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OVERVIEW ON DENGUE HEAMORRAGIC FEVER
1.
International Research Journal
of Engineering and Technology (IRJET) e-ISSN: 2395-0056 Volume: 10 Issue: 01 | Jan 2023 www.irjet.net p-ISSN: 2395-0072 © 2023, IRJET | Impact Factor value: 7.529 | ISO 9001:2008 Certified Journal | Page 828 OVERVIEW ON DENGUE HEAMORRAGIC FEVER Harshita Kalal1, Sherin Mary Rajan2, Dr. Priyadarshini Kamble3 1PharmD VI Year Student, Bhupal Nobles’ College of Pharmacy, Rajasthan, India 2 PharmD VI Year Student, Bhupal Nobles’ College of Pharmacy, Rajasthan, India 3Assistant Professor, Bhupal Nobles’ college of Pharmacy, Rajasthan, India ---------------------------------------------------------------------***--------------------------------------------------------------------- Abstract - The flaviviridae family, which is an arthopoda, is mostly responsible for flaccid fever. The word denga, which signifies fever andhaemorrhages, isborrowedfromAfrica. The virus is typically transmitted through mosquito bites, specifically those from the Aedes Aegypti species. The rainy season is when this disease is most prevalent. DHF causes cutaneous and intestinal haemorrhages as a result of thrombocytopenia, hemoconcentration, hypovolumicchanges, and neurologic abnormalities. DHF causes focal haemorrhages, congestion that increases vascular permeability, oedema in a specific organ, coagulopathy with thrombocytopenia, and hemoconcentration intheorgansthat are affected by the virus. Serologic testing is used to detect it. Symptoms of DHF include severe malaise, high fever, and nausea, vomiting, athralgia, flushing, and severe abdominal pain. DHF NASAIDS PCM (antipyretic) and non- pharmacological treatment are also incorporated in the management of DHF. Key Words: NSAIDS, Thromobocytopenia, Haemorrhages, and Dengue fever. 1. INTRODUCTION The most prevalent arthropod infection, dengue fever, is brought on by the flaviviridae family.Feveristheresult1.The word "Denga" is an African word that signifies fever with haemorrhages and means fever. The virus that causes it is most frequently spread via the bite of the Aedes aegypti mosquito. This virus spreads most quickly during the rainy season, when mosquito populationsareattheirhighest2.Itis correlated with climatic and environmental factors and exhibits both geographical and temporal patterns3. Major routes run through the tropical and subtropical regions4. 1.1 Epidemiology: Dengue illness has afflicted 50 million people worldwide, with 20,000 deaths and 50,000 severe cases annually. For dengue fever, there is no vaccination available5. 1.2 DHF DHF is a severe kind of fever that is almost always deadly and is characterised by cutaneous and intestinal bleeding brought on by thrombocytopenia, hemoconcentration, hypovolemicshock,andneurological abnormalities.Children under the age of 15 are the most affected by it. Monocytes, lymphocytes, and endothelial cells in the blood are affected by dengue. It results in thrombocytopenia and complement activation, which together make up consumptive coagulopathy. This procedure moves forward considerably more quickly, taking only a few hours. Starting the appropriate treatment at this point will result in a rapid and significant recovery, but in untreated instances, dengue shock syndrome will develop, and death may result. PATHOLOGICAL CHANGES The DHF-affected organs exhibit specificchangesinthistype of fever, including focal haemorrhages, congestion that increases vascular permeability and results in oedema in particular organs,coagulopathywiththrombocytopenia,and hemoconcentration. DIAGNOSIS DHF is confirmed by immunofluorescence methods, monoclonal antibodies, rapid methods such reverse transcriptase-PCR and fluorogenic-ELISA, and serologic testing for the identification of antibodies6. 1.3 DENGUE FEVER Either a primary infection or a secondary infection results from dengue fever. Hyperpyrexia, severe headaches (especially in the retro-orbital area), athralgia, myalgia, anorexia, abdominal discomfort, and occasionally macular papular rashes are unanticipated symptoms. The fever can be biphasic7,8 and it lasts for 2–7 days. Coryza is particularly common in children and may be the primary symptom9. Dengue fever recovery canbeprolonged,especiallyinadults, although it can also be monotonous10. High temperature, severe headache (mostly in the retroorbital area), flushing, myalgia, athralgia, vomiting, anorexia, and abrupt stomach discomfort are all clinical signs of DHF11,12. Indicators of bleeding include nasal bleeding, gingivitis, bruises (ecchymosis), vomiting blood, dark blood in the stool, and spotting or menorrhagia in females. Indicators of plasma leakage include circulation abnormalities (low BP), quick heartbeat, and bruising, low pulse pressure, slow capillary refill time, pleural effusion, ascites, and occasionally pericarditis can lead to complications such as neurological diseases, brain disease (encephalopathy), brain inflammation, persistent liver failure, heart muscle inflammation, and consumptive coagulopathy.
