SUPLEMENTAL TOPICS.docx

7/30/2019 SUPLEMENTAL TOPICS.docx

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SUPPLEMENTAL NOTE

Lecturer : Galileo B. Bayos RM, RN, MAN

DIABETES MELLITUS- a hereditary endocrine disorder characterized by

inadequate production of insulin by pancreas to regulate body glucose.

Brief review of anatomy of physiology of pancreasPancreas- islet of langerhans(beta cell)- produce insulin- serve as

mediator to enter the glucose to cell)

Carbohydrate as main source of energy, fats and protein are

converted to store on subcutaneous tissue that form as body fats,

1st trimester- concentration of maternal glucose and fluctuation in

insulin production, increases fetal demand cause decrease insulin level in

mother.2nd trimester- maternal tissue sensitivity to insulin begin to decline

because of human placenta lactogen. Resulting to increase level of glucose

in mother resulting to gestational DM.

HPL- increase availability of glucose to fetus by decreasing maternal

tissue sensitivity to glocuse.

Classification of diabetes Mellitus

Type 1 Insulin dependent diabetes Mellitus

Destruction of beta cell of the pancreas that lead toabsolute insulin insufficiency

Usually associated with birth defect. Birth defect usually

originate on first trimester

Type 2 Non insulin dependent diabetes mellitus

A state that usually arise because of insulin resistance

combined with relative deficiency of insulinGestational

diabetes

Abnormal glucose metabolism that arises during

pregnancy. Generally does not cause birth defect,

because gestational diabetes arise on later part of

pregnancy.

Classic sign and symptoms

o Hyperglycemia- the most enable insulin function is to mediateglucose to enter the cell to utilizes as main source of energy.

With the damage of pancreas, which produce insulin. The

glucose will accumulate to the bloodstream resulting to

hyperglycemia.

o Glycosuria- when glucose exceed to renal threshold, glucosewill expel in the urine.

o Polyuria- expel of glucose in the urine, elicit increase of urineoutput because, glucose attracts water.

o Polydips ia- the excretion of large amount of fluid in thebody lead to dehydration.

o Polyphadgia- due to starvation of cell for food/glucose.o Weight loss- since glucose cannot used by the body as

source of energy, gluconeogenesis will occur, fats andprotein will be used as source energy resulting to muscle

wasting and weight loss

o Ketoacidosis- breakdown of fats and protein will end toketones.

Effect to mother Effect to babyPreeclampsia/eclampsia Macrosomia

UTI/ candidiasis- due to

increase glycogen tovagina

Hydramious- glocuse attract

water

Hydramious PrematurityDiabetic nephropathy Hypocalcemia

Diabetic retinopathy Hypoglycaemia-considering

mother blood sugar level

consistently, causing fetal high

insulin level in i ts circulation,

after birth, baby continue tohave high level f insulin, but it has

no longer high level of sugar

from the mother, resulting to

blood sugar level become very

low.

Pre term labor Respiratory distress- increase

insulin delay lung maturity.L/S ratio- give false positive

result, the ratio tend not to show

maturity as early as other

pregnancy because of synthesis

of phosphatidylglycerol, thecompound the stabilizes

surfactant.

MANAGEMENT

Pre natal

o Screening through family history of DM in the family Case of unexplained of repeated abortion


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Glysuria Obesity Give birth of large infant, more than 10 lbs

o Glucose test OGTT- FBS RBS Benedict test- not reliable due to false positive result-

lactose from mothers milk

o Diet Caloric intake of pregnant woman- 1800 to 2400

cal/day

Excess would result to CPD, macrosomia Total Weight gain24 lbs

o Exercise Liberal cardiovascular conditioning exercise Eat complex carbohydrate prior to exercise to avoid

hypoglycaemia

Exercise lower blood sugar and decrease the needof insulin

o Insulin therapy Oral hypoglycaemic agent- diamecron and

tolbutamide contraindicated- teratogenic effect

that can cross the palcenta that may cause fetal

and newborn hypoglycemia

Gestational diabetes mellitus- can be treated by dietand exercise.

Insulin requirement increase at 3rd trimester

o Post partum Fetal hypoglycaemia- during intrauterine life, the

fetus were used to have an increase glucose level

because of mother diabetes mellitus, the pancreas

of the baby secreted more insulin, after delivery, the

baby own body produce it own glucose causing to

have hypoglycaemia due increase insulin level

secrete by the pancreas.

