Revision Phase 4

5/1/2012

Nephrotic syndrome in childhood

Criteria for diagnosis Early morning urine protein/creatinine ratio >200mg/mmol (urine protein loss of >40 mg/m2 H) UPCI Hypoalbuminaemia <25 g/L Oedema Hypercholestremia +/-

Primary causes
Pos-tinfectious etiologies Collagen vascular disease (systemic lupus erythematosus, rheumatoid arthritis, polyarteritis nodosa) Henoch-Schnlein purpura Hereditary nephritis Sickle cell disease Diabetes mellitus Amyloidosis Malignancy (leukemia, lymphoma, Wilms tumor, pheochromocytoma) Toxins (bee sting, poison ivy and oak, snake venom) Medications (probenecid, fenoprofen, captopril, lithium, warfarin, penicillamine, mercury, gold, trimethadione, paramethadione) Heroin use

Secondary causes
Related to post-infectious causes : Group A beta-hemolytic streptococci Syphilis Malaria Tuberculosis Viral infections (varicella, hepatitis B, HIV type 1, infectious mononucleosis)

Standard definitions in SSNS

Remission Urine protein dipstick (Albustix) reading 0 or trace for 3 consecutive days Relapse Albustix reading 2+ or more 3 consecutive days having previously been in remission Frequently relapsing 2 or more relapses within 6 months of initial response or 4 or more within any 12 month period Steroid dependent 2 consecutive relapses occurring during corticosteroid treatment or within 14 days after its cessation Steroid sensitive Normalization of proteinuria within 4 weeks after start of standard initial therapy of daily oral prednisolone Steroid resistant Failure to achieve remission in spite of 4 weeks of oral prednisolone of 60mg/m2/day to maximum of 80 mg/day

Complications?
Acute complications Hypovolaemia Infection : Peritonitis / Septecemia / cellulitis Thrombosis: Arteial / venous Others Acute renal failure: Prerenal uremia / acute tubular necrosis Hyperlipidaemia: Hypercholesterolaemia / increased plasma LDL and VLDL Protein malnutrition (cachexia)

Atypical features?
Age <1 year or > 12 years Persistent hypertension Gross haemeturia (microscopic in 25%) Renal impairment not due to hypovolaemia (plasma creatinine) Plasma C3

AGN Complications
Acute renal impairment Hypertensive encephalopathy Acute left ventricular failure

Vesico ureteric reflux

Idiopathic Immune Thrombocytopenia

Conjunctival hemorrhage

Extensive petechiae and purpura on the legs

Haemarthrosis

HenochSchonlein purpura
Classification criteria for HSP: Palpable purpura (mandatory) in the presence of at least one of the following four features: Diffuse abdominal pain Arthritis (acute) or arthralgia Renal involvement (any haematuria and/or proteinuria) Any biopsy showing predominant IgA deposition Palpable purpura often symmetrically distributed over the extensor, dependent surfaces of the lower limbs and buttocks. It may involve the arms, face and ears but usually spares the trunk.

Dengue Fever and Dengue Haemorrhagic Fever

Aedes aegypti Mosquito

Clinical Case Definition for Dengue Hemorrhagic Fever

4 Necessary Criteria:
Usually develops around 3rd 7th day of illness Fever, or recent history of acute fever Hemorrhagic manifestations Low platelet count (100,000/mm3 or less) Objective evidence of leaky capillaries:
elevated hematocrit (20% or more over baseline) low albumin pleural or other effusions

Four Grades of DHF

Grade 1
Fever and nonspecific constitutional symptoms Positive tourniquet test is only hemorrhagic manifestation

Grade 2
Grade 1 manifestations + spontaneous bleeding

Grade 3
Signs of circulatory failure (rapid/weak pulse, narrow pulse pressure, hypotension, cold/clammy skin)

Grade 4
Profound shock (undetectable pulse and BP)

Warning Signs for Dengue Shock

Alarm Signals: Severe abdominal pain Prolonged vomiting Abrupt change from fever to hypothermia Change in level of consciousness (irritability or somnolence)

Four Criteria for DHF: Fever Hemorrhagic manifestations Excessive capillary permeability 100,000/mm3 platelets Initial Warning Signals: Disappearance of fever Drop in platelets Increase in hematocrit

When Patients Develop DSS: 3 to 6 days after onset of symptoms

SEROLOGY
10 dengue Infection: IgM produced by 5th day of symptoms and persists for 30-60 days. IgG appears by 14th day and persist for life.
20 dengue Infection: Induces IgM response after 20 days of infection. IgG rises within 1-2 days after onset of symptoms

Criteria for admission (any of the following) in the presence of suspicion of dengue fever
Restlessness or lethargy Cold extremities or circumoral cyanosis Bleeding in any form Oliguria or reluctance to drink fluids Rapid and weak pulse Capillary refill time > 2 seconds Narrowing of pulse pressure <20mmHg or hypotension Haematocrit of 40%, or rising Platelet count of <100,000 Acute abdomianl pain Evidence of plasma leakage: pleural effusion, ascitis

Fever
Enhances immune functioning Antipyretics
length of illness and viral shedding Negative impact on bacterial illness vaccine antibody response

John Mc Intyre Arch Dis Child 2011;96:1175-1179

Paracetamol
Clinical phases after toxic ingestion. 1 Early symptoms (1st day): nausea, vomiting 2 Latent phase (1-2days): may have some improvement over the next 48 hours but liver enlarges and LFT rises 3 Liver failure (3-5 days): enlarged tender liver, jaundice, hypoglycemia, hypotension, varied cardiac arrhythmia and metabolic acidosis, acute haemolytic anaemia and hypothrombinaemia

Iron
Acute poisoning occurs in stages:

1.

