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When to start ART in children
- • All children infected with HIV below five years of age, regardless of WHO clinical stage or CD4 cell count and infants diagnosed in the first year of life.
- • All children infected with HIV five years of age and older with CD4 cell count≤500 cells/mm3, regardless of WHO clinical stage.
- • All children with HIV with severe or advanced symptomatic disease (WHO clinical stage 3 or 4) regardless of age and CD 4 count
- • Any child younger than 18 months of age who has been given a presumptive clinical diagnosis of HIV infection
What ART regimens to start
- • First-line ART- 2 (NRTIs) plus 1(NNRTI).
- • TDF + 3TC + EFV as a fixed-dose combination -preferred option to initiate ART
- • If contraindicated or not available, one of the following options is recommended:
- - Age < 3yrs ABC or AZT + 3TC + EFV
- - Age 3-10 yr ABC + 3TC + NVP
- - Age >10 yrTDF + 3TC + NVP
Diagnosis of HIV in Children Child aged < 18 months:
- • HIV can be diagnosed : two positive virological assays* obtained from two different blood samples, excluding cord blood.
- • HIV can be excluded:
- 1. 2 negative HIV virological tests, 1 performed age >1 month and the other age > 4 months.
- 2. 2 negative HIV antibody tests performed after age 6 months, obtained one month apart.
- • HIV viral culture, HIV PCR DNA/RNA
- • NAT
Diagnosis of HIV AGED >18 MONTHS
- • HIV can be diagnosed by:
- • 1)A repeatedly positive HIV antibody test , followed by a confirmatory test (western blot).
- • 2) A positive HIV virological test result: HIV PCR RNA/DNA, viral culture.
- • HIV can be excluded: 1 negative HIV antibody, in the absence of hypoglobulinemia with negative virological tests and no clinical symptoms of HIV
Presumptive clinical diagnosis of HIV infection may need to be made as follows:
- • Infant is confirmed HIV-antibody positive; and Diagnosis of AIDS-indicator condition(s) can be made or The infant is symptomatic with two or more of the following:
- - Oral thrush
- - Severe pneumonia.
- - Severe sepsis.
- • Other factors that support the diagnosis of severe HIV disease in an HIV seropositive infant include:
- - Recent HIV-related maternal death or Advanced HIV disease in the mother;
- - CD4 <20%.
Monitoring ART response and diagnosis of treatment failure
- • Viral load is recommended as the preferred
- • Monitoring approach to diagnose and confirm ARV treatment failure.
- • If viral load is not routinely available, CD4 count and clinical monitoring
Comprehensive and integrated four prong approaches to prevent HIV infection in infant and young children
- • Prevent HIV infection among women of childbearing age;
- • Prevent unintended pregnancies among women living with HIV;
- • Prevent HIV transmission from infected mothers to their infants:
- - Antiretroviral treatment for mother and infant prophylaxis
- - Safer delivery practices
- - Safer infant feeding choices;
- - Provide appropriate treatment, care and support to women living with HIV and their children and families.
First-line ART for pregnant and breastfeeding women
- • A once-daily fixed-dose combination of TDF + 3TC+ EFV is recommended as first-line ART.
- • Infants of mothers who are receiving ART and are breastfeeding should receive six weeks of infant prophylaxis with daily NVP.
- • If infants are receiving replacement feeding-six weeks of infant prophylaxis with daily NVP.
Multi Drug Resistant TB
At least resistant to Isoniazid and Rifampcin
Extended Drug Resistant TB
- • Resistant to almost all 2nd line drugs, i.e resistant to
- • Atleast Rifampcin and Isoniazid
- • Resistant to Fluoroquinolones
- • Resistance to one or more of IV drug: Amikacin, Capreomycin, Kanamycin
CORTICOSTEROIDS IN TB
- • Indications:
- a) Tuberculous meningitis – reduces vasculits, inflammation and ICP
- b) Endobronchial tuberculosis that causes respiratory distress, localized emphysema or segmental pulmonary lesions.
- c) Acute tubercular pericardial effusion
- d) Miliary TB (with alveolocapillary block)
- e) Pleurisy with severe distress
- Most commonly prescribed regimen is Prednisolone 1-2mg/kg/day in 1-2 divided doses orally for 4-6wks followed by gradual tapering.
Latent TB Infection:
- -A reactive tuberculin skin test (TST) and the absence of clinical and radiographic manifestations are the hallmark of this stage.
