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ERYTHEMATOSUS
GENERAL DATA
• PM
• 9 y/o
• Female
• EDD/PA
• Roman Catholic
• Born on 22 May 2008
• Zamboanga del Sur
• Admitted for the first time on13 August 2017
CHIEF COMPLAINT
• Increased Blood Pressure (160/100)
HISTORY OF PRESENT ILLNESS
(+) Abdominal
enlargement
↑ in abdominal girth
Discharged after 2
weeks
HISTORY OF PRESENT ILLNESS
Medications
Self-medicated
withSambongand Banaba
leaves
HISTORY OF PRESENT ILLNESS
Recurrence of bilateral
edema and ascites
1 MONTH PTA
Progression of bilateral
pitting edema and ascites
HISTORY OF PRESENT ILLNESS
Consult with
Pediatrician
Advised to transfer to
AFPMC
Admission at our
institution
PAST MEDICAL HISTORY
• (-) Hypertension • No allergies to food and drugs
• (-) Diabetes Mellitus • No previous hospitalizations
• (-) Bronchial Asthma • No previous surgeries
• (-) Blood Dyscrasia • No history of blood transfusion
• (-) PTB
• (-) Thyroid Diseases
• (-) Cancer
FAMILY HISTORY
PATERNAL SIDE MATERNAL SIDE
• (+) Hypertension • (+) Hypertension
• (+) Diabetes Mellitus • (+) Diabetes Mellitus
• (+) Bronchial Asthma • (-) Bronchial Asthma
• (-) Cancer • (-) Thyroid Diseases
• (-) Cancer
FAMILY PROFILE
• Father: 35 y/o, active military for 14 years (SSG), asthmatic
• Mother: 37 y/o, housewife, apparently well
• Brother: 8 y/o, NSD, Grade I, apparently well
SOCIAL AND ENVIRONMENTAL HISTORY
• Lives with parents, grandparents, and brother in
Zamboanga del Sur
• Currently in Grade III
• Drinking water: Distilled Water
• Has no food preference
• Water supply: Zamboanga del Sur Water District
Physical Examination
General Survey
• Conscious, coherent not in cardiorespiratory distress
• GCS 14 (E4V4M6)
• BP- 110/70
• PR-130
• RR- 25
• Temp- 37.0
• O2 Sat- 96%
Visual Acuity
• Patient has difficulty on verbalizing
Nystagmus Headache
Vomiting
Vision loss
Enlarging head
circumference
OPTIC NEURITIS
Preferential gaze
Nystagmus
History of
autoimmune
disorder (lupus
nephritis)
COURSE IN THE WARD
DATE S O PLAN
15 AUG 17 (+) Generalized Wt: 28.2 • Low Salt Low Fat diet
body weakness BP: 130/100 • BP monitoring strictly q2
3RD HD Ti: 390 • Referred to pedia-nephro:
T0: 300 Start albumin 25% 100cc x 4H
UO: 0.44cc/kg Furosemide 20mg/TIV mid and post albumin
BSA: 0.96 w/ strict bp prec
T: 38.4 Hold captopril
Start amlodipine 5mg/tab q12
• bipedal and Nifedine 10mg/tab q6H
facial Diazepam 8mg TIV for active seizure
edema Start ceftriaxone 700mg TIV q12H—(50mkd)
• increased • Fluid was restricted to 200cc q8H
abdominal • (Paracetamol 250mg/ 5ml, 6ml q4 (T> 37.8)
girth, • Diagnostic: TPAG now
Date S O Plan
16 AUG 17 Loss of BP: 140/100 Transfer to PICU
vision CR: 96 Medications:
RR: 30 1. Albumin 25% 100c x 4H
T:36.9 2. Furosemide 20mg/TIV mid and post
O2sat: 97% albumin
AC: 73.5 3. Furosemide 20mg/TIV q8
4. Amlodipine 5mg/tab, 1 tab q12
5. Nifedine 10mg/tab q6H
4th HD; DX: Nephrotic 6. Metoprolol 50mg/tab, 1 tab OD
1st PICU Syndrome; t/c 7. Ceftriaxone 700mg/TIV q12
Lupus Nephritis 8. Diazepam 8mg/TIV for active seizure
Date S O Plan
17 (+) bipedal and Wt: 28.2 • Diagnostic: Mantoux test, Repeat UA
AUG facial edema AC: 73.5 • Medications:
17 T:36.6 1. Albumin 25% 100c x 4H
increased UO 1.12cc/hr 2. Furosemide 20mg/TIV mid and post albumin
abdominal girth 3. Furosemide 20mg/TIV q8
4. Amlodipine 5mg/tab, 1 tab q12
discoid rash on the 5. Nifedine 10mg/tab q6H
extremities 6. Metoprolol 50mg/tab, 1 tab OD
(bilateral) DX: Lupus 7. Ceftriaxone 700mg/TIV q12
Nephritis 8. Diazepam 8mg/TIV for active seizure