2.
International Research Journal
of Engineering and Technology (IRJET) e-ISSN: 2395-0056 Volume: 10 Issue: 01 | Jan 2023 www.irjet.net p-ISSN: 2395-0072 © 2023, IRJET | Impact Factor value: 7.529 | ISO 9001:2008 Certified Journal | Page 829 Dengue Hemorrhagic Fever Although it can affect adults, DHF is primarily a condition of children under the age of 15. A number of vague signs and symptoms, including a sudden onset of fever that typically lasts 2 to 7 days, describe it. It might be challenging to identify DHF from dengue fever and othertropical infections during the acute stage of the illness. Measles, rubella, influenza, typhoid, leptospirosis, malaria, and other viral hemorrhagic fevers should be included in the differential diagnosis during the acute phase of the illness, any other illness that can manifest during the acute stage as an undifferentiated viral condition. Upper respiratory symptoms in children are usually caused by concomitant infections with several virusesandbacteria.Duringtheacute stage, there is no pathognomonic sign or symptom for DHF; however, when the fever subsides, distinctive signs of plasma leakage occur, often allowing for a precise clinical diagnosis. Defervescence is when DHF enters its critical stage,however symptoms of circulatory failure or hemorrhagic manifestations might appear up to 24 hours before or after the temperature reaches normal or below. Indicators of a vascular leak in the patient's blood include thrombocytopenia (platelet count, 100,000/mm3) and hemoconcentration compared to baseline. syndrome. Skin haemorrhages such petechiae, purpuric lesions, and ecchymoses are typical hemorrhagic symptoms. Less commonly, epistaxis, bleeding gums, GI haemorrhage, and hematuria happen. The tourniquet test, which shows that the patient's capillaries are more fragile, may aid the doctor in making a diagnosis. The most prevalent hemorrhagic symptom is scattered petechiae, which most frequently affects the limbs but can also affect the trunk, other body regions, and the face in those withseveredengue shock syndrome (DSS). Although purpuric lesions can develop everywhere in the body, they often occur where venipuncture is performed. Large ecchymotic lesions may form on the trunk and extremities in some individuals, whereas venipuncture sites in other patients may bleed actively, sometimes excessively. Patients who are more seriously unwell suffer GI bleeding. Although patients may experience extensive, open upper GI bleeding as well, frequently before to the start of shock, the classic hematemesis with coffee-ground vomitus and melena typically occurs after protracted shock. Without early detection and appropriate treatment, some patients experience shock from blood loss, which may be mild or severe. More commonly, shock is caused by plasma leakage; it may be mild and transient or progress to profound shock with undetectable pulse and blood pressure. Children with profound shock are often somnolent, exhibit petechiae on the face, and have perioral cyanosis. Patients with severe DHF or DSS typically experiencea fever and vague constitutional symptoms for a few days before their health abruptly deteriorates. The patient's skin may turn chilly, blotchy, and congested during, right before, or right after the temperature drop. Circumoral cyanosis is usually seen, and the pulse becomes weak andfast.Although some patients first seem sluggish, they quickly transition into a severe stage of shock after becoming restless. They typically feel severe stomach discomfort just before going into shock. All indications and symptoms disappear in people with moderate DHF quickly after the temperature goes down. However, the onset of fever may be followed by excessive sweating, slight variations in blood pressure and pulse rate, coldness in the extremities, and skin congestion. These alterations represent brief, minor circulatory disruptions brought on by plasma