kundenlogo case discussion fau erlangen 13.12.2002 wolfgang freisinger a 54-day-old premature girl...
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Kundenlogo
Case Discussion
FAU Erlangen 13.12.2002
Wolfgang Freisinger
A 54-Day-old Premature Girl with Respiratory Distress and
Persistent Pulmonary Infiltrates
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Chief Complaint
• A 54-day-old girl was admitted to the hospital because of recurrent respiratory distress and failure to gain weight
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SH - Mother
• 38-year old woman ( gravida 2, para 0 )– Group B, Rhesus positive blood– Immune to rubella, negative serologic test for syphilis
• Smoking during pregnancy – Less than 1 pack a day
• Respiratory tract infection several weeks before delivery– Treatment with erythromycine was successfull
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PMH - Child
• Delayed fetal growth
• Born at 35 ½ weeks gestation by urgent cesarean section, performed after detection of meconium on amniocentesis and increased fetal heart rate
• Birth weight was 1520g
Is she a high-risk-infant ?
– Yes, because of underweight, premature birth, mother smoking, meconium stained fluid
• APGAR: 7 after one minute, 8 at five minutes, no resuscitation was required
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PMH - Child (2)
• Stable during and after brief administration of supplemental oxygen
• No evidence of meconium aspiration
• Placenta was small and showed a small, healed infarct
• Tests for CMV and toxoplasmosis were negative
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9.400 – 34.000
54-623-5
25-33
3-71-30-0,75
1,500-3,000/mm³84,000-478,00048-69
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HPI – 4th day of life
• child was transferred elsewhere for feeding and growth
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HPI – 8th day of life
• Development of a diaper rash
• No response to multiple measures
– Alternatives to cow milk don‘t bring any benefit
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HPI – 26th Day of Life
• Child is in tachypnea, with intercostal retractions
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CXR 26th day of life
Anteroposterior Film of the Chest on the 26th Day of Life. The lungs are hyperinflated, with bilateral streaky opacities in a parahilar, peribronchial distribution. The heart appears normal, and the superior mediastinal contour is narrow. There is a bone-within-bone appearance of the vertebral bodies and anterior flaring of the ribs.
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CXR 26th Day of Life
Lateral Film of the Chest on the 26th Day of Life. The lungs are hyperinflated, with bilateral streaky opacities in a parahilar, peribronchial distribution. The heart appears normal, and the superior mediastinal contour is narrow. There is a bone-within-bone appearance of the vertebral bodies and anterior flaring of the ribs.
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HPI – 26th Day of Life
Management ?
• Specimens were obtained for culture
• Administration of Gentamicin and Ampicilline
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CXR 30th day of life
Air – space Disease in the right upper lobe, a finding consistent with the presence of atelectasis
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HPI – 30th Day of Life
• Blood cultures were positive for coagulase-negative streptococci
• Administration of antibiotics for additional 11 days
• Condition improved
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HPI – 36th Day of Life
• Radiographic findings had improved
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HPI – 40th Day of Life
• Three days after the end of the antibiotic treatment : tachypnea recurred
• But : another radiograph still shows improvement
What would you do?
