The document discusses dengue virus, its transmission and clinical manifestations. Some key points:
- Dengue virus is transmitted by Aedes aegypti mosquitoes and has 4 serotypes. It causes dengue fever and the more severe dengue hemorrhagic fever/dengue shock syndrome.
- The disease progresses through febrile, critical, and recovery phases. During the critical phase, plasma leakage and bleeding can cause shock.
- Symptoms range from mild fever to severe bleeding, organ impairment and shock. Thrombocytopenia is common.
- Diagnosis is based on clinical criteria and confirmed with serology, antigen or PCR testing. There is no vaccine and treatment focuses
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Dengue (pronounced DENG-gay) can affect anyone but tends to be more severe in people with compromised immune systems. Because it is caused by one of four serotypes of virus, it is possible to get dengue fever multiple times. However, an attack of dengue produces immunity for a lifetime to that particular serotype to which the patient was exposed.
A mosquito-borne viral disease occurring in tropical and subtropical areas.
Spreads by animals or insects
Requires a medical diagnosis
Lab tests or imaging often required
Short-term: resolves within days to weeks
Those who become infected with the virus a second time are at a significantly greater risk of developing severe disease.
Symptoms include high fever, headache, rash and muscle and joint pain. In severe cases there is serious bleeding and shock, which can be life threatening.
Treatment includes fluids and pain relievers. Severe cases require hospital care.
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Dengue (pronounced DENG-gay) can affect anyone but tends to be more severe in people with compromised immune systems. Because it is caused by one of four serotypes of virus, it is possible to get dengue fever multiple times. However, an attack of dengue produces immunity for a lifetime to that particular serotype to which the patient was exposed.
A mosquito-borne viral disease occurring in tropical and subtropical areas.
Spreads by animals or insects
Requires a medical diagnosis
Lab tests or imaging often required
Short-term: resolves within days to weeks
Those who become infected with the virus a second time are at a significantly greater risk of developing severe disease.
Symptoms include high fever, headache, rash and muscle and joint pain. In severe cases there is serious bleeding and shock, which can be life threatening.
Treatment includes fluids and pain relievers. Severe cases require hospital care.
A mosquito-borne viral disease occurring in tropical and subtropical areas.
Those who become infected with the virus a second time are at a significantly greater risk of developing severe disease.
Symptoms include high fever, headache, rash and muscle and joint pain. In severe cases there is serious bleeding and shock, which can be life threatening.
Treatment includes fluids and pain relievers. Severe cases require hospital care.
As an intern house officer, I prepared this presentation after I came across a rare case of dengue fever complicated by hemophagocytic lymphohistiocytosis (HLH). Dengue fever itself is a rare disease entity in the UAE, as a developed country; and the presence of such a complication merely added to the complexity of the diagnosis. Therefore, I am delighted to share this lively PowerPoint Presentation about dengue, which was initially supplemented with an interesting case presentation but was removed for confidentiality purposes when sharing the document. I hope you enjoy it!
PS: Use the slideshow button in Microsoft PowerPoint for the best experience.
Dengue virus rarely causes death. However, the infection can progress into a more serious condition known as severe dengue or dengue hemorrhagic fever. Symptoms of dengue hemorrhagic fever include: bleeding under the skin. frequent vomiting.