leakage. Usually, patients get well on their own or after receiving fluid and electrolyte treatment. Without proper care, patients who are in shock risk dying. The patient may pass away within 8 to 24 hoursofgoinginto shock, however recovery from shock is typically swift after receiving antishock treatment. With or without shock, convalescence for individuals with DHF is often brief and uncomplicated. Once the first shock has passed, even those with undetectable pulse and blood pressure will usually recover within 2 to 3 days. Leukopenia is typical, similar to dengue fever, and thrombocytopenia and hemoconcentration are ongoing observations in DHF and DSS. It is typical to find a platelet count of 100,000/mm3 between days 3 and 8 of sickness. In traditional DHF, hemoconcentration, a sign of plasma leakage, is usually always present, althoughitismoresevere in shock patients. Hepatomegaly is a typical, though not always present, finding. Most individuals with proven DHF and DSS have enlarged livers in various nations. Hepatomegalyinothernations,however,fluctuatesfrom one pandemic to another, suggesting that liver involvement might vary depending on the virus's strain and/or serotype. Elevated levels of liver enzymes are typical. An abrupt increase in vascular permeability that causes plasma to leak into the extravascular compartment, causing hemoconcentration and a dropinbloodpressure,isthemain pathophysiologic aberration found in DHF and DSS. Studies on plasma volume have revealed a drop of morethan20%in serious instances. Serous effusion discovered postmortem, pleural effusion shown on an X-ray, hemoconcentration,and hypoproteinemia are all supporting evidence of plasma leakage. Fatality rates can be reduced to 1% or less with early diagnosis, vigorous fluid replacement treatment, and competent nursing care. IndividualswithmoderateDHFand DSS can utilise normal saline or lactated Ringer's solution; however, patients with severe cases may require plasma or plasma expanders. Information on the efficient handling of DHF and DSS has previously been provided. Since there are no obvious destructive vascular lesions, it is likely that a short-acting mediator is to blame for the temporary functional vascular alterations. The extravasated fluid is
3.
International Research Journal
of Engineering and Technology (IRJET) e-ISSN: 2395-0056 Volume: 10 Issue: 01 | Jan 2023 www.irjet.net p-ISSN: 2395-0072 © 2023, IRJET | Impact Factor value: 7.529 | ISO 9001:2008 Certified Journal | Page 830 quickly reabsorbed when the patient is stabilised and starts to recover, which results in a decrease in the hematocrit. Vascular abnormalities, thrombocytopenia, and coagulation issues all contribute to hemostatic alterations in DHF and DSS. The majority of DHF patients have abnormal coagulograms, increased vascular fragility, and thrombocytopenia, all of which suggest disseminated intravascular coagulation.Concomitantthrombocytopenia,a prolonged partial thromboplastin time, a decreased fibrinogen level, and increased levels of fibrinogen degradation products are additional signs of disseminated intravascular coagulation. The majorityofpatients whopass away had GI bleeding, according to autopsies.21 1.4 LABORATORY FINDING S IN DHF Hematological analysis: Thrombocytopenia (100*109/L), abnormal lymphocytosis >15%, odd coagulation blood profile, drop in WBC quantity during early illness (extended activated partial thromboplastin time, prothrombin time, raised fibrinogen degradation products and lower serum complement range. Investigating biologically: acidosis, elevated liner enzymes, and hypoalbunemia13. PATHOGENESIS OF DHF Dengue can be caused by any of its viral serotypes, but when one is infected, it gives rise to future defence immunity against that serotype but not for others.Additionally,whena different serotype is infected for the second time, a more severe infection occurs. This is due to an occurrence known