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CLINICOPATHOLOGIC

CASE PRESENTATION

By: Edwin John C. Limjuco


Senior Clerk
Informant:Patient
% Reliability: 90%

General Data:
A.M., 30 years old, G5P4004, LMP: July
25,2006, PMP: June 25, 2006, AOG: 9 4/7
weeks, EDC: April 30,2007 admitted for
the first time at Sacred Heart Hospital due
to vaginal bleeding.
Chief Complaint:

Vaginal Bleeding
History of Present Illness (HPI):

10 days prior to admission, the


patient noted vaginal bleeding
characterized as intermittent,
scanty, bright red, non-foul
smelling, using 2-3 pads a day,
moderately soaked.
The condition is not aggravated by
physical activity and emotional stress;
however, this was associated with mild,
crampy, intermittent hypogastric pain,
non-radiating. No headache, no
dizziness, no blurring of vision, no
anorexia and no weakness noted. Since
condition was tolerable, no consult was
made and no medications were taken.
The said condition persisted until 18
hours prior to admission, patient had
passage of meaty tissues associated with
profuse vaginal bleeding and severe
hypogastric pain, crampy, intermittent,
non-radiating . This prompted the
patient to seek consult at Toledo City
Hospital, where a pregnancy test was
done with positive result. She was then
referred to Sacred Heart Hospital for
further management and was advised
admission.
Antenatal course:

Unremarkable
Review of Systems:
 Skin- no jaundice, no pallor, no rashes, no
pruritus, no bruising
 HEENT- no migraine, no history of head
trauma, no visual disturbances, no
abnormal lacrimation, no difficulty of
hearing, no epistaxis, no sinusitis, no nasal
discharges, no gum bleeding, no mouth
sores, no tongue sores, no hoarseness.
 Neck- no history of lumps and masses, no
stiffness.
 Breast- no history of trauma, no lumps, no
discharges.
 Respiratory system- no shortness of
breath, no chronic cough, no hemoptysis,
no wheezing.
 Cardiovascular system- no chest pain, no
palpitations, no edema, no dizziness.
 Gastrointestinal tract- no change in
bowel habits, no mass.
 Urinary tract- no dysuria, no urgency
 Genitalia- vaginal bleeding noted 10 days
PTA, no dyspareunia, no post-coital
bleeding, no pruritus.
 Nervous system- no paralysis, no
disturbances in smell or vision, no history
of loss of consciousness.
 Metabolic- no weight loss, no weight
gain, no fever.
 Psychiatric- no nervousness, no
memory loss, no hallucinations, no
insomnia.
Menstrual history:

The patient had her first


menstruation at the age of 13 years
old, in approximately 28-30 day
cycles with 3-4 days of duration
noted to be moderate in flow. This
was usually associated with
dysmenorrhea. LMP: July 25, 2006,
PMP: June 25, 2006.
Obstetrical History:

Birth Year of AOG Condition BW Place of Sex Type Handled Compli


order delivery of the baby delivery cations

1 1988 FT Good 6.5 lbs Hospital M NSVD MD None


cry
2 1989 FT Good 6.1 lbs Hospital M NSVD MD None
cry
3 1992 FT Good 6.8 lbs Hospital M NSVD MD None
cry
4 1995 FT Good 6.3 lbs Hospital F NSVD MD None
cry
Contraceptive History:

 The patient and her spouse used


condom as contraception.
 No history of OCP use
Sexual History:

Her first sexual contact was at the


age of 17 years old, single partner.
No history of post-coital bleeding,
no history of dyspareunia. Her last
sexual contact was 2 weeks prior to
admission.
Past Medical History:

M- hypertensive, non-asthmatic, non-


diabetic, no thyroid dysfunction, no
history of abnormal vaginal bleeding.
M- None
A- No food and drug allergy
S- None
H- acute gastroenteritis with mild
dehydration in 2006 at Toledo City
Hospital.
Family History:

Heredofamilial disease include


hypertension, on both maternal and
paternal side of the patient.
Personal and Social History:
- The patient is a college graduate and is
presently working as a teacher
- She resides at Toledo City
- She has been married for the last 15 years,
a Roman Catholic and lives with her
husband
- She has no history of alcohol ingestion,
cigarette smoking or drug/substance
abuse.
- Her husband is 36 years old, a
businessman and is currently in good
health with single sexual partner.
Nutritional History

 Breakfast: 1 glass milk, 1 pc.