- - The following treatment options are recommended for the treatment of LTBI:
- a) 6-month isoniazid, or
- b) 9-month isoniazid, or
- c) 3-month regimen of weekly rifapentine plus isoniazid, or
- d) 3–4 months isoniazid plus rifampicin, or
- e) 3–4 months rifampicin alone.
Indication of IVIG
- Immunoglobulin is a highly purified and sterile antibody containing solution, usually derived through cool ethanol fraction of large pool of human plasma from adults.
- IVIG is more than 95% IgG and is tested to ensure minimum Ab titers to Corynebacterium Diphtheriae, Hepatitis B Virus, Measles Virus and Polio Virus
- INDICATION ARE
- • Replacement Therapy for Primary Immunodeficiency Disorders
- • Kawasaki Disease to prevent coronary artery abnormalities and shorten the clinical course
- • Replacement therapy for prevention of serious bacterial infection in children infected with HIV
- • Prevention of Serious bacterial infection in people with hypogammaglobinemia in Chronic B-lymphocytic leukemia
- • ITP to increase platelet Count
- • Prophylaxis of infection following BM transplant
- • Severe TSS
- • Guillan Barre Syndrome
- • Anemia by Parvo Virus B19
- • Varicella Post Exposure Prophylaxis
Three Circumstances in which the diagnosis of ARF can be made without strict adherence to Jones Criteria:
- • When Chorea occurs as the only Major Manifestation of ARF
- • When Indolent Carditis is the only manifestation in patients who first come to medical attention only months after the apparent onset of ARF
- • In a limited number of patients with recurrence of ARF in particularly high risk population
- Two of 4 Criteria, 1 of which must be abnormal temperature or abnormal leukocyte count
- 1. Core temp >38.5*C (101.3*F) or < 36*C(96.8*F) (Rectal, Bladder, Oral or Central Catheter
- 2. Tachycardia: Mean HR > 2 SD above normal for age in the absence of external stimuli, chronic drugs or painful stimuli OR
- Unexplained persistent elevation over 0.5 – 4 hr OR
- In children < 1 yr old, persistent bradycardia over 0.5 hr (Mean HR <10th percentile for age in the absence of vagal stimuli, B-blocker or CHD)
- 3. Respiratory Rate >2SD above normal for age or acute need for mechanical ventilation not related to NM disease or GA
- 4. Leukocyte count elevated or depressed for age (not secondary to chemotherapy) or to >10% immature neutrophils
SIRS plus a suspected or proven infection
- Sepsis plus 1 of the following
- 1. Cardiovascular organ dysfunction, defined as
- Despite>40ml.kg of isotonic IV fluid in 1 hr:
- Hypotension <5th percentile for age or SBP <2SD below normal for age
- Need for vasoactive drug to maintain BP
- 2. 2 of the following:
- Unexplained Metabolic acidosis : Base Deficit >5 mEq/L
- Increased arterial lactate: >2 times upper limit of normal
- Oliguria: Urine Output <0.5 ml/kg/hr
- Prolonged CRT >5 sec
- Core to peripheral temp. gap >3*C (5.4*F)
Varicella Zoster Virus
- Primary Infection is manifested as Varicella(Chickenpox) and results in establishment of a lifelong latent infection of sensory ganglion neurons. Reactivation of the latent infection causes herpes zoster(Shingles).
- Varicella predispose to Staph. Aureus and Group A streptococcus, Encephalitis and Cerebellar Ataxia, Pneumonia.
- Progressive Varicella Syndrome is a dreaded complication in immunocompromised individual, neonates, even healthy adults and adolescents. Characterized by continued vesicular lesion development after 7 days, hemorrhagic lesions, coagulopathy and visceral organ involvement including hepatitis, pneumonia and encephalitis.
- Neurotropic DNA Virus, present in respiratory secretion and skin lesions of affected children and is transmitted by airborne or direct contact. Disease is highly contagious with secondary attack rate of 80% among household contacts.
- Herpes Zoster in children tends to be milder than in adults, is less frequently associated with acute pain and post herpetic neuralgia does not occur in healthy children. Average no of Varicella lesion is 300 but healthy children may have fewer than 10 to more than 1500.
- Break through Varicella is a disease that occurs in a person vaccinated more than 42 days before rash onset and is caused by wild type virus.
- IV therapy is indicated in Disseminated varicella including pneumonia, Severe hepatitis, Thrombocytopenia and Encephalitis
Relapse and Recrudescence
- The term for recurrence of infection with other species, P. falciparum, P. malariae and P. knowlesi, which lack hypnozoites, is "recrudescence", meaning that the infection (unless a new infection) has recurred from persistent blood stages of the malaria parasite.