as antibody dependent enhancement, in which the antibody from one serotype infection amplifies infection with a different serotype14. While there is currently no proof that certain persons can cause symptoms of illness, active study has been done in this area. The dengue virus enters the human body by the bite of an infected person, where it replicates inside macrophages, monocytes, and B cells. Additionally, it is known that mast cells, dendritic cells, and endothelial cells can get infected15,16,17. The virus must mature for 7–10 days before it maystartaninfection.Patient exhibits signs of febrile illness during the viremia phase, which is followed by the leakage phase, which results in bleeding (DHF) for dengue shock syndrome. When viruses appear in plasma and reach maximal plasma level, the disease worsens18. Factors Responsible for the Increased Incidence Unprecedented worldwide population expansion and the ensuingunplannedandunregulatedurbanisation,particularly in tropical developingnations,havebeentwokeycontributing reasons. Unplanned urbanisation has resulted in subpar housing, overcrowding, and a decline in water, sewer, and waste management systems, which have created the perfect environment for increasing mosquito-borne disease transmission in tropical metropolitan areas. The absence of efficient mosquito control in places where dengue is endemic has been a third significant contributing factor.21 2. MANAGEMENT OF DENGUE FEVER Dengue fever and the febrile stage of DHF are closely associated in terms of control. PCM is the only antipyretic that is intended, unlike NSAIDS like aspirin and diclofenac sodium might cause GI bleeding or cause gastrointestinal discomfort. If the fever continues to be high after the administration of PCM, teped, sponging is indicated as the progression to hepatic damage associatedwithdenguevirus infection may be worse. The dose of PCM (60 mg/kg/day) should not be increased. If a soft diet is refused, non- pharmacological therapy is indicated, such as switchingoral rehydration solution. Cimetidine is prescribed to patients who have stomach bleeding or a low platelet count. Domperidone, an antiemetic, is used to treat vomiting.Exceptforpatientswith severe vomiting or dehydration, IV fluid management is not advised for patients in the febrile phase. Platelet count and packed cell volume should be performed daily as soonasthe fever starts on the third day in order to determine if the patient is entering the plasma leaking phase or not. Significant plasma loss is defined as platelet count 100*109/L and an increase in packed cell volumeof>20%19. The following is the Halliday and Segar formula for the fluid demand in DHF20: • Body weight under 10 kg: 100 mg/kg • Body weight between 10 and 20 kg: 1000 ml plus 50 ml for each kg over 10 kg • For body weights of 20 kg or more, add 20 ml to 1500 ml. 2.1 Vaccine Development The first candidate dengue vaccines were developed shortly after the viruses were first isolated by Japanese and American scientists. Despite considerable work over the years, an effective safe vaccine was never developed. The World Health Organization designated the developmentofa tetravalent dengue vaccine a priority for the most cost- effective approach to dengue prevention. Effective vaccination to prevent DHF will most probably require a tetravalent vaccine, because epidemiologic studies have shown that preexisting heterotypicdengueantibodyisa risk factor for DHF. In recent years, significant work has been made in creating a vaccine for dengue and DHF withthehelp of the World Health Organization. Phase I and II studies in Thailand have examined promising candidate attenuated
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International Research Journal
