RCNIC ORIENTATION

1
RCNIC ORIENTATION

• CARE OF THE NEONATE WITH A HEMATOLOGIC DISORDER
• M.VICTORIA DECASTRO,
• RNC, BSN, Clinical Coordinator, CNIII

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Care of Neonate with Neonatal Hyperbilirubinemia
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Hyperbilirbinemia

• Definition
• physiological jaundice
• the yellow discoloration of the skin,
  conjunctivae, and sometimes mucous membranes
• Occurs in more than 50 of all newborns
• (Deacon ONeill, 1999)
• affects full-term infants within 2 to 4 days of
  birth and lasts until about day 6 (Kenner Lott,
  2003)
• preterm infants have higher peak levels occurring
  at about 5 to 7 days of life (Kenner Lott,
  2003) jaundice lasts longer in preterm infants
  the more preterm an infant is the lower the
  lightlevel

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Hyperbilirbinemia

• Pathophysiology
• Bilirubin is produced by the breakdown of
  hemoglobin at the end of a red cells lifespan
• Because the neonates liver is immature, the
  bilirubin level exceeds the livers ability to
  conjugate bilirubin (convert bilirubin to
  soluble form for excretion)
• This bilirubin then free floats in the plasma
• At high levels, bilirubin can cross the
  blood-brain barrier and damage brain cells
  causing kenicterus

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Hyperbilirubinemia

• Serum bilirubin levels (unconjugated) are greater
  than 12 mg/dl and generally occurs after the
  first 36 hours
• A bili level above 12 mg/dl within the first 24
  hours is not considered physiological
• Bili levels in general are considered
  physiological if
• Full-term-12mg/dl or greater by 3 days of life
• Preterm-10 to 12 mg/dl or greater by 5 days of
  life
• Treatment depends on the bili level, the infants
  gestational and actual age, and the severity of
  the infants condition

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Causes of Hyperbilirubinemia

• (Kenner and Lott, 2003)
• ABO incompatibilities
• RBC breakdown
• Sepsis
• Drug reaction-such as Vitamin K
• Extravasation of large quantities of blood
• Bilirubin conjugation interference
• Breastmilk conjugation

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Causes of Hyperbilirubinemia

• (Kenner and Lott, 2003)
• Transplacental and neonatal drug interactions
• Hypothyroidism-affects up to 3 to 4 weeks
• Acidosis and hypoxia
• Decreased bowel motility or hepatocellular damage
  can cause abnormal bilirubin excretion
• Congestive heart failure can cause abnormal
  bilirubin excretion

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What will you see in a jaundiced infant?

• Yellow discoloration that starts on the face and
  spreads caudally
• Yellow discoloration of the sclera and mucus
  membranes
• Signs and symptoms of kenicterus

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Hyperbilirubinemia

• Kenicterus is the yellow staining of brain tissue
  and leads to brain damage, such as cerebral palsy
  and deafness.
• Kenicterus occurs in 50 of infants with bili
  levels of 30 of greater and in 10 with bili
  levels 20 to 25

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Hyperbilirubinemia

• Risk factors (Kenner and Lott, 2003)
• Inadequate intake/dehydration
• Acidosis and hypoxia
• Certain drugs and substances may compete with
  available bilirubin binding sites such as
  sufisoxazole, salicylates and sodium benzoate
• Hypoproteinemia (lower albumin levels)-places
  preterm infants at higher risks

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Hyperbilirubinemia

• Clinical manifestations of kenicterus
• usually evident in the first 5 days of life
• In a sick or preterm neonate, kenicterus can
  occur at levels as low as 5 mg/dl (Nathan Oski,
  1998)

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Hyperbilirubinemia

• Generally, the neonate is stable and otherwise
  healthy
• Because of early discharge, physiological
  hyperbilirubinemia is often diagnosed in the home
  care setting
• Key to diagnosis is parent education
• Home phototherapy can be used

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Hyperbilirubinemia

• Treatment and management
• PREVENTION!!
• Double volume exchange transfusion
• Nursing Standard of Care Infant with Neonatal
  Hyperbilirbinemia
• Phototherapy
• Hydration
• Phenobarbital administration

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Phototherapy

• Phototherapy lights causes the bilirubin to
  become more water-soluble this bilirubin can be
  excreted in bile/stool and urine
• May use bank lights and/or bili blanket

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Phototherapy

• Use bank lights and/or bili blankets
• Use bili mask to protect eyes.
• Monitor temperature closely by using continuous
  skin temperature monitoring take temperature Q
  2-4 hours
• Bili levels at least every 8-12 hours, turning
  off phototherapy lights with lab draws only

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Phototherapy

• Important to expose as much skin as possible,
  covering only genitals and eyes for protection
• Turn infant frequently to allow for maximum
  exposure
• Avoid use of ointments and lotions

