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Case Presentation
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General Data
A case if C.C 19 years old, female, single,Filipino, Roman Catholic. Born on March6, 1990. presently residing at San NicholasMambaling Cebu City. Admitted for the
first time at CPCMHI on September 10,2009
Chief complaint: elevated blood pressure
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History of present illness
Advised to
Consult at CPMH admitted
revealed
130/100 mmhg 120/100 mmhg
3 hours prior to admission
Saint Anthony Hospital BP monitoring
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Past medical history
Not hypertensive
Not diabetic
Non-asthmatic
No food and drug allergies No history of previous hospitalization
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Family history
Hypertension maternal side
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Personal and social history
Youngest among 8 siblings
2nd year HRM student
Non smoker
Non alcoholic drinker
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OB-Gyne History
Menarche at the age of 12 years old,moderate flow, duration of 3-5 days,
consumed 2 pads per day with irregularcycle
Coitarche at the age of 17 years old withfour sexual partners. No associateddyspareunia, no post coital bleeding
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OB-Gyne History
Had history of Misoprostol intake 3 tabletsorally and 3 tablets inserted vaginally. Noconsultation done.
1st prenatal check-up at 5 months AOG,with regular visits. No associated maternalillness. With supplements: Dellefer,Calciumade, Folic Acid.
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OB-Gyne History
Ultrasound: at 3 months AOG and 8months AOG
Papsmear done: at 5 months AOG whichrevealed normal findings
Contraceptive method: condom and
withdrawal method
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OB-Gyne History
G1 P0
LMP: December 21, 2008
PMP: November 2008 EDC: September 28, 2009
AOG: 37 4/7 weeks
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P.E
Examined patient conscious, coherent,cooperative. Oriented to person, place andtime. Not in respiratory distress. With thefollowing vital signs:
BP: 130/90 mmHg
PR: 80
Temp: 36.2 RR: 25
Wt: 79.1 kg
Ht: 55
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P.E
Skin: warm, good turgor
HEENT: pinkish palpebral conjunctivae,
anicteric sclerae. No dilatation of alae nasi.No lymphadenopathy.
Chest and lungs: clear breath sounds,
equal chest expansion
Cardiovascular: distinct heart sounds,normal rate regular rhythm
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P.E
Abdomen: gravid abdomen with fundalheight = 34 cm
FHT 132 bpm
presentation: cephalic
Dilatation: 1.5 cm
Effacement: slightly effaced
Station: -3IBOW
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Friedmans Curve
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Admitting CTG
Reassuring fetal heart beat with baselineof 140, acceleration of 160 with milduterine contraction
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LABS
Urinalysis 9/10/09 9/11/09
Color yellow yellow
Specific gravity 1.010 1.025
Albumin - +1
Character Sl. cloudy cloudy
Ph 6.5 6.0
Sugar - -
Pus cells 2-4 0-2
RBC - 2-4Epithelial cells many rare
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LABS
Hematology Result reference
WBC 12.8H 4.0-11.0
RBC 3.93 3.80-6.50
HgB 12.0 11.5-18.0
HcT 36 37-50
PLATELET 283 150-400
Res % Reference RES k/ul Ref
Lymphocyte 13L 20-45 1.7 1.5-4.0
Neutrophil 76H 40-75 9.7H 2.0-7.5Eosinophil 5 0-6 0.6H 0.0-0.4
Basophil 0 0-1 0.0 0.0-0.1
monocyte 6 0-10 0.8 0.0-0.8
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Ultrasound result
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Pregnancy uterine, 37 weeks and 4 days(+3 weeks) by FL biometry, live singleton,cephalic presentation.
Adequate amniotic fluid volume (AFI = 16.2cm)
Posterior placenta, grade II, high lying
Consider hydranencephaly
Short cervix (cervical length 1.0 )
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Doctors order
Please admit patient under service case
Secure consent
TPR every 4H
Labs: CBC, U/A, admitting CTG Meds:
Methyldopa 250 mg tablet every 8H
Cefazolin 1 gm IVTT ANST now then
500 mg every 8H Monitor BP every hour, FHT
Eclampsia precaution
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For congenital scan tomorrow am
Refer for bp >140/100 mmhg, blurring ofvision, epigastric pain and others
Refer accordingly
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Schedule for stat CS
AP prep
Secure signed consent
Secure 1 unit of FWB of patients bloodtype screened and crossmatched
Inform OR, Pedia, Anes
Pre-op meds
Famozidine 1 amp IVTT Placil 1 amp IVTT
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Post-op Analgesics
Tramadol 50 mg slow IVTT q6h x 4
doses to start at 5pm Ketorolac 25 mg slow IVTT q6h x 4
doses to start at 8 pm
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Pre-op Diagnosis
PUFT, in labor, CPD secondary tohyrdanencephaly
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Intra-op Diagnosis
Gravid uterus, adequate clear amnioticfluid, delivered a live baby girl, BW=3.9 kg,AS 8-9-10, placenta posterofundal inlocation, both fallopian tubes and ovaries
are grossly normal EBL=600cc
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Post-Op Diagnosis
PUFT, in labor, CPD Secondary toHydranencephaly, Delivered a Live BabyGirl, BW=3.9 kg, AS 8-9-10
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Discussion
Hydranencephaly
It is a rare type of cephalic disorder,isolated abnormality occurring in lessthan 1 per 10,000 births worldwide
It is the most severe form of bilateralcerebral cortical destruction.