- Reappearence of asexual parasite with 28 days of treatment is defined as recrudescence or late treatment failure. Causes are wrong drug, wrong dose, poor compliance, drug resistance, artemisin monotherapy
Why P. falcifarum is dangerous
High Parasitemia in P. falcifarum upto 60% and it infect both immature and mature erythrocytes while P.vivax and Ovale infect only immature and P.malariae infect mature.
Erythrocyte containing HbS resist
Malarial parasite growth.
Erythrocyte lacking Duffy blood group Ag resist
Erythrocyte containing HbF and Ovalocytes resistant
Investigation of Malaria
- • PBS: Thick Smear: Concentration in thick smear is 20-40 times is used to quickly scan large no of erythrocytes. Thin Smear: Positive identification of malarial parasite, Determination of percentage of Infected erythrocytes, Prognosis (Mature Schizonts and pigmented neutrophil indicate poor prognosis) Useful in following response to therapy
- • Quantitative buffy Coat
- • Rapid Diagnostic Tests: (PfHRP2, PMA, PLDH). Optimal Test based on detection of parasite LDH. P.falcifarum Histidine rich protein. Aldolase is used for testing testing P.falcifarum and P.vivax
- • Polymerase Chain Reaction
T/tof uncomplicated P. falcifarum
- Artemisin based combination therapy(ACT)
- Artemether + Lumefantrine
- Artesunate + Amodiaquine
- Dihydroartemisin + Piperaquine
- Astesunate + Sulfadoxine – Pyrimethamine
- Artemether Lumefantrine (Tab. Contain 20mg A + 120mg L) 5-14: 1 tab, 15-24: 2 tab, 25-34:3 tab, ≥35: 4 tab. 6 times to be given 0,8,24,36,48,60 hours
- Dengue Fever is a benign syndrome characterized by biphasic fever, myalgia or arthralgia, rash, leukopenia and lymphadenopathy.
- Dengue haemorrhagic fever is a severe often fatal febrile disease caused by 1 of 4 dengue viruses, characterized by capillary permeability, abnormalities of hemostasis and in severe cases a protein losing shock syndrome( Dengue Shock Syndrome)
- Aedes Aegypti (Day time Biting Mosquito).Transovarial Transmission A. Aegypti is highy urbanized, breeding in water stored for drinking or bathing and in rainwater collected in container
- Tourniquet Test
- Joints Symptoms may be particularly severe in patients with chikungunya or o’nyong nyong infection (Joint pain often sever in intensity, polyarticular, migratory predominantly involve the small joints of hands, wrist, ankle and feet with less involvement of large joints)
Dengue Hemorrhagic Fever:
- Fever (2-7days in duration or Biphasic)
- Minor/Major haemorrhagic Manifestation
- Objective evidence of increased capillary permeability (Hct increase by 20%)
- Pleural effusion or Ascites or Hypoalbuminemia
Dengue Like Illness Virus Disease
- Toga Virus Chikungunya
- Toga Virus O’nyong-nyong
- Flavi Virus West Nile Fever
Dengue Shock Syndrome:
DHF as well as hypotension, tachycardia, narrow pulse pressure and signs of poor perfusion
- Clinical Criteria: acute onset high grade fever, Haemorrhagic Manifestation (+ve Torniquet test), Tender Hepatomegaly, Effusion in body cavities or in shock
- Laboratory Criteria: Thrombocytopenia < 1 lakh cells per cubic mm or < 1-2 platelet per oil immersion field, Rising Hematocrit
Abdominal pain and Tenderness, Prolonged Vomiting, Clinical Fluid Accumulation, Hepatomegaly >2cm, Lethargy and Restlessness, Mucosal Bleeds, Laboratory features like increase in PCV with concurrent with rapid decrease in platelet count
- • Severe plasma leakage leading to shock, Fluid accumulation with respiratory distress
- • Bleeding manifestation as evidenced by Clinician
- • Severe Organ involvement
- Liver: AST/ALT > 1000 U/L
- CNS: Impaired Consciousness
- Heart and other organs
Management of Bleeding
- • Petechieal Bleeding or mild mucosal bleed but hemodynamically stable
- • Severe Bleeding and Hemodynamically instable, excessive mucosal bleed
Management of Fluid Overload
- • Fluid overload with stable hemodynamically stable and is out of critical phase
- • Fluid overload with stable hemodynamically stable and is still in critical phase
D/D of Dengue
Chikungunya, Leptospirosis, Meningococcemia, Enteric Fever, Influenza, Malaria. In event of haemorrhagic manifestation, meningococcemia, scrub typhus and leptospirosis.