Bread
 Lunch: 1 cup rice, 1 serving
fish “tinola”
 Dinner: 1 cup rice, 1 serving
vegetables
 weight:55 kg
 height:5’1” =61”

 IBW = (61x2.5) – 104.75 = 48 kg

 TCR= (IBWx30) + 300

= 1740 kcal
 BMI= 55 / (1.52)2 = 24 kg / m2
 She has no change in appetite, no
dentures, chews food properly,
 Has no allergy to food. She does not
have preference to food.
 Their budget per meal is P200.00
PHYSICAL EXAMINATION
 General Survey:
Examined conscious, coherent,
cooperative, ambulatory, afebrile,
not in respiratory distress and with
the following vital signs:

BP: 130/70 mmHg HR: 89 BPM


RR: 18 CPM Temp: 37° C
 Skin: warm, good turgor
 Head: normocephalic

 Eyes: pinkish palpebral


conjunctivae, anicteric sclerae,
no periorbital edema
 Ears: no discharges

 Nose: no alar flaring,

 Throat: moist lips and tongue


 Breast: asymmetrical, slightly
engorged, no nipple discharge
 Chest and Lungs:
I- symmetrical, equal chest expansion,
no skin lesions
P- equal tactile fremitus in all lung
fields, no mass
P- Resonance at both lung fields
A- Vesicular sound in all areas, no
abnormal breath sounds, no rales, no
wheeze
 CVS:
I- symmetrical, no bulging of the
precordium
P- PMI at L 5th ICS, MCL, no
tenderness
P- cardiac dullness within normal limits
A- No murmur and friction rub,
normal rate (89 bpm) and regular
rhythm
 Abdomen:
I- flabby, positive silvery striae
gravidarum, no scar
P- soft, nontender, no mass palpated,
urinary bladder not distended
P- dullness on uterine area
A-normoactive bowel sounds
 Genitalia: non-gaping with myrtiform
caruncles, minimal vaginal bleeding
Speculum Exam:
– Cervix: smooth, pinkish, no erosions, no active
bleeding, no mass.
Bimanual Pelvic Examination:
– Cervix: admits tip, movable, nontender
– Uterus: slightly enlarged, anteverted, non-tender
– Adnexae: no mass, nontender
– Discharge: minimal vaginal bleeding, non-foul
 Extremities: no edema, no clubbing, strong pulses,
no limitation of movement, no deformities.
Neurologic Examination:

– Cerebral function: conscious, coherent,


oriented to time, place & person
– Cerebellar function: no disturbances in gait
or balance, no nystagmus
– Motor Function: full motor strength (5/5),
both upper and lower extremities
– Sensory Function: intact pain and tactile
sensation
– Cranial Nerves: within the normal limits
– Reflexes: Normoreflexia (++), no
pathologic reflexes
Laboratory
Examinations
LABORATORY EXAM
RESULTS:
 CBC:
– WBC = 11.6 K/uL
– Hemoglobin = 13.0 g/dL
– Hematocrit = 39.1%
– Platelet count = 237K/uL
 BLOOD TYPING: “B POSITIVE”
 Urinalysis:
– WBC = 0 – 2/ HPF
SALIENT FEATURES:

36 YEARS OLD


2 MONTHS AMENORRHEA

9 WEEKS AGE OF GESTATION

VAGINAL BLEEDING (intermittent,


scanty, bright red, non-foul smelling,
using 2-3 pads a day, moderately
soaked)
 HYPOGASTRIC PAIN (severe,
crampy, intermittent, non-radiating)
 POSITIVE PREGNANCY TEST
 NO HISTORY OF OCP USE

 CERVIX ADMITS TIP ON


INTERNAL EXAM
 UTERUS: SLIGHTLY ENLARGED,
NONTENDER
Differential Diagnosis:

 Submucous Myoma
 Ectopic Pregnancy

 Hydatiform Mole (Partial Molar


Pregnancy)
Submucous Myoma:
Etiology
 The etiology of submucous myoma is
incompletely understood.
 Genetic determinants definitely
contribute to its development.
Pathophysiology
 ↑ estrogen and progesterone, epidermal
growth factor, insulin-like growth factor-1,
platelet-derived growth factor