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Phototherapy

• Important that the phototherapy light levels are
  within acceptable range
• Bilimeter readings q shift with approximate goal
  of 25 to 45 (combined readings of biliblanket
  and bili lights)

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Phototherapy

• Side effects-(Kenner and Lott, 2003)
• Parental teaching-signs and symptoms of
  hyperbilirubinemia and dehydration
• Dermal Rash
• Lethargy
• Abdominal distention
• Possible eye drainage
• Dehydration
• Thrombocytopenia
• Hypocalcemia
• Temporary lactose intolerance
• Bronze baby syndrome

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Nursing Standard of Care

• Patient will not experience neurological injury
• Assess and document skin color from head, sclera,
  and trunk in daylight or under fluorescent light
  at least q shift
• Obtain bili levels as ordered
• Observe for and report abnormal neurological
  findings
• Check bilimeter readings

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Nursing Standard of Care

• Patient will not experience injury from
  phototherapy
• Cover eyes
• Inspect eyes q 2 hours and prn with phototherapy
  lights off, notify physician of any drainage
• Change eye shields prn
• Avoid tight head band on eye shield to reduce the
  risk of increased ICP, especially in preterm
  infants
• Maximize exposed skin surface, protecting
  genitalia
• Avoid exposure of skin temperature probe to
  phototherapy lights

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Nursing Standard of Care

• Patient will be adequately hydrated
• Maintain parenteral nutrition as ordered
• Encourage feedings ASAP, including breastfeeding
  if held for feeds can discontinue overhead lights
  for a short time and wrap biliblanket with
  infant.
• Accurate Is and Os
• Assess for signs of dehydration, account for
  insensible water losses
• Daily weights

22
Nursing Standard of Care

• Patient will maintain thermoregulation
• Provide neutral thermal environment
• Maintain axillary temperature of at least 36.5
  degrees Celsius
• Avoid cold stress
• Q 4 hour vitals and prn
• Properly secure temperature probe to abdomen or
  back

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Nursing Standard of Care

• The parents/caregivers will participate in the
  childs care and health goals/outcomes
• Provide information and explanations of
  hyperbilirubinemia and phototherapy to the
  parents/care givers
• Explore with parents/caregivers their willingness
  to provide care

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Phototherapy

• Follow-up Care
• Maintain adequate hydration, including enteral
  feeds if possible
• Check bili levels at least 4-8 hours after
  phototherapy is D/Ced there is a chance for
  rebound

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Exchange Transfusion

• Early exchange transfusion is indicated with the
  presence of hemolytic disease
• Carefully monitor fluid and electrolyte status
• Provide adequate hydration

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Exchange Transfusion

• Double volume Exchange Transfusion
• Purpose-to remove the infants bilirubin and
  antibody-coated red blood cells from circulation
  by removing the infants blood volume and
  replacing the volume with blood or another volume
  expander

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Phenobarbital Administration

• Increases the uptake and conjugation of bilirubin
  by the liver and increasing its excretion by
  increasing bile flow

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Care of the Neonate with Anemia
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Anemia

• Definition
• low hemoglobin concentration and/or decreased
  number of red blood cells diminishes the
  oxygen-carrying capacity of the blood and the
  level of oxygen available to tissues (Blanchette
  Zipursky, 1994 Hume, 1997 Miller, 1995
  Oski, Brugnara, Nathan, 1998)

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Anemia

• Physiology
• removal or loss of 10 or more of total blood
  volume over 24 to 48 hours can lead to anemia
• In general, there are 100 ml of blood volume per
  kg in a preterm infant and 82-85 ml of blood
  volume per kg in a term infant (Kenner and Lott,
  2003)
• Hgb and HCT levels determine the type and degree
  of anemia in general, Hct less than 40 is
  considered anemia
• Hgb may not accurately the extent of acute blood
  loss
• low HCT or Hgb may be acceptable if retic count
  is NL

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Anemia

• Clinical findings
• Acute anemia-signs and symptoms are emergent and
  life-threatening most common causes are
  hemorrhage, RBC destruction and hemolysis, and
  frequent blood sampling/draws
• Chronic anemia in preterm and term infants
  results from dietary deficiencies may not need
  immediate intervention, but close monitoring for
  signs of decompensation is necessary

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Anemia

• Risk factors and indications
• Frequent lab draws
• Family history of anemia or jaundice
• History of bleeding, splenectomy, consanguinity,
  and/or blood group incompatibilities
• Some ethnic groups and natives of specific
  geographical origins, such as African-American
  population and sickle cell anemia
• Maternal history
• Presence of cephalohematoma
• Abnormal distention of mass-damage or ruptured
  liver, spleen , adrenal, kidney
•   Cardiovascular abnormalities-tachycardia,
  murmur, gallop rhythm
• Hydropic changes

