dengue management
TRANSCRIPT
DENGUE
Presented by:Lt SaroshDengue – derived from Swahili ki denga pepo
CASE DEFINITION
A probable case is an acute febrile illness with 2 or more following features:• Headache• Retro orbital pain• Myalgia• Arthralgia• Nausea vomiting• Rash• Heamorrhagic manifestation• Supportive serology
A confirmed case is with virus isolation, demonstration of 4 fold increase in antibody titre, IgM & IgG antibody positivity, demonstration of dengue antigen by immunochemistry or PCR
992- Chinese Encyclopedia –water poison
1780- Philadelphia “break-bone fever”- Benjamin Rush
Dengue Fever has a long history…
Spread of the vector and the disease go hand in hand
Transatlantic Slave Trade
World War IIhttp://neatorama.cachefly.net/images/2007-09/world-war-2.jpg
EPIDEMIOLOGY
Global situation
WHO –
Disease is now endemic in more than
100 countries in Africa, the Americas,
the Eastern Mediterranean, South - East
Asia and the Western Pacific.
Pathophysiology
VECTOR
AGENT
ENVIRONMENT
Dengue Virus
Flavi Virus
Serotypes 1-5
Post - monsoon period
High temperature and high humidity..
Areas friendly for mosquito breeding
Human behaviour, climate and movement of humans
Day time biter Mosquito
breeding area
Aedes aegypti
Disease process
Infected female Mosquito bites human
Extrinsic incubation period 8-10 days
Mosquito acquire virus from infected person
Virus circulate in humans 2-7 days
Transovarian transmission Maintains virus in nature
Humans are only main Host of virus
Transmission of disease
Phases
Febrile phase
Critical phase
Recovery phase / Severe phase
ACUTE VIREMIA
FEBRILE PHASE
CAP PERMEABILITYPLATELETS
WBCs
A B
B USUALLYPRECEDES A
RECOVERY PHASE
WORSENS DUETO PLASMA LEAK
CRITICAL VOLLOSS
DIC
SEVERE H’AGEHEMATOCRIT
METAB ACIDOSIS
ORGANIMPAIRMENT
Febrilephase
Critical phase
HEMATOCRIT
IF PATIENT SURVIVES CRITICAL PHASE
SITUATION IMPROVES
REABS OF FLUID IMPROVES WELLBEING
HEMODYNAMICSSTABILISES
Recovery phase
Severe dengue
Hypovolemia worsens
Hypovolemic Shock
Compensatory
Systolic pressure normal Pulse pressure narrows
Tachycardia Peripheral vasoconstriction Cold extDelayed cap refil
Hypovolemic Shock
Decompensatory
Prolonged hypotensive Shock & Hypoxia
Vascular permeability progresses
Multi Organ FailureDIC Acidosis
Patient with severe dengue may have coagulation abnormalities but usually not sufficient to cause
major bleeding
Major bleeding usually assoc with prolonged shock along With thrombocytopenia, hypoxia and acidosis leading to
Multi Organ Failure
CLINICAL FEATURES
Clinical spectrum Undifferentiated fever
Dengue fever
Dengue hemorrhagic fever
Dengue shock syndrome
SEARO – REVISED
Undifferentiated fever
Dengue fever
Dengue hemorrhagic fever
Expanded dengue syndrome
Undifferentiated Fever May be the most common manifestation
of dengue
Commonly diagnosed as viral fever
Dengue guidelines for diagnosis, treatment, prevention and control, WHO, 2009
Classical Dengue Fever Prodrome
2 days malaise and headache
Acute onset (Febrile phase) Fever, continuous/saddleback(break on 4/5th day) Backache,arthralgia,generalized musculoskeletal pains
(“break bone fever”) Pain on eye movement Anorexia, nausea, vomiting, Depression, prostration Relative bradycardia, postural hypotension Lymphadenopathy, hepatosplenomegaly
Probable Dengue
Live in /travel to dengue endemic area. Fever and 2 of the following:
• Nausea, vomiting • Rash • Aches and pains • Tourniquet test positive • Leukopenia
Laboratory-confirmed dengueDengue guidelines for diagnosis, treatment, prevention and control, WHO, 2009
Warning signs
Clinical • Abdominal pain or tenderness • Persistent vomiting • Clinical fluid accumulation • Mucosal bleed • Lethargy, restlessness • Liver enlargment >2 cm
Laboratory: Increase in hematocrit concurrent with rapid decrease in platelet count
Dengue guidelines for diagnosis, treatment, prevention and control, WHO, 2009
SEVERE DENGUE
Severe dengue is defined by one or more of the following: plasma leakage that may lead to shock
(dengue shock) and/or fluid accumulation, with or without respiratory distress, and/or
severe bleeding, and/or severe organ impairment.
