PROLONG FEVER

Siti hamidah

Nurfarhana

Medical students UniSZA

Year 3 (2013)

DATAName:---------

Age: 8 months

Gender: Female

Race: Malay

Religion: Islam

Address: kuala berang

Date of Admission: 6/1/2014 ;16:46

Date of Clerking: 16/1/2014

Date of Discharge: -

Informant: Mother

CHIEF COMPLAINT

Fever 1 day prior to admission

HISTORY OF PRESENTING ILLNESS

•Fever 1/7 prior to admission. Fever since 5 months of age. It was on and off without chill and rigor. Currently, The fever was associated with runny nose and sore throat. Documented temperature was 38°C at home.

•Worsening noisy breathing and rapid breathing 1/7 which preceded by cough 2/7. the cough chesty in nature with no facial congestion and no paroxysmal cough.

•Went to hospital hulu terengganu at 11.30am

•Less active and reduce oral intake.

•At hospital hulu terengganu treated as severe croup and was given neb adrenaline once and iv hydrocort.But at 2pm there was worsening respiratory distress + sridor.

•Admitted to PICU hsnz at 4.50pm, was ventilated and sedated, Condition pink, not tachpneic, rashes whole body.

• Transfer to general ward on 8/1/2014, spiking temperature

• 10/1/2013 admitted again to PICU due to respiratory distress + stridor + hyperextended neck with tongue protuded, was given iv dexa 1.6mg + iv ig infusion 12g over 16h on allergic reaction develop.

• Vital sign was stable and afibrile.

SYSTEMIC REVIEW

CNS= no fit/seizure, no abnormal movementCVS= no cyanosis, no pedal edema, no shortness of breath.GIT= reduced oral intake and vomiting with no altered bowel habit, no abdominal distension, no loss of weight.Genitourinary= normal colour urineHematology= not sudden bruise and sudden bleeding.

ANTENATAL HISTORY

•Attend check up regularly.

•Mother has asthma and taking inhaler

•Mother had no diabetes, no hypertension and no complication during pregnancy.

BIRTH HISTORY

•born at preterm (36 weeks) via spontaneous vaginal delivery at hospital.

•Weighing 2.3 kilogram.

NEONATAL HISTORY•Neonatal jaundice for 4 days

•No treatment of phototheraphy

FEEDING AND DIETARY HISTORY

•breast fed from birth until 3 months and was on formula milk.

•4 ounces 4-3 times per day

DEVELOPMENTAL HISTORY

Gross Motor: She was able to control head but unable to crawling or standing unsupported.

Vision and Fine Motor: She was able to reach object.

Hearing, Speech and Language: babbles

Social, Emotional and Behavioural: She was able to smile

IMMUNIZATION HISTORY

•Miss immunization for hep B dose 3 at 6/12 due to fever.

•last immunization at 5 months old was the acellular pertussis vaccine dose 3 (DTaP), inactivated polio vaccine dose 3 (IPV) and Haemophilus influenza b vaccine dose 3 (Hib).

PAST MEDICAL AND SURGICAL HISTORY

•No chronic illness.

•3rd hospitalization = 1st hospitalization was during after birth due to neonatal jaundice, 2nd hospitalization last month due to fever.

•Never done any surgical procedure before.

DRUG AND ALLERGY

•Not in regular medication

•No known history of allergic

FAMILY HISTORY

•Father = 29 years old works as officer at primary school, healthy.

•Mother = 27 years old works as officer at KK Putrajaya, has asthma on medication

•She is 1st child in family

•No known history of cancer/ same illness in family.

SOCIAL HISTORY

•She had taken care by her grandmother in a house with adequate facilities.

•Father not a smoker and no other risk exposure of cigarette smoke.

•Father financial status is stable.

•No history of travelling to endemic area

CASE SUMMARY

My patient 8 months old malay girl, admitted to hospital due to fever 1/7. she has fever since 5 months old which is on and off + URTI symptoms. Currently fever associated with noisy breathing and rapid breathing. Cough chesty in nature. There had rashes whole body

Management for patient

Iv dexamethasone1.5mg

Sy paracetamol 100mg

Sy piriton 0.6 mg

Calamine lotion

syrup aspirin 50mg

Iv globulin infusion 12g over 16h

Monitor vital sign

Iv penicillin

NON INFECTIOUS CAUSES OF PROLONGED FEVER

What is Kawasaki Disease?