of Engineering and Technology (IRJET) e-ISSN: 2395-0056 Volume: 10 Issue: 01 | Jan 2023 www.irjet.net p-ISSN: 2395-0072 © 2023, IRJET | Impact Factor value: 7.529 | ISO 9001:2008 Certified Journal | Page 831 vaccine viruses in monovalent, bivalent, trivalent, and tetravalent formulations. The tetravalent vaccine formulation is presently conducting follow-up phase I trials in the United States, and a commercializationagreement has been struck. A current evaluation of the live attenuated dengue vaccine's development is available.21 CONCLUSION Reviewing dengue hemorrhagic fever's impact on public health, which has made it one ofthe mostprevalentillnesses, is the key goal. This review article is concerned with different clinical manifestations, diagnoses, and effective treatment strategies. The development of a vaccine and an antiviral medication regimen are the next directions in the fight against this terrible illness. REFERENCES 1. Murthy JM, Rani PU. Biological activity of certainbotanical extracts as larvicides against the yellow fever mosquito, Aedes aegypti L. J Biopest. 2009; 2:72-76. 2. Mohan Harsh, Dengue hemorrhagic fever. 5th edition of textbook of pathology, Jaypee Brothers Medical publishers (P) LTD New Delhi2005 ;190. 3. Vanessa Racloz , Rabecca Ramsey , Shilv Tong , Wenbiao HU . Surveillance of dengue fever virus: A Review of Epidemiological Models and Early Warning systems. 2012. doi:10.137/journal. pntd. 0001648 . 4. Dengue fever treatment with carica Papaya leavesextract, Asian Pac. J Trop Bioned , 2011 August ;1(4); 330-333 . 5. Shu - Wen Wan, Robert Anderson, Chiou- Feng Lin. Current progress in dengue vaccines. Journal of Biomedical Science 2013, 20:37 doi : 10 .1180/ 1423- 0127- 20-37. 6. Mohan Harsh, Dengue hemorrhagic fever. 5th edition of textbook of pathology, Jaypee Brothers Medical publishers (P) LTD New Delhi 2005 ;190-191. 7. Ahmed FU, Mahmood CB, Sharma JD, et al . Dengue fever and dengue haemorraghic fever in children the 2000 outbreak in Chittatong , Bangladesh . Dengue Bulletin 2001; 39:1027-33. 8. Narayanan M, Arvind MA, Thilothammal N , et al . Dengue fever epidemic in Chennai – a study of clinical profile and outcome. India Pediatr2002; 39:1027-33 . 9. Hongsisriwon S. Dengue hemorrhagic fever in infants. Southeast Asian J Trop Med Public Health 2002; 33:49-55. 10. WHO .Prevention and control of dengue and dengue hemorrhagicfever:comprehensiveguideline.WHORegional publication, SEARO No 29 1999. 11. Mendez A, Gonzalez G. Dengue hemorrhagic fever in children: ten years of clinical experience . Biomedica 2003; 23:180-93. 12. Srivastava VK, Suri S, Bhasin A, et al. An epidemic of dengue hemorrhagic fever and dengue shock syndrome in Delhi : a clinical study . Ann Trop Paediatr 1990; 10:329-34. 13. Kalayanarooj S, Vaughn DW, Nimmannitya S, et al. Early clinical and laboratory indicator of acute dengue illness. J Infect Dis1997; 176:313-21. 14. Guzman MG, Kouri G. Dengue : an update. Lancet Infect Dis2002; 2:33-42. 15. King CA , Marshall JS, Alshurafa H, et al. Release of vsoactive cytokines by antibody- enhanced dengue virus infection of a human mast cell /basophil line . J virol2000; 74:7146-50. 16. Ling Jun Ho, Wang JJ, Shaio MF, et al. Infection of human dendritic cells by dengue virus causes cell maturation and cytokine production. J Immunol2001; 166:1499-506. 17. Huang YH, Lei HY, Liu HS, et al. Dengue virus infects human endothelial cells and induces IL-6 and IL-8 production. Am J Trop Med Hyg2000; 63:71-5. 18. Libraty DH, Young PR, Pickering D, et al. High circulating levels of dengue virus nonstructural protein NS1 early in dengue illness correlate with the development of dengue hemorrhagic fever. J Infect Dis2002; 186:1165-8. 19. Workshop on case management of dengue hemorrhagic fever, June 2002, Bangkok, Thailand. 20. Halliday MA, Segar WE. Maintenance need for water: in parenteral fluid therapy. Pediatrics1957;19:823. 21. Gubler DJ. Dengue and dengue hemorrhagic fever. Clin Microbiol Rev. 1998 Jul;11(3):480-96. doi: 10.1128/CMR.11.3.480.PMID:9665979;PMCID:PMC88892.
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