MACROSOMIA: (477)
- birthweight > 4500g
- Common with:
- prepregenancy maternal obesity
- excessive maternal weight gain
- maternal diabetes
- prior hx of macrosomia
- male fetus
- grand multiparity
- prolonged gestation
- Hispanic background
- erythtroblastosis fetalis (when an RH-negative mother is pregnant with an RH-positive fetus and maternal antibodies cross the placenta, enter fetal circulation, and destroy the fetal RBC's resulting in jaundice, anemia, and compensatory erythropoiesis. Marked in increases in immature RBC's occurs, hence name erythroblastosis fetalis. RhoGAM has contributed to the decrease of this)
- Maternal implications of macrosomia:
- CPD (cardiopulmonary disease)
- dysfunctional and prolonged labor
- soft tissue laceration during birth
- post-partum hemmorhage
- Fetal/Neonatal Implications
- meconium aspiration
- asphyxia
- shoulder dystocia
- upper brachial plexus injuries, fractured clavicles
- hypoglycemia, polycythemia, hyperbillirubinemia
- Clinical Therapy
- problems can be lessened by identifying macrosomia before onset of labor
- carefully evaluate pelvis
- estimate weight by palpation, ultrasound, and x-ray
- planned cesarian to avoid shoulder dystocia
- shoulder dystocia marked by presence of "turtle sign", fetal head emerges then quickly retracts as the shoulder becomes wedged beneath the pubic bone
- McRoberts Maneuver may relieve
- NEVER use fundal pressure
- Nursing Management:
- assist in identifying women at risk
- assess FHR for signs of distress
- evaluate rates of cervical dilation and fetal descent
- apply fetal monitor
- lack of fetal descent or early decelerations due to fetal head compression are signs the infant is too large for a vaginal both
- inspect macrosomic newborns for cephaltohematoma, Erb's palsy, and fractured clavicles
- monitor blood glucose of fetus since macrosomia is usually associated with gestational diabetes
- after birth overstretched uterus may not contract well (uterine atony) and may feel boggy (soft), uterine hemorrhage likely
- may need IV or IM Pitocin
- monitor for signs of shock
DIABETIC KETOACIDOSIS, (1549):
- primarily occurs in children with type 1 diabetes
- Causes include:
- incorrect insulin doses
- incorrect administration of insulin
- illness, trauma, or surgery
- new onset diabetes
- Insulin deficiency is accompanied by a compensatory increase in hormones (epi, nor-epi, cortisol, growth hormone, and glucagon) that are released when inadequate glucose is released to the cells.
- The muscle cells break down protein into amino acids that are then converted into glucose by the liver, leading to hyperglycemia.
- The adipose tissue releases fatty acids that are transformed by the liver into ketone bodies and their accumulation leads to ketoacidosis.
- The hyperglycemia causes an osmotic diuresis resulting in dehydration, acidosis, and hyperosmolality.
- DKA is associated with severe metabolic, electrolyte, and fluid imbalances.
- Signs of DKA include:
- polyuria
- polydipsia
- weight loss
- abdominal pain
- nausea and vomitting
- tachycardia
- dehydration
- flushed ears and cheeks
- Kussmaul respirations
- acetone breath
- altered level of consciousnes
- hypotension
- hyperglycemia, glycosuria, and ketonuria are also present
- Children may complain of chest pain, nausea, and vomiting
- may progress to electrolyte disturbances, arrhythmias, altered consciousness, pupillary changes, irregular respiration, widening pulse pressure
- DKA is present with th following finidings:
- blood glucose level > 250 mg/dL
- serum ketones
- acidosis (pH < 7.3 and HCO3 < 15 mEq/L
- child usually hospitalized
- medial management includes:
- isotonic IV fluids
- short acting insulin (0.1 unit/kg/hr) by continuous infusion pump to decrease serum glucose at rate not to exceed 100mg/dL/hr; faster reduction increases risk for cerebra edema. When glucose is lowered too rapidly, water is freed and attracted to the glucose, which has accumulated in the brain.