Dengue fever is the fastest emerging arboviral infection spread
by Aedes mosquitoes with major public health consequences in
over 100 tropical and sub-tropical countries in South-East Asia,
the Western Pacific, and South and Central America. Up to 2.5
billion people globally live under the threat of dengue fever and its
severe forms—dengue hemorrhagic fever (DHF) or dengue shock
syndrome (DSS). More than 75% of these people, or approximately
1.8 billion, live in the Asia-Pacific Region. As the disease spreads to
new geographical areas, the frequency of the outbreaks is increasing
along with changing disease epidemiology. It is estimated that 50
a million cases of dengue fever occur worldwide annually and half a
million people suffering from DHF require hospitalization each year,
a very large proportion of whom (approximately 90%) are children
less than five years old. About 2.5% of those affected with dengue
die of the disease.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. Virus
Is an arbovirus composed of single-stranded RNA
Has 4 serotypes (DEN-1, 2, 3, 4)
3. Vector
• Is an arbovirus composed of single-stranded RNA
• Has 5 serotypes (DEN-1, 2, 3, 4 and 5)
• Transmitted by mosquitoes of the Stegomyia family,
• Aedes aegypti, a daytime biting mosquito,
4. Aedes aegypti
• Dengue transmitted by infected female
mosquito
• Primarily a daytime feeder
• Lives around human habitation
• Lays eggs and produces larvae preferentially in
artificial containers
5. Replication and Transmission
of Dengue Virus
1. Virus transmitted to human
in mosquito saliva
2. Virus replicates
target organs
3. Virus infects white
blood cells and
lymphatic tissues
4. Virus released and
circulates in blood
3
4
1
2
Infectivity Period
(about 7 days)
Extrinsic Incubation
Period (8–12 days)
Intrinsic Incubation
Period (3–14 days)
6. Replication and Transmission
of Dengue Virus (Part 2)
5. Second mosquito
ingests virus with blood
6. Virus replicates
in mosquito midgut
and other organs,
infects salivary
glands
7. Virus replicates
in salivary glands
6
7
5
7. Modes of Transmission
Mosquito bite
Perinatal transmission
Blood transfusion
Organ transplantation
Needle stick injury or
laboratory accident
8. Vertical transmission &
Neonatal dengue infection
Incidence 1.6 - 64%
peripartum maternal infection may increase the likelihood of
symptomatic disease in the newborn
Antibodies to the dengue virus in the dengue infected mother can cross
the placenta and can cause severe dengue in newborn infants
Clinical:
• Mild illness such as fever with petechial rash, thrombocytopenia and
hepatomegaly, to severe illness with pleural effusion, gastric bleeding, circulatory
failure, massive intracerebral haemorrhage
9. Case Definition
Dengue Fever:
An acute febrile illness of 2-7 days duration with
two or more of the following manifestations:
Headache, retro-orbital pain, myalgia, arthralgia,
rash, haemorrhagic manifestations.
10. Case Definition
Probable DF/DHF:
A case compatible with clinical description of dengue Fever during
outbreak:
OR
Non-ELISA based NS1 antigen/ IgM positive.
(A positive test by RDT will be considered as probable due to poor
sensitivity and Specificity of currently available RDTs.)
11. Case Definition
Confirmed dengue Fever:
A case compatible with the clinical description of dengue fever with at
least one of the following
• Isolation of the dengue virus (Virus culture +VE) from serum, plasma,
leucocytes.
• Demonstration of IgM antibody titre by ELISA positive in single serum
sample.
• Demonstration of dengue virus antigen in serum sample by NS1-ELISA.
• IgG seroconversion in paired sera after 2 weeks with Four fold increase of
IgG titre.
• Detection of viral nucleic acid by polymerase chain reaction (PCR).
12. Grading of DF/DHF (old)
DF: Fever of 2-7 days with two or more of following- Headache, Retro orbital pain,
Myalgia,
Arthralgia with or without leukopenia, thrombocytopenia and no evidence of plasma
leakage.
DHF II Above plus some evidence of spontaneous bleeding in skin or other organs (black
tarry stool, epistaxis, gum bleeds) and abdominal pain.
Thrombocytopenia with platelet count less than 100000/ cu.mm and Hct rise more
than 20% over baseline.
DHF III
(DSS):
Above plus circulatory failure (weak rapid pulse, narrow pulse pressure < 20 mm
Hg, Hypotension, cold clammy skin, restlessness).
Thrombocytopenia with platelet count less than 100000/ cu.mm and Hct rise more
than 20% over baseline.