• Administration of Cefuroxime, Clindamycin and Cisapride
• Baby‘s conditon improves again
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HPI – 44th Day of Life
• CXR again shows abnormalities
• Infant ist transferred to hospital this day
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PE
• Axillary Temp. 36,2°C
• Pulse: 99
• Respirations 70 / min while breathing oxygen by nasal cannula
• BP: 105/90
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PE
• Length 41cm (below 2 SD of new born)
• Weight 2100g (below 2 SD of new born)
• Head circumference: 34.5 cm (1 SD below the mean)
• Lungs: occasional wheezes and scattered fine crackles are heard bilaterally
• Minimal subcostal retractions
• Liver edge palpable 5mm below right costal margin
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Assessment
44-day-old premature girl with recurrent respiratory distress, severe lymphopenia and failure to gain weight
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Cultures and serologic studies
• No evidence of
– Chlamydia
– RSV
– Adenovirus
– Influenza A Virus
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Stool specimen
• No ova or parasites
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Initial Treatment
• Erythromycine and multivitamin
• Albuterol by nebulizer
• Axillary temperature does not exceed 37.7° but is normal on most occasions
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Stained blood smear
• Anisocytosis (+)
• Poikilocytosis (+)
• Polychromatophilia (+)
• Hypochromia (+)
• Many microcytes
• Few macrocytes
• Rare teardrop cells and schistocytes
• 2 nucleated red cells per 100 white cells
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Effect of the therapy
• Infant‘s condition improves and remains stable for several days
• Considerable mucus production and coughing
• Moderate respiratory distress (50-60/min)
• Axillary temp 36,4°C
• Pulse 179 /min
• SpO2: 89 %
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ABG
While breathing supplemental oxygen
• Oxygen: 137 mmHg
• Carbon Dioxide: 46 mmHg
• pH 7.39
• Bicarbonate 28 mmol/l
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CXR After Initial Treatment
• Resolution of pulmonary abnormalities
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Upper GI Series
• Normal findings
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DD
• AIDS/ HIV Infection
• Intestinal Lymphangiectasia
• Severe Combined Immunodeficiency SCID
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AIDS
• Could explain this form of prolonged and profound lymphopenia in adults
• But in this case– There is no evidence for HIV-Infection of the mother
– No risk factors of the mother are known
– CD4+ Lyomphopenia is manifested later in life
– No clinical features or lymphadenopathy characterisic of pediatric AIDS
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Intestinal lymphangiectasia
• Leads to extensive lymphopenia and accumulation of lymphocytes in the gut
• BUT:
– Infants are immunocompetent and do not aquire early opportunistic infections
– The absence of diarrhea makes this diagnosis unlikely
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Forms of Severe Combined Immunodeficiency ( SCID )
• SCID with deficient T- cells and normal or high levels of B-cells
– X-linked form (common -chain-deficiency)
– Autosomal recessive form: Janus kinase 3 (JAK3) deficiency
• SCID with deficient T-cells and B-cells– Adenosine deaminase (ADA) deficiency
– Defect in Recombinase activating gene (RAG) 1 or 2
– Reticular dysgenesis
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Red Cell Studies
• Absence of adenosine deaminase activity and elevated levels of deoxyadenosine triphosphate
• Levels of purine nucleoside phosphorylase normal
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Peripheral blood lymphocytes
• No proliferative response to phytohemagglutinin
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SCID due to ADA-Deficiency
• Autosomal - recessive form; 20% of all SCID patients
• Due to various mutations in the ADA gene
• Accumulation of adenosine, deoxyadenosine deoxyadenosine triphosphate and S-Adenosy-L-homocysteine are toxic to lymphocytes this causes the immunodeficiency
• ADA-SCID presents with a more severe lymphopenia than other forms of SCID (absol. counts < 500/mm³)
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Clinical Presentation of SCID due to ADA
• Lymphopenia with marked depletion of T and B lymphocytes
• Normal or increased NK Cells
• No corticomedullary demarcation of the thymus (Absence of Hassall‘s bodies and thymocytes)
• Lymphnodes retain their normal architecture but contain only very few lymphocytes
• Rib cage abnormalities similar to rachitic rosary, predominantly at the costochondral junctions, the apophyses of the iliac bones and in the vertebral bodies
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Clinical Presentation of SCID due to ADA (2)
• Circulating B-cells may present in some patients
• Severity depends on the type of mutation in the ADA gene and the resulting degree of the ADA definciency
• Growth and developmental abnormalities, including neurologic and osseous findings, have been observed
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SCID Treatment of the Patient
• Our patient was treated with polyethylene-glycol – modified adenosine intramuscularly, initially twice a week, guided by the levels of ADA and the toxic metabolites
• She began smiling and interacting with the environment already after two doses of ADA
• Suspected P. carinii infection was treated with Trimethoprim-Sulfamethoxazole i.v.
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SCID Treatment
• HLA identical or haploidentical bone marrow transplantation without chemotherapy
– first perfomed in 1969
– graft-versus-host disease is uncommon
– Survival ~100% for HLA identical and 78% for haploidentical graft
• Gene therapy
• Substitution of the enzyme
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Follow Up
• 500 mg immunoglobuline per kilogram every three or four weeks will give her enough protection
• No live vaccinating agents
• She is expected to grow and develop normally
• The cartilaginous abnormalities should disappear
• She can have a normal diet
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Thank you for your attention