Sign of hypoglycaemia- shrill cry, weakness- giveglucose water

Sign of hypocalcemia- tetany, tremors- calciumgluconate

Observe for congenital anomalies- oesophagealatresia, neural tube defect

HEART DISEASE

Cardiac disease can affect mainly the left and right side heart failure

Left side heart failure- it compromises the left side of the heart which mainly

affect the heart itself and the lung, it is characterized by passes of fluid from

pulmonary membrane to interstitial spaces causing pulmonary oedema anddecrease oxygen and carbon dioxide exchange. As the oxygen supply

decrease, chemoreceptor stimulate respiratory centre to increase respiratory

rate. The woman may experience orthopnea, paroxysmal nocturnal dyspnea.

Right sided heart failure- right side failure occurs when the output of the right

ventricle less than the blood volume received by the right atrium. Backpressure from this may result to congestion of system organ. The woman may

experience generalized edema, splenomegaly and hepatomegaly.

Classification of Heart disease from functional capacity of the heart

Classs 1 No limitation of physical activity; regular activity does

not produce symptoms.

Class II Slight limitation; asymptomatic at rest but regular

activities produce palpitations, fatigue, dyspnea and

angina pain.

Class III Marked limitation of activities, less than regular

/ordinary activities cause symptoms

Class IV Mark limitation of activities symptomatic at rest

Sign and Symptoms

Dyspnea Palpitations Fatigue Syncope

Sign of cardiac decomposition

moist cough pedal edema dyspnea increasing with minimal activity cyanosis

Management

Pre Natal Care


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Frequent prenatal visit and consultation to specialist Rest- both physical and mental. Allow 8 hours sleep at night

and frequent rest period at day, Overcrowded places, Heavy work, high altitude, smoking and

alcohol consumption should be avoid- it decrease

oxygenation

Diet should be low salt, high iron, and protein. Avoid constipation- take high fiber fruit and vegetable to

have regular bowel( walking is the best)Intra partum Care

Early hospitalization- hospitalized prior to labor to promote restand close watch

Left lateral position- optimal uteroplacental perfusion Other position include- semi recumbent, semi fowler, but

lithotomy is contraindicatedAdequate analgesia/analgesic- to eliminate pain and spontaneous pushing

Forcep delivery and episiotomy- shorten second stage oflabor

CS is the least option due to potential infection and increaseblood loss

Administered oxygen if necessary Strict I and O- to monitored fluid overload

Note:

Class I and class 2 may proceed to pregnancy without cardiac symptoms;

class 3 and 4, pregnancy should be guarded to insure safety of the

mother.

Post partal Care

CARDIAC FAILURE AND DECOMPOSITION LIKELY OCCUR IN

EARLY POSTPARTAL PERIOD DUE TO:

Loss of placental circulation. 30 to 50 % in blood volumereabsorbed by general circulation causing fluid overload

Rapid decrease of intraabdominal pressure cause of rapid risecardiac output.

Pre term rupture of membraneRupture of fetal membrane with loss of amniotic fluid before

37 weeks

Risk factors

Infection ( chorioamnionitis) Cord prolapsed Cord compression- due to pressure on umbilical cord due

loss of amniotic fluid

Management

Prophylactic administration of broad spectrum antibiotic-delay the onset of labour and infection

Administration of Betamethasone- for lung maturityMultiple Gestations

Gestation of two or more foetuses; carrying more than one fetus

during the same pregnancy

Type of multiple gestations

Monozygotic or identical twin-develop from one ovum and one

sperm cell that undergo rapid cellular division that result from 2 or more

individual. The individual always posses the same sex and genetic traits.

Twinning happen within 72 hours- there will be diamnionic, dichorionic andtwo

embryo(monozygotic)

Twinning happen 4 to 8 days- there will be diamnionic, monochorionic and 2

embryo ( monozygotic

Twinning after 8 days -there will be monoamnionic , one chorion and 2

embyo.Twinning happen after embryonic disc formed- conjoined twin will develop

Posterior- pyopagus Cephalic- craniopagus Caudal- ischiopagus

Monozygotic twinning does not influenced by heredity, race, parity and

maternal age.

Dizygotic Twin or fraternal twin- develops from two or more ovum fertilized by

sperm cell in the same time. They have different sex and genetic trait. Theirembryos have their own chorion and amnion.