Diagnosis of Dengue
- Increased PCV, Low platelet count and decreasing leukocyte (Malaria, Typhoid) with lymphocytosis. Mild acidosis, increased transaminases value and hypoproteinemia. HCT >20%, thrombocytopenia, prolonged BT and a moderately decreased prothrombin level
- Confirmation of Diagnosis
- - Direct method Virus Isolation by Culture, Genome detection by PCR, NS1 antigen detection
- - Indirect method including IgM detection and IgG detection
SCRUB TYPHUS Clinical Feature and D/D
- Orientia Tsutsugamushi, Transmitted through chigger(Larval Bite)
- Fever for 9-11 days. Regional or generalized lymphadenopathy 23-93%, hepatomegaly in two thirds, splenomegaly in one third, GI Symptoms including abdominal pain, vomiting and diarrhea upto 40%, Single Painless eschar, Maculopapular rash, Thrombocytopenia in one third and Leukocytosis in 40%
- D/D FUO, Enteric Fever, Dengue Haemorrhagic Fever, Rickettsioses, Tularemia, Anthrax, Dengue, Leptospirosis, Malaria and Infectious Mononucleosis.
CYSTICERCOSIS manifestation and Classifiaction
- Ingestion of undercooked pork containing the larval cysts.
- Seizure: MC. Others: Hydrocephalous, Diffuse Cerebral Edema, Focal Neurologic findings.
- Classified as, Intraventricular, subarachnoid, spinal or ocular
Diagnosis of NCC
- MRI: Information about Cyst location, viability and associated inflammation, sometime detect protoscolex pathognomic of NCC. MRI also detects Basilar arachnoiditis, intraventricular cyst and cyst in spinal cord
- In children from endemic regions, the presentation of a single enhancing lesionthat is round <2cm in diameter, absence of symptoms or signs of other disease(eg: no fever or lymph node) no focal findings and no evidence of raised ICT highly specific for NCC.
D/D of NCC:
Brain Abscess, Granuloma(TB, Fungal Infection, Lymphocytic histiocytosis, Toxoplasmosis), Tumors
Differential Diagnosis of Ring Enhancing lesion
- Infection: Toxoplasmosis, Cysticercosis, Tuberculoma, Brain abscess
- Neoplasm: Brain tumors, Metastatic, Primary CNS Lymphoma
- Demyelinating Disease: MS, ADEM
- Others: SLE, Sarcoidosis
Herpes Simplex Virus:
Variety of illness depending on the anatomic site where the infection is initiated, the immune status of host and whether the symptoms reflects primary or recurrent infection. Commonly affect skin, eye, oral cavity and genital tract. Mild and self limiting except in the immunocompromised and neonate. HSV remain latent infection in the regional sensory ganglion neuron and can cause recurrent infection
HSV1 vs HSV2
- HSV-1 has a greater propensity to cause recurrent oral infection where as HSV-2 to cause recurrent genital infection. For this reason HSV-1 infection typically results from contact with oral secretion, whereas HSV 2 most commonly result from anogenital contact.
- Viral Infection typically begins at a cutaneous portal of entry such as the oral cavity, genital mucosa, ocular conjunctiva or breaks in keratinized epthelium
Clinical Manifestation of Herpes:
- Skin vesicles small 2-4 mm vesicles that may be surrounded by erythematous base, may perisit for a few days before evolving into shallow, minimally erythematous ulcer.
- Acute Oropharyngeal Infection: Gingivostomatitis, Pharyngitis, Tonsillitis
- Herpes Labialis
- Cutaneous Infection
- Genital Herpes
- Ocular Infection: Conjuctivits, Kerato Conjuctivitis
- CNS Infection: HSV Encephalitis: Acute Necrotizing infection generally involving the frontal temporal and limbic system beyond neonatal period, almost always caused by HSV1. Injury to frontal temporal or limbic system may produce finding more predictive of HSV encephalitis, anosmia, memory loss, peculiar behavior, expressive aphasia and other change in speech, hallucination and focal seizure
- It is passed to humans by the bite of an infected mosquito Culex. These mosquitoes often feed on pigs and wading birds So Japanese encephalitis is more common in areas where pigs and wading birds are found. In particular it is common in areas of rice fields (paddy fields) and pig farms.
- Japanese encephalitis virus–specific immunoglobulin M (IgM) capture enzyme-linked immunoassay (ELISA) on serum or cerebrospinal fluid (CSF) is the standard diagnostic test for Japanese encephalitis. MRI and CT scanning of the brain may show bilateral thalamic lesions with hemorrhage.
- Altered mental status may rapidly follow and can range from mild confusion to agitation to overt coma. Seizures develop more often in children, while headache and meningismus are more common in adults. Acute encephalitis is the most common neurologic manifestation. RAPIDLY CHANGING NEUROLOGICAL SIGNS( e.g: HYPERREFLEXIA FOLLOWED BY HYPOREFLEXIA OR PLANTAR RESPONSES THAT CHANGES). Usually Affect B/L Thalamic Region
- Mutism has been reported as a presenting symptom. Acute flaccid paralysis has also been described, attributed to the involvement of anterior horn cells resulting in a poliomyelitis-like presentation. Fevers disappear by the second week, and parkinsonian features (choreoathetoid movement, tremor, dystonia) develop as the other neurologic symptoms disappear.
Clinical Criteria for Diagnosis of HLH
- One of the two is required to establish a diagnosis
- 1. Presence of pathogenic mutation in PERF, SAP, MUNU gene
- 2. Five of following 8 criteria are fulfilled
- - Fever
- - Splenomegaly
- - Cytopenia in at least 2 cell lineages
- - Hypertriglyceridemia (Fasting TG >265 mg/dl) or hypofibrinogenemia(fibrinogen<1.5g/l)
- - Hemophagocytosis in BM, spleen or lymph node
- - Low or absent activity of NK cells
- - Serum Ferritin > 500mcg/l
- - Soluble IL-2 receptor(CD25) >2400 units/ml
Clinical Feature of Polio
- 90-95% of individual, polio virus is inapparent. In remaing 5-10% of individual, one of the following syndromes may occur ABORTIVE POLIO(4-8%), NON-PARALYTIC ASEPTIC MENINGITIS(1-2%), PARALYTIC POLIOMYELITIS(0.5-1%), SPINAL PARALYTIC POLIOMYELITIS(80%)
- RESIDUAL PARALYSIS: Following an acute phase of illness lastin 1-4 week, recovery of paralyzed muscle occurs. Extent of recovery variable ranging from mild to severe residual paralysis. Maxm recovery takes place in 1st 6 month, slow recovery upto 2 yr. After 2 year no more recovery is expected and the child is said to have post polio residuial paralysis
High Risk for Influenza complication
Children < 2yr of age, Pt. with chronic disease, Person with immunosuppression, including that caused by medication or by HIV infection, Adolescents who are pregnant or post-partum (within 2 week after delivery), Pt. younger than 19 yr of age who are receiving long term aspirin therapy
Commonest complication of Diphtheria
- Resp. failure d/t occlusion of airway by membrane. Myocarditis in the form of CCF and Arrythmia
- Neurological Complication(Palatal Palsy, ocular palsy, loss of accomdation manifested by visual blurring and inability to read, generalized polyneuritis)
C/F of Pertusis
- I.P 7-14 days
- Catarrhal Phase (1-2 wks): Most infective phase, distinguishable from URTI, Cough, Coryza, with little nasopharyngeal secretion.
- Paroxysmal Phase (2-6 wks): Cough progress to episodic paroxysm of increasing intensity ending with high pitched inspiratory whoop
- Convalescent phase
Complication of Pertusis
- o Neurological Complication: Seizure, Encephalopathy
- o Bleeding Manifestation: Epstaxsis, Retinal or conjunctival Haemorrhage, ICH
- o Inguinal hernia, Rectal Prolapse
- o Malnutrition d/t persistent vomiting and disinclination to eat d/t fear of paroxysm of cough with attempts at feeding
- PCV 7 4, 6B, 9V, 14, 18C, 19F, 23F
- PCV 10 1, 4, 5, 6B, 7F, 9V, 14, 18C, 19F, 23F
- PCV 13 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, 23F
Staph. Aureus, Kliebsella Pneumoniae, M. TB
Prognosis of Neonatal tetanus is worse if
- o Onset of symptoms within 1st wk of life.
- o Interval between lock jaw and onset of spasm is less than 48 hours
- o High fever and Tachycardia
- o Spasm especially of larynx result in apnoea are severe and frequent.