DHF IV
(DSS):
Profound shock with undetectable blood pressure or pulse. Thrombocytopenia with
platelet count less than 100000/ cu.mm and Hct rise more than 20% over baseline
13. Dengue Epidemiology - WHO
• Dengue is now endemic in over 100 countries.
• As many as 3.6 billion people
• 40% of the world's population, reside in dengue-endemic areas.
• Each year, 400 million people are infected with dengue virus,
• 100 million become ill with dengue
• 21,000 deaths attributed to dengue are detected.
• Early identification of cases and timely initiation of correct clinical
management can reduce the case fatality rate from 10% to 1%.
14. Pathogenesis
• Circulation of infection‐enhancing antibodies at the time of
infection e strongest risk factor for development of severe disease.
• Rapid activation of the complement system.
• Capillary damage ‐ internal redistribution of fluid, resulting in
• hemoconcentration,
• hypovolemia,
• increased cardiac work,
• tissue hypoxia,
• metabolic acidosis, and
• hyponatremia.
15. Pathogenesis of Severe Dengue
Antibody-dependent enhancement (ADE)
• Occurs when nonneutralising antiviral antibodies enhance viral entry
into host cells. Once inside the white blood cell, the virus replicates
undetected, eventually generating very high virus titers leading to
more severe disease .
• In Dengue - nonneutralizing heterotypic IgG anti-DENV antibodies
produced during a person's first DENV infection (or sub-neutralizing
level of antibodies in the case of infants who acquired IgG passively
in utero) can form antibody-DENV complexes in the second
infection that can allow uptake of DENV by macrophages.
• DENV then replicates in these macrophages thereby increasing viral
production.
19. Dengue viral infection
Symptomatic Asymptomatic
Mild Moderate Severe
A. Undifferentiated
DF
B. Fever without
complication like
bleeding,
hypotension and
organ
involvement
C. Without evidence
of capillary
leakage
Home Management
DF with high risk and
comorbid conditions
DF with warning signs and
symptoms
• Infants
• Old age
• Diabetes
• Hypertension
• Pregnancy
• CAD
• Hemoglobinopathies
• Immunocompromized
patient
• Patient on steroids,
anticoagulants or
immunosuppressants
A. DF warning signs and
symptoms
• Recurrent vomition
• Abdominal pain/tenderness
• Generalized weakness /
letharginess / restless
• Mild pleural effusion /
ascites
• Hepatomegaly
• Increased Hct > 20%
B. DHF I & II with minor
bleeds
A. DF/DHF with significant
hemorrhage
B. DHF with shock (DHF III &
IV – DSS)
C. Severe organ involvement
(Expanded dengue
syndrome)
D. Severe metabolic disorder
Choose Monitoring and possibly Hospitalization Tertiary level care
2009 Dengue
Case Definitions
22. CRITERIA FOR DENGUE ± WARNING SIGNS
• Nausea, vomiting
• Rash
• Aches and pains
• Tourniquet test positive
• Leukopenia
Any warning sign
Warning signs*
23. CRITERIA FOR SEVERE DENGUE
• Shock
Severe plasma leakage - leading to:
• as evaluated by clinician
Severe bleeding
• Liver: AST or ALT >=1000
• CNS: Impaired consciousness
• Heart and other organs
Severe organ involvement
25. The course of dengue illness
1. Febrile Phase
2. Critical Phase
3. Recovery Phase
26. The course of dengue illness
Febrile Phase
- Dehydration
- High fever
- Neurological
disturbances & febrile
seizures in young children
Critical Phase
- Shock from plasma
leakage;
- Severe haemorrhage;
- Organ impairment
Recovery Phase
- Hypervolaemia
- Worsening effusions
- Acute pulmonary
edema
Probable adverse events
27. Febrile Phase of Dengue
Typical duration
of 0–7 days
Biphasic fever
possible
Monitoring
for defervescence
and warning signs
crucial to identify
progression into
the critical phase.