 Somatic mutation of normal myometrium

 Growth of myoma
 Leiomyomas are benign tumors of
muscle cell origin. It is the most
frequent pelvic tumor.
 Initially, most myomas develop from
the myometrium beginning as
intramural myomas (only 5%-10% of
myomas become submucosal).
 As they grow, they remain attached to the
myometrium with a pedicle of varying
width and thickness.
 Continued growth in one direction
determines which myomas will be located
just below the endometrium (submucosal)
and which will be found just beneath the
serosa (subserosal).
 The exact stimulus for growth of myomas
is unclear, however the growth may be
influenced by relative levels of estrogen
and progesterone.
 Myomas often enlarge during pregnancy
and occasionally enlarge secondary to oral
contraceptive therapy.
 Estrogen and progesterone receptors are
found in higher concentration in myomas
than in the surrounding myometrium
 The amount of fibrous tissue is
proportional to the extent of atrophy and
degeneration that has occurred overtime
 The eventual rate of some myomas is
determined by their relatively poor
vascular supply
 Types of degeneration:

– Hyaline: the most common type of


degeneration, it is the mildest form
– Myxomatous
– Calcific
– Cystic
– Fatty
– Red: the most acute form of
degeneration
Clinical Characteristics
 The incidence of intrauterine myoma is
common in 20-44 years of age
 About 30% of women in the reproductive
years may develop myoma of the uterus
and accessory organs
 The highest prevalence occur during the
5th decade of a woman’s life
 Myomas are prone to grow and become
symptomatic in multiparous women
 Myomas may vary in size from small to
large enough to fill the entire abdominal
cavity
 Large myomas may put pressure on the
bladder neck, causing acute urinary
infection
 The more common symptoms are the
following:
1. Pressure from an enlarging mass
2. Abdominal pain including
dysmenorrhea
3. Abdominal uterine bleeding – occurs in
30% of women with myomas
 The most common symptoms is
menorrhagia
 The diagnosis is usually confirmed by
palpating an enlarged, firm, irregular
uterus during pelvic exam
 The uterine cavity is generally enlarged
and often irregular with myomas
Basis for inclusion
 36 years old
 Multiparous

 Vaginal bleeding associated with


hypogastric pain
Basis for Exclusion
 No history of Oral contraceptive pills used
 Uterus slightly enlarged but not irregular,
no mass palpated
Diagnostic Procedures
 Vaginal ultrasound – serial ultrasound is
used to evaluate the progression in size of
myomas or its response to therapy.
 Hysteroscopy
Ectopic Pregnancy
Ectopic Pregnancy

 Implantation of the fertilized


ovum outside the
endometrium, lining the
uterine cavity.
Etiology

 Tubal pathology (acute salpingitis


- major cause of ectopic
pregnancy)
 Contraception failure – occurs
with tubal sterilization (1.85%)
 Hormonal alterations – 1.5%
ectopic pregnancy rate after
ovulation has been reduced with
clomiphene citrate
 Previous abortion – prior abortion
increases the risk of ectopic
pregnancy
Pathophysiology
 Transplantation of the blastocyst in the
mucosa