9. Calcium Carbonate 500mg/tab, 1 tab BID
10.Calcitriol 0.25mg/tab, 1 tab ODHS
11.Prednisone20mg/tab, 1 tab OD in am
12.Paracetamol 250mg/5ml, 6ml q4 for T:37.8
Date S O Plan
25 2 days PTC: • GCS: 12 (E3V6M3) • For referral to: Neuro service for Acute Visual
AUG • preferential • VA: No visual threat Loss probably Central in origin
gaze, left • Pupils: 5-6mm dilated NRTL • For Cranial MRI with Orbital Cuts
17 • EOM: Preferential gaze, right • Refer back once with MRI Result or if once
1 day PTC: even on L lateral decubitus but stable for full Ophtha exam or re-assessment
• preferential observed some central and
gaze, right left gaze
• Fundus: (+ROR), clear media,
well defined margin, AVR 2:2,
CDR 0.3
DX:
• Normal fundus finding at time
of examination
• Preferential right gaze
• T/C Acute Visual Loss probably
Central
Date S O Plan
08 Awake, • (-) Edema, CRT <2s Rheuma consult was done w/ following
Sept not in • CR: 107 suggestions:
17 distress • RR: 22-24, O2Sat:98% Increase: Prednisone 20mg/tab, 2
• (-) fever (36.1- 36.7) tabs OD after meal
• BP: 110/80 Secure Cyclophosphamide & start
• (-) bleeding 500mg IV once a month for 6 months,
• GCS 15 then 3 mos there after
Hgb 101 86
Eo 0 0.01
K 5.9
Imaging
Cranial MRI with Orbital - Moderate diffuse parenchymal loss involving the cerebral hemispheres bilaterally.
cutz This is frequent intracranial manifestation of systemic lupus erythematous or maybe
09/18/2017 a consequence of a prior episode of lupus cerebritis
- There is a focal cortical encephalomacia involving the left parietal lobe, which is
probably a residua from a prior inflammatory or vascular injury.
- MRI of the orbits demonstrate abnormal enhancement involving the left optic
nerve, consistent with left optic neuritis. There also appears to be mild abnormal
enhancement of the intraorbital segment of the right optic nerve. These are of
uncertain etiology.
KUB Ultrasound -Negative ultrasound study of both kidneys and urinary bladder
09/20/17
OPHTHALMOLOGY NOTES
Date S O Plan
DX:
• Optic Neuritis, resolving
OPHTHALMOLOGY NOTES
Date S O Plan
4 Oct (-) fever (-) cough For possible Renal Biopsy on 11 October 2017 @
2017 (-) weakmess (-) colds PCMC
(-) decreased (-) seizure For possible transfer to PCMC on 10 Oct 2017
vision FOR BT: BT A+
(+) Good
appetite
(+) Good
Activity
OPHTHALMOLOGY NOTES
Date S O Plan
Seg 0.69
Lymp 0.22
Eo 0.01
Mono 0.07
Baso 0.01
Plt 289
Systemic Lupus
Erythematosus
Systemic Lupus Erythematosus
• chronic autoimmune disease characterized by
• multisystem inflammation
• presence of circulating autoantibodies directed against self-antigens
• occurs in both children and adults
• disproportionately affecting females of reproductive age
• most commonly involved organs: skin, joints, kidneys, blood-forming
cells, blood vessels, and the central nervous system
• Children and adolescents more severe disease and more widespread
organ involvement
Etiology
• Factors influencing risk and severity: genetics, hormonal milieu and
environmental exposures
• Specific Genetic Abnormalities: congenital deficiencies of C1q, C2, and C4, as
well as several polymorphisms, familial clustering of SLE or other autoimmune
disease, and human leukocyte antigen (including HLA-B8, HLA-DR2, and HLA-
DR3)
• Hormonal Factors: preferentially affects females during the reproductive
years; Estrogen exposure promotes B-cell autoreactivity
Epidemiology
• Prevalence of SLE
• children and adolescents 1-6/100,000
• Adults 20-70/100,000
• highest among African-Americans, Asians, Hispanics, Native