Defervescence
occurs between
day 3 and day 8 of
the illness.
28. Febrile Phase of Dengue
Abrupt onset of high temperature + any of the
following:
• Severe headache
• Retro orbital pain
• Myalgia
• Arthralgia
• Transient macular or maculopapular rash
• Minor hemorrhagic manifestations, for
example petechiae, ecchymosis,
purpura, epistaxis, bleeding gums, hematuria,
or a positive tourniquet test
• Facial flushing or erythema
• Injected oropharynx
• Anorexia
• Some persons with dengue may only have fever
Laboratory findings
• Leukopenia
• Mild to moderate thrombocytopenia
• h aspartate aminotransferase (AST)
• h alanine aminotransferase (ALT)
• Hyponatremia
29. Febrile Phase – Medical Complications
Dehydration
Hyponatremia
Febrile seizures in young children
Neurologic disease manifestations,
including encephalitis and aseptic meningitis
30. Critical Phase – Clinical Manifestations
Rapid decline in platelet count with a rise in hematocrit (HCT)
Leukopenia up to 24 hours before platelet drop is recognized
Presence of warning signs for severe disease
Warning signs
• Clinical fluid accumulation, such
as ascites, pleural effusion
• Liver enlargement > 2 cm
• Severe abdominal painPersistent
vomiting (at least 3 vomiting
episodes within 24 hours)
• Mucosal bleed
• Lethargy or restlessness
31. Bleeding Manifestations in Patients with Dengue
Mild hemorrhagic manifestations (in 1/3 cases)
• petechiae,
• purpura,
• epistaxis, and
• gingival bleeding Might be due to increased capillary fragility as a
result of thrombocytopenia or platelet dysfunction.
Major mucosal bleeding
• gastrointestinal or vaginal - in dengue patients can be occult and is often
associated with prolonged shock and metabolic acidosis.
32. Causes of Bleeding in DF/DHF
• Abnormal coagulogram
• Thrombocytopenia
• Platelet dysfunction •
• Prothombin complex deficiency
secondary to Liver involvement
• Endothelial injury
• DIC and Prolong aPTT
• Decrease fibrinogen level
• Increase level of fibrinogen
degradation product (FDP)
• Increase level of D-Dimer
• Consumptive coagulopathy
(activation of mononuclear
phagocytes)
• Sequestration of platelets
33. Coagulopathy
Due to loss of essential coagulation proteins due to plasma
leakage.
Interactions between dengue virus nonstructural protein 1 (NS1)
and the endothelial glycocalyx layer may cause a change in
filtration characteristics, resulting in leakage of plasma proteins
and release of heparan sulfate into the circulation.
Heparan sulfate, which can function as an anticoagulant, might
contribute to the coagulopathy
34. Thrombocytopenia
Thrombocytopenia is defined by the World Health Organization
(WHO) as a platelet count of less than or equal to 100,000/μL.
Causes
• Early pancytopenic suppression of the bone marrow either by direct
infection of progenitor cells or by macrophages that activate T-cells that
release cytokines that suppress hematopoeisis.
• Peripheral immune mediated platelet destruction via dengue virus binding
to platelet in presence of NS1 antibody, so that the half-life of platelets
are decreased in dengue patients.