Severe Dengue
Severe plasma leakage leading to: • Shock (DSS) • Fluid accumulation with respiratory distress
Severe bleeding Severe organ involvement
• Liver: AST or ALT >=1000 • CNS: Impaired consciousness • Heart and other organs
Dengue guidelines for diagnosis, treatment, prevention and control, WHO, 2009
Dengue Hemorrhagic Fever Fever: 2-7 days Hemorrhagic
tendencies Thromboctopenia
<100000/mm3 Plasma leakage
Clinical Case Definition for Dengue Shock Syndrome
All criteria of DHF, plus Evidence of circulatory failure
manifested indirectly by all of the following: Rapid and weak pulse Narrow pulse pressure (<20 mm Hg) OR
hypotension (<90mmHg) Cold, clammy skin and altered mental
status
Dengue guidelines for diagnosis, treatment, prevention and control, WHO, 2009
Unusual Presentationsof Severe Dengue Fever
Differentials
LABORATORY EVALUATION AND
SUPPORT
INVESTIGATIONS
Etiological Diagnosis
Severity of illness and guide to
management
Investigations: Etiological Diagnosis Antigen detection
Antibody detection
Virus isolation and characterisation
Viral nucleic acid detection
General time line of a primary infection from virus isolation to detection of IgM & IgG
Rapid test for NS1 Antigen, IgM & IgG
Primary infection IgM antibodies
detectable in 50% by days 3-5 80% by day 5 99% by day 10
Anti-dengue serum IgG - Low titers at the end of 1st week Detectable after several months, and probably
even for life
Secondary infection Antibody titres rise rapidly and react
broadly against many flaviviruses.
The dominant immunoglobulin isotype is IgG
To distinguish primary and secondary dengue infections
IgM/IgG antibody ratios Haemagglutination-inhibition test (HI)
Investigations: Severity of illness
Complete Blood Count Leucopenia Thrombocytopeni
a Rising Hematocrit
- Plasma leakage/critical phase of the disease
Additional tests LFT RFT Plasma Glucose Serum electrolytes,
bicarbonate/ lactate
Cardiac enzymes urine specific
gravity/microscopy
Interpretation of Dengue Diagnostic Tests
Highly suggestive Confirmed
One of the following:
1. IgM +ve in a single serum sample
2. IgG +ve in a single serum sample with HI titre of 1280 or greater
One of the following:
1. NS1 Ag detection
2. PCR + ve
3. Virus culture +ve
3. IgM seroconversion in paired sera
4. IgG seroconversion in paired sera OR fourfold IgG titer increase in paired sera
Summary of Diagnostic tests
MANAGEMENT
Group A – OPD management
1. Able to tolerate adequate volumes of oral fluids
2. Pass urine at least once every six hours3. Do not have any of the warning signs,
particularly when fever subsides
Daily review for disease
Group B – Requires Admission These include patients with
Warning signs Comorbidities Social circumstances
Group C Require urgent ICU admission Complicated cases
DSS DHF Multi organ failure
Management of patient with no shock Hematocrit before fluid therapy Give only isotonic solutions- 0.9% NS, RL
Start with 5–7 ml/ kg/hour for 1–2 hours
3–5 ml/kg/hr for 2–4 hours
2–3 ml/kg/hr or less
Management of patient with compensated shock Hematocrit before fluid therapy
i.v bolus infusion @ 10 ml/kg
Assess after 1 hr
Maintenance fluid 2nd i.v. bolus for 24-48 hrs
Improvement No improvement
reassess
Management of patient with hypotensive shock Hematocrit before fluid therapy
i.v bolus infusion @ 10 ml/kg
Assess after 1 hr
Improvement 2nd i.v. bolus
Maintenance fluid Colloid for 24-48 hrs 10-20 ml/kg for ½-1 hr
Treatment
Complications Hemorrhagic complication Hyperglycaemia /hypoglycaemia Electrolyte and acid-base imbalances
Hyponatraemia, hypokalaemia, hyperkalaemia,
Co-infections and nosocomial infections
Patients at risk of major bleeding Prolonged/refractory shock Hypotensive shock and renal or liver failure
and/or severe and persistent metabolic acidosis Use NSAIDS/anti coagulants Pre-existing peptic ulcer disease Trauma / IM inj Patients with haemolytic conditions are at
risk of acute haemolysis with haemoglobinuria and will require blood transfusion
Treatment of haemorrhagic complications
Minimal mucosal – wait and watch Profound thrombocytopaenia- ensure
strict bed rest and protect from trauma to reduce the risk of bleeding
No intramuscular injections- haematoma Prophylactic platelet transfusions for
severe thrombocytopaenia in otherwise haemodynamically stable patients - NO ROLE
Treatment Blood transfusion is life-saving - the risk
of fluid overload Do not wait for the haematocrit to drop
too low Indication for platelet transfusion
Active bleeding Platelet <10,000/ml
Discharge criteria All to 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 haematocrit without intravenous fluids
Vaccine… National Institutes of Health - human
clinical testing. National Institute of Allergy and
Infectious Diseases (NIAID) and is undergoing clinical study at the Johns Hopkins Bloomberg School of Public Health in Baltimore
Thank You