latest Dengue.pptx

AnkitKumar814 316 views 53 slides Jan 29, 2023
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About This Presentation

dengue mangement in children
latest guidelines, fluid management in dengue


Slide Content

Dengue Dr Ankit Kumar PG JR 1 Dept of Pediatrics GMC Haldwani

At least 100 countries are endemic for DHF About 40% of world population (2.5 billion) are at risk in tropics and subtropics INDIA alone accounts for 34% of Global Dengue burden.

Epidemiological Triangle The Host The Virus The Vector Interaction

Initial epidemics in INDIA were due to serotype 2 or 4 but serotype 1 was predominant serotype in Delhi during 2007-2010. Recently serotype 2 & 4 in Delhi Infection with one serotype provides lifelong immunity against the same serotype but does not provide immunity against other serotypes. Subsequent infection by another serotype results in severe dengue because of preformed antibodies. Severity of epidemics caused by serotype 1 has been reported to be maximum.

ENVIRONMENTAL FACTORS The population of Aedes aegypti fluctuates with rainfall and water storage Between 16 degree C and 30 degree C Relative humidity of 60–80%. Altitude between 0 ft and 1000 ft above sea level A nthropophilic and rests in cool shady places.

HOST Severe dengue occurs with high frequency in Infants Children having experienced a previous dengue infection Bronchial asthma, HIV Certain HLA types :- HLA1(A04, A24, B46), HLA2(DR1, DR4, DQ) Polymorphisms in TNF ἀ , TGF-ẞ G6PD deficiency Thalassemia Obesity, DM, Renal failure

PATHOGENESIS

Dengue virus infection Production of antibodies/presence of enhancing antibodies Antigen antibody rxn with compliment activation Deposition on vessels various tissues and platelets Clinical manifestation of coagulopathy Hypotension/shock Pleural effusion Ascites Bleeding organ involvement Activation of T cells Production of chemical mediators,cytokines,TNF , interferons. Increase vascular permeability Manifestation of vasculopathy

Natural course of dengue Infection The illness passes through the following three phases: Febrile phase Critical phase Convalescent phase CLINICAL MANIFESTATIONS

Incubation period is 4 – 7 days A febrile patient/measly look/ blanchable rash Suffused swollen face, injected eyes, reddened ears Crimson malar area, swollen and purplish lips Absence of significant catarrh Sudden onset of fever, chills, headache Back pain with severe myalgia , arthralgia Retro-orbital pain, break bone fever, headache Maculo-papular rash on trunk/extremities may supervene Epistaxis and scattered petechiae Febrile phase

Photophobia, extreme weakness, dragging pain in inguinal region Anorexia, Nausea, vomiting Pain on eye movements Pain on palpating abdominal muscles Rash may be associated with itching & hyperasthesia Rash lasts for 2hrs to several days & may be followed by desquamation Primarily not a respiratory illness Complete recovery is the rule. Illness is about 2–7 days. Other manifestations- DF

Inflate blood pressure cuff to a point midway between systolic and diastolic pressure for 5 minutes Positive test: 1 0 or more petechiae per 1 inch² (6.25 cm²) Tourniquet Test

DF patients usually go to critical phase after 3 to 4 days of onset of fever. During this critical phase plasma leakage and high haemoconcentration are documented and patients may develop hypotension. Abnormal haemostasis and leakage of plasma leads to shock, bleeding, accumulation of fluid in pleural and abdominal cavity Critical phase

High morbidity and mortality are commonly associated with various organ involvements and metabolic derangement. The period of plasma leakage usually persists for 36-48 hrs.

SHOCK Around the time of defervescence , in some patients increase in capillary permeability sets in resulting in extravasation of plasma. Patients with prolonged & prolific leak would deteriorate & manifest signs of impending shock i.e. cold & clammy extremities , feeble pulses, Prolonged CRT, narrow PP & falling BP. Extravasated fluid collects primarily into serous cavities like peritoneum, pleura & pericardium which may present as large ascites and pleural effusion

During the recovery phase the extracellular fluid which was lost due to capillary leakage returns to the circulatory system and signs and symptoms improve. This phase usually after 6-7 days of fever and last for 2-3 days . Longer convalescence may be expected in some of the patients with severe shock, organ involvement and other complications which may require specific treatment. Convalescent phase Patient may develop pulmonary oedema due to fluid overload if the fluid replacement is not optimised carefully.

Termination of the illness is marked by a distinctive acral exanthem . A bright red confluent petechial rash erupts along the lateral margins of palms & soles. Ascending upwards and medially, the rash assumes a confluent character. Peripheral pruritus , asthenia & bradycardia can occur

Children without warning signs can also develop severe dengue

Group A patients:- ( probable Dengue without warning signs) 1. accepting orally & passing urine adequately 2. No associated risk factor like CRF, DM Group B patients :( Patients with warning signs) Coexisting conditions like infancy, DM, Renal failure Social circumstances such as living alone or living far from hospital 3. Poor oral intake or decreased urine output Those having severe dengue GROUP C PATIENTS :

PROBABLE DENGUE A case compatible with clinical description of dengue fever with one or more of the following: -Supportive serology ( reciprocal haemaglutination -inhibition titre,comparable IgG ELISA titre or positive IgM antibody test in late acute or convalescent-phase serum specimens). - Occurance at same locations and time as other confirmed cases of dengue fever CONFIRMED DENGUE A case compatible with the description with atleast one of the following : Isolation of virus from serum,plasma , leucocytes IGM ab titer by ELISA Dengue virus NSI antigen by ELISA IgG seroconversion in paired sera after 2 wks with four fold rise. Viral nucleic acid detection by PCR Case definition

Hematological tests An Hct level rise of greater than 20% is a sign of hemoconc . & precedes shock TCP :- plat count < 100,000/mm3 indicates onset of critical phase WBC count can be Normal or show leukocytosis during initial phase. Leukopenia often with lymphopenia precedes TCP & is observed near the end of the febrile phase of the illness Biochemical profile PT, aPTT are prolonged Low fibrinogen & elevated FDP levels may be seen(DIC) Hyponatremia is the most common electrolyte abnormality in critical phase. SGOT, SGPT levels may be raised INVESTIGATIONS

Non structural protein1 (NS1) IgM antibodies to dengue IgG antibodies in paired samples (fourfold rise ) Serodiagnosis :-

Only test that shows hemoconcentration or increased vascular permeability & response to therapy. Measure a base line hematocrit . An increase in hematocrit with a rapid drop in platelet indicates warning sign. >50% in men and above base line in children and women indicates plasma leakage. <40 to 45 %in males ,<35 to 40% in children and women and <30 to 35 % in infants indicates bleed . HEMATOCRIT

Management of dengue illness Includes: suspicion of disease assessment & management of early febrile phase identify patients with warning signs recognise early critical phase & initiate fluid therapy Recognise & manage severe dengue

Depending on the clinical manifestations & other Circumstances p atients may be divided into three groups Group A – sent home Group B – require in hospital management Group C – require emergency management

Group A patients (probable Dengue without warning signs ) 1. accepting orally & passing urine adequately 2. No associated risk factor like CRF, DM These constitute majority of dengue patients and can be managed at home, however they need close clinical observation during febrile period & 2-3 days beyond defervescence

1. Ensure adequate fluid intake 2. Assess urine output in relation to fluid intake i.e. scanty urine output with adequate oral fluid intake should alert you about vascular leak 3. Use only PCM for pain & fever 4. Warn patients for warning signs ---- if appear report to hospital 5. Child deteriorating or failing to improve with subsidence of fever should alert you about progression to critical phase Outpatient management

When to report back to hospital immediately:- Scanty urine, giddiness Inability to walk, diaphoresis Abdominal distention, respiratory distress, abdominal pain. Abnormal mentation, impaired conciousnes , convulsion. Petechiea , purpura, ecchymosis

Coexisting conditions like infancy, DM, Renal failure Social circumstances such as living alone or living far from hospital Poor oral intake or decreased urine output Group B patients : Patients with warning signs