 Blastocyst invade the lamina propria and
subsequently the muscularis

 Blastocyst grows mainly between the
lumen of the tube and mesosalpinx

 Trophoblast invades blood vessels


 Retroperitoneal tubal hemorrhage

 Extrusion from the fimbriated end

 Tubal rupture
Clinical Characteristics

 A classic triad of symptoms is usually


described by a patient with ectopic
pregnancy, namely:
1. abdominal pain
2. amenorrhea
3. vaginal bleeding
 The abdominal pain is described as
colicky, unilateral or bilateral, and in
most instances, it is on the same side
of the ectopic gestation.
 Subjective symptoms of pregnancy
are seen in about half of patients
 On pelvic exam, tenderness of the cervix
is elicited
 Decidual casts can be noted plugging the
cervical os
 The uterus is smaller than the AOG except
in cases of cervical or interstitial
pregnancies
 The cul-de-sac may be full due to
substantial hemo-peritoneum
 A discrete mass or fullness of the adnexa
is noted in half of the cases
Basis for Inclusion
 (+) abdominal pain
 (+) amenorrhea
 (+) vaginal bleeding
 Positive pregnancy test
Basis for Exclusion
 Adnexae: nontender
 Cervix: nontender
 No history of OCP used and smoking
Diagnostic Procedures
 hCG assays: hCG level in ectopic
pregnancy is >6,500 mIU/mL
 Culdocentesis: the presence of non-
clotting blood in the posterior cul-de-sac is
indicative of hemoperitoneum.
 Laparoscopy: direct visualization of the
pelvic organs is the gold standard in the
diagnosis of ectopic pregnancy.
HYDATIDIFORM MOLE
Hydatidiform Mole
 Characterized histologically by abnormalities of
the chorionic villi consisting of varying degrees
of trophoblastic proliferation & edema of villous
stroma.
 Types:
– Complete- fetus absent, diffuse villous edema, slight
to severe trophoblastic proliferation
– Incomplete (Partial)- fetus often present, focal villous
edema, slight to moderate trophoblastic proliferation
Incomplete Mole: Etiology
 Incomplete or partial moles are usually
triploid and have 69 chromosomes of
both maternal and paternal origin. The
most common mechanism for the
origin of a partial mole is a haploid egg
being fertilized by two sperm, resulting
in 3 sets of chromosomes alternatively,
triploidy could result when an
abnormal diploid sperm fertilizes the
haploid egg.
 It is also possible for an abnormal
diploid egg to be fertilized by a
haploid sperm, but this latter
mechanism usually results in an
abnormal conceptus with congenital
abnormalities rather than a partial
mole.
Clinical Characteristics
 In incomplete mole, the uterus is usually
small for date, and if there is a fetus, it has
multiple congenital defects, is stunted and
does not survive. The contents are usually
expelled in 10 – 26 weeks.
 Normal signs and symptoms of pregnancy
may be present.
 There may be evidence of a fetus in
incomplete mole by ultrasonography.
 Bleeding is the common sign, found in
86% of cases.
 There is disparity in the size of the uterus
and the age of gestation.
 Grossly the mole appears like a bunch of
grapes, they are smooth and transparent on
the surface.
 The risk of malignancy in incomplete
mole is low.

Basis for Inclusion
 (+) vaginal bleeding
 (+) pregnancy test
 (+) History of hypertension
Basis for Exclusion
 Normal signs and symptoms of pregnancy
are absent.
 No history of Thyroid dysfuntion.
Diagnostic Procedures
 B – HCG titer: In H – mole, the BHCG titer
is higher to normal pregnancy and can even
reach > 100,000 IU/L on the 100th day
from the LMP.
 Hysteroscopy through the cervix is a simple
and rapid procedure to identify mole cysts
easily when present.
 Pelvic Ultrasonography- snowstorm
appearance
Final Diagnosis:

Incomplete Abortion
Non-septic; non-induced
Abortion
 Termination of pregnancy before 20 weeks
based upon the date of the first day of last
normal menses.
 The delivery of a fetus-neonate that weighs
less than 500 g.
 The fetus and placenta are likely to be
expelled together before 10 weeks, but
separately thereafter. When the placenta, in
whole or in part, is retained in the uterus,
bleeding ensues sooner or later
incomplete abortion.
Incomplete Abortion: Etiology
 Genetic