Fraternal twin are influence by race, heredity, age and parity(sia), takingovulation induction drugs ( clomediphine), common on woman who stop

from oral contraceptive cause excitement to pituitary gonadotrophin to

release greater amount. Assisted reproduction such as in vitro fertilization.

Complication

Miscarriage Death of one fetus Pre term labor- as the number of fetus increase, the duration

of pregnancy decrease.

Low birth weight

Hydramious PIH


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Condition should be avoided by

pregnant mother with cardiac

disease.

Infection, anemia, excessiveweight gain and edema

Twin to twin transfusion- fetus share vascular communication,possibly of leading overgrowth one fetus and under growth of

another fetus. Common on monoamnion Cord entanglement, prolapsed, compression

Sign and symptoms

Abdominal size is larger than date Auscultate of 2 or more FHT

Hyperemesis gravidarum

Defined as persistent nausea and vomiting start the end of first

trimester (10-12 weeks) and resolve about 22 weeks that require intervention.

Other term; pernicious vomitingCause

Unknown but is somewhat related to;

a. Hormonalincrease HCG and estrogen level.b. Emotionalunwanted pregnancyc. Endocrine due to thyroid stimulating properties of

human chorionic gonadothrophin.d. Bacterial- helicobacter pylori

Sign and symptoms

1. Severe nausea and vomiting not relieved by ordinary remedies.2. Sign of dehydration- scanty urine, thirst, dry skin, weight loss

Management

Woman with sign of dehydration should be hospitalized-to correctdehydration, fluid and electrolytes balance by administration IV fluids.

o Blood chemistryto determine electrolytes imbalances If condition improved-

o Start food graduallyo SFF- 5 to 6 divided mealo Do not force to eat, remove food if nausea and vomiting

recurs.

o Cracker toast bread, before rising to bedo Do not serve strong odorous, spicy, greasy

RESPIRATORY DISTRESS SYNDROME (RDS)

Define as; difficulty in respiration due to insufficient lung surfactant, leading to

collapsed lungs (atelectasis), which prevent adequate gas exchange.(RPS)

Incidence

common in pre term, 1000 grmas- 1500 grams diabetic mother, CS delivery, ante partal bleeding

Assesment silverman-anderson scale

o 0- normalo 10- most difficult in respiration

Sign and symptomso Tachycardia- more than 70 breath/min. Early signo Nasal flaring-early signo Retraction- sternal and intercostals due the use of accessory

muscle to aid respiration.

o See-saw breathing- flattening of the chest during inspirationwith bulging of abdomen

o Grunting- major sign, late signDIAGNOSIS

o Historyo Assessment(

silverman)

o Blood gasstudies

COMPLICATIONo Hypoxiao Retrolental fibroplasias- from high

oxygen concentration more than 40 %

o AlelectasisAMNIOTIC FLUID EMBOLISM

Define as ;Amniotic fluid are forced to entered the open maternal

sinus through some defect in the membrane.

RISK FACTORSo PROM, normal rupture of BOWo Abruptio placentao Difficult labour( hypertonic contraction)

INCIDENCE

Rare but fatal, mortality happen on first 24 hours in 25% of woman.

ASSESSMENTo Maternal respiratory distress

o acute dyspneao cyanosiso

sudden chest paino pulmonary shock

Normal ratio of lecithin-

sphingomyelin 2:1


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Amniotic fluid

AFI normal- 8 23 cm.

POLYHYDRAMIOUS

Mild- 25-30 cmModerate- 30.1- 35 cm

Severe more than 35 cm

o circulatory collapse, followed by severe bleeding and DIC

TREATMENTo Oxygenationo Hydration

o IV fluid replacemento Blood transfusiono Monitor I and O

o Digitalis for failing cardiac functiono Heparin- antidote protamine sulphate

INTRODUCTION OF AMNIOTIC FLUID

Sources of amniotic fluid

1. Fetal urine2. Fluid transported from maternal blood

Kidney start to produced urine at 10 weeks

OLIGOHYDRAMIOUS-

Defined as; amniotic fluid less than 300 ml or amniotic fluid index is less

than 5 cm.