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Anemia

•   Normal values for the neonate (0 to 30 days)
• RBC-4.1 to 6.1
• Hemoglobin (Hgb)-16 to 21
• Hematocrit (Hct)-44 to 60
• Reticulocyte count (Retic)-2 to 6
• Values vary depending on infants gestational age
  and actual age

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Anemia

• Acute Anemia
• Symptoms are more emergent and life-threatening
• Most common causes include hemorrhage, RBC
  destruction and hemolysis, and frequent blood
  sampling

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Acute Anemia

• Signs and Symptoms of Acute Anemia
• Pallor
• Tachycardia
• Shallow, rapid, irregular respirations
• Low or absent blood pressure, low venous
  pressures
•  Weak or absent peripheral pulses
•   Poor perfusion

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Acute Anemia

• Signs and Symptoms of Acute Anemia
• Capillary refill time greater than 4 seconds
• Mottling
• Lethargy
• Low HCT
• Hgb may be initially NL, with decline over the
  next 6-12 hours

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ANEMIA

• Chronic Anemia in preterm and term infants is a
  result in dietary deficiencies and may not need
  immediate intervention
• Close monitoring for signs of decompensation is
  necessary

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Anemia

• Signs and symptoms of chronic anemia
• Pallor without signs of acute distress
• Increased incidence of apneic and/or bradycardic
  episodes or increased severity of apneic and/or
  bradycardic episodes 
• Hepatosplenomegaly 
• Signs of congestive heart failure
• Tachycardia 

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Anemia

• Signs and symptoms of chronic anemia
• Increased oxygen requirement
• Increased respiratory effort (dyspnea) or
  tachypnea 
• Lethargy, decreased activity/energy level-infant
  just does not seem like oneself
• Poor feeding
• Poor weight gain
• Low RBCs, HCT, and Hgb levels Retic counts may
  be low, normal, or high

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Anemia

• Management of acute anemia
• Remember your ABCs of resuscitation!!
• Hemodynamic support
• CBC with differential, type and cross, Coombs
  testing
• Blood transfusion
• acute-CMV safe, HgbS negative, and O-negative
  PRBCs
• in infants less than 1 kg or immuno-suppressed
  use irradiated

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Anemia

• Management of acute anemia
• Provide warmth, monitoring of vital signs, and
  continuous and accurate assessment of Is and Os
• Lab tests and physical exams are necessary in
  order to determine the cause of acute anemia
• Modifications in care that eliminate recurrence
  of precipitous events and prevent blood loss

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Anemia

• Chronic anemia
• Goal of treatment-the control or eradication of
  the cause or symptoms

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ANEMIA

• Management of chronic anemia
• Nutritional management/replacement therapy
• Iron-ferrous sulfate (Ferinsol), iron-fortified
  formulas
• Folic acid
• Vitamin E (Aquasol E)
• Erythropoeiten
• Transfusion therapy

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Transfusion Therapy

• Blood products for neonates are CMV safe,
  leukofiltered, and Hgb-S negative irradiated for
  immunosuppressed infants such as micropreemies
  (less than 1 kg) and septic infants
• Use MDX (minimal donor exposure) protocol for
  infants less than 1 kg
• The decision to transfuse is dependent on many
  factors

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Transfusion Therapy

• Assess for S/S of transfusion reactions-usually
  occurs during the first 15 minutes of the
  transfusion
• Shivering/chills -Vomiting
• Dyspnea -Presence of blood in urine
• Hyperthermia  -Tachycardia
• Hypertension -Rash
• Irritability

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Transfusion Therapy

• Vitals
• TPR and B/P before(within 5 minutes of the start
  of the transfusion) and after administration
  (within 5 minutes of the end of the transfusion),
  at 15 minutes of the start of the transfusion,
  and every hour until transfusion is complete

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Transfusion Therapy

• If signs of transfusion reaction appear
• Stop transfusion immediately
• Immediately send transfused blood and
  administration set to blood bank.
• Follow instructions on report of transfusion
  reaction form

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Anemia

• Long-term follow-up and prognosis
• Continue to assess for S/S of anemia
• Maintain adequate nutritional support
• Improved oxygenation and control or eradication
  of symptoms are indicative of a positive
  prognosis
• Long-term prognosis is determined by the
  underlying causes degree of anemia and the
  infants response to interventions

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Care of the Neonate with Polycythemia
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Polycythemia

• Definition
• the condition in which an excess mass of RBCs is
  in circulation, resulting in increased blood
  viscosity
• Venous HCT greater that 65 and venous Hgb is
  greater than 22 g/dl
• Occurs in the first week of life

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Polycythemia

• Incidence (Kenner and Lott, 2003)
• 4-5 of all infants
• 2-4 of AGA infants
• 10-15 of SGA and LGA infants
• Not seen in infants less than 34 weeks gestation