• Idiopathic multisystem disease characterized by vasculitis of small & medium blood vessels, including coronary arteries

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Diagnostic Criteria• Fever for at least 5 days fever is usually high,

greater than 102°F, does not respond well to antipyretics, and can last 1-2 weeks.

• At least 4 of the following 5 features: 1. Changes in the extremities

Edema, erythema, desquamation

2. Polymorphous exanthem, usually truncal

3. Conjunctival injection

4. Erythema&/or fissuring of lips and oral cavity

5. Cervical lymphadenopathy (early disease)

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Atypical or Incomplete Kawasaki Disease

• Present with < 4 of 5 diagnostic criteria• Compatible laboratory findings• Still develop coronary artery aneurysms• No other explanation for the illness• More common in children < 1 year of

age

Phases of Disease• Acute (1-2 weeks from onset)

– Febrile, irritable, toxic appearing– Oral changes, rash, edema/erythema of feet

• Subacute (2-8 weeks from onset)– Desquamation, may have persistent arthritis

or arthralgias– Gradual improvement even without treatment

• Convalescent (Months to years later)- In this phase remaining symptoms resolve &

laboratory values normalize.

Acute changes =erythema and edema of hands and feet, usually on the dorsal surfaces.Erythema of palms & soles Usually start 3-5 days after onset of fevers

desquamation in subacute phaseBeau lines may be seen 2-3 months after onset

Polymorphous, non-vesicular rash

Present in 99% of cases Usually maculopapularCharacteristic confluence in perineum (60%)Often not pruritic

the first week, patients can develop bilateral,

painless bulbar conjunctival injection

without exudate.erythema and cracking

of lips, a strawberry tongue

Trager, J. D. N Engl J Med 333(21): 1391. 1995.

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JIA

Systemic JIA• Definition:

– Arthritis with, or preceded by, daily fever of at least 2 weeks’ duration

– Fevers are quotidian (daily) for at least 3 days and is accompanied by one or more of the following:

• Evanescent, non-fixed, erythematous rash• Generalized lymph node enlargement• Hepatomegaly and/or splenomegaly• Serositis

Overview of Systemic JIA• 10-15% of all JIA patients• Broad peak of onset 1-5 years• M:F 1:1• Variable number of joints• Il-6 is elevated and correlates with disease activity

• Extra articular symptoms: – Fever 100 %– Rash 95%– Hepatosplenomegaly, 85%– Lymphadenopathy 70%– Pericarditis 35%– Pleuritis 20%

• It begins with repeating fevers that can be 103°F or higher + salmon-colored rash that comes and goes.

• Systemic onset JIA= cause inflammation of the internal organs as well as the joints.

Quotidian fever Intermittent fever of systemic JIA .The fever spikes usually occurred daily in the late evening to early morning (quotidian pattern), returned to normal or below normal, and were accompanied by severe malaise, tachycardia, and rash.

• Rash - – Salmon colored– Maculopapular –

flat to slightly raised– Trunk and

extremities– Migratory– Pruritic 5%– Persistent with

fever spike

investigation

• Anemia (a low red blood cell count) and elevated white blood cell counts are also typical findings in blood tests

• negative rheumatoid factor blood test

treatment

Medications

• NSAID= naproxen (Naprosyn) or ibuprofen (like Motrin or Advil)

•Disease-Modifying-Anti-Rheumatic-Drugs (DMARDs)= methotrexate (Rheumatrex) and sulfasalazine (Azulfidine)

•Steroids, such as prednisone

• Physical and Occupational Therapy

• Surgery

• Diet and Exercise

Systemic Lupus Erythemotosus

causes lupus in children• Genetics• Environmental exposures?• Medications:

– Minocycline (an antibiotic often used for acne in adolescents) is a well-known cause of positive ANA and lupus-like syndromes. Symptoms often resolve after discontinuation.

