Case presentation

Dulawe, Anne
Gumiran, Jefferson
Kotla, Chaitanya Kumar
Munda Cruz, Reiden Flynn

Informants: Reliability
JF, mother of patient 95%
RF, the patient herself 100%

General Data
Patient RF
11 year old
Filipino
Female,
a Roman Catholic
from Atulayan sur, Tuguegarao city
admitted at Cagayan Valley Medical Center
for the first time on 8:55pm of June 26, 2014.
referred from Peoples General Hospital on the
same day.

Chief complaint:
Pain and edema of left foot.

History of present illness
10 days prior to admission
4 nonpruritic flat circumscribed rashes
with a diameter of 2mm on patients left
leg
No fever

Before
After
Six days prior to admission
pain on left ankle
Confluent rashes on both legs and dorsum of both
feet
loss of appetite
consultation at Peoples General Hospital
diagnosed with Hypersensitivity reaction
Cetirizine, 10 mg per tab 1 tab bedtime for 7
days.
On the night of the same day
nausea and vomiting
Mefenamic acid 1 capsule orally given by the
mother.
epigastric pain
Four nights prior to admission
Nausea
vomiting (once)
abdominal pain graded as 8 in a scale of 1 to 10
where 10 is the most intense.
Mefenamic acid given by mother with
subsequent relief.
Two days prior to admission
Edema of Left foot
Arthralgia on left ankle pain
massaged with oil with no relief
Rashes on both thighs.

Few hours prior to admission
patients ankle pain and foot edema worsened
hence consultation was sought at Peoples general
Hospital but was referred to CVMC hence
admission.

Past medical History
generally healthy as a child
several episodes of fever with no associated convulsions
few episodes of cough and colds but was never
hospitalized prior to current hospitalization.
Two years ago:
rashes on lower extremities with unrecalled
accompanying signs and symptoms
diagnosed with Urinary Tract infection
given unrecalled medicines
said rashes disappeared after 3 days.
no known allergies to drugs or specific foods but was
advised to avoid seafoods, dairy products, coffee and
junkfoods.

Personal and Social History
youngest of four children
father is a 49 year old government
employee
mother is a 53 year old elementary school
teacher
siblings had no history of manifesting
similar signs and symptoms of current
condition
Active in school organizations
Prenatal history
regular prenatal check-ups at Atulayan health center.
given one dose of Tetanus toxoid intramuscularly
Ferrous and folic supplementation
diet consisting mainly of rice, vegetables and meat and milk excluding
coffee and soft drinks
did not smoke cigarettes nor consumed alcoholic beverages.
No history of infections, fall/accident, and exposure to radiation
8th month of pregnancy
mild vaginal bleeding
consultation at CVMC but was referred to St. Paul Hospital
given unrecalled medicine
advised on bed rest after which the bleeding subsided

Birth History

Full term
Born to a 42 year old G4P4 (4004)
Normal spontaneous delivery
at home
attended by a midwife


Post natal History
born with pinkish body
minimal vernix caseosa
loud cry
good suck
Immediate post natal care was administered
by midwife.


Immunizations
Completed before 1 year old
single dose of BCG
3 doses of DPT, OPV and Hepa-B
single dose of Measles

BCG booster was not given
Nutritional history
breast fed for the first 2 months
mixed fed thereafter
Solid foods introduced 6 months of age
normally has good appetite
preferred soft drinks and junk foods for
snacks

Developmental milestones
Patient is an academic achiever ranking first in her
class.



Classic theories
Age Psychosexual
theory
Psychosocial
theory
Cognitive theory
School age (6-12
y/o)
latency Industry vs
inferiority
Concrete
operational
Family history
Paternal side:
(+) HPN (+) DM (-) Asthma (-) Ca (-) Tuberculosis
Maternal Side:
(+) Ca- an uncle died due to liver caner
(+) HPN- Both grandparents died of stroke


Review of systems
Integumentary: no pruritus, no burning sensation
CNS: no convulsions, no faintness or loss of
consciousness,
HEENT: no headache, no blurring of vision, no
tinnitus or ear ache
Cardio-Respiratory: no cough, no difficulty of
breathing, no palpitations
GIT: no dysphagia, no constipation nor diarrhea
GUT: no dysuria, no hypogastric pain
Review of systems (cont.)
Musculoskeletal: No muscle weakness or muscle pain
Hematology: no unexplained bruises
Endocrine: no excessive sweating, no sensitivity to hot or
cold temperature
Reproductive: Menarch- 10 y/o
Duration of menstrual cycle: 28 to 32 days
Character of menstrual bleeding:
duration: 6 days
quantity : first two days- 3 almost fully soaked pads
per day then
succeeding days- 3 half soaked to minimally soaked
pads per day for the

PHYSICAL EXAMINATION
General Survey:
Patient is awake, conscious, coherent and
afebrile, not irritable, active and not in respiratory
distress.
Vital Signs:
Temperature: 36.5 C
Heart rate: 76bpm
Respiratory rate: 18 cpm
Anthropometric Measurements:
Weight: 35kgs
Head Circumference : 53cms

Skin: (+) pallor, (-) jaundice, moist and cold to touch.

HEENT:
Head : normocephalic with moist scalp, abundant and
evenly distributed dark hair
Eyes : pale conjunctiva, pupils equally round and reactive
to light accommodation, no periorbital edema
Ears: symmetrical and no discharges
Nose: no discharges and (-) nasal flaring
Mouth: no hyper salivation
Neck: no cervical lymphadenopathy, no mass and no
nuchal rigidity
Lungs: Breathing spontaneously with symmetrical
chest expansion, no rales on all lung fields
Heart: adynamic precordium, PMI at 5
th
intecostal
left midclavicular line,normal rate, regular rhythm
a no murmur.
Abdomen: soft, globular abdomen with
normoactive bowel sound, no tenderness , (-)
palpable mass
Genitalia: Tunner stage III
Extremities: no edema, pinkish nail beds, CRT 1-2
seconds, full and equal pulses, 10 toes and hand
digits


Neurological Examination
Cerebral: conscious and coherent
Cerebellar: (-) nystagmus

Cranial Nerves:
CN1: able to smell
CN2: pupils equally round and
reactive to light
CN3,4, and 6: no ptosis
CN5: grimaces
CN7: no facial symmetry
CN8: respond to verbal
commands and inquiries appropriately
CN9 and 10: good gag reflex
CN11: can shrug her shoulder and
turn face against resistance
CN12: no tongue deviation

Motor System: (Muscle bulk, tone, and strength)
Able to move extremities in all
directions (grade 5/5)
Sensory System: (pain, temperature, light touch,
vibration, discrimination)
All fours 100%


SALIENT FEATURES:
General Data:
Adolescent (11 years old),
female
History:
Skin: Macular rashes
GI: Abdominal pain, nausea
and vomiting
Muskuloskeletal: (+) arthralgia,
edema of dorsum left foot

IMPRESSION

Henoch- Schonlein Purpura

RULE IN RULE OUT
arthralgia biphasic fever
Macular
purpura/ rash
myalgia
Abdominal pain Lymphadenopa
thy
DIFFERENTIAL DIAGNOSES

DENGUE FEVER
It is a benign syndrome caused by several anthropod- borne viruses.
RULE IN RULE OUT
abdominal pain Weight loss
purpura painful nodules
Arthralgias myalgias
testicular pain
POLYARTERI TI S NODOSA
is a systemic necrotizing vasculitis affecting small and medium-sized arteries.
RULE IN RULE OUT
Age at onset <16 years
old
Quotidian fever for at
least 3 days and
accompanied by 1 of
the following:
1. Evanescent (nonfixed)
erythematous rash.
2. Generalized lymph
node enlargement.
3. Hepatomegaly or
splenomegaly or both.
4. Serositis.
Arthritis Easy fatigability
Nonpruritic rash
J UVENI LE I DI OPATHI C ARTHRI TI S
formerly juvenile rheumatoid arthritis) is the most common rheumatic disease
in children and one of the more common chronic illnesses of childhood. JIA is
an autoimmune disease associated with alterations in both humoral and cell-
mediated immunity.
RULE IN RULE OUT
Arthritis, arthralgias, Fatigue, anorexia,
weight loss, fever,
lymphadenopathy
tendonitis,
myositis, myalgias,
avascular necrosis,
osteoporosis
Nonpruritic rash Malar rash, discoid
rash
SYSTEMI C LUPUS ERYTHEMATOSUS
is a chronic autoimmune disease characterized by multisystem inflammation and the presence of
circulating autoantibodies directed against self-antigens.

Case
Discussion


HENOCH SCHONLEIN PURPURA
is the most common vasculitis of childhood and is
characterized by leukocytoclastic vasculitis and
immunoglobulin (Ig) A deposition in the small vessels
in the skin, joints, gastrointestinal tract, and kidney.