Causes:

o Fetal renal agenesis or potter syndrome-decrease fetal urineformation is the most common cause.

o Maternal dehydrationo Premature rupture of membraneo Exposure to angiotensin coverting enzymeso Uterine abnormalities

Note: fetus start to produce urine at 10 weeks

Characteristic of newborn Cord compression- lead to decrease blood flow to fetus

subsequently IUFD

o Compression deformities Squash looking face Flattened nose Micrognathia-deformed jaw Skin is dry and leathery Pulmonary hypoplasia

Managements

Oligohydramious sometimes related to post term pregnancy- linked to

placental insufficiency and fetal organ including the kidney. Decrease fetal

urine formation.

Rule out for renal agenesis

Other cause of oligohydramious like pre term rupture ofmemebrane, diarrhea

Simple maternal hydration is the cause is diarrhea Prophylactic amnioinfusion with normal saline, ringer lactate

perform to prevent compression deformities and hypoplastic

lung disease.

PRE TERM RUPTURE OF MEMBRANE( PROM)-

Defined as ; rupture of fetal membrane with the loss of amniotic fluid

during pregnancy before 37 weeks of pregnancy.

Causes;

Unknown

But associated with;

Infection- chorioamnionitis

Assessment finding

Maternal report of passage of fluid per vaginaDetermination of alkaline amniotic fluid and not acidic urine

Diagnosis

Nitrazine test- change in colour, yellow- acidic, bluealkaline Ferming test- amniotic fluid, high in sodium content ferming

pattern when dried in slide.

Sterile speculum examination- direct visualization of fluid fromcervical os- most reliable diagnosis of PROM.

Effect of PROM Infection- grave threat to fetus since the barrier has

been rupture. Cord compression-due to loss of amniotic fluid will

result to pressure to umbilical cord that cause to

decrease oxygen and nutrient supply.

Cord prolapsed- due to small fetal headNote:

Do not allow woman to ambulate-prevent cord prolapsed

POLYHYDRAMIOUS

Defined as; amniotic fluid exceeding

2000 ml or AFI of 24 cm, consideredhydramious


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Fact

People with Rh positive-has Rh antigen

Negative Rh-do not have antigen

When a person who are Rh positive enter the

body of Rh positive. Rh body reacts and

produce antibodies to destroy the invading

antigen, hence. Rh are part of b lood, it destroy

blood component.

Maternal sensation- expectant mother hasbeen exposed to Rh positive blood and has

been develop antibodies.

Causes

Esophageal atresia Open neural tube defect

o Anencephalyo Spina bifida

Multiple pregnancy- monozygotic twin Diabetes mellitus- hyperglycemia cause increase fetal urine

output-Glucose attract water

Manifestation

Uterus is larger than AOG Shortness of breath Abdominal skin appear to be stretch and shiny and marked of

straie gravidarum

Confirmed by ultrasound by computing the amniotic fluid index through

pocket index or amniotic fluid volume.

Complication

Premature labor and delivery- the increase uterine pressure causerupture of membrane

Abruption placenta Post partum haemorrhage- due to over distension Cord presentation and prolapsed Mal presentation

Management

Amniocentesis- removal of amniotic fluid to relieve maternaldistress

Indomethacin therapy- a drug that decrease the fetal urineformation. the side effect include premature closure of ductusarteriosus.

Amniotomy- removal of amniotic fluid per cevix, the danger ofthe procedure is cord prolapsed and abruption placenta.

HEMOLYTIC DISEASE OF THE NEWBORN

Defined as; the mother produced antibodies against fetal blood

resulting in destruction or hemolysis of fetal red blood cells which result tosevere fetal anemia and hyperbilirubenemia

TYPE OF HEMOLYTIC DISEASE

1. Rh incompatibility- mother is negative and baby is positive

2. ABO incompatibility- mother is blood type O and baby blood type Aor B

Sensation- means that the expectant mother has been exposed to Rh

positive blood and has develop antibodies.

Rh compatibility

Mother is Rh negative, fetus Rh positiveTheoretically, there is no mixing of maternal circulation and

fetal circulation

Mixing of maternalblood and fetal

blood during

placental

Separation and

other procedure

that would havechance to mix

maternal and fetal

blood.

Circumstances of fetal and maternal

blood mixing;

o Amniocentesio Chrionic villi samplingo Abortiono Feto-maternal transfusiontrauma

ABO INCOMPATIBILITY

Occurs when the maternal blood is type O and fetus is typeType A-most common

Type B- most serious has protein component (

antigen )

Type AB- rare

The principal source of bilirubin is hemolysis of erythrocytes-unconjugated bilirubin,

non water soluble, converted to conjugated bilirubin by small intestine and excreted

by the liver.

ABO incompatibility may happen on the first pregnancy due to;

People with type O blood develop anti A and anti B bodiesnaturally as result of exposure in the food or to infection, as a result


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.some woman develop high serum of anti A, anti B bodies prior to

pregnancy. The anti bodies may be Ig G and IgM . when a woman

become pregnant . the IgG cross the palcenta and cuase hemolysis

of fetal red blood cell.Diagnosis

o Direct coombs test- presence of antibodies in maternalcord= Percuteneous umbilical sampling

o Indirect coombs test- presence of antibodies inmaternalblood.

o Amniocentesis-evaluate the optic density of amniotic fluid, itmeasure the amount of reflect bilirubin present in amniotic

fluid.

o Ultrasound-o Dopplerevaluate cardiac function

Assessment finding Antibodies destroy fetal RBC- produce un conjugated

bilirubin( icterus gravis), lead to neurologic disease(

bilirubin encephalopathy

Initiate rapid production of immature RBC, which doesnot carry oxygen( erythroblastosis fetalis)

Fetus become anemic, leading to generalized anemia, (hydrops fetalis) Cardiac decomposition

Management

Suspension of breastfeeding-during first 24 hours to preventpregnanediol-interfering with conjugation of indirect bilirubin

to direct bilirubin.

Phototherapy-speed up the maturation of RBC to preventaccumulation.

o Single quart halogen lamps, day bright positioned 12to 30 inches above the infant

Nursing care Cover eye with dressing Expect stool to be loose bright green from

bilirubin excretion

Provide good skin care Expect urine to be dark color because of

urobilinogen formation

Assess for dehydration, monitor I and O Maintain body temperature between 36 to

37C

o Home therapy Exchange transfusion

DYSTOCIA- a general erm for difficult labor, arise from the 3 component of

labor process

(a) Power, (b) passenger, (c) passageway.Complication with the power-

Inertia- sluggishness of contraction or more current is

dysfunctional labor

Dysfunctional labor

Classified as primary- onset of laborSecondary- occurring later in labor

Hypertonic contraction Hypotonic contraction

Contraction less than 2 to 3 per 10

minutes. Usually occur in active labor

Contraction is more common, and

intensity is may be not longer, usually

seen in active phase.

Contraction; strong and painful Contraction ; weak and painless

Causes; improper use ofoxytocin Causes; administration of analgesia,especially if cervix is not more than 3-

4 cm, bladder and bowel distention,-cause engagement, overdestintion

due to multiple pregnancy andhydramoius.

Management- rest and pain relief

such as morphine sulphate, decreasestimulus.

Management- oxytocin infusion,( rule

out first CPD prior to administration.

ABNORMAL LABOR PATTERN

type description treatment

Prolonged

latent phase

Latent phase more than 20

hours-nulli 14 hours- multi

Causes; hypertonic

contraction, false labor,

excessive sedation and

analgesia, poor cervical

condition- rigid, unripe, firm

cervix-most common

Therapeutic rest

Protractiondisorder


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Protracted

active phase

Protracted

descent phase

Less than 1.2 cm r dilatation

per hour-nulli

Less than 1 cm per dilatation

per hpur-multi

Less than 1 cm fetal descent

per hour-nulli

Less than 2 cm fetal descent

per hour -multi

Causes;

Excessive sedation

Conduction of analgesia

Persistent OP

Assess pelvic size,

presentation,

position, provide

support to mother

Arrest disorder

Arrest of

dilatation

Absent of cervical dilatation

for more than 2 hours in nulli

and 1 hour for multi

Arrest of

descent

Absent ofprogress of fetal

descent for more than 1 hour

in nulli and multi

Failure of

descent

Absent of fetal descent in

second stage of labor

Prolong second

stage of labor

More than 50 minute for nulli

Mor than 20 minutes for multi

Causes

POP

Epidural anesthesia

COMPLICATION OF LABOR

PRE TERM LABOR

Labor that occurs after 20th weeks and before 37 weeks of gestation.

Risk factors

Maternal factors Maternal infection PROM Bleeding

Uterine abnormalities/overdistention/incompetentcervix

Previous CS Trauma, poor nutrition Extreme age, decrease weight 100 lbs, less than 5ft.