– Antiseizure medications, antihypertensive (blood-pressure), and several other medications can have similar effects, though are less commonly used in children and teens.

presentation• Common initial presentations:

– Unexplained fevers or prolonged general illness without explanation

– Swollen lymph nodes

• Other initial presentations:– Kidney disease

• up to 80% of patients eventually.– Neurologic symptoms

• Seizures, psychosis, movement problems, etc.– Blood clots

• Antiphospholipid antibodies are relatively common.– Other

• Heart disease• Lung disease• Organ enlargement

Diagnosis of lupus in childrenSymptoms:

• Photosensitivity•Malar rash•Discoid rash•Oral ulcers•Arthritis•Pleurisy or pericarditis, •Seizures or psychosis•Raynaud’s phenomenon•Hair loss

Lab tests:• Proteinuria, hematuria, other urine abnormalities• Low white blood cells, low platelets, hemolytic anemia•Positive ANA•Positive anti-Smith or anti-dsDNA•Anti-Ro, anti-La, anti-RNP, anti-histone•Coombs test•Low complements•Elevated inflammatory markers

Treatment of lupus in children

• Generally similar to that of adults.corticosteroids (e.g. prednisone or SoluMedrol) to control symptoms–Mild lupus

• Often responds to hydroxychloroquine (Plaquenil).

• May benefit from NSAIDs (ibuprofen, naproxen, etc.) for musculoskeletal symptoms.

–Moderate lupus• azathioprine (Imuran) or mycophenolate (CellCept). These are often

used for hematologic or renal involvement of the disease.

–Severe lupus• cyclophosphamide (Cytoxan) or sometimes rituximab (Rituxan), for

involvement of the central nervous system or for severe kidney or hematologic disease.

MALIGNANCY

• Leukemia results from an event in a bone marrow precursor cell which gives rise to immature progeny that have lost the capacity to differentiate and proliferate in an uncontrolled manner

• Immature progeny (blasts) expand in marrow and impair normal hematopoiesis

LEUKEMIA

Childhood Leukemia

• Leukemia is the most common form of cancer of childhood (30%)

• Peak incidence 2-5 years of age• males > females• Incidence of ALL (acute lymphoblastic

leukemia) is 5 times higher than incidence than AML (acute myeloid leukemia)

Causes of acute leukemias

• idiopathic (most)

• chemicals, drugs

• ionizing radiation

• viruses (HTLV I)

• hereditary/genetic conditions

Classification of leukemias

Acute Chronic

Myeloid origin

Lymphoid origin

Acute Myeloid Leukemia (AML)

Acute Lymphoblastic Leukemia (ALL)

Chronic Myeloid Leukemia (CML)

Chronic Lymphocytic Leukemia (CLL)

Common Presenting Signs and Symptoms

• Expanding blast population in bone marrow causes bone and joint pain

• Pallor and fatigue due to anemia• Bruising, petechiae and bleeding due to

thrombocytopenia• Fever due to infection and cytokines from leukemia • Adenopathy, hepatomegaly and splenomegaly due

to blasts migrating out of marrow

Clincal manifestations

• symptoms due to:– marrow failure– tissue infiltration– leukostasis– constitutional symptoms– other (DIC)

• usually short duration of symptoms

Marrow failure

• neutropenia: infections, sepsis

• anemia: fatigue, pallor

• thrombocytopenia: bleeding

Infiltration of tissues/organs• enlargement of liver, spleen, lymph nodes• gum hypertrophy• bone pain• other organs: CNS, skin, testis, any organ

Leukostasis

• accumulation of blasts in microcirculation with impaired perfusion

• lungs: hypoxemia, pulmonary infiltrates

Constitutional symptoms

• fever and sweats common

• weight loss less common

Laboratory features

• WBC usually elevated, but can be normal or low

• demonstrate anemia, thrombocytopenia, leukocytosis or leukopenia with circulating blasts

• normocytic anemia

• DIC

Distinguishing AML from ALL

• light microscopy– AML: Auer rods, cytoplasmic granules– ALL: no Auer rods or granules.

