however, certain nonhuman primates in Africa and Asia also serve as hosts. Mosquitoes acquire the

virus when they feed on a carrier of the virus. The mosquito can transmit dengue if it immediately bites another host. In addition, transmission occurs after 8-12 days of viral replication in the mosquitos salivary glands (extrinsic incubation period). The mosquito remains infected for the remainder of its 15- to 65-day lifespan. Vertical transmission of dengue virus in mosquitoes has been documented. The eggs of Aedes mosquitoes withstand long periods of desiccation, reportedly as long as 1 year, but are killed by temperatures of less than 10C. Once inoculated into a human host, dengue has an incubation period of 3-14 days (average 4-7 d). Following incubation, a 5- to 7-day acute febrile illness ensues. Recovery is usually complete by 7-10 days. DHF or DSS usually develops around the third to seventh day of illness, approximately at the time of defervescence. The major pathophysiological abnormalities that occur in DHF and DSS are plasma leakage and bleeding. Plasma leakage is caused by increased capillary permeability and may be manifested by hemoconcentration, as well as pleural effusion and ascites. Bleeding is caused by capillary fragility and thrombocytopenia and may present various ways, ranging from petechial skin hemorrhages to life-threatening gastrointestinal bleeding. Most patients who develop DHF or DSS have had prior infection with one or more dengue serotypes. In individuals with low levels of neutralizing antibodies, nonneutralizing antibodies to one dengue serotype, when bound by macrophage and monocyte Fc receptors, have been proposed to result in increased viral entry and replication, and increased cytokine production and complement activation. This phenomenon is called antibody-dependent enhancement. In addition, certain dengue strains, particularly those of DEN-2, have been proposed to be more virulent, in part because more epidemics of DHF have been associated with DEN-2 than with the other serotypes.

6. Prevention a. Vaccine development There is no commercially available vaccine for the dengue flavivirus. However, one of the many ongoing vaccine development programs is the Pediatric Dengue Vaccine Initiative which was set up in 2003 with the aim of accelerating the development and introduction of dengue vaccine(s) that are affordable and accessible to poor children in endemic countries. Thai researchers are testing a dengue fever vaccine on 3,000-5,000 human volunteers within the next three years after having successfully conducted tests on animals and a small group of human volunteers. And, a number of other vaccine candidates are entering phase I or II testing. b. Mosquito control Primary prevention of dengue mainly resides in eliminating or reducing the mosquito vector for dengue. Public spraying for mosquitoes is the most important aspect of this vector. Application of larvicides such as Abate to standing water is more effective in the long term control of mosquitoes. Initiatives to eradicate pools of standing water (such as in flowerpots) have proven useful in controlling mosquitoborne diseases. Promising new techniques have been recently reported from Oxford University on rendering the Aedes mosquito pest sterile. US and British researchers have also genetically engineered a strain of flightless mosquito that may help curb the spread of Dengue fever. Recently, researchers at the Federal University of Minas Gerais, in Brazil, have developed a world-awarded new technology to monitor and control the mosquito, using traps, chemical attractants, handheld computers and GPS georeferenced maps. The MI Dengue system can show precisely where the mosquitoes are inside the urban area, in a very short period of time. c. Personal protection

Personal prevention consists of the use of mosquito nets, repellents containing NNDB or DEET ((N,N-Diethyl-meta-toluamide; also known as N,N-Diethyl-3methylbenzamide), covering exposed skin, use of DEET-impregnated bednets, and avoiding endemic areas. 7. Treatment The mainstay of treatment is supportive therapy. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant hemoconcentration if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion. It is very important to avoid aspirin and non-steroidal anti-inflammatory medications. These drugs are often used to treat pain and fever though in this case they may actually aggravate the bleeding tendency associated with some of these infections. Patients should instead receive acetaminophen preparations to deal with these symptoms if dengue is suspected.Having a strong immune system also benefits recovery from dengue. 8. Complications Neurologic manifestations such as seizures and encephalitis/encephalopathy have been reported in rare cases of dengue infection. Some of these cases did not manifest other typical features of dengue infection. Other neurological complications associated with dengue infection include neuropathies, Guillain-Barr syndrome, and transverse myelitis.

Liver failure has been associated with DHF/DSS epidemics. Whether this is a viral effect or a product of prolonged liver hypoperfusion remains

unclear.Overhydration is a well-recognized complication of DF and DHF/DSS.

NURSING MANAGEMENT FOR DENGUE HEMORRHAGIC FEVER (DHF)

1. Definition Dengue is a tropical virus disease transmitted by mosquitoes and characterized by fever, headache, pain in the limbs, and rash (Brooker, 2001).Dengue fever is a disease primarily in children, adolescents, or adults, with clinical signs of fever, sore muscles, or joints accompanied by leukopenia, with / without rash (rash) and lymphadenopathy, biphasic fever, severe headache, pain on the movement of the eyeball, taste menyecap impaired, mild thrombocytopenia, and bleeding spots (ptekie) spontaneous (Noer, et al, 1999).Dengue hemorrhagic fever is a disease caused by dengue viruses (arboviruses) that enters the body through the bite of the mosquito Aedesaegypti (Suriadi&Yuliani, 2001).

2. Pathophysiology Dengue virus enters the body through the bite of aedesaegypti mosquito and then reacted with the antibody and virus-antibody complexes formed in circulation will activate the complement system (Suriadi&Yuliani, 2001).Dengue virus enters the body through mosquito bites and infection first causes dengue fever. Body reaction is a reaction commonly seen in infections by viruses. A very different reaction would seem, when someone gets repeated infections with different dengue virus types. And DHF can occur when a person is infected after the first time, got the other dengue virus infection recurs. Re-infection will cause an anamnestic antibody reaction, giving rise to the concentration of antigen-antibody complex (virusantibody complexes) is high (Noer, et al, 1999).

A. Nursing Assessment of Dengue Hemorrhagic Fever (DHF) 1. Identity Dengue Hemorrhagic Fever (DHF) is a tropical disease that often causes the death of children, adolescents and adults (Effendy, 1995). 2. Main complaint Patients complain of fever, headache, weakness, heartburn, nausea and decreased appetite. 3. History of present illness Medical history showed headache, muscle pain, soreness throughout the body, pain on swallowing, weakness, fever, nausea, and decreased appetite. 4. History of previous illness No illness in specific. 5. Family history of disease A history of DHF disease on other family members is crucial, since DHF disease is a disease that can be transmitted through mosquito bites aigepty aides. 6. Environmental Health History Normally less clean environment, lots of clean water puddles like tin cans, old tires, where the drinking water of birds that are rarely changed the water, the tub is rarely cleaned. 7. Historical Growth Physical Examination for Dengue Hemorrhagic Fever (DHF)

B. Nursing Diagnosis of Dengue Hemorrhagic Fever (DHF) 1. Hyperthermia related to dengue virus infection process. 2. Risk for fluid deficit related to movement of the intravascular to the extravascular fluid. 3. Risk for fluid volume deficit related to excessive bleeding, intravascular to the extravascular fluid displacement.

4. Risk for impaired nutritional needs less than body requirements related to inadequate nutritional intake due to nausea and decreased appetite. 5. Risk for hemorrhage related to a decrease of blood clotting factors (thrombocytopenia). 6. Anxiety: parents related to the child's condition. 7. Knowledge deficit: about disease, prognosis, the effect of the procedure, and the care of sick family members associated with less exposure / recall information.

C. Nursing Care Plans DP 1: Hipertermie associated with the dengue virus infection Purpose: Normal body temperature Criteria: body temperature between 36-37, lost muscle pain Intervention: 1. Assess the patient's body temperature Rational: find an increase in body temperature, facilitate intervention 2. Give a warm water compress Rational: reduce heat by conduction heat transfer. Warm water slowly to control heat transfer without causing hypothermia or shivering. 3. Provide / instruct the patient to drink plenty of 1500-2000 cc / day (as tolerated) Rational: To replace fluids lost due to evaporation. 4. Instruct patient to wear clothing that is thin and easy to absorb sweat Rational: To provide a sense of comfort and clothes that easily absorb sweat and thin does not stimulate an increase in body temperature. 5. Observation of intake and output, vital signs (temperature, pulse, blood pressure) every 3 hours or as indicated Rationale: Early detection and knowing the lack of fluid and electrolyte balance in body fluids. Vital Signs is a reference to determine the patient's general condition.

6. Collaboration: intravenous fluid and drug administration according to the program. Rational: Fluid is very important for patients with high body temperature. Drugs, especially to reduce the patient's body heat.

DP 2: The risk of fluid volume deficit related to intravascular fluid into the extravascular emigration. Objectives: There was no fluid deficit volume Criteria: Input and output balanced, Vital signs within normal limits, no sign pre shock, Capilarry refill Intervention: 1. Keep an eye on vital signs every 3 hours / as indicated Rational: Vital signs help identify fluctuations in intravascular fluid 2. Observation of capillary refill. Rational: Indications adequacy of peripheral circulation 3. Observation of intake and output. Record the color of urine / concentration, BJ Rational: The decline of concentrated urine output with an increase in BJ suspected dehydration. 4. Advise to drink 1500-2000 ml / day (as tolerated)

Rationale: To meet the needs of body fluids/oral 5. Collaboration: intravenous fluid administration 6. Rational: May increase the amount of body fluids, to prevent hipovolemic shock.

DP 3: The risk of hypovolemic shock associated with excessive bleeding, intravascular fluid into the extravascular emigration. Objectives: There was no hypovolemic shock Criteria: Vital signs within normal limits Intervention:

1. Monitor the patient's general condition Rational: To monitor the condition of the patient during treatment, especially when paused bleeding. Nurses immediately know the signs pre shock / shock. 2. Observation of vital signs every 3 hours or more. Rationale: Nurses need to continue observation vital sign to ensure it does not happen pre shock / shock. 3. Explain to the patient and family sign of bleeding, and report immediately if there is bleeding Rational: By involving the patients family and signs of bleeding can be identified and appropriate action is fast and can be given. 4. Collaboration: intravenous fluid administration Rationale: Intravenous fluids needed to overcome the great loss of body fluids. 5. Collaboration: checks: HB, PCV, platelet Rational: To determine the rate of leakage of blood vessels that experienced by patients and for reference to further action.

DP 4: Risk of impaired nutritional needs less than body requirements related to inadequate nutritional intake due to nausea and decreased appetite. Objectives: There was no need for nutritional disorders Criteria: There are no signs of malnutrition, weight-balanced show. 1. Intervention: Review the history of nutrition, including food preferences Rationale: Identify deficiencies, assuming the possibility of intervention 2. Observation and record the patient's food intake Rational: Keep an eye on calorie input / lack of quality of food consumption 3. BB Weigh each day (if possible)

Rational: Keep an eye on weight loss / monitor the effectiveness of interventions. 4. Give a little but often and the food or eat between meals Rationale: Food may slightly decrease and increase input weaknesses also prevent gastric distention. 5. Give and Bantu oral hygiene. Rationale: Increased appetite and input/oral 6. Avoid foods that stimulate and contain gas. Rational: Reduce distension and gastric irritation.

DP 5: The risk of bleeding associated with a reduction factor of blood clotting factors (thrombocytopenia) Objectives: There was no bleeding Criteria: BP 100/60 mmHg, N: 80-100x/s regular, strong pulse, No sign of further bleeding, platelets increase. Intervention: 1. Monitor signs of decreased platelets are accompanied by clinical signs. Rational: Decreased platelet count is a sign of leakage of blood vessels at some stage can cause clinical signs such as epistaxis, ptike. 2. Instruct patient to take plenty of rest (bed rest) Rational: the patient activity can lead to uncontrolled bleeding. 3. Provide information to clients and families to report any signs of bleeding such as hematemesis, melena, epistaxis. Rational: The involvement of patients and families can help to handling early if there is bleeding. 4. The anticipation of bleeding: use a soft toothbrush, pet oral hygiene, given the pressure took 5-10 minutes after each blood. Rational: To prevent further bleeding. 5. Collaboration, monitor platelets every day

Rational: The platelets are monitored every day, it can be seen the rate of leakage of blood vessels and the possibility of the patients experienced bleeding.

DP 6: parental anxiety associated with the child's condition. Purpose: anxiety is reduced / controlled. Criteria: the client reported no physical manifestations of anxiety, there is no manifestation of behavior due to anxiety. Intervention: 1. Assess and document the patient's anxiety level. Rational: to facilitate intervention. 2. Assess patient's coping mechanisms used to cope with anxiety in the past. Rational: maintaining adaftif coping mechanisms, increasing the ability to control anxiety. 3. Do the approach and provide motivation to patients to express their thoughts and feelings. Rational: the approach and motivation to help the patient to externalizing perceived anxiety. 4. Patient's motivation to focus on the reality that exists today, positive expectations for therapy that in lead. Rational: a tool to identify the coping mechanisms needed to reduce anxiety. 5. Give positive reinforcement to continue their daily activities while in a state of anxiety. Rational: create trust in the patient that he was able to overcome the problem and give confidence in myself as evidenced by the self recognition others in his abilities. 6. Instruct the patient to use relaxation techniques. Rational: creating a sense of calm and comfortable.

7. Provide factual information (real and true) to patients and families regarding diagnosis, treatment and prognosis. Rational: increase knowledge, reduce anxiety. 8. Collaboration of anti anxiety drugs. Rational: reduce anxiety as needed.

D. Implementation 1. Prevent the lack of fluid volume a. Observe signs - vital signs at least every 4 hours b. Monitor sign - a sign of the increasing shortage of liquid: turgor is not elastic, crown - sunken fontanel, decreased urine production c. Observe and record intake and output d. Provide adequate hydration according to the needs of the body e. Monitoring laboratory values: electrolyte / blood, BJ urine, serum body f. Maintain an adequate intake and output g. Monitor and record the weight h. Monitor the provision of intravenous fluids per hour through i. Reducing fluid loss does not appear (insesible water loss / IWL) 2. Adequate tissue perfusion a. Assess and record the signs - Vital signs (quality and frequency of pulse, blood pressure, capillary refill) b. Assess and record the circulation in the extremities (temperature, humidity and color) c. Assess the possibility of the death of tissue in the extremities such as cold, pain, swelling of the feet) 3. The need for adequate nutrition a. Allow the child to eat foods that can be tolerated child. Plan to improve the nutritional quality at the child's appetite increases. b. Give the food is accompanied by a nutritional supplement to improve the quality of nutritional intake

c. Advised the parents to provide food with a small portion technique but often d. Weigh every day at the same time and with the same scale e. Maintaining a patient's oral hygiene f. Explain the importance of adequate intake nutrition to cure 4. Maintain normal body temperature a. Measure signs - body temperature of vital signs b. Teach the family in the temperature measurement c. Perform "tapid sponge" (wipe) with plain water d. Increase fluid intake e. Provide therapy to lower the temperature 5. Adaptive support family coping a. Assess feeling and parent or family to full stress situation. b. Allow parent and family for give the response be completely and identification factor about most parents worried c. Identification coping that usually be used and how to manage situation

E. Evaluation 1. Normal body temperature 2. Fluid does not occur deficit volume 3. Hypovolemic shock does not occur 4. Nutritional needs are not an interruption occurs 5. No bleeding 6. Anxiety is reduced / controlled 7. parents understand about the conditions, procedures and effects of the treatment process.

CONCLUSION

Dengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases, that occurs in the tropics. Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. Dengue is transmitted to humans by the Aedesaegypti (rarely Aedesalbopictus) mosquito, which feeds during the day. Arthropod-borne virus belonging to the family Flaviviridae. There are four known serotypes: DEN-1, DEN-2, DEN-3, and DEN-4. Symptomsof dengue haemorrhagic fever:Fever within 5 to 6 days after you have been bitten by an infected mosquito, high fever, up to 105 degrees Fahrenheit, severe headache, retro-orbital (behind the eye) pain, severe joint and muscle pain, sausea and vomiting and rash.

BIBLIOGRAPHY

http://en.wikipedia.org/wiki/Dengue_Haemorrhagic_Fever.html http://corex-c.blogspot.com/2011/01/DHF.html http://nursingbegin.com/DHF/html http://id.wikipedia.org/wiki/dengue-hemorrhagic-fever http://www.edtech.vt.edu/edtech/id/assess/assess.html http://www.state.mn.us/mn/externalDocs/dengue_hemorrhagic_fever.pdf http://www.york.ac.uk/res/dec/resources/papers/cog%20comp%20DHFt.pdf