• DIC
• Peripheral sequestration of platelets
35. Dengue virus infection
Production of
antibodies/presence of
enhancing antibodies
Antigen antibody reaction
with complement
activation
Deposition on vessels,
various tissues and
platelets
Clinical manifestations of
coagulopathy (bleeding)
Activation of T- cells
Production of various
chemical mediators
Increased vascular
permeability
Clinical manifestations of
vasculopathy (capillary
leakage)
• Hypotension/shock
• Pleural effusion
• Ascites
• Bleeding
• Organ involvement
Patho-physiology
of DF/DHF
36. Clinical Features of of DF/ DHF
• Undifferentiated dengue Fever (UDF)
• Severe dengue Fever
• Dengue Fever with warning signs and symptoms:
• Expanded dengue Syndrome (EDS)
37. Critical Phase – Lab Findings and Medical Complications
Laboratory findings
• Increase in HCT or hemoconcentration
• Moderate to severe thrombocytopenia
• Leukopenia
• Transient increase in activated partial-
throboplastin time (aPTT) with decrease
in fibrinogen
Medical complications during the critical
phase include the following:
• Hypovolemic shock from plasma leakage
• End organ impairment due to prolonged shock
• Severe hemorrhage
• Encephalopathy
38. Recovery Phase of Dengue
Patient improvement
Gradual reabsorption of extravasated fluid (such as from plasma leakage)
over 48–72 hours
Increased diuresis (patient might wet bed)
Hemodynamic status stabilizes
Patient can temporarily become bradycardic (but hemodynamically stable)
39. Recovery Phase - Clinical Manifestations
A second rash that might be macular or
erythematous with small circular
islands of normal, unaffected skin.
This convalescent rash can be very
pruritic and desquamate.
Severe fatigue
Laboratory findings
• HCT stabilizes or is slightly lower due to a dilutional
effect of reabsorbed plasma (hemodilution)
• White blood count (WBC) begins rising soon after
defervescence
• Platelet count increases following WBC recovery
40. Recovery Phase - Medical Complications
Hypervolemia and acute pulmonary edema can occur if intravenous fluid
(IVF) therapy has been excessive or extended too long.
Organ impairment can result in the event of prolonged
or refractory shock. This might include ischemic hepatitis and hepatic
encephalopathy.
Nosocomial or hospital-acquired infections, can occur, especially in
infants and elderly patients.
41. Causes of Death
Unrecognized dengue without appropriate medical
management
Unrecognized or prolonged shock
Unrecognized occult hemorrhage
Fluid overload
Nosocomial infections
Liver failure
43. Tourniquet Test
1. Take the patient's blood pressure and
record it, for example, 100/70.
2. Inflate the cuff to a point midway between
SBP and DBP and maintain for 5 minutes.
3. Reduce and wait 2 minutes.
4. Count petechiae below antecubital fossa.
A positive test is 10 or more petechiae per
1 square inch.
• More likely to be positive near time of defervescence
• Less likely to be positive in patients with shock
Pan American Health Organization: Dengue and Dengue Hemorrhagic Fever: Guidelines for
Prevention and Control. PAHO: Washington, D.C., 1994: 12.
44. Lab tests
Antigen NS1 test
ELISA- IgG, IgM antibodies
Blood cultures- isolate the virus
Full blood count
Hct
Liver function test
PCR- Nucleic acid detection
45.
46. Dengue diagnostic and sample characteristics
Clinical sample Diagnostic method Methodology Time to results
Virus
detection
and its
components
Acute serum (1-
5 days of fever)
and necropsy
tissue
Viral isolation Mosquito or mosquito cell
culture inoculation
One week or more
Nucleic acid
detection
RT-PCR and real time RT-
PCR
1 to 2 days
Antigen detection NS1 Ag rapid tests Minutes
NS1 Ag ELISA 1 day
Immuno-histochemistry 2-5 days
Serological
response
Paired sera
(acute serum 1-
5 days and 2nd
serum 15-21
days after)
IgM or IgG
seroconversion
ELISA
HIA
1-2 days
Neutralization test Min 7 days
Serum after day
5 of fever
IgM detection
(recent infection)
ELISA 1 or 2 days
Rapid tests Minutes
IgG detection IgG ELISA
HIA
1 or 2 days
47. Interpretation of dengue diagnostic tests
[adapted from Dengue and Control (DENCO) study]
Highly suggestive Confirmed
One of the following:
1. IgM +ve in a single serum
sample
2. IgG +ve in a single serum
sample with a HI titre of
1280 or greater
One of the following:
1. PCR +
2. Virus culture +
3. IgM seroconversion in
paired sera
4. Four fold IgG titer increase
in paired sera
50. Step I 1. History, including information on symptoms, past medical & family
history
2. Physical examination, including full physical and mental
assessment
3. Investigation, including routine laboratory and dengue-specific
laboratory
Step II Diagnosis, assessment of disease phase and severity
Step III 1. Disease notification
2. Management decisions.
Depending on the clinical manifestations and other circumstances,
patients may:
– be sent home (Group A);
– be referred for in-hospital management (Group B);
– require emergency treatment and urgent referral (Group C).
