case presentation ob maternity

8/2/2019 Case Presentation Ob Maternity

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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.full


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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

case presentation ob maternity

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