• flow cytometry

• special stains (cytochemistry)

TREATMENT

Choice of Rx is influenced by:

• type (AML vs ALL)• age

Treatment of leukemias – – There are 2 goals:

• Eradicate the leukemic cell mass• Give supportive care

There are four general types of therapy• Chemotherapy – usually a combination of drugs is

used• Bone marrow transplant• Radiotherapy• Immunotherapy – stimulate the patients own

immune system to mount a response against the malignant cells

• Monoclonal antibodies – examples include Rituxin

LYMPHOMA

HODGKINS NON-HODGKINS

LYMPHOBLASTIC LYMPHOMA

BURKITT’SLYMPHOMA

LARGE CELLLYMPHOMA

IMMUNOBLASTIC ANAPLASTIC

(40%) (60%)

(<15%) (30-40%) (40-50%)

(50%) (50%)

Non-Hodgkin’s Lymphoma

Malignant solid tumor of immune system Undifferentiated lymphoid cells Spread: aggressive, diffuse, unpredictable Lymphoid tissue; BM and CNS infiltration High growth fraction and doubling time Dx and Rx ASAP Rapid CTX response; tumor lysis concern

Incidence/Etiology - NHL

6% childhood cancer 60% of childhood lymphomas

Peak age of 5-15; M:F ratio of 2.5:1 Increased with

SCIDS, HIV, EBV post solid organ transplant

Geographic, viral, genetic & immunologic factors

Types of NHL

Lymphoblastic (30-35%)– 90 % immature T cells (very similar to

T-ALL)• remainder pre-B phenotype (as in ALL)

– 50-70% anterior mediastinum– neck, supraclavicular, axillary

adenopathy– Classic: older child with

intussusception

Large-cell lymphoma (15-20%)- Diffuse Large B-cell lymphoma

(DLBCL)- frequent Mediastinal involvement- More like Hodgkin lymphoma than other

NHLs- “Peripheral T-cell” lymphoma- Often involves skin, CNS, lymph

nodes, lung, testes, muscles, and GI tract

Burkitt Facts• 100 new cases/year in US, 2-3:1

male:female; mean age 11 years (in non-endemic form)

• small, noncleaved cell; mature B phenotype; intraabdominal (sporadic) or jaw (endemic) most common primary site

• Extremely rapidly-growing; tumor lysis issues

Clinical Presentations Abdomen: (35%): pain, distention,

jaundice, GI problems, mass Head/neck (13%): lymphadenopathy,

jaw swelling, single enlarged tonsil, nasal obstruction, rhinorrhea, cranial nerve palsies

Mediastinum (26%): SVC syndrome CNS (rare): HA, V, irritability,

papilledema+Fever, malaise, night sweats, wt. loss,

Hodgkin’s Disease

Immune system malignancy, involving B or T lymphocytes

Reed-Sternberg cells Spread: slow, predictable, with

extension to contiguous lymph nodes

Infiltration to non-lymphoid organs is rare

Hodgkin’s disease with Reed Sternberg celloften CD20+

Incidence and Etiology

Hodgkin’s 5% of childhood cancers Bimodal peaks, at 15-35 and >50;

rare < 5 M:F ratio of 3:1; variation r/t

geography and SES, and type Increased in immunologic

disorders, HIV, EBV

Types of Hodgkin’s Lymphoma

Nodular sclerosing (NS), 40-60%, lower cervical, supraclavicular, mediastinal nodes

Mixed cellularity (MC), 15-30%; advanced disease with extranodal involvement

Lymphocyte predominance (LP), 5-15%, presents as localized disease

Lymphocyte depletion (LD) (<5%); widespread disease

Clinical Presentation

Painless lymph node swelling (90%) that persists despite antibiotic therapy

Palpable non-tender, firm, mobile, rubbery nodes; Mediastinal adenopathy (60%); SVC

Bulky: when mass is > 1/3 thorax diameter

symptoms: Fever of >38C for 3 days, drenching night sweats, 10% weight loss

Treatment

Surgery Radiation TherapyChemotherapy: with overall cure rates

60-80+%