It is a condition which the cerebralhemispheres are absent and replacedby sacs filled with cerebrospinal fluid.
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Differential Diagnosis
Severe hydrocephalus
Alobar holoprosencephaly (adevelopmental anomaly).
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Causes:
Hydranencephaly is an extreme form ofporencephaly, which is characterizedby a cyst or cavity in the cerebralhemispheres, and may be caused by
vascular insult or injuries, infections, ortraumatic disorders after the 12th weekof pregnancy.
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Causes
While the pathogenesis ofhydranencephaly is thought to be avascular accident, this cannot always beconfirmed because internal carotid arteries
are not always occluded at autopsy. Intrauterine infections, particularly
toxoplasmosis and viral infections(enterovirus, adenovirus, parvovirus,
cytomegalic, herpes simplex, Epstein-Barr,and respiratory syncytial viruses), havebeen implicated in a number of cases.
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Causes
Toxic exposures and cocaine abuse havebeen reported, and hydranencephaly hasbeen described in rare syndromes (5).
http://radiology.rsna.org/content/210/2/419.fullhttp://radiology.rsna.org/content/210/2/419.full8/2/2019 Case Presentation Ob Maternity
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Pathophysiology
Hydranencephaly occurs after the brainand ventricles have fully formed, usually inthe second trimester.
The brain destruction is complete or
almost complete in a bilateral internalcarotid artery distribution, with the cerebralhemispheres replaced by fluid coveredwith leptomeninges and dura.
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Pathophysiology
During the destructive phase, unusualmasses of hemorrhage and soft tissue
may be seen. Because the ventricles havealready been formed, the falx cerebri is
present. The cerebellum, midbrain, thalami, basal
ganglia, choroid plexus, and portions ofthe occipital lobes, all fed by the posterior
circulation, are typically preserved.
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Presentation
Usually the cerebellum andbrainstem are formed normally,although in some cases thecerebellum may also be absent.
An infant with hydranencephaly mayappear normal at birth or may havesome distortion of the skull andupper facial features due to fluid
pressure inside the skull
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Presentation
With most of the cerebral cortex absent,the fetal head would be expected to besmall.
Although this may occur, the head is more
often normal or increased in size becausethe choroid plexuses within the lateralventricles continue to produce cerebralspinal fluid that is not adequately
absorbed. This causes increased pressure, which
may expand the head and lead to ruptureof the falx cerebri.
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Presentation
The infant's head size and spontaneousreflexes such as sucking, swallowing,crying, and moving the arms and legsmay all seem normal, depending on the
severity of the condition However, after a few weeks the infant
usually becomes irritable and hasincreased muscle tone (hypertonia).
After several months of life, seizuresand hydrocephalus may develop
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Other symptoms may include visualimpairment, lack of growth, deafness,blindness, spastic quadriparesis(paralysis), and intellectual deficits.
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Hydranencephaly may, on first impression,mimic severe hydrocephalus (dilatedlateral ventricles). Depending on the levelof obstruction, concomitant dilatation of the
third and fourth ventricles may be seen. Hydrocephalus is often not an isolated
anomaly and can be associated with otherintracranial abnormalities, multiple
anomaly syndromes, and abnormalkaryotype.
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With hydrocephalus, as withhydranencephaly, the head is normal toenlarged with an identifiable falx cerebri,which may be disrupted in severe cases.
Unlike in hydranencephaly, an intact rim ofcortex is always present even in the mostsevere forms of hydrocephalus. It may,however, be difficult to identify prenatally.
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Holoprosencephaly is a developmentalanomaly resulting from absent orincomplete diverticulation of the forebrain(prosencephalon) and occurs in 1 in
16,000 live births worldwide. Alobar, its most severe form, shows no
separation of the ventricles, an absent falx,and partial fusion of the thalami.
The head is often considerably smallerthan the body, and there are oftenadditional and marked abnormalities.
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Diagnosis
Diagnosis may be delayed for severalmonths because the infant's earlybehavior appears to be relativelynormal.
Transillumination, an examination inwhich light is passed through bodytissues, usually confirms the diagnosis.
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Preliminary diagnosis may be made inutero via standard ultrasound.
It can be confirmed with a level II orhigher ultrasound
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Treatment
There is no standard treatment forhydranencephaly.
Treatment is symptomatic andsupportive.
Hydrocephalus may be treated with ashunt.
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Prognosis
The prognosis for children withhydranencephaly is generally quitepoor.
Death usually occurs in the first year of
life