- bicarb is not routinely used as it places the child at risk for hypokalemia, acidosis, and cerebral edema
- as insulin is administered, potassium shots to the cells, resulting in hypokalemia. Potassium supplement is given only after confirmation of renal function
- Cerebral edema is the most common cause of DKA related death
- Nursing Management:
- monitor vitals'monitor for arrhythmia associated with hypokalemia
- assess for dehydration
- monitor blood glucose levels hourly or as ordered
- monitor electrolytes, urine glucose, ketone levels
- I/O hourly
- monitor for signs of hypoglycemia from continuous infusion
- Fluid Management:
- if child is in shock IV fluid boluses of 10-20 mL/kg given rapidly over 5 minutes
- give adequate fluids
- titrate insulin infusion to control gradual reduction of hyperglycemia
- taper off IV insulin and transition to subQ when clinically stable
- oral feedings are reintroduced when child is alert and glucose level is stable
- Teaching:
- teach parents that increased blood glucose and ketone monitoring is important when the child has significant stress or illness
- insulin is required even when child is not eating to counter the hormones secreted in response to stressors
HYDRAMNIOS, (460):
- also called polyhydramnios
- more than 2000 mL of amniotic fluid
- occurs in about 1% of all pregnancies
- often occurs in cases of major congenital abnormalities
- associated with fetal malformations that affects fetal swallowing and disorders in which the fetal meninges are exposed in the amniotic cavity
- also found in cases of anencephaly when the fetus is thought to have urinated excessively because of overstimulation of the cerebrospinal centers
- 2 types of hydramnios; chronic and acute
- Chronic type- fluid gradually increases and is a problem of the third trimester; accounts for most cases
- Acute type- volume increases rapidly over a few days; usually diagnosed between 10 and 24 weeks
- Maternal Implications:
- when fluid is over 3000 mL the woman experiences shortness of breath and edema in the lower extremeties due to compression of the inferior vena cava
- associated with diabetes Rh sensitization, and multiple gestation pregnancies
- can also occur as result of infection such as syphillis, toxoplasmosis, cytomegalovirus, herpes, and rubella
- if removed rapidly before birth, abrupt placentae can occur from too sudden a change in the size of the uterus
- over detention of uterine muscles can cause uterine dysfunction is the intrapartum period and increase incidence of postpartum hemorrhage
- Fetal/Neonatal Implications:
- fetal malformations and preterm birth are common with hydramnios
- perinatal mortality is fairly high
- prolapsed cord can occur when membrane is ruptured creating further complication
- incidence of malpresentation increases
- incidence of preterm labor and cesarean section significantly increases
- Clinical Therapy
- managed with supportive treatment unless intensity of women's distress and symptoms dictate otherwise (dyspnea, pain)
- fluid can be removed vaginally or via amniocentesis
- dangers of removing vaginally are prolapsed cord and inability to remove fluid slowly
- if amnio is performed, it should be with aid of sonography to prevent injury to fetus and placenta
- fluid should be removed slowly to prevent abruption
- Nursing Managemant:
- suspected when fundal height increases out of proportion to gestational age
- as fluid increases it may be difficult to palpate fetus and auscultate FHR
- in sever cases maternal abdomen appears tense and tight
- on ultrasound large spaces can be identified between fetus and uterine wall
- maintain sterile technique during amniocentesis
- offer support by explaining the procedure
- if fetus has congenital defect, collaborate with social services to offer family additional help
OLIGOHYDRAMNIOS, (461):
- defined as less than normal amount of fluid (~ 500mL is considered normal)
- affects 1-3% of all pregnancies
- diagnosed when the largest vertical pocket amniotic fluid on ultrasound is 5cm (2 inches) or less
- cause unknown
- found in cases of:
- maternal hypertensive disorders with IUGR
- post maturity
- fetal renal malformations
- renal aplasia with dysplastic kidneys
- obstructive lesions of lower urinary tract
- if present during first part of pregnancy there is a danger of fetal adhesions (one part of fetus may adhere to another part)
- Maternal implications:
- dysfunctional labor
- hypertensive disorders
- Fetal/Neonatal Implications:
- skin and skeletal abnormalities due to impaired fetal movement
- pulmonary hypoplasia (less fluid to use during fetal breathing movement)
- reduced cushioning effect for umbilical cord during labor, high incidence of cord compression
- fetal head compression
- Clinical Therapy:
- suspected when uterus does not increase in size and fetus is easily palpated
- as soon as fetus is term a delivery is schedule due to higher risk for fetal demise
- continuos fetal monitoring during labor
- some practitioners advocate for amnioinfusion (transcervical intimation of warmed sterile saline followed by continuos transfusion rate) after membranes have ruptured to decrease frequency of variable decelerations and gives more fluid to cushion cord
- Nursing Management:
- continuous fetal monitioring
- evaluate EFM for non reassuring signs
- if variable decelerations noted, change woman's position to relive pressure on cord and notify MD/CNM
CARE OF THE NEWBORN WITH JAUNDICE:
- the most common abnormal physical finding
- some degree of jaundice resulting from elevated unconjugated bilirubinemia occurs in ~85% of healthy term infants an most preterm infants
- physiologic or neonatal jaundice is: a normal process that occurs during transition from intrauterine to extrauterine life and is caused by the newborn's shortened red blood cell span (90 days as compared to 120 in adulthood), slower uptake by the liver, lack of intestinal bacteria, and/or poorly established hydration by initial breastfeeding
- ja
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