Fetal factors

Multiple pregnancy Infections Polyhydramious Fetal malformation Placental separation/disorder

Complication

Prematurity Fetal death SGA/IUGR Increase perinatal/mortality

Treatment---- to prevent pre mature delivery

Bed rest, on left lateral position Adequate hydration Administration of tocolytic to arrest labor by relaxation of

the uterus( terbutaline, magnesium sulphate, ritrodrinesulphate

Administration of cortecosteriod( celestone,betamethasone)enhance maturation of fetal lungs by

stimulating production of surfactant

DYSTOCIA- general

DYSFUNCTINAL LABOR-

Hypertonic contraction Hypotonic contraction

Contraction less than 2 to 3 per 10

minutes. Usually occur in active labor

Contraction is more common, and

intensity is may be not longer, usuallyseen in active phase.

Contraction; strong and painful Contraction ; weak and painless

Causes; improper use ofoxytocin Causes; administration of analgesia,

especially if cervix is not more than 3-

4 cm, bladder and bowel distention,-cause engagement, overdestintion

due to multiple pregnancy and

hydramoius.

Management- rest and pain relief

such as morphine sulphate, decrease

stimulus.

Management- oxytocin infusion,( rule

out first CPD prior to administration.


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UTERINE RUPTURE-

Defined as; rupture of the uterus because of the stress of labor.

Risk Factors

Previous CS-most common ( uterine thickness less than .6cm)

Improper use of oxytocin Over destintion of the uterus Hypertonic contraction Mal presentation Traumatic manoeuvres like forcep delivery and traction

Assessment finding

Sign of impending rupture- pathologic retraction ring, astrong uterine contraction without cervical dilatation,

o Experience sudden, severe pain, during strongcontraction, and report of tearing sensation

Complete rupture- complete rupture of endometrium,myometrium, perimetrium leaving peritoneum intact.

o Uterine contraction immediately stop Incomplete rupture- woman experience only localized

tenderness, an persistent aching, pain over the lower

uterine segment.

Sign of external bleedingComplication

Hemorrhagic shock Maternal and fetal death

Treatments

CS manner of delivery Hysterectomy- unless otherwise if the rupture is on lower

uterine segment

IV oxytocin- attempt to contract the uterus to preventbleeding

Administer emergency fluid replacementNursing implementation

Stay with the patient Applied support measures

o Shock positiono Provision of warmth

Advised mother not to conceive again. Reposition mother to left lateral position

UTERINE INVERSIONDefined as; turning inside out with either birth of fetus or delivery of

placenta

Causes;

Traction applied to umbilical cord to remove placenta Fundal pressure applied when uterus is not contracted Passage of the fetus with short umbilical cord that pull the

fundus down

Assessment finding Total inversion- uterus protrude to the vagina Partial inversion- lie within the uterine cavity Large amount of blood sudden gushes to vagina Sign of shock, dizziness, paleness Exsanguinations

Treatment

Never attempt to replace the uterus-may cause additionalbleeding

Never attempt to replace the placenta- may cause largesurface area of bleeding

Administer oxygen by mask Antibioticexposure of endometruim

PRECIPITATE LABORShort labor that lasts for 2 to 3 hours or less

Or 5 cm per hour- nulli

Or 10 cm per hour- multiRisk factors

Multiparity- most common Trauma Large pelvis/lax soft tissue Small fetus Labor induction( amniotomy, oxytocin)

Assessment finding Titanic-like contraction Rapid labor and delivery

Nursing intervention

Never leave the patient Monitor FHT, to detect distress from the fetal hypoxia

secondary titanic contraction


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Never hold the baby back Have the client to pant not to push Deliver the head in between contraction Support the fetal head during delivery

Complication

Maternal Fetal

Maternal laceration Hemorrhage Infection

Hypoxia,anoxia Sepsis Intracranial hemorrhage

Treatment

Episiotmy Delivery

BANLS RING (pathological retraction ring)

Defined as;

PROLAPSED UMBILICAL CORD

Defined as; loop of umbilical cord slip down in front of the presenting

part. happen after the membrane rupture.

Causes;

PROM Mal presentation Placenta previa Small fetus CPD- prevent engagement Hydramious Multiple gestation

Cord prolapsed automatically lead to cord compression

Assessment finding

Cord may be felt as a presenting part AFTER BOW, RUPTURE THE INITAL MANAGMENT IS TO PERFORM

IE and

o monitor FHT-variable deceleration FHT patternsuddenly become apparent.