– major cause of abortion


– Cytogenetic studies indicate that
incidence of chromosomal anomalies is
about 50%. The most common type of
anomaly is autosomal trisomy, followed
by polyploidy. The rate of chromosomal
abnormalities is highest when abortion
occurs between 8 and 15 weeks AOG.
The incidence increases markedly after
35 years old,rising to>30% after age 40.
 Environmental- congenital uterine
anomalies
– About 20-25% of women with
anomalies of uterine fusion have
problems with reproduction’
– Bicornuate and septate uteri are the
anomalies most frequently
associated with abortion.
 Uterine Anomalies after Diethylstilbestrol
(DES)
– The endometrial cavity of women
exposed to DES in utero had a
significantly smaller surface area than
normal contributing to the increased
rate of spontaneous abortion.
– It is associated with uterine anomalies
particularly uterus didelphys as well as
anomalies produced by fetal DES
exposure.
 Cervical incompetence
– Characterized by an asymptomatic
dilation of the internal cervical os,
leading to dilation of the cervical canal
and external os during the 2nd trimester
of pregnancy. The consequent lack of
support of the fetal membranes leads to
their spontaneous rupture, which is
usually followed by the expulsion of the
fetus and placenta.
 Acquired uterine defects
– Leiomyomas: submucosal leiomyoma is
associated with repetitive abortion.
– Intrauterine adhesions can cause partial
or complete obliteration of the
endometrium and amenorrhea, as well
as being a cause of abortion. On
occasion, IUA’s develop after
diagnostic curettage, as well as in
women with genital tuberculosis.
 Endocrine causes
– Progesterone deficiency: thyroid disease
(there is no definite evidence that
hypothyroidism is a cause of spontaneous
abortion); and diabetes mellitus (diabetes
without good metabolic control is associated
with an increased risk of early pregnancy loss,
and a direct correlation exists between the
level of hemoglobin A, and the rate of
abortion.
– Hypersecretion of LH: the incidence of
spontaneous abortion was only increased in
those women with polycystic ovarian
syndrome who had elevations of follicular
phase plasma LH levels.
 Immunologic Factors
– Lupus anticoagulant – the presence of
either the lupus anticoagulant or the
anticardiolipin antibodies has been
found to be associated with an increased
rate of spontaneous abortion and IUFD.
– Increased activated protein C resistance
– hyperhomocystenemia
 Infectious
– T. gondii may infect the embryo
and cause abortion
– Mycoplasma, U. urealyticum, M.
hominis can cause abortion.
– U. urealyticum was associated with
recurrent abortions
 Environmental Factors
– Cigarette smoking – women who smoked
more than 14 cigarettes/day has 1:7 times
greater risk of having abortion than for
women who do not smoke.
– Coffee, caffeine, and cocaine – there are some
epidemiologic data suggesting that each of
these substances may be an independent risk
factor for abortion, but the data are
inconsistent.
– Irradiation- teratogenic effect is dose-related
– Environmental toxins- little valid information
exists concerning the effect of environmental
toxins on human abortion.
 Paternal Factors
– Chromosomal translocation in
sperm can lead to abortion
– Adenovirus and Herpes simplex
virus are found in semen samples of
sterile men in nearly 40%
Pathophysiology
 Hemorrhage into the decidua basalis and
necrotic changes in the tissues adjacent to
the bleeding

 The ovum becomes detached


 Stimulation of uterine contraction

Expulsion
Clinical Characteristics
 Incomplete abortion refers to the passage
of some but not all fetal or placental tissue
from the uterine cavity through the
cervical canal before 20 weeks’ gestation.
Most abortions that occur between 8-14
weeks AOG are incomplete.
 If only a portion of the products of
conception have been expelled and the
cervix remains dilated, a diagnosis of
incomplete abortion is made.
 In many cases, the retained placental
tissue simply lies loose in the cervical
canal and can be lifted from an exposed
external os with ovum or ring forceps
 Hemorrhage from incomplete
abortion is occasionally severe
but rarely fatal
Basis for inclusion
 Vaginal bleeding
 (+) pregnancy test
 18 hours prior to admission, had passage
of meaty tissues
 Cervix admits tip
Management
 Curettage
– Indicated if missing products of
conception are evident
– It is often unnecessary to dilate the
cervix before curettage
– In many cases, the retained placental
tissue simply lies loose in the cervical
canal and can be lifted form an exposed
os with ovum or ring forceps
Management
 A woman with a more advanced pregnancy,
or a woman who is bleeding heavily, should
be hospitalized and the retained tissue
removed without delay.
 Fever is not a contraindication to curettage
once appropriate antibiotic treatment has
been started.
COURSE IN THE WARD

 Day 1 (Oct. 1 ,2006)


– Admitted due to vaginal bleeding
– IVF: D5LR
– DAT
– Laboratory exams requested: CBC, UA,
BT, TVS in am
– No medications given
COURSE IN THE WARD
 Day 2 (Oct. 2, 2006)
– TVS done with the following results:
 Slightly enlarge-sized, anteverted uterus
 Thickened & intact heterogenous endometrium (1.2
cm) with minimal mixed echoes suggestive of
bloodclots
 No gestational sac intra nor extrauterine

– Final diagnosis Complete Abortion


– Discharged with take home medications:
 Cefalexin 500 mg 1 cap q8h x 7 days
 Ferrous sulfate 1 cap OD

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