Patients with warning signs These patients are likely to pass to critical phase Close clinical observation Obtain PC & Hct before starting I/V fluids Start I/V fluid NS/RL @ 6ml/kg/hr for 1-2hr Hemodynamically stable, Hct remains same or rises minimally NS/RL 3ml/kg/hr for 2-4 hr 3-1.5 ml/kg/hr for another 2-4 hr Stop I/V fluids when child demands and accepts adequate oral fluids and food

Any time if there is worsening of hemodynamic status Check HCT Hct rises HCt falls Bolus 10ml/kg/hr may be given for 2 hr. Then modify fluid therapy as per response Those who worsen or develop profound shock, bleeding or Multisystem involvement, manage as group C

Severe dengue :- I/V fluid therapy is the most important aspect of management Fluid sufficient enough to maintain effective circulation & perfusion is advised Idea is use minimal intravenous fluid volume required To maintain good perfusion Use only isotonic fluids( NS,RL)

Choice of fluid Two commonly used fluids in dengue are Crystalloids :- should be used for initial resucitation Colloids:- reserved for patients presenting with a) Hypotensive shock b) Recurrent shock c) Refractory hypotensive shock

DENGUE SHOCK Compensated ( Nr Systolic BP, incresing DBP, Narrowing PP, postural hypotension) NS/RL 10 -20ml/kg over one hour and after 1hr reassess vitals, CRT, Hct , UO Still unstable . . Improving With increasing Decreasing Hct . Hct 10 ml /kg/hr for 1-2hr crystalloid / colloid Blood transfusion 10-20ml /kg over1hr (no improvement) 6 ml /kg/hr for2-4hr ( Improvement) 1 0ml/ kg/hr for 1-2hr 3-1.5 ml/kg/ hr for 2-4hr (stable ) Maintainance fluid for 24-48 hrs . Taper if improving

IV inotropes with crystalloid maintenance fluid according to Holiday–Segar formula Refractory hypotension Assess A irway /Bleeding/ Calcium/ Sugar (No Improvement )

PROFOUND SHOCK (DSS IV) NS/RL 10-20ml/kg over 15-30 min Shock persists improves NS/RL 10ml/kg over 1hr Review Hct stable Low high taper fluid gradually over 6-8 hours Indicates bleeding I/V colloids 10-20ml/kg over 60min continue maintainance Give transfusion fluid for 24-48 hrs Repeat 10–20 ml/kg crystalloid/colloid* second bolus over 15–30 mins

Improves unstable 10ml/kg/hr (colloid for 1-2hr) Hct Improves increasing decreasing Change to crystalloids further colloid Blood transfusion Taper gradually IV inotropes with crystalloid maintenance fluid according to Holiday–Segar formula Refractory hypotension Assess A irway /Bleeding/ Calcium/ Sugar (No Improvement )

MONITORING Hourly till patient is hemodynamically stable At least 4 hrly if patient is hemodynamically stable till fluid infusion is complete & patient is totally out of risk Hct :- before & after fluid boluses till stable than 4-6 hourly

PR/RR/BP pulse pressure :- most significant parameter for defining dengue shock. PP should be maintained >20 PP if <20 – indication for stepping up fluid therapy Abdominal girth monitoring urine output monitoring- at least once in 6 hrs. Monitor

Increase in RR > 10. Increase in PR >20 Basal crackles. Gallop rhythm. Increase in liver size. Periorbital puffiness. SIGNS OF FLUID OVERLOAD

Platelet count less than10000/ cu.mmin absence of bleeding manifestations (Prophylactic platelet transfusion). In case of systemic massive bleeding, platelet transfusion may be needed in addition to red cell transfusion. Platlet transfusion

Absence of fever for at least 48 hours Return of appetite Visible clinical improvement Good urine output Minimum 2 to 3 days after recovery from shock , no respiratory distress from pleural effusion or shock. Discharge criteria

COMPLICATIONS Hepatitis 1. hepatomegaly 2. raised AST & ALT – AST(SGOT) > ALT, inc by 3 rd day, max by 8-9 days, Normal by 3-8 wks 3. rarely fulminant hepatic failure can occur Neurological complications convulsions, impaired consciousness, myositis, spasticity & paresis Cardiac complications Global hypokinesia , low ejection fraction, rhythm disturbances

25 C ± 5 degree Celcius , Relative humidity around 80% Innumerable small water collection

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