Management

If fully effaced and dilated cervix- physician choose to deliverit quickly by forcep delivery

o If not, CS is indicated Aimed to relieve pressure to umbilical cord

o Manually elevate the presenting part off the cordo Placing in knee-chest positiono Tredelenburg position

If exposed to room air, drying will begin leading to atrophy ofumbilical cord.

o DO NOT ATTEMPT TO PUSH BACK TO VAGINA- result tokinking and knotting of cord

o cover exposed umbilical cord with saline solutionPOST PARTUM COMPLICATION

POST PARTUM HEMORRHAGEThe most important maternal mortality associated with childbearing.

Blood loss greater than 500 ml.

There are four main causes of post partal hemorrhage.

1. Uterine atony2. Laceration3.

Retained placental fragment4. subinvolution

UTERINE ATONY-

Defined as; relaxation of uterus, most common post partal

hemorrhage

Condition that increase a woman risk for post partal hemorrhage

o distended uteruso multiple gestationo hydramoiuso large babyo presence of uterine mayoma

o cause cervical and uterine lacerationo operative birtho Rapid birth

o Varied placental site or attachmento Accrete,previao Premature separation of placenta/abruption

placenta

o Retained placental fragmento Unable to contract readily

o Deep anesthesiao Maternal ageo Prolonged laboro Secondary to maternal illness( anemia)


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o Prolonged used of magnesium sulphate andtocolytic agent

o High parityManagement

Identify for the source of bleeding. Manual evacuation is necessary if the cause is retained placenta

o Cautious with placenta accreta Massage the uterus in circular motion Placed icepack over fundus Administered oxytocin or methergine with caution Bimunual uterine compression and compression of aorta

Comparison of two common used uterotonic drugs

oxytocin Methergin(ergot)

action Rhythmic uterine contraction Sustained tonic

contraction

Onset 2-3 minutes 6-7 minutes

Side effects Water retention, hypotension Hypertension, headache,

vomiting

availability By prescription By prescription

LACERATIONDefined as; tear on birth canal is common and considered normal

consequence of childbearing, however large laceration are complication.

Common on;

Difficult or precipitate labor Primigravidas Large infant Lithotomy position and instrument

Cervical laceration

Vaginal laceration

Perineal laceration

Defined as; perineal laceration are injuries or tears in the vaginal

canal and outlet that occurs during delivery of the baby.

Classification of perineal laceration

First degree Skin, vaginal mucus,

2nd degree Skin, vaginal mucus, perineal muscle3rd degree Skin, vaginal mucus, perineal muscle, anal sphincter

4th degree Skin, vaginal mucus, perineal muscle, anal sphincter,

rectal lumen

Predisposing factors

Face presentation Rigid and scarred perineum Precipitate labor

Rapid breech extraction Big baby

RETAINED PLACENTA- a placenta does not deliver completely. Some portion

of the placenta left behind keeping the uterus from not contracting well.

Causes;

Succenturiate placenta- a placenta with accessory lobes

Placenta accrete- placenta fuses with the myometrium because ofabnormal deciduas basalis.

Therapeutic management

Removal of placental fragment is necessary to prevent bleeding.

Usually dilatation and curettage is performed to remove retained placentalfragment.

Methotrexateprescribe to destroy retained placenta.

SUBINVOLUTION- is incomplete return to its pre pregnant state, shape and

size. Result to retained placental fragment, myoma, mild enometriois

PUERPERIAL INFECTION-

Defined as; infection from the genital tract happening at any time

between rupture of BOW up to 42 weeks post partum.

Assessment finding

Fever Pelvic pain Abnormal lochia with foul smelling

Predisposing factors

Episiotomy and laceration Endometritis Abscess formation Breast infection Wound infection PROM Prolonged labor


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Puerperal infection may lead to maternal infertility- due to ascending

infection to internal genital area that would lead to PID.

HEMATOMAS- perineal hematomas, is accumulation of blood in subcutaneoustissue layer of perineum. Ccurs in episiotmy site, or during repair if the vein has

been puncture during repair.

Management

Report the size and degree of woman discomfort.Administered mild analgesia

Applied ice pack

Bleeding vessel should be ligate.

If the hematoma is small

Observe hematoma, applied ice pack, assess of degree of pain.

Hematoma is reabsorbed after 6 weeks/

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