EPIDEMIOLOGY
- HSP occurs worldwide and affects all ethnic groups.
- incidence of HSP is estimated at 14-20/100,000
children per year and affects males more than
females, with a 1.2-1.8 : 1 male: female ratio. usually -
- between the ages of 3 and 10 yr.
- more common in the fall, winter, or spring and is
unusual in summer months.
- Many cases of HSP follow a documented upper
respiratory infection.
PATHOLOGY

- In all tissues, immunofluorescence identifies
IgA deposition in walls of small vessels,
accompanied to a lesser extent by
deposition of C3, fibrin, and IgM.

PATHOGENESIS
The exact pathogenesis of HSP remains
unknown.
Given the frequency of preceding upper
respiratory infections, including group A
streptococcal infections, an infectious trigger is
suspected.
The common finding of deposition of IgA,
specifically IgA1, suggests that HSP is a disease
mediated by IgA and IgA immune complexes.
Suggestive of genetic components
CLINICAL MANIFESTATIONS
The hallmark of HSP is its rash: palpable purpura starting as pink
macules or wheals and developing into petechiae, raised
purpura, or larger ecchymoses. Occasionally, bullae and
ulcerations develop.
The skin lesions are usually symmetric and occur in gravity-
dependent areas (lower extremities) or on pressure points
(buttocks).
The skin lesions often evolve in groups, typically lasting 3-10
days, and may recur up to 4 mo after initial presentation.
Subcutaneous edema localized to the dorsa of hands and
feet, periorbital area, lips, scrotum, or scalp is also common.
Musculoskeletal involvement, including arthritis and
arthralgias, is common, occurring in up to 75% of children with
HSP.
The arthritis tends to be self-limited and oligoarticular, with a
predilection for the lower extremities, and does not lead to
deformities.
DIAGNOSIS
The diagnosis of HSP is a clinical one and is
often straightforward when the typical rash
is present. However, in at least 25% of cases,
the rash appears after other manifestations,
making early diagnosis challenging. The
differential diagnosis for HSP depends on
specific organ involvement but usually
includes other small vessel vasculitides,
infections, coagulopathies, and other acute
intra-abdominal processes.

LABORATORY FINDINGS
No laboratory finding is diagnostic of HSP. Common but
nonspecific findings include leukocytosis,
thrombocytosis, mild anemia, and elevations of
erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP). Occult blood is frequently found in stool
specimens. Autoantibody testing is not useful
diagnostically except to exclude other diseases. Serum
IgA values are often elevated but are not routinely
measured.
Assessment of renal involvement with blood pressure,
urinalysis, and serum creatinine is necessary. Ultrasound
is often used in the setting of gastrointestinal complaints
to look for bowel wall edema or the rare occurrence of
an associated intussusception. Barium enema can also
be used to both diagnose and treat intussusception.
Although often unnecessary in typical HSP, biopsies of
skin and kidney can provide important diagnostic
information, particularly in atypical or severe cases.
TREATMENT
Treatment of HSP is supportive, with an emphasis on
assuring adequate hydration, nutrition, and analgesia.
Controversy continues concerning the appropriate use of
glucocorticoids in the management of HSP, but steroids
are most often used to treatsignificant gastrointestinal
involvement or other life-threatening manifestations.
Empiric use of prednisone (1 mg/kg/day for 1 to 2 wk,
followed by taper) reduces abdominal and joint pain but
does not alter overall prognosis nor prevent renal disease.
Chronic HSP renal disease is managed with a variety of
immunosuppressants, including azathioprine,
cyclophosphamide, and mycophenolate mofetil. End-
stage renal disease develops in up to 8% of children with
HSP nephritis.

COMPLICATIONS
Acutely, serious gastrointestinal involvement
such as intestinal perforation imparts
significant morbidity and mortality. Renal
disease is the major long-term
complication, occurring in 1-2% of children
with HSP. Renal disease can develop up to 6
mo after diagnosis but rarely does so if the
initial urinalyses findings are normal. It is
recommended that children with HSP
undergo serial monitoring of blood pressure
and urinalyses for 6 mo after diagnosis,
especially those who presented with
hypertension or urinary abnormalities.


PROGNOSIS
Overall, the prognosis for childhood HSP is
excellent, and most children experience an
acute, self-limited course. About 30% of children
with HSP experience one or more recurrences,
typically within 4-6 mo of diagnosis. With each
relapse, symptoms are usually milder than at
presentation. Children with a more severe initial
course are at higher risk for relapse. Chronic renal
disease develops in 1-2% of children with HSP, and
approximately 8% of those with HSP nephritis go
on to have end-stage renal disease.


THANK YOU
Po..