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Polycythemia-Risk factors (Kenner and Lott, 2003)

• PIH, pre-eclampsia/eclampsia
• Increased maternal age
• Maternal renal or heart disease
• Severe maternal diabetes
• Oligohydramnios
• Maternal smoking
• Placental infarction

• Placental previa
• Viral infections, especially TORCH infections
• Postmaturity
• Placental dysfunction leading to SGA
• Cyanotic cardiac abnormalities
• Trisomies 13, 18, 21
• Beckwith-Wiedemann Syndrome

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Polycythemia

• Physiology
• Active-results as a response to tissue hypoxia,
  usually in utero
• Passive-results from increased blood volume
  secondary to maternal-fetal or twin-twin
  transfusion.
• Clinical findings
• infants may be asymptotic

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Polycythemia- Clinical findings

• Respiratory distress
• Pleural effusions
• Pulmonary congestion and edema
• Central cyanosis
• Plethora (extreme ruddiness)

• Cardiomegaly
• Arrhythmias, dysrhythmias, ECG changes
• Tachycardia
• Lethargy
• Elevated reticulocyte count

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Polycythemia- Clinical Findings

• Seizures
• Apnea
• Vomiting
• Poor suck
• Exaggerated startle
• Tremors
• Hypotonia

• Jitteriness
• Hypocalcemia
• Hypoglycemia
• hyperbilirubinemia
• Hepatospleno-megaly
• Thrombocytopenia

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Polycythemia

• Management
• Basic resuscitation and stabilization
• Adequate hydration
• Assessment of symptoms determines treatment
• Venous Hgb and Hct, CBC with differential, blood
  cultures
• Thorough H P
• Partial volume exchange transfusion

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Partial Volume Exchange Transfusion

• Also known as Single Volume Exchange
• Generally similar to double-volume exchange
  transfusion, except for the use of 5 Albumin or
  crystalloid instead of RBCs for blood
  replacement and the partial removal of blood

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Partial Volume Exchange Transfusion

• Goals
• Relieves congestive failure and helps improve CNS
  function
• Corrects hypoglycemia
• Reduces cyanosis
• Improve renal function
• Desired decrease in HCT less than 60

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Polycythemia

• Long-term follow-up/prognosis
• Early treatment and management of symptoms can
  prevent persistent problems and adverse effects
• Problems are related to
• The underlying causes or disease processes
• The extent of the CNS complications-gross and
  fine-motor delays may occur speech delays may be
  evident around the age of 2 and learning
  deficits may be seen in school age children

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Care of the Neonate with Thrombocytopenia
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Thrombocytopenia

• Definition-the disease process in which the
  platelet count is less than 100,000
• infants may be asymptotic
• most common bleeding disorder of the neonate
• Physiology
• Normal-150,000 to 450,000
• Abnormal-less than 150,000 watch for active S/S

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Thrombocytopenia

• Decisions for platelet transfusion are dependent
  on the infants specific condition, underlying
  disease process, severity of symptoms, and the
  ability of the infant for hemostasis

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Thrombocytopenia- Neonatal Risk Factors

• Birth asphyxia
• Giant hemangiomas
• Presence of thrombosis
• Side effect of exchange transfusion
• Cold stress
• polycythemia

• Sepsis/infection
• Some congenital diseases or syndromes
• Apgars less than 7
• DIC
• Meconium aspiration syndrome

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Thrombocytopenia- Neonatal Risk Factors

• Hepatic disease
• Cardiopulmonary bypass
• Congenital Anomalies such as Trisomies 13,18,
  21, Fanconi Anemia, Congenital Leukemia

• NEC
• PPHN
• SGA
• Isoimmune (Rh incompatibility
• Cephalohematoma
• Absence of Vitamin K administration
• Renal failure

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Thrombocytopenia-Maternal Risk Factors

• Maternal autoantibodies (immune-mediated) causing
  destruction of platelets or Idiopathic
  Thrombocytopenia (ITP)-maternal IgM of IgG
  attaches to platelets, when IgG crosses the
  placental barrier, fetal platelets can be
  destroyed

• PIH, pre-eclampsia, eclampsia
• Placental infarction
• Maternal systemic lupus erythematosus
• Maternal thrombocytopenia

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Thrombocytopenia-Risks from Drug Side Effects

• Maternal or Neonatal
• Indomethacin
• Demerol
• Phenergan
• Aspirin
• Sulfonamides

• Quinide
• Quinine
• Nitric Oxide-prevents adhesion of platelets to
  endothilial cells

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Thrombocytopenia

• Clinical Findings
• Presence of petichiae, purpura, ecchymosis
• Bleeding (GU, GI, umbilical, wound, puncture
  sites, integumentary)
• Hepatosplenamegaly
• Jaundice
• Septic shock in severe cases
• Anemia
• