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M Day/Date: Tuesday/30th November 2010 Supervisor : dr.Hj.Tiangsa br.Sembiring,SpA(K)
INTRODUCTION Dengue fever (DF) or Dengue haemorrhagic fever (DHF) is a growing public health problem in the subtropics. In South-East Asia, with a total population of 1.5 billion, approximately 1.3 billion people live at risk of acquiring DF or DHF. Currently, DHF is the leading cause of hospital admissions and death among children in this region.1 Dengue, the most common arboviral illness transmitted worldwide, is caused by infection with 1 of the 4 serotypes of dengue virus, family Flaviviridae, genus Flavivirus ,single-stranded nonsegmented RNA viruses. 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).9 Most patients with dengue infection have only mild disease or classic dengue fever, with influenza-like symptoms, severe headache, and aching joints and muscles. However, in a small percentage of patients maybe half a million people every year potentially lethal forms of dengue called dengue hemorrhagic fever and dengue shock syndrome develop.2
Dengue virus transmission follows two general patterns which is 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. Transmission appears to begin in urban centers and then spreads to the rest of a country. 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.2 At present, the only method of controlling or preventing dengue and DHF is to combat the vector mosquitoes. Aedes aegypti breeds primarily in man-made containers like earthenware jars, metal drums and concrete cisterns used for domestic water storage, as well as discarded plastic food containers, used automobile tyres and other items that collect rainwater. It can also breed extensively in natural habitats such as tree holes and leaf axils. In recent years, Aedes albopictus, a secondary dengue vector in Asia, has become established in the United States, several Latin American and Caribbean countries, in parts of Europe and in one African country. The rapid geographic spread of this species has been largely attributed to the international trade in used tyres. Dengue continues to be a global challenge because the pathogenesis of DHF is not fully understood, there is no immediate prospect of a vaccine and the mosquito control measures are inadequate. The wide spread DHF epidemics during 2003 reinforces the belief that DHF has come to stay in this country and will continue to spread to newer areas unless vector control measures are taken up on war footing.3
EPIDEMIOLOGY Dengue haemorrhagic fever is now endemic in more than 100 countries in Africa, the Americas, the Eastern Mediterranean, Southeast Asia and the Western Pacific, Southeast Asia and the Western Pacific are most seriously affected. Some 2500 million people two fifths of the world.’s population are now at risk from
dengue. WHO currently estimated 50 million cases of dengue infection worldwide every year and during epidemics of dengue, attack rates among susceptibles are 40 to 90%. An estimated 500,000 cases of DHF require hospitalization each year, of whom a very large proportion are children.3 Figure 1: Dengue, countries or areas at risk, 2008
Indonesia is the largest country in the region with a population of 245 million. Almost sixty per cent of the people live on the island of Java, which is most severely afflicted by periodic outbreaks of dengue disease. However, the disease is endemic in many large cities and small towns throughout the country and has also spread to certain smaller villages, where population movement and density are high.Epidemic DF has been reported in all 27 Indonesian provinces, whereas in 1968 only two provinces had reported dengue cases.1
Figure 2: The incidence rate and case-fatality rate of DHF in Indonesia in 2005.
An increase in commercial air travel has subsequently aided the transmission of the virus between populations so that dengue is now endemic in over 100 countries throughout tropical and sub-tropical areas of the world. The main vector Aedes aegypti is found worldwide between latitudes 35ºN and 35ºS .The principle areas affected include the Caribbean, South and Central America, Mexico, Africa, the Pacific Islands, South East (SE) Asia, Indian sub-continent, Hawaii, and Australia (see Figure 1). By 2002, more than 2.5 billion people were at risk of infection (roughly 40% of the world’s population). An estimated 50-100 million illnesses occur annually, 250,000-500,000 of which are dengue haemorrhagic fever, many of these in children. The estimated global mortality rate is 25,000 per annually.4 VIROLOGY The genome of Dengue virus consists of a single stranded, non segmented, positive sense ribonucleic acid (RNA) of about 11 kb in length . The genome is translated into a single polypeptide which is co- and posttranslationally processed by host signalases as well as the virus encoded serine protease into the three structural and seven non structural proteins (NS) in the order C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5 that traverse the Endoplasmic Reticulum (ER) membrane .Dengue and other flaviviruses are thought to replicate in the cytoplasm, mature on intracellular membranes and egress by exocytosis and in some cases by budding at the plasma membrane . The host ER is the primary site of envelope glycoprotein biogenesis, genomic
scutellaris and Ae. other Aedes species also transmit disease in specific areas. It is most widely transmitted by Ae. although nonhuman primates in Asia and Africa may also be infected. thus overwhelming the ER folding capacity. Humans are the main reservoir for the dengue virus.replication.2. polynesiensis (Society Islands) and Ae. Ae. As a natural consequence. a large amount of flaviviral proteins are synthesized in infected cells.5 TRANSMISSION Transmission occurs following a bite from an infected Aedes mosquito. niveus (Philippines). flaviviruses induce proliferation and hypertrophy of the ER membranes Moreover. Philippines and Japan). we hypothesize that these events will lead to the activation of the ER stress response which in turn will modulate various signaling pathways resulting in cell survival or death decisions. Ae. and particle assembly of flaviviruses.4 The cycle of transmission typically involves humans and mosquitoes. The virus is spread from an infected human to a mosquito and then to another human.4 Figure 3: Mechanism of transmission 5|Page . The mosquito can transmit dengue if it immediately bites another host. In the course of productive infection. pseudoscutallaris (Pacific Islands and New Guinea). Ae. often in areas where there are dense human populations. polynesiensis. aegypti and Ae. albopictus (Asia.
and buckets.4 Figure 4: Vector 6|Page . The mosquito can transmit dengue if it immediately bites another host. pots. in bathrooms and under beds) and breed in clean. is the principal vector. usually close to human habitation.g. such as tires. however. stagnant water in containers that collect rainwater. aegypti. They often rest in dark rooms (e. Mosquitoes acquire the virus when they feed on a carrier of the virus. The Aedes mosquito prefers to breed in water-filled receptacles. found worldwide in the tropics and subtropics.Humans serve as the primary reservoir for dengue.2 VECTORS A. tin cans. certain non human primates in Africa and Asia also serve as hosts but do not develop dengue hemorrhagic fever.
the virus replicates in regional lymph nodes and is disseminated through the lymphatic system and blood to other tissues.2 PATHOGENESIS After an infected mosquito has bitten a person. but it is usually 4 to 7 days.3 7|Page . shock and haemorrhagic manifestations. and is capable of biting several people in a short period for one blood meal. The incubation period ranges from 3 to 14 days. A rapid increase in the levels of cytokines and chemical mediators apparently plays a key role in inducing plasma leakage. Replication in the reticuloendothelial system and skin results in viremia. The mosquito remains infected for the remainder of its 15. often with the help of enhancing antibodies in secondary infection.Female Aedes are highly susceptible to dengue virus. and then triggered by rapidly elevated cytokines and chemical mediators produced by intense immune activation.6 Viral virulence and immune responses have been considered as two major factors responsible for the pathogenesis of DHF. It is likely that the entire process is initiated by infection with a socalled virulent dengue virus. depending largely on the patient’s age and immunologic condition.3 In addition. The eggs of Aedes mosquitoes withstand long periods of desiccation. but are killed by temperatures of less than 10°C. making them efficient vectors. feeds preferentially on human blood. reportedly as long as 1 year. Infection with dengue virus of any of the four serotypes causes a spectrum of illness. The immunopathological mechanisms appear to include a complex series of immune responses. 6 They inflict an innocuous bite and are easily disturbed during a blood meal. Vertical transmission of dengue virus in mosquitoes has been documented. has an almost imperceptible bite. is a daytime feeder. Virological studies areattempting to define the molecular basis of viral virulence. causing them to move on to finish a meal on another individual. ranging from no symptoms or mild fever to severe and fatal hemorrhage. transmission occurs after 8-12 days of viral replication in the mosquito's salivary glands (extrinsic incubation period).to 65-day lifespan.
occurring as a phe. The level of T-cell activation in a secondary dengue infection is also enhanced. C5a.15 the subneutralizing concentration of the crossreacting antibody from the previous infection may opsonize the virus and enhance its uptake and replication in the macrophage or mononuclear cells. Profound T-cell activation and death during acute dengue infection may suppress or delay viral elimination. upon the second infection with a heterotypic dengue virus.16. probably previously encountered serotypes. DHF caused by primary or secondary dengue infection is due to the occurrence of abnormal immune response involv ing production of cytokines or chemokines.The pathogenesis of DHF is poorly understood. interferon-α and histamine. IL-10. activation of T-lymphocytes and disturbance of the hemostatic system.17 and is undergoing programmed cell death.9–14 Halstead described the antibody-dependent enhancement whereby. The elevated mediators include C3a. In 8|Page . tumor necrosis factor-α. Many dengue.nomenon known as original antigenic sin. interleukin (IL)-2. 7 Most patients who develop dengue hemorrhagic fever or dengue shock syndrome have had prior infection with one or more dengue serotypes. Secondary infection with a heterotypic dengue virus is associated with increased risk of developing DHF in individuals who have recovered from a primary dengue virus with a ﬁrst serotype. IL-6. leading to the higher viral loads and increased immunopathology found in patients with DHF.speciﬁc T-cells are of low afﬁnity for the infected virus and show higher afﬁnity for other.
ascites. small proteins. and. Capillary damage allows fluid. Bleeding tendency The bleeding diathesis is caused by vasculopathy. threatened shock and profound shock.7 b. Evidence of plasma leakage The plasma leakage is due to the increased vascular permeability induced by several mediators such as C3a. red cells to leak into extravascular spaces. in some instances. nonneutralizing antibodies to one dengue serotype. The rising hematocrit may not be evidenced because of either severe bleeding or early intravenous fluid replacement. This phenomenon is called antibody-dependent enhancement.3 The evidence of plasma leakage includes hemoconcentration. have been proposed to result in increased viral entry and replication and increased cytokine production and complement activation. electrolytes. It may be a direct effect of dengue virus as it appears in the first few days of illness during the viremic phase.individuals with low levels of neutralizing antibodies. hypoproteinemia/ hypoalbuminemia. Thrombocytopenia is most prominent during the toxic stage.6 a. C5a during the acute febrile stage and prominent during the toxic stage. pleural effusion. The mechanisms of 9|Page . platelet dysfunction and coagulopathy.7 Thrombocytopenia and platelet dysfunction Patients with DHF usually have platelet counts less than 100 × 10 9/L.2 Vasculopathy A positive tourniquet test indicating the increased capillary fragility is found in the early febrile stage. thrombocytopenia. when bound by macrophage and monocyte Fc receptors.2 PATHOPHYSIOLOGY Two main pathophysiological changes occur in DHF/DSS are increase in vascular permeability that gives rise to loss of plasma from vascular compartment and disorder in haemostasis.
erythroblast and myeloid precursors. antithrombin and α-antiplasmin. the increased peripheral destruction is markedly prominent during 2 days before defervescence. The bone marrow then revealed hypercellularity with an increase in the megakaryocyte. VII. in 1989 also demonstrated the impaired platelet aggregation response to ADP that returned to a normal response 2–3 weeks later.Survival of patients and transfused platelets was markedly decreased because of immune-mediated injury of platelets.7 Coagulopathy During the acute febrile stage. Platelet dysfunction as evidenced by the absence of adenosine diphosphate (ADP) release was initially demonstrated in patients with DHF during the convalescent stage by Mitrakul et al. Elevated levels of tissue factor. IX and X. An increase in plasma β-thromboglobulin and platelet factor 4.thrombocytopenia include decreased platelet production and increased peripheral destruction. The subsequent study during the febrile and early convalescent stages by Srichaikul et al. in 1977. indicating increased platelet secretory activity. mild prolongation of the prothrombin time and partial thromboplastin time. The coagulation abnormality is well compensated for in the 10 | P a g e . was observed. 3 Additionally. Variable reductions in the activities of several coagulation factors. Fibrin degradation product or D-dimer is slightly elevated. lymphocytes and platelets was observed. as well as reduced fibrinogen levels. including prothrombin. The platelet dysfunction might be the result of exhaustion from platelet activation triggered by immune complexes containing dengue antigen. presumably due to plasma leakage. factors V. Hemophagocytosis of young and mature erythroid and myeloid cells. thrombomodulin and plasminogen activator inhibitor-1 reflect endothelial.9 Low levels of anticoagulant proteins C and S and antithrombin III were found to be associated with increasing severity of shock. platelet and/or monocyte activation and may be a secondary response to direct activation of fibrinolysis by the dengue virus. VIII. have been demonstrated in several studies. have been demonstrated.
especially of the knees and shoulders. respectively. and legs.106°F). A rash.majority of patients without circulatory collapse.4 – 41. particularly of the lower back. and arthralgias. and fatigue. pain behind the eyes (retroorbital pain). and mild respiratory and gastrointestinal symptoms. erythematous mottling of the skin. and facial flushing (a sensitive and specific indicator of dengue fever). and may be accompanied by scaling and pruritus.3 The fever typically begins on the third day and lasts 5-7 days. abating with the cessation of viremia. arms. Patients are at risk for development of dengue hemorrhagic fever or dengue shock syndrome at approximately the time of defervescence. Most of the patients have serum aspartate transaminase (AST) and alanine transaminase (ALT) levels threeand twofold higher than normal. Proliferation of mononuclear leucocytes and less frequently polymorphonuclear leucocytes occurs in the sinusoids and occasionally in the portal areas. the fever abates for a day and then returns. Other signs and symptoms include flushed facies (usually during the first 24 to 48 hours). an inflamed pharynx. often lasts for two to four days. Occasionally.2 11 | P a g e . 6 Fever in persons with symptomatic dengue fever may be as high as 39.1°C (103 . lymphadenopathy. a pattern that has been called saddleback fever.The fever usually lasts five to seven days. Fever is often preceded by chills. swelling appearance of Councilman bodies and hyaline necrosis of Kupffer cells. accompanied by a severe headache. and more commonly in children. and it is often associated with severe myalgias.9 CLINICAL FEATURES Classic dengue or “breakbone fever” is characterized by a sudden onset of high-grade fever. injected conjunctivae.2. There is focal necrosis of hepatic cells. typically macular or maculopapular and often confluent with the sparing of small islands of normal skin has been reported in about half of infected persons. It usually appears near the time of defervescence.
epistaxis. Very rare complications of dengue fever include myocarditis. leukopenia with lymphopenia. and neurologic abnormalities. Laboratory findings commonly associated with dengue fever include thrombocytopenia. such as encephalopathy and neuropathies. and gastrointestinal hemorrhage are only occasionally seen. mild-to-moderate elevations of hepatic aminotransferases and lactate dehydrogenase.cmenorrhagia.Gum bleeding. and hyponatremia.6 DIAGNOSIS The WHO guidelines propose the following classification for symptomatic dengue infection : 12 | P a g e . hepatitis.
signs of plasma leakage such as pleural effusion. indicated by raised diastolic pressure and increased PVR in an alert patient. bleeding from the mucosa. 2. haemorrhagic 13 | P a g e . a rise in the haematocrit equal or greater than 20% above average for age. occasionally biphasic. The onset of shock may be subtle. haematemesis or melena 3. Thrombocytopaenia (100. the following must all be present. manifested by at least one of the following: a. and hypoproteinaemia. a drop in the haematocrit following volume-replacement treatment equal to or greater than 20% of baseline c. evidenced by at least one of the following: a. sex and population b.000 cells per mm3 or less) 4. petechiae. ascites. injection sites or other locations d.9. Evidence of plasma leakage due to increased vascular permeability. the four criteria above for DHF (fever. or purpura c.10 1. lasting 2-7 days. Bleeding (haemorrhagic tendencies). gastrointestinal tract. a positive tourniquet test (TT) b. ecchymosis.2 To fulfil the case definition for Dengue Shock Syndrome (DSS). Fever or history of acute fever.Figure 1 Manifestation of dengue virus infection To fulfil the WHO case definition for DHF.
These disappear after 6-12 wk. b. Crossreactions with other flaviviruses interfere with serologic testing.6 The most commonly used test for the diagnosis of dengue is the IgM capture ELISA.) d. and plasma leakage) must all be present plus evidence of circulatory failure manifested as: 10 a. but this test is negative early in the course of the disease.10 In 2nd primary dengue infections.tendencies. including those previously vaccinated against flavivirus infections. Rapid and weak pulse Narrow pulse pressure (<20 mmHg) Hypotension for age (this is defined as systolic pressure < 80 mmHg for those less than five years of age. Cold clammy skin and restlessness. between acute and convalescent sera or positive test for dengue-specific IgM/IgG performed by enzyme-linked immunosorbent assay (ELISA). Usually such samples should be collected not earlier than 5 14 | P a g e .6 The secondary dengue infection is defined when the hemagglutination inhibition titer was 1:2560 or more. should be performed only four to five days after the onset of symptoms.6 In both primary and secondary dengue infections. c. thrombocytopaenia. polymerase chain reaction (PCR) from the clinical specimens such as serum in the early febrile stage. or serological studies. or neutralization test. enzyme immunoassay. complement fixation. most antibody is of the IgG class. or <90 mmHg for those five years of age and older. and gives only a probable diagnosis. The positive serological studies define as a fourfold or more increase in the hemagglutination inhibition test. such as yellow fever and Japanese encephalitis. which can be used to time a dengue infection. there is a relatively transient appearance of antidengue immunoglobulin M (IgM) antibodies. The diagnosis of dengue infection is confirmed by testing positive for either virus isolation using culture. particularly the ELISA for IgG. and this affects the interpretation of test results in travelers exposed to other flavivirus infections.8. or the ratio of IgG and IgM was >1.
6 CLASSIFICATION DHF is lassified into four grade of severity. with the presence of cold.6. The presence of thrombocytopenia with concurrent haemoconcentration differentiates grades I and II DHF from DF: 9 1. pulse. the only haemorrhagic manifestation is a positive TT and/or easy bruising. IgM antibodies are detectable for three to six months. whereas levels of IgG antibodies rise rapidly in secondary infections. clammy skin and restlessness. whereas IgG antibodies remain detectable for life. 3. and narrowing of the pulse pressure or hypotension. even during the acute phase. the level of IgM antibodies is lower than in primary infections and the antibodies are sometimes even absent. 4. Grades III and IV are define are as DSS. Grade IV is profound shock with undetectable blood pressure or 15 | P a g e . Thus. where grades III and IV are considered to de DSS. weak pulse usually in the form of skin or other haemorrhages. the presence of high titers of IgG early in the course of the disease is a criterion for secondary infection. Rheumatoid factor may lead to an IgM capture assay that is false positive for dengue. Grade III is circulatory failure manifested by a rapid.10 Primary infections are characterized by an increase in dengue-specific IgM antibodies 4 to 5 days after the onset of fever and by an increase in IgG antibodies only after 7 to 10 days. In secondary infections. 2. Grade I is defined as fever and non-specific constitutional signs and symptoms. Grade II is the same as grade I but includes spontaneous bleeding.days nor later than 6 wk after onset.
Chikungunya fever may be difficult to differentiate clinically from DF and mild or early cases of DHF. the differential diagnose for DHF/DSS includes a wide spectrum of viral.8 DIFFERENTIAL DIAGNOSIS Early in the febrile phase. meningococcemia and other viral hemorrhagic fevers. hepatomegaly. shock. The of shock in a patient with a provisional diagnosis of DHF supports the diagnosis of DSS. laboratory findings may establish a diagnosis before shock occurs. plus one of the laboratory findings establishes a provisional diagnosis of DHF. ideally before the onset of shock but are not intended to be substitutes for the case definitions. bacterial and parasitic infections. the guidelines list indicators that may be used to guide the diagnosis of DHF/DSS.8 In addition. hemorrhagic manifestations (at least a positive TT).Figure 2 The spectrum of dengue illness In addition. hantavirus infections.8 By the third or fourth day. Shock virtually rules out a diagnosis of chikungunya fever. thrombocytopaenia. DHF can also mimic Kawasaki disease. These indicators may help clinicians to establish an early diagnosis. 16 | P a g e . The listed indicators of DHF/DSS are: high fever of acute onset. yellow fever. The first two clinical observations. and hemoconcentration.
10 Other abnormalities include moderate elevations of the serum transaminase levels.10 In dengue fever. Leukopenia.Marked thrombocytopenia with concurrent haemoconcentration differentiates DHF/DSS from diseases such as endotoxin shock from bacterial infection or meningococcaemia. thrombocytopenia. Rift Valley fever. pancytopenia may occur after the 3-4 days of illness. and hypoalbuminemia. Fibrinogen levels may be subnormal and fibrin split products elevated. Platelet counts of less than 100.000 cells/μL are seen before defervescence and the onset of shock. neutrophil. and platelet counts than patients with other febrile illnesses in dengue-endemic populations. slight elevation of serum urea nitrogen. sandfly fever.2 Neutropenia may persist or reappear during the latter stage of the disease and may continue into convalescence with white blood cell counts of <2. viral hepatitis.10 The most common hematologic abnormalities during dengue hemorrhagic fever and dengue shock syndrome are hemoconcentration with an increase of >20% in hematocrit. The platelet count and hematocrit level should be monitored at least every 24 hours to facilitate early recognition of dengue hemorrhagic fever and every 3-4 hours in severe cases of dengue hemorrhagic fever or dengue shock syndrome.9 The differential diagnosis of dengue fever includes viral respiratory and influenza-like diseases. mild metabolic acidosis with hyponatremia. Four arboviral diseases have dengue-like courses but without rash: Colorado tick fever. mild yellow fever. occasionally hypochloremia. prolonged bleeding time. scrub typhus. often with lymphopenia.2 17 | P a g e . and moderately decreased prothrombin level that is seldom <40% of control. and Ross River fever.3 Thrombocytopenia has been demonstrated in up to 50% of dengue fever cases. consumption of complement. the early stages of malaria. A recent systematic review found that patients with dengue had significantly lower total WBC. is observed near the end of the febrile phase of illness.000/mm3. and leptospirosis.
CSF. Thickening of the gallbladder wall may presage clinically significant vascular permeability. oxygenation. including complement fixation (CF). neutralization test (NT). Serodiagnosis is made based on a rise in antibody titer in paired IgG or IgM specimens. The IgM capture enzyme-linked immunosorbent assay (MAC-ELISA) has become the most widely used assay. ectopic ventricular foci. hemagglutination inhibition (HI).2. Typing and crossmatching of blood should be performed in cases of severe dengue hemorrhagic fever or dengue shock syndrome because blood products may be required. Arterial blood gas should be assessed in patients with severe cases to assess pH.10 MANAGEMENT There is no specific treatment for DHF.Cultures of blood. and only supportive care is required. and other body fluids should be performed as necessary to exclude or confirm other potential causes of the patient's condition. The electrocardiogram may show sinus bradycardia. Therapy for DHF is wholly symptomatic and aims at controlling the clinical manifestations of shock and hemorrhage. and viral isolation. Bilateral pleural effusions are common in patients with dengue shock syndrome. and prolongation of the P-R interval. as there are no specific antiviral medications for dengue infections. and a thickened gallbladder wall.2 Positive and reliable ultrasonographic findings include fluid in the chest and abdominal cavities.10 Imaging Studies Chest radiography of the chest reveal pleural effusions (left > right) in nearly all patients with dengue shock syndrome. Results vary depending on whether the infection is primary or secondary.2 Serum specimens should be sent to the laboratory for serodiagnosis. although other tests.7 18 | P a g e . PCR. flattened T waves. and ventilation. Dengue fever is usually a selflimited illness. pericardial effusion. and IgG ELISA are also used. urine.
dengue hemorrhagic fever. These signs are as follows: Rapid pulse with no fever Prolonged capillary refill time Cold clammy skin. fruit juice. Table 1 shows high risk patients and some indication for admission to hospital. Bedrest is recommended for patients with symptomatic dengue fever. Patients may become dehydrated from fever. thalassemia. cannot eat or drink. Return of appetite after dengue hemorrhagic fever or dengue shock syndrome is a sign of recovery.9 Table 1 . Patients who are able to tolerate oral fluids should be encouraged to drink oral rehydration solution. heart disease Indication for admission Excessive family concern or cannot be followed up Very weak. not drinking/feeding poorly Spontaneous bleeding Platelet counts ≤ 100.No specific diet is necessary for patients with dengue fever.High-risk dengue patients and indication for admission to hospital/ICU High-risk dengue patients that need special attention Infants under 1 year of age Overweight/obese patients Massive bleeding Change of consciousness. mottling 19 | P a g e . especially restlessness and irritability or coma Presence of underlying diseases e. or dengue shock syndrome. G-6-PD deficiency. lack of oral intake. or vomiting.g.000 cells/mm3 and/or rising Hct 10-20% Clinical deterioration in defervescence Severe abdominal pain/vomiting Significant dehydration requiring intravenous fluids Admit immediately if there are signs of shock. or water to prevent dehydration.
Steps to the management of the febrile phase Resting.6 Patients who do not receive a proper treatment usually die within 12–24 hours after shock ensues.recommended in case of gastrointestinal bleeding 20 | P a g e .Avoid black. nutritious diet. every 4 to 6 hours Nutritional support: Soft. Salicylates and other nonsteroidal antiinflammatory drugs should be avoided as these may predispose a child to mucosal bleeding. balanced. e. juice and electrolyte solution plainwater is not adequate.8 Table 2 . no urine for 4-6 hours Change of consciousness: drowsiness to stupor. Fever is treated with paracetamol.or red-colored food or drinks (may be mistaken for bleeding) Other supportive and symptomatic treatment • Domperidone -1 mg/kg/day in three divided doses in case of severe vomiting for 1-2 days. 100/80 Hypotension Oliguria. irritability (encephalopathy) World Health Orgnization. The most important aspect in managing patients with DHF is close observation by the attending physicians and nurses with frequent clinical and laboratory monitoring. One single dose may be adequate • H2-blockers (ranitidine) . oral fluids Reduction of fever: Tepid sponge after a dose of paracetamol 10-15 mg/kg/day for high fever ≥ 39oC.Narrowing of pulse pressure ≤ 20 mmHg.g. restlessness. Dengue Haemorrhagic Fever: 1997 The treatment of dengue fever in the febrile phase is symptomatic (Table 2).
fluid intake. vomiting. It may cause harm Intravenous fluids: In case of doubt.000 cells/cumm – indicates progression to critical phase. and urine output • Physical examination: vital signs. decreased urine output or no urine for 4-6 hours • Behavioral changes e. just correct dehydration.g.from the 3rd day until afebrile for 24-48 hours. Important points to evaluate are : • History of bleeding. Rising Hct of 1020% . acute abdominal pain. provide intravenous fluids. appetite. confusion. altered mental status. decreased urine output. liver size and tenderness • Blood counts: WBC ≤ 5. cool or mottled skin. diminished pulse amplitude. use of foul language Follow up preferably everyday . and urine output levels. Dengue Haemorrhagic Fever: 1997 Patients who develop signs of dehydration. restlessness. confusion and irritability World Health Orgnization. desire for sleeping all the time • Refusal to eat or drink • Cold. prolonged capillary refill time. rise in 21 | P a g e . irritability. The volume of fluid should be targeted at treating mild to moderate isotonic dehydration (5-8% deficit). and discontinue it as soon as possible If sent home. clammy skin and extremities. guided by serial hematocrit.not necessary.indicates that the patient has progressed to the critical phase • Liver function tests in every patient who shows a change in consciousness. it may lead to complications • Steroid is ineffective in preventing shock DHF.Advise about warning signs and symptoms of shock and ask to report immediately if any of the following symptoms occur • Clinical deterioration in defervescence (no fever or low-grade fever) • Any type of bleeding • Severe vomiting/abdominal pain • Intense thirst • Drowsiness. such as tachycardia. abdominal pain. blood pressure.• Antibiotic . restlessness.000 cells/mm3 with lymphocytosis and increase in atypical lymphocytes – and platelet counts ≤ 100. restlessness.
If no improvement is observed in vital parameters and hematocrit level at the end of 3 hours. as indicated by normal blood pressure.9 22 | P a g e . if hematocrit level decreases and vital parameters improve.hematocrit levels. Once the hematocrit level and vital parameters are stable the infusion rate should be gradually reduced and discontinued over 24-48 hours. the fluid infusion rate should be increased to 10 mL/kg over the next hour. should be hospitalized as require admission for intravenous fluid administration. satisfactory oral intake and urine output. After 1 hour. the fluid infusion rate should be decreased to 5 mL/kg over the next hour and to 3 mL/kg/hour for 24-48 hours. the fluid infusion rate should be further increased to 15 mL/kg over the third hour.8 If at 1 hour the hematocrit level rises and vital parameters do not show improvement. or hypotension.8. colloids or plasma infusion (10 mL/kg) should be administered (Figure 3). When the patient is stable. the child can be discharged. narrowed pulse pressure. In case of no improvement.9 Ringer’s lactate is infused at a rate of 7 mL/kg over 1 hour.
Figure 3 Management for DHF grade I and II Intravenous fluids should be stopped when the hematocrit level falls below 40% and adequate intravascular volume is present.8.9 23 | P a g e . and level of consciousness (Table 3). patients reabsorb extravasated fluid and are at risk for volume overload if intravenous fluids are continued. With adequate and appropriate fluid replacement. Do not interpret a falling hematocrit value in a clinically improving patient as a sign of internal bleeding. platelet count. DSS is rapidly reversible. hemorrhagic manifestations. hematocrit levels.2 The most important element of treatment in a critically ill patient or in a patient with DSS is providing intensive care with close monitoring of blood pressure. At this time. urinary output.
no nasogastric tube insertion. and every 1-2 hours thereafter • Hematocrit levels must be checked every 2 hours for 6 hours.g. • Long-acting sedatives should be avoided Monitoring of children with DHF/DSS • Vital signs should be checked every 15-30 minutes until the patient is stable. NCPAP should be preferred if there is acute respiratory failure associated with DSS • Frequent monitoring • Stop bleeding with proper techniques e. then every 4 hours until the patient is stable. Monitoring at every 12 hours during recovery • Fluid balance sheet: type of fluid. rate etc • Accurate measurement of urine output • Serum electrolytes and blood gases should be checked every 12 hours • DIC profile and liver function tests as and when indicated • Weight should be measured every 12 hours Obtain laboratory tests 24 | P a g e . anterior nasal packing for massive epistaxis • Avoid blind invasive procedures e. amount. is recommended. orally or rectally.Table 3 Steps to the management of the critical phase/DHF and dengue shock syndrome General measures • Give oxygen via face mask/nasal cannula in case of shock/impending shock. no gastric lavage • Essential nursing care • Sedation is needed in some cases to restrain an agitated child.g.5-50 mg/kg). Chloral hydrate(12.
. if possible. 25 | P a g e . excess amount will leak into the pleural and peritoneal spaces Initial rate of administration • DSS grade III – 10 mL/kg/hour for 1-2 hours • Grade IV – Free flow or 20 mL/kg/dose IV bolus until BP can be measured (usually within 5-15 minutes).000. K. then reduce the rate to 10 mL/kg/hour for 1-2 hours • Non-shock patients: normal maintenance or + 5%deficit and then reduce the rate to minimum after 2-4 hours. uric acid) Blood gas Coagulogram (PTT.g. CO2) Liver function test Renal function test (BUN. Body weight < 15 kg: 4-7 mL/kg/hour. but may cause fluid overload Type of IV fluid used: isotonic salt solution (normal saline or Ringer 's lactate) In young infants without shock-N/2 saline in 5% dextrose. Ca. IV fluid before critical phase cannot prevent shock. rising Hct of 10-20%. Body weight 15-40 kg: 3-5 mL/kg/hour • Colloids: The initial rate is 10 mL/kg/hour. PT.• In uncomplicated DHF cases. After that. this will reduce Hct by about 10 percentage points e. creatinine.e. colloid solutions in patients who already have volume overload. TT) IV fluid IV fluids should be given only when the patient enters the critical phase: thrombocytopenia ≤ 100. i. massive pleural effusion Fluid replacement rate – minimum necessary to maintain effective circulatory volume. reduce to 5. Hematocrit and platelet counts are the only necessary tests • In those at high risk of complicated DHF Blood grouping/cross matching Blood glucose Blood electrolyte (Na. from 53 to 43%.