A stepwise approach to the management of dengue
51. Patient Assessment Steps
Step 1
• History Taking
Step 2
• Clinical Examination
Step 3
• Investigation
Step 4
• Diagnosis, phase of disease and severity
52. Patient Assessment Steps
Step 1 : History Taking
• Date of onset of fever
• Symptoms and severity
• Three Golden questions
• How much fluid intake: Quantity and quality
• How much urine output: Frequency, volume and time of most
recent voiding?
• What activates could the patient do during the illness
53. Patient Assessment Steps
Step 1 : History Taking
• Other fluid losses: diarrhoea, vomiting
• Present of Warning Signs
• Family or neighbour with dengue OR travel to dengue-endemic
area
• Risk Factors
• Infancy, pregnancy, obesity, diabetes mellitus, hypertension, etc.
54. Patient Assessment Steps
Step 2: Clinical Assessment
General Assessment:
• Mental state
• Hydration state
• Hemodynamic state
Clinical e/o. warning signs
• Bleeding manifestations: mucosal
bleeding
• Abdominal tenderness
• Liver enlargement
• Fluid accumulation,: pl effusion,
ascites
Other imp signs:
• Rash
• Tachypnoea/acidotic
breathing: indicates shock
• Torniquet test: repeat if –
ve
57. Parameters Stable condition Compensated shock
Conscious level Clear and lucid Clear and lucid
Capillary refill
time
Brisk(less than 2 sec) Prolonged (>2 sec)
Extremities
(color, temp)
Warm and pink Cold peripheries
Peripheral
Pulse volume
Good volume
Weak & thready
Heart rate
(HR)
Normal HR for age Tachycardia for age
Pulse pressure
(PP)
Normal PP for age Normal systolic pressure
Rising diastolic pressure
Blood pressure
(BP)
Normal BP for age Narrowing of PP
Postural hypotension
Respiratory rate
(RR)
Normal RR for age
‘Quiet tachypnea’
Urine output
Normal Reducing trend
Normal brain function
Reduced kidney perfusion
Tissue acidosis
Reduced
Peripheral
perfusion
Reduced cardiac
output
58.
59.
60.
61. Parameters Stable condition Compensated shock Hypotensive shock
Conscious level Clear and lucid Clear and lucid Restless, combative
Capillary refill
time
Brisk(less than 2 sec) Prolonged (>2 sec) Very prolonged, mottled skin
Extremities
(color, temp)
Warm and pink Cold peripheries Cold and clammy
Peripheral
Pulse volume
Good volume
Weak & thready Feeble or absent
Heart rate
(HR)
Normal HR for age Tachycardia for age
Severe tachycardia or
bradycardia in late shock
Pulse pressure
(PP) Normal PP for age Normal systolic pressure
Rising diastolic pressure
Hypotension
Unrecordable BP
Blood pressure
(BP)
Normal BP for age Narrowing of PP
Postural hypotension
Narrowed pulse pressure
(< 20 mm Hg)
Respiratory rate
(RR)
Normal RR for age
‘Quiet tachypnea’ Kussamal breathing
Urine output
Normal Reducing trend
Oliguria or
anuria
Reduced brain function
Reduced
Peripheral
perfusion
No kidney perfusion
Severe tissue acidosis
Reduced
cardiac
output
62. Definition of hypotension
Adults:
• Systolic blood pressure of < 90 mm Hg or
• Meal arterial pressure < 70 mm Hg or
• Systolic blood pressure decrease of > 40 mm Hg or
• < 2 SD below normal for age (Hypertensive patients)
Children upto 10 year of age:
• The 5th centile for systolic pressure
• 70 + (age in years X 2) mm HG
63. Pearls in clnical examination of dentue patients
The “5-in-1 maneuver” magic touch – CCTV-R
Hold patient’s hand to evaluate peripheral perfusion
Save life in 30 seconds by recognizing shock
1
Color
2
Capillary
refill
3
Tempera
ture
4
Pulse
Volume
5
Pulse
Rate
65. Group A
Outpatient Management
During the febrile phase (may last 2–7 days) and subsequent
critical phase (1–2 days), your clinic should
• Follow CBCs
• Watch for dehydration Watch for warning signs, including
decreasing platelet count and increasing hematocrit
• Watch for defervescence (beginning of critical phase)
66. Group A
Advise patient or their family to do the following
Control the fever
Prevent dehydration
Prevent spread of dengue within your house
Watch for warning signs as temperature declines 3 to 8 days after
symptoms began.
• Severe abdominal pain or persistent vomiting
• Red spots/patches on skin
• Bleeding from nose or gums
• Vomiting blood, Black, tarry stools
• Drowsiness or irritability
• Pale, cold, or clammy skin
• Difficulty breathing
67. Group B - Pts with Waning Signs
Admit
Obtain baseline
CBC
Monitor fluid I/O
Encourge oral fluids
Monitor vital sings q4h
Adequate?
• Check Hct
• IV fluids (NS.RL)
• 5-7 ml/kg/hr for 1-2 hrs
• 3-5 ml/kg/hr for 2-4 hrs
• Keep monitoring
• Check Hct
• Observe for shock,
warning signs of severe
dengue
• Group C management
If NO improvement or
Compensated or Hyootensive shock
If improvement - YES
• Reduce isotonic crystalloids
in stepwise manner
1. 5–10 ml/kg/hour for 1–2 hours
2. 3–5 ml/kg/hour for 2–4 hours
3. 2–3 ml/kg/hour for 2–4 hours
68. Group B - Pts with Waning Signs
Some patients in Group B have warning signs and are
hemoconcentrated but are not in shock. If they are in shock, they are in
group C. Before giving them IVFs, obtain a reference or baseline HCT.
Follow the algorithm below.
• Give isotonic IVFs at 5–7 mL/kg/hr.
• Reduce after 1–2 hours to 3–5 mL/kg/hr for 2–4 hours if clinical status allows and reassess the
patient’s condition (vital signs, capillary refill, urine output).
• Repeat the HCT.
• If the HCT remains the same or rises minimally, reduce rate to 2–3 mL/kg/hr for 2–4 hours, then
reassess HCT.
• If vital signs worsen and HCT rapidly rises, increase rate to 5–10 mL/kg/hr for 1–2 hours.
• Reassess the clinical status; repeat HCT and revise IVF rates accordingly.
