DENGUE FEVER BY DR.RADHE.pptx CIVIL HOSPITAL NEPAL

RAMJIBANYADAV2 480 views 39 slides Apr 02, 2024
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About This Presentation

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DENGUE FEVER Prepared by : Dr.Radheshyam sah FCPS medicine resident

INTRODUCTION Dengue is a mosquito borne viral disease that has rapidly spread in many countries worldwide in recent years. In nepal, dengue is a rapidly emerging disease. Endemic across most provinces,dengue incidence has increased in recent years largely due to expansion of the vector Aedes aegypti and Aedes albopictus,as well as the movement of people and the introduction of imported cases. All 4 dengue serotypes exist in nepal,wt DENV1 historically contributing the highest burden.

EPIDEMIOLOGY It is estimated to infect 390 million people annually of which 96 million manifest clinically One study on prevalence of dengue estimates that 3.9 billion people in 128 countries are at risk of infection wt dengue viruses. Before 1970,only 9 countries had experienced severe dengue epidemics ,today the disease is endemics in more than 100 countries.

In nepal Dengue has been identified as one of the youngest emerging infectious disease in nepal . The first case of dengue was reported in 2004. in 2006,large no. of probable cases and 32 lab confirmed cases were reported across hospitals in central and western terai as well as kathmandu.most cases were confirmed the presence of all 4 serotypes . Sincethan no. of outbreaks reported each year in many districts.

Transmission VIRUS – DENV is a small ss RNA virus comprising four distinct serotypes ( DENV1-DENV4 ).The virus belong to the genus Flavivirus ,family Flaviviridae.They encodes three structural proteins (capsid c,membrane M,and envelope E) and seven nonstructural proteins (NS1,NS2a,NS2b,NS3, NS4a,NS4b,NS5). The NS1protein can be detected in the early stages of infection and mark virus replication. VECTOR- Aedes aegypti > Aedes albopictus . HOST-humans are the main carriers and multipliers of the virus. TRANSMISSION-the virus circulating in the blood of viraemic humans is ingested by female mosquitoes during feeding .after virus incubation for 8-10 days,an infected mosquito is capable of transmitting the virus for the rest of life.

Natural course of dengue illness Febrile phase Critical phase Recovery phase

Febrile phase(3-7 days) Sudden high grade fever usually lasts 3-7 days Headache Retro orbital pain Myalgia/ arthalgia Facial flushing Skin erythema Anorexia/nausea and vomiting Positive tourniquet test Mild hemorrhagic like petechiae and nose ,gums bleed Rash generally occur two to five days after onset of fever,typically macular or maculopapular and may occur over face,thorax,abdomen and extremities ,a/w pruritus. The liver is often enlarged and tender after few days of fever CBC-progressive leucopenia and thrombocytopenia

Continue.. Serum aspartate transaminase (AST) level are frequently elevated ( 2 to 5 times the upper limit of normal value ), occasionaly marked elevation ( 5 to 15 times the upper limit value ) Elevated aPTT and decrease fibrinogen Physical examination may demonstrate conjunctival injection,pharyngeal erythema,lymphadenopathy,hepatomegaly .

DENGUE RASH

TORNIQUET TEST

CRITICAL PHASE(24-48 hrs ) The vast majority of infections that progress to critical phase result from second DENV infection that occur more than 18 months after resolved first infection . Moderate to severe thrombocytopenia , nadir platelet count <20,000 cells/mm3 Plasma leakage – eg pleuraleffusion , ascities Hemorrhagic manifestations – bruising,bleed Shock-organ hypoperfusion lead to progressive organ impairement,metabolic acidosis Severe organ impairement -hepatitis, encephalitis or myocarditis etc

Recovery phase During the recovery phase ,plasma leakage and hemorrhage resolve,vital signs stabilize and accumulated fluids are resorbed. An additional rash( a confluent ,erythematous eruption with small islands of unaffected skin that is often pruritic) may appear during the recovery phase within 1 to 2 days of deferervescence and lasting 1 to 5 days Recovery phase typically lasts 2 to 4 days ,adult may have profound fatigue for days to weeks after recovery .

WHO 1997 CLASSIFICATION Dengue fever Also known as break-bone fever It defined by the presence of fever and two or more of the following: Headache,retroorbital pain,myalgia,bone pain,arthralgia,rash,leukopenia

Dengue hemorrhagic fever fever or h/c of acute fever lasting 2 to 7 days,occasionally biphasic The cardinal feature of DHF is plasma leakage d/t increased vascular permeability as evidenced by hemoconcentration (>20% rise in hematocrit above baseline),pleural effusion ,ascites. Petechiae,ecchymoses,purpura , hematemesis or melena,thrombocytopenia

Dengue shock syndrome DSS is DHF with marked plasma leakage that leads to circulatory collapse (shock)as evidence by narrowing pulse pressure or hypotension .

WHO 2009 classification of dengue 1.Dengue without warning sign The person lived or travelledin an area of dengue transmission in the last 14 days,has a sudden high fevertypically of 2 to 7 duration and presents two or more of the following: manifestations nausea,vomiting Exanthem /rash Myalgia/ arthalgia Headache/ retroorbital pain Peteciae or tourniquet test positive leucopenia

Dengue with warning sign Abdominal pain or tenderness Persistent vomiting Fluid accumulation( ascities,pleural effusion) Mucosal bleeding Lethargy,restlessness Liver enargement >2cm Lab-increase in hematocrit,decrease in paltelet

Severe dengue DENGUE wt atleast 1 of the following Severe plasma leakage leading to shock( dss )or fluid accumulation wt respi distress Severe bleeding Severe organ involvement( ie AST or ALT 1000 or greater, impaired consciousness,organ failure)

Differential diagnosis flu like syndromes- influenza,infectious mononucleosis Illness wt rash-scarlet fever,meningococcal infection, Chikungunya fever,zika virus infection,malaria,parvovirusB19 Diarrheal disease AGE Typhoid Leptospirosis Septic shock Viral hepatitis Scrub typhus

D iagnosis During the early stage of the disease virus isolation, nucleic acid or antigen detection can be used. At the end of the acute phase of infection ,serology is the method of choice . Note-NS1 test is positive when pt have fever. The sensitivity of the test is the highest in the first day of fever (90%), then declines as fever days.by day 5 of fever the test is less sensitive and may b negative from day6.