Americans, and Pacific Islanders
• Female:Male ratio
• Prior to puberty 2-5:1
• during reproductive years 9:1
Clinical Manifestations
• Any organ system can be involved
• Most common presenting complaints of children fever, fatigue,
hematologic abnormalities, arthralgia, and arthritis
• Course: periods of flare and disease quiesence or more smoldering
course
Diagnosis
• Presence of 4 of the 11 American College of Rheumatology (ACR)
1997 Revised Classification Criteria for SLE
• MUSCULOSKELETAL MANIFESTATIONS
• Intermittent polyarthritis
• characterized by soft tissue swelling and tenderness in joints, most commonly in hands, wrists, and
knees
• CUTANEOUS MANIFESTATIONS
• Lupus dermatitis can be classified as:
• Discoid lupus erythematosus(DLE)
• Systemic rash
• Subacute cutaneous lupus erythematosus (SCLE), or
• Other.
• Discoid lesions
• roughly circular with slightly raised, scaly hyperpigmented erythematous rims and depigmented,
atrophic centers in which all dermal appendages are permanently destroyed.
• Malar Rash
• butterfly rash, one of the most common signs.
• Fixed erythema over the malar eminence, usually spares the nasolabial folds.
• RENAL MANIFESTATIONS
• Nephritis
• Most serious manifestation of SLE
• Classification of lupus nephritis is primarily histologic
• Patients with dangerous proliferative forms of glomerular damage (ISN III and IV)
usually have microscopic hematuria and proteinuria (>500 mg per 24 h)
• One-half develop nephrotic syndrome, and most develop hypertension
• NERVOUS SYSTEM MANIFESTATIONS
• Cognitive dysfunction most common manifestation of diffuse CNS lupus
• Difficulties with memory and reasoning.
• Headaches
• Seizures
• Psychosis
• VASCULAR OCCLUSIONS
• Prevalence of transient ischemic attacks, strokes, and myocardial infarctions is
increased in patients with SLE
• PULMONARY MANIFESTATIONS
• Pleuritis with or without pleural effusion
• most common pulmonary manifestation
• Life-threatening pulmonary manifestations include
• Interstitial inflammation leading to fibrosis
• Shrinking lung syndrome, and
• Intra-alveolar hemorrhage
• CARDIAC MANIFESTATIONS
• Pericarditis
• most frequent cardiac manifestation;
• More serious cardiac manifestations
• Myocarditis
• Fibrinous endocarditis of Libman-Sacks.
• HEMATOLOGIC MANIFESTATIONS
• Anemia (usually normochromic normocytic)
• most frequent hematologic manifestation
• Leukopenia
• also common
• almost always consists of lymphopenia
• Thrombocytopenia
• may be a recurring problem
• GASTROINTESTINAL MANIFESTATIONS
• Nausea, vomiting, diarrhea
• Diffuse abdominal pain
• caused by autoimmune peritonitis and/or intestinal vasculitis.
• Vasculitis involving the intestine
• Perforations, ischemia, bleeding, and sepsis are frequent complications
• OCULAR MANIFESTATIONS
• About 1/3 of patients with SLE have ocular manifestations
• Sicca syndrome (Sjogren’s syndrome) and nonspecific conjunctivitis
• common in SLE and rarely threaten vision
• Retinal vasculitis and Optic neuritis
• serious manifestations:
• blindness can develop over days to weeks
Etiology:
A. Genetic factors
a. Certain HLA associations are more common in people with SLE than in the
general
b.population (e.g., HLA-A1, HLA-DR3).
Etiology:
Etiology:
• Immunologic Factors
• Recent studies in animal models and patients
have revealed several immunologic aberrations
that collectively may result in the persistence
and uncontrolled activation of self-reactive
lymphocytes
Etiology:
Mechanisms of injury
MANAGEMENT
Treatment for SLE