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/