69. Initiate Intravenous therapy @ 10ml/kg over 1 hour
Reassess Clinical Status
Reduce IV fluids stepwise
6ml/kg/hr for 2-4 hours
3 ml/kg/hr for 2-4 hours
3-1.5 ml/kg/hr for 2-4 hrs
Further improvement
If worsening 10-20
ml/kg for 1 hour
If improvement after 2nd bolus, reduce
to 7-10 ml/kg for 1-2 hours
If no improvement & if HCT decreases > blood
transfusion
Group C - Pts with Compensated Shock
HDHF Grades I & II
Hemodynamic status improved
Discontinue IV after 24-48 hr
Hemorrhagic tendencies, thrombocytopenia, Hct rise > 20%
70. Check Hematocrite
Improvement
Crystalloid/Colloid
10 ml/kg for 1 hr, then reduce to
o 5-7 ml/kg 1-2 hrs
o 3-5 ml/kg/hr for 2-4 hrs
o 2-3 ml/kg/hr for 2-4 hrs
If Hct increases or is high
adm 3rd bolus fluid (colloid)
10-20 ml/kg over 2 hrs
HCT decreasing
Consider significant
occult /overt bleed
Initiate blood transfusion
HCT increasing or high
Adm 2nd bolus fluid
(colloid) 10-20 ml/kg
over ½ to 1 hr
No improvement
Yes No
Stop
After
48 hrs
Group C - Pts with Hypotensive Shock
Fluid resuscitation with 20 ml/kg over 15 minutes isotonic crystalloid or colloid
71. Targets of fluid resuscitation
Improving central and peripheral circulation
• Decreasing tachycardia
• Improving BP and pulse volume
• Warm and pink extremities with a capillary refill
• time < 3 seconds
Improving end-organ perfusion
• Achieving a stable conscious level (more alert or less restless)
• Urine output ≥ 0.5 ml/kg/hour
• Decreasing metabolic acidosis.
72. Points to remember in fluid resuscitation
1) No hypotonic fluids.
2) Cautious with glucose containing fluids like DNS.
3) Targeting a minimally acceptable hourly urine output (0.5–1 mL/kg/hr) is an
effective and inexpensive monitoring modality.
4) A urine output of more than 1.5–2 mL/kg/hr should prompt reduction in fluid
infusion rates, provided hyperglycemia has been ruled out.
5) In case of persistent shock, after fluid resuscitation, if the hematocrit
continues to decline, internal bleeding should be suspected.
6) Blood transfusion is life-saving and should be given as soon as severe
bleeding is suspected or recognized.
7) Do not wait for the haematocrit to drop too low before deciding on blood
transfusion.
8) Prefer fresh blood.
9) Use Ideal Body Weight to calculate IV fluid rates in Obese children.
73. WHEN TO STOP INTRAVENOUS FLUIDS
Features of intra vascular compartment overload •
• Hypertension with good volume pulse.
• Breathing difficulties, pulmonary edema.
48 hours after defervescence.
74. Management of Dengue Patient - Summary
GROUP-A GROUP-B GROUP-C
Give anticipatory guidance prior
to sending patient home (Refer
to patient handout)
Admit patient to hospital In addition to Group B
management, do the following:
Follow-up daily Monitor hemodynamic status
frequently
Use colloids for refractory shock
Do serial CBCs Use HCT to determine
interventions
Monitor for occult bleeding
Identify warning signs early Use isotonic IVFs judiciously
Correct metabolic acidosis and
electrolyte abnormalities as
needed
*Do not use prophylactic platelet transfusions.
75. Discharge criteria
(all of the following conditions must be present)
Clinical • No fever for 48 hours.
• Improvement in clinical status
• general well-being,
• appetite,
• haemodynamic status,
• urine output,
• no respiratory distress
Laboratory • Increasing trend of platelet count.
• Stable haematocrite without intravenous fluids.
76. Dengue Vaccine?
No licensed vaccine at present
Effective vaccine must be tetravalent
Field testing of an attenuated tetravalent vaccine currently
underway
Effective, safe and affordable vaccine will not be available
in the immediate future
77. • Avoid mosquito bites when traveling in tropical areas:
• Use mosquito repellents on skin and clothing.
• Wear long-sleeved shirts and long pants tucked into socks.
• Avoid heavily populated residential areas.
• When indoors, stay in air-conditioned or screened areas.
• Use bednets if sleeping areas are not screened or air-conditioned.
• If you have symptoms of dengue, report your travel history
• Eliminate mosquito breeding sites in areas where dengue might occur:
• Eliminate mosquito breeding sites around homes.
• Discard items that can collect rain or run-off water, esp. old tires.
• Regularly change the water in outdoor bird baths and pet and animal
water containers.
Prevention