It should be discontinued when the hematocrit level falls to approximately 40%.000/mm3 (10-20 mL/kg of platelets). urine output In case of no response to IV fluids: consider and correct • Massive plasma leakage • Concealed internal bleeding – decrease in Hct • Hypoglycemia – Blood sugar < 60 mg% • Hyponatremia. Blood and platelet transfusion • The indications for fresh whole blood or packed red cell transfusion are significant blood loss > 10% (6-8 mL/kg). and hypervolemia. hypocalcemia – electrolytes • Acidosis – indicates metabolic acidosis in blood gas analysis Duration of IV fluid infusion: between 24-48 hours as plasma loss may continue for 24-48 hours. concealed internal bleeding • Dose: Fresh whole blood 10 mL/kg/dose. hemolysis. Platelets return to normal within 726 | P a g e .then to 3 mL/kg/hour Increase or decrease the rate of IV fluid depending on: clinical signs of shock. The return of the patient’s appetite is also a sign of recovery. It is extremely important that a drop in hematocrit levels at this later stage is not interpreted as a sign of internal bleeding.Strong pulse and blood pressure and adequate dieresis are good signs at this stage. packed red cells 5 mL/kg/dose • Indication for platelet transfusion: significant bleeding with thrombocytopenia or if platelet count is less than 10. Reabsorption of extravasated plasma occurs 48 hours after the termination of shock (manifested by a further drop in hematocrit levels after intravenous fluid administration has been stopped). pulmonary edema or heart failure may occur if more fluid is given. Mild reductions in platelet counts are usually not associated with significant bleeding. hematocrit level. with stable vital signs. A good urine flow indicates sufficient circulating volume.
should be infused over 1 hour or given as bolus 20 mL/kg if blood pressure is unrecordable (DSS grade IV). If the hematocrit level is falling without improvement in vital parameters. Only 0. Once improvement starts. the fluid infusion rate should be gradually decreased. If there is no improvement in vital parameters and hematocrit level rises. 10-20 mL/kg. which may be easily detected by echocardiography. platelet infusion does not alter the outcome. colloids 10 mL/kg should be rapidly infused. Infusion of fresh frozen plasma and platelet concentrates may be beneficial in patients with disseminated intravascular coagulation. Ringer’s lactate solution. In children with severe thrombocytopenia in absence of significant bleeding. Dengue Haemorrhagic Fever: 1997 In children with hypotension (DSS grade III).4% of DHF patients need platelet transfusion World Health Orgnization. Low platelet count may not be predictive of bleeding.8. presuming that lack of improvement is due to occult blood loss (Figure 4). The bolus may be repeated twice if there is no improvement. blood transfusion is necessary. Platelets or blood should not be transfused based upon platelet count alone.9 27 | P a g e .9 days.9 Patients who are unresponsive to fluids may have myocardial dysfunction and decreased left ventricular performance.
Judicious fluid removal using colloids with controlled diuresis (furosemide 1 mg/kg infusion over 4 hours) or dialysis overload.Figure 4 Management for DSS COMPLICATIONS The complications can occur from DHF include 2. Non-reduction in the rate of IV fluid after initial resuscitation d. Electrolyte imbalance : Hyponatremia.9 1. Excessive use of hypotonic solutions c. Hypocalcemia Fluid overload (overhydration) : avoid the common causes of fluid a. Early IV fluid therapy. Blood loss replaced with fluids in cases with occult bleeding e.in the febrile phase b. 2. which are: 28 | P a g e .
fluid overload and acute liver failure with encephalopathy. Most deaths from DHF/DSS are caused by prolonged shock. 9. 8. Severe refractory shock. 3.3. clinically improved condition Adequate urine output Stable hematocrit level At least 48 hours since recovery from shock: stable pulse. ARDS. 7. blood Absence of respiratory distress from pleural effusion and no ascites Platelet count greater than 50. 6. If left untreated. If shock is identified when pulse pressure starts to drop and intravenous fluids are administered.9 1. Patients with dengue hemorrhagic fever or dengue shock syndrome may be discharged from the hospital when they meet the following criteria:2. there is residual brain damage caused by prolonged shock or occasionally by intracranial hemorrhage. DIC. PROGNOSIS Significant morbidity and mortality can result if early recognition and monitoring of severe forms are not done. the outcome will be excellent. Early recognition of illness. Infrequently. massive bleeding. 5. The outcome may not be so good if the patient develops cold extremities.000 cells/μL No evidence of external or internal bleeding Convalescent confluent petechial rash pressure and breathing rate 29 | P a g e . ascites Disseminated intravascular coagulation CRITERIA FOR DISCHARGING IN PATIENTS Patients who are resuscitated from shock rapidly recover. the mortality of DHF or DSS patients may be as high as 40-50%. 2. Large pleural effusions. 4.10 Recovery is fast and most patients recover in 24-48 hours without any sequelae. liver failure and neurological manifestations singly Afebrile for at lease 24 hours without antipyretics Good appetite. 4. careful monitoring and appropriate fluid therapy alone have decreased mortality to 1%.
9 PREVENTION AND CONTROL At present. 3) Biological control: by larvivorous fish: Gambria affinis and Peorilia reticulate. pirimiphos (only in major DHF epidemics). insecticide-treated mosquito nets and curtains.8. The case fatality rate is high with shortage of experienced medical teams. 30 | P a g e .9 1) Environmental changes: improved water supply. fenitrothion.or in combination were the commonest causes of death in a recent series. cisterns and underground reservoirs. mats.g. permethrin impregnated in cloth. DEET. no specific drug or vaccine is available against the dengue virus. Space sprays – malathion. aerosol coils (pyrethrum). 2) Personal protection: protective clothing. Bacteria – Bacillus thuringiensis H-14. 4) Chemical control: 1% temephos sand granules. Insect growth regulators – interfere with development of the immature stages of the mosquito in larvae or disruption of pupal stage. mosquito proofing of overhead tanks.1. The control is primarily dependent on vector control.. Bacillus sphaericus – in polluted water. repellents e.
Nausea and vomiting were found since 3 days ago with a frequency of 3x/day.4% (normoweight) Body Temperature : 38. cyanosis (-). dyspnea (-) 31 | P a g e .Cefadroxil.The aim of doing this paper is to report a case of grade II dengue hemorrhagic fever of an 6 year-old girl that was admitted at the Infection Unit of Pediatric Ward Haji Adam Malik General Hospital. icteric (-). Micturition and defecation were normal. Volume: ¼ Aqua cup.Hadrianus Sinaga for the diagnosis of the Dengue Haemorrhagic Fever. Small red patches were found on hands and legs since a day ago. The fever occured suddenly since 3 days ago with a characteristic of high fever which relieved with fever relieving medication. Neither gingival bleeding and black stool. Shivers and seizures were not found.Ranitidine PHYSICAL EXAMINATION Generalized Status: Body weight (BW) : 19 kg BW/ BL : 90. Patient experienced epistaxis 1 day ago.Parasetamol. History of previous illness: This patient was referred from RSU Dr. CASE EN. History of drugs usage : Ringer Lactat. 2010 at 02. a 6 year-old girl.6 ۫C Consciousness: Was Clear Body length (BL) : 120 cm Anemic (-). was admitted to the Infection Unit of Pediatric Ward Haji Adam Malik General Hospital on October 29th. oedema (-). 19 kg. 116 cm.Patient complained of fatigue since 3 days ago. . Pain behind the eyes was not found.00 am with chief complaint was fever.
no murmur RR: 20 rpm.20% 11.80pg 33. CRT < 3’’ cold acral.Localized Status: Head : Eye: light reflexes (+/+). regular. pressure/volume: adequate BP: 90/50 mmHg. regular. no rales Abdominal : Soepel.60% 0.20 g% 5. regular.90 % 55x 103/ mm3 80. pale inferior conjunctival palpebral (-/-). ptechiae (+) o/t superiorinferior dextra-sinistra extremities Rumple leed : (+) Urogenital : Female. within normal limit Laboratorium Findings (October 29th 2010) from Emergency Unit of Adam Malik Test Hemoglobin (Hb) Erytrocyes (RBC) Leucocytes (WBC) Hematocrit Thrombocyte MCV MCH MCHC RDW Neutrophil Lymphocyte Monocyte Eosinophil Basophil Result Complete Blood Count 12.2 x 106/mm3 2.000x103/mm3 36-46% 150-400x103mm3 83-103fL 28-34pg 32-36g% 39-46% 37. retraction of epigastric (-) HR: 123 bpm.200% Normal Value 11-15g% 3. Liver : Not palpable Spleen: Not palpable Extremities : Pulse: 123 bpm.5 x 103/ mm3 45. JVP: R-2cmH₂O : Symmetrical fusiformic. peristaltic was normal.70 fL 26.000-10. palpebra edema (-/-) Mouth/Ears /Nose: Within normal limit Neck Chest : Lymph node enlargement (-).00% 1.20g% 13.30 % Cell Count 52% 35.80% 20-40% 2-8% 1-6% 0-1% 32 | P a g e . isochoric pupil (right=left).0-5.3x106mm3 5.
ptechiae (+) o/t superior-inferior A P dextra-sinistra extremities DHF Grade II • IVFD RL 5 cc/BW/hour 95 gtt/i micro Paracetamol 3x250 mg • 33 | P a g e . BP :90/60mmHg. Liver / Spleen: Not palpable Extremities: Pols 100 bpm.0 ۫C BW: 19. pale inferior palpebral conjunctiva (-). regular. red spots in body (+) Consciousness: Was Clear T: 38.00 am Fever (+) 4 day. JVP: R-2cmH₂O : Symmetrical fusiformic. epistaxis (+). regular. • • Investigation Plan : Routine Blood Count/6 hour Follow Up S O Follow Up October 29th 2010 06. no murmur RR : 30 rpm.0 kg th BL: 116cm BW/BL: 90.Differential diagnosis :.DHF grade II Working diagnosis Management : • Chikugunya : DHF grade II IVFD RL 5 cc/BW 95gtt/i micro Paracetamol 3x250 mg Diet porridge 1450kkal with 38 grams of protein. epigastrial pain (-). Neck Chest : Lymph nodes enlargement (-). retraction of epigastrial (-). Pressure/Volume:adequate.4 % (normoweight) Head : Eyes: Light reflexes (+/+). isochoric pupil. CRT < 3” warm acral. Ears/Nose/Mouth: Within normal limits. regular. no rales Abdomen : Soepel. normal peristaltic. HR : 100 bpm.
7 g% Ht : 44.4 % Head : Eyes: Light reflexes (+/+). no rales 34 | P a g e .80 % L : 3. epistaxis (-). pale inferior palpebral conjunctiva (-).84 x 103/ mm3 Plt : 47 x 103/ mm3 S O Follow Up October 30th 2010 06. JVP: R-2cmH₂O : Symmetrical fusiformic.• Diet porridge 1450 kkal with 38 grams of protein Investigation plan : - Routine Blood Count / 6 hours consult to Infection Division Lab examination IgG and IgM anti dengue Laboratory findings at 12. regular.17 x 103/ mm3 Plt : 51 x 103/ mm3 Laboratory findings at 06. no murmur RR : 26 rpm.1 ۫C BW: 19 kg BL: 116cm th BW/BL: 90. regular.40 % L : 3. retraction of epigastrial (-). HR : 100 bpm. red spots in body (+) Consciousness : Was Clear T: 37.00 g% Ht : 45. Ears/Nose/Mouth: Within normal limits.00 pm: Hb : 12. isochoric pupil. Neck Chest : Lymph nodes enlargement (-).00 am Fever (-) 5 day.00 pm: Hb : 13.
Liver / Spleen: Not palpable Extremities : Pols 98 bpm.80 % L : 5.40 g% Ht : 45.00 am : Hb : 12.60 g% Ht : 42.00 pm : Hb : 13.11 x 103/ mm3 Plt : 66 x 103/ mm3 Laboratory findings at 00. epigastrial pain (-). BP :90/60mmHg. ptechiae (+) o/t superior-inferior dextra-sinistra extremities Investigation plan : Waiting for IgG and IgM anti dengue lab result A P DHF Grade II • IVFD RL 3cc/BW 57 gtt/i micro • Diet porridge 1450 kkal with 38 grams of protein Laboratory findings at 06.35 x 103/ mm3 Plt : 41 x 103/ mm3 Laboratory findings at 12. CRT < 3” warm acral.00 am : Hb : 12.19 x 103/ mm3 Plt : 57 x 103/ mm3 Laboratory findings at 06.30 g% Ht : 42. regular.10 g% Ht : 44.50% L : 6. Pressure/Volume:adequate.10 % L : 9. normal peristaltic.80% L : 7.00 pm: Hb : 12.Abdomen : Soepel.54 x 103/ mm3 35 | P a g e .
00pm - 36 | P a g e . Ears/Nose/Mouth: Within normal limits. no murmur RR : 24 rpm.4%. CRT < 3” warm acral.Routine Blood Count at 06.Plt : 72 x 103/ mm3 Imunoserologi : Virus Anti DHF IgM : Positif Anti DHF IgG : Positif S O Follow Up October 31st 2010 06. pale inferior palpebral conjunctiva (-). Liver / Spleen: Not palpable Extremities: Pols 86 bpm. Neck Chest : Lymph nodes enlargement (-). Pressure/Volume:adequate. JVP: R-2cmH₂O : Symmetrical fusiformic. HR : 86 bpm.7C BW: 19 kg BL: 116cm th BW/BL: 90. normal peristaltic. retraction of epigastrial (-). regular. epigastrial pain (-). ptechiae (+) o/t superior-inferior dextra-sinistra extremities A P DHF Grade II • • IVFD RL 3 cc/BW/hour 57 gtt/i micro Diet porridge 1450 kkal with 38 grams of protein Investigation : . isochoric pupil. BP :90/60mmHg. regular. regular. no rales Abdomen : Soepel. red spots in body (+) Consciousness : Was Clear T: 36.00 am Fever (-) 6 day. Head : Eyes: Light reflexes (+/+).
22 x 103/ mm3 Plt : 64 x 103/ mm3 Laboratory findings at 06. Neck Chest : Lymph nodes enlargement (-).4% Head BL: 116cm : Eyes: Light reflexes (+/+).39 x 103/ mm3 Plt : 65 x 103/ mm3 S O Follow Up October 1st 2010 06. pale inferior palpebral conjunctiva (-). normal peristaltic. regular. no rales Abdomen : Soepel.50 % L : 7. Ears/Nose/Mouth: Within normal limits.4 g% Ht : 38.00 pm : Hb : 11.60 % L : 7. epigastrial pain (-). A CRT < 3” warm acral.00 pm : Hb : 11.50 g% Ht : 39.8C BW: 19 kg BW/BL: 90. JVP: R-2cmH₂O : Symmetrical fusiformic. regular. Liver / Spleen: Not palpable Extremities: Pols 88 bpm. BP :90/60mmHg DHF Grade II 37 | P a g e . regular. retraction of epigastrial (-). isochoric pupil. HR : 88 bpm.00 am Fever (-) Consciousness : Was Clear T: 36.Laboratory findings at 12. Pressure/Volume:adequate. no murmur RR : 24 rpm.
96 x 103/ mm3 Plt : 93 x 103/ mm3 Patient is discharged from the hospital. In this patient all of the criteria were found. and from the laboratory 38 | P a g e . all 4 criteria must be fulfilled to make the diagnosis of DHF.P • • IVFD RL 3 cc/BW/ hour 57 gtt/i micro Diet porridge 1450 kkal with 38 grams of protein Laboratory findings at 06. which are: 1) fever or history of acute fever lasting 2-7 days. DISCUSSION According to WHO. 2) small red patches (petechies) on hands and legs and history of bleeding nose as haemorrhagic tendencies.40 g% Ht : 37.000 cells per mm3 or less). and 4) evidence of plasma leakage due to increased vascular permeability.00 am : Hb : 11. which were 1) sudden of high-grade fever since 3 days ago. 2) bleeding (haemorrhagic tendencies). 3) thrombocytopaenia (100.40 % L : 6.
3.Specimens that may be suitable for virus isolation include acute phase serum.000/mm3) and 4) raised of hematocrit (44. The severity of DHF are classified into 4 gradings according to WHO guidelines which are: 1. In this patient. whereas IgG antibodies remain detectable for life.IgM and IgG were checked on day 5th .9%) as the evidence of plasma leakage. Grade I is defined as fever and non-specific constitutional signs and symptoms. clammy skin and restlessness. Isolation of most strains of dengue virus from clinical specimens can be accomplished in which the sample is taken in the first few days of illness and processed without delay to know the serotype of the dengue virus . autopsy tissues from fatal cases. IgM antibodies are detectable for three to six months. and mosquitoes collected in nature. lymph nodes and thymus. Grade III is circulatory failure manifested by a rapid. plasma or washed buffy coat from the patient. spleen. especially liver. usually in the form of skin or other haemorrhages.serotype of the denque virus could not been found as isolation of virus were not done. weak pulse and narrowing of the pulse pressure or hypotension.results were 3) thrombocytopaenia (platelet 55. Grade II is the same as grade I but includes spontaneous bleeding. 2. 39 | P a g e . Laboratory examinations of IgM and IgG are important to find out whether its primary or secondary infections. the only haemorrhagic manifestation is a positive TT and/or easy bruising.In this patient. with the presence of cold. Primary infections are characterized by an increase in dengue-specific IgM antibodies 4 to 5 days after the onset of fever and by an increase in IgG antibodies only after 7 to 10 days.Both IgM and Ig G were positive and this concludes that this patient has been exposed with one of the dengue serotypes earlier and currently suffering the secondary infection.
P. REFERENCES 1. only supportive care is required. Setiati. Mairuhu. This patient was discharged from hospital after the routine blood count showed that platelet and hematocrit level were in normal value (93000/mm3 and 37. This patient was given intravenous fluid (RL) and paracetamol.. and laboratory findings. van Gorp. C. D. de Kruit. M. M. J. F.r. This patient was discharged from hospital after the condition the routine blood count of platelet and hematocrit level were in normal value. A.searo. Changing Epidemiology of Dengue Haemorrhagic Fever in Indonesia.. 2006.. Available from : http://www. T. E. T. the patient was diagnosed as DHF grade II. SUMMARY It has been reported a case of a 6-year-old girl with dengue haemorrhagic fever grade II... A.. The diagnosis was established based on history taking..who.. Soemantri. Therapy for DHF is wholly symptomatic and aims at controlling the clinical manifestations of shock and hemorrhage.4..pdf October 30th 2010] [Accessed 40 | P a g e ... Grades III and IV are define are as DSS. Thus.int/LinkFiles/Dengue_Bulletins_c1. E.. Spontaneous bleeding (petechiaes and history of epistaxis) was found because the girl had petechiaes on her extremities. Treatment for this patient was only supportive and symptomatic.40%). Grade IV is profound shock with undetectable blood pressure or pulse. clinical manifestation.. There is no specific treatment for DHF. Wagenaa.
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