Dengue diagnostic methods A. Direct diagnostic methods Virus isolation Nucleic acid detection Viral antigen detection B.Indirect diagnostic methods Igm antibodies IgG antibodies

Virological and serological markers in realtion of dengue infection An incubation period of 4-10 days occurs after mosquito bites resulting in an asymptomatic or symptomatic dengue infection. During this period the virus replicates and an antibody response is developed. In general viraemia is detectable in most cases at the same time when symptoms appear, and is no longer detectable at the time of defervescence.the development of Igm antibody is coincident wt disappearnce of fever and viraemia . Accordingly dengue infection is A.primary dengue infection -affects individuals wtout prior flavivirus exposure B.secondary infection -occurs mainly in individuals previously infected by any of the remaining virus serotypes .

Case management Depending on the clinical manifestations and other circumstances pt may either 1.Be sent home(group A )-dengue wtout warning sign 2.Be referred for in hospital management(group B)- dengue wt warning sign 3.Require emergency treatment and urgent referral(group C)- severe dengue

Group A management Advice for - 1.Adequate bed rest 2.Adequate fluid intake 3.PCM 4gm max,per day 4.Monitor daily a.wbc b.defervescence c.warning signs 5.Advice for immediate return to hospital if development of any warning signs 6.Avoid aspirin,NSAIDS

Group B management Treatment Encourage oral fluids. If not tolerated start iv fluid therapy 0.9% saline or ringer lactate at maintenance rate. Obtain reference Hct before fluid therapy Give isotonic solutions 0.9% saline or RL start wt 5-7 ml/kg/ hr for 1-2 hrs then reduce to 3-5 ml/kg/ hr for 2-4 hrs then reduce to 2-3 ml/kg/ hr or less based on clinical response Reasses clinical status and repeat Hct If hct remains same or rises only minimally continue wt 2-3ml/kg/ hr for another 2-4 hrs. If worsening of vital signs and rapidly rising hct increase rate 5-10ml/kg/ hr for 1-2 hrs. Reasses clinical status repeat hct and review fluid infusion rates accordingly Reduce iv fluids gradually when the rate of plasma leakage decreases towards the end of the critical phase. This is indicated bya.adequate urine output and/or fluid intake b.hct decreases below baseline in a stable pt. Monitoring- vitals,I /O chart,warning signs,hct,wbc,platelet Blood glucose,rft,lft .

Group c management 1.Treatment shock Start iv fluid at 5-10 ml/kg/ hr over 1hr If pt improves than reduce gradually ie 5-7 ml/kg/ hr for 1-2 hrs then 3-5ml/kg/ hr for 2-4 hr then 2-3ml/kg/ hrfor 2-4 hrs then reduced depending on hemodynamic status Iv fluid can be maintained for upto 24-48 hrs If pt still unstable check hct after first bolus –if hct increases /still high(>50%)then repeat second bolus at 10-20 ml/kg/ hr for 1 hr Hct decreases indicates bleeding and need to crossmatch and blood transfuse

Management of bleeding Gastrointestinal bleeding ,epistaxis, heavy menstrual bleeding may be severe enough to warrant blood transfusion . Significant internal bleeding should be suspected in patients with sign of intravascular hypovolemia without evelation of hematocrit . Platelet transfusion has not been shown to be effective at preventing or controlling hemorrhage but may be warranted in patient with severe thrombocytopenia (<10000/mm3)and active bleeding Administration of iv vitamin K is warranted for patient with severe liver dysfunction or prolonged PT.

Discharge criteria No fever for 48 hrs Improve in clinical status Increasing trend of platelet count Stable hct wtout iv fluids No respi distress

Vector control 1.anti larval measures-biological larvicides,chemical control 2.Reducing breeding site 3.anti adult –spray chemical 4. personal protection-mosquito net,repellants,protective clothing 5. community engagement 6.active mosquito and virus surveillance 7.CYD-TDV( Dengavaxia ) vaccine –in 2018, CYD-TDV vaccine was approved by European authorities and recommended by the WHO for persons aged 9 to 45 years with confirmed previous dengue infection who live in endemic area.

Risk factors Previous infection wt DENV increases the risk of the individual developing severe dengue Previous infection wt DENV1 followed by infection wt DENV2 is more fatal than infection wt DENV4 followed by infection wt DENV2. Unplanned urbanization Community risk to dengue due to lack of knowledge,attitude and poor control of vector.

SAGE journals on vaccine Vector control has achieved only limited success in reducing the transmission of dengue and there are currently no licensed antivirals to treat dengue. The most effective way to control dengue in future include the use of safe and effective vaccine. Although no licensed dengue vaccine is yet available, several vaccine are under development including live attenuated virus vaccine,live chimeric virus vaccine, inactivated virus vaccine,live recombinant. The live chimeric virus vaccine is undergoing a phase 3 clinical trial.

References WHO journal for dengue and severe dengue National guidelines on dengue 2019 nepal Davidsons23rd Medscape UPTODATE

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