2.

3.

Stage I (30 mins-12 hrs) Local toxicity: Acute GIT upsets with epigastric pain, nausea, vomiting, dehydration, haemetemesis and bloody diarrhoea Stage II (8-16 hrs) Systemic toxicity: Signs of acute encephalopathy (severe headache, confusion, delirium, convulsions and coma), acidosis and circulatory collapse and hepatic impairment may occur Stage III (2-5 wks) Late complications: GIT stricture

Salicylate
Stimulates CNS directly to cause hyperpnoea and produce metabolic derangement with accumulation of organic acids Blood pCO2, HCO3 and pH fall progressively At therapeutic doses interferes with platelet aggregation- > bleeding time Toxic doses lowers plasma PT levels by interfering with utilization of vitamin K in the liver Gastric mucosal injury and gastric bleeding (presence of alcohol increases mucosal injury)

Clinical features acute poisoning

Severe
Severe hyperpnea, coma, cyanosis, oliguria, uremia, pulmonary oedema, and respiratory failure. Hypoglycemia

Anaphylactic reaction
Asthmatics should avoid

Salicylate Monogram

Contraindications for lumbar puncture in suspected acute bacterial meningitis

Signs suggesting raised intracranial pressure Reduced or fl uctuating level of consciousness (Glasgow coma scale score <9 or a drop of 3 or more) Relative bradycardia and hypertension Focal neurological signs Abnormal posture or posturing Unequal, dilated, or poorly responsive pupils Papilloedema Abnormal dolls eye movements Shock Extensive or spreading purpura Convulsions Coagulation abnormalities
Coagulation results (if obtained) outside the normal range Platelet count below 100109/litre Receiving anticoagulants

Local superfi cial infection at the lumbar puncture site Respiratory insuffi ciency

Stridor
Comfortable position with parent Oxygen-nasal prong only + oximetry Steroid 0.6 mg/im (max 12 mg) stat, then prednisolone 1 mg/kg 8-12 hourly Epinephrine 1/1000, 0.5 ml/kg/dose (max 6 ml) repeat in 2 hours if required (improves in 30 min lasts 2 hours) Encourage oral fluids Intubation and tracheostomy

Aetiology

Viruses causing croup

PI (commonest), RSV, Inlfuenza virus, measles virus

Bacterial
Staph, streptococcus Diphtheria H. influenza

FB and inhalation of hot gases Acute angioneurortic oedema Expanding mediasternal masses tetany

Characteristic findings in Bronchiolitis

Sharp dry cough following coryzal Cyanosis or pallor Tachypnoea, apnoea <4mo Subcoastal, intercostals recession Hyperinflation of chest
prominent sternum Liver displaced downwards

Auscultation
Fine end-inspiratory crackles Prolonged expiration

Bronchiolitis treatment

Oxygen by nasal cannula Pulse oximetry and apnoea monitor Nebulised ipratropium, bronchodilator Fluids by NG or IV Observe: colour, RR Ventilation 2% and pattern of breathing Oxygen saturation Ribavirin
Shortens viral excretion and clinical sympoms In cardiopulmonary disorders, immune deficiency

Palivizumab- high risk preterms

PEFR: (5 X Height cm) 400 50

Acute asthma Mx.

Give oxygen
Nasal prong/cannula 1-2L/min Partial rebreathing mask, 10-12L/min-50-60% Non-rebreathing mask, 10-15L/min-95% Venturi-type, room air with O2 25-60%

Monitoring + pulse oximeter Hydration Nebulised bronchodilator

6-9L of oxygen driven, volume of 4 ml over 20 min and 3X in 1 hour

Steroids
Oral 1-2 mg/kg/day or IV 4mg/kg hydrocortisone

Agents causing pneumonia in children

Viruses RSV,PI: infants and young children
Mycoplasma, commonest in school going children

Bacteria
Pneumococcus all ages common Haemophilus influenza Staphylococcus aureus

World Health Organization Revised 1990

MANAGEMENT OF THE PATIENT WITH DIARRHOEA

Loose or watery stool loose stools with blood

FIRST, ASSESS YOUR PATIENT FOR DEHYDRATION

1.LOOK AT: CONDITION EYES TEARS MOUTH AND TONGUE THIRST

Well, alert Normal Present Moist Drinks normally not thirsty

Restless, irritable Sunken Absent Dry Thirsty, drinks eagerly

Lethargic or unconscious, floppy Very sunken and dry Absent Very dry Drinks poorly or not able to drink
Goes back very slowly

Goes back quickly 1.FEEL 1.DECIDE SKIN PINCH The patient has NO SIGNS OF DEHYDRATION

Goes back slowly

If the patient has two or more signs including at least one sign there is SOME DEHYDRATION

If the patient has two or more signs including at least one sign, there is SEVERE DEHYDRATION

1.TREAT

Use Treatment Plan A

Weigh the patient, if possible, and use Treatment Plan B

Weigh the patient AND USE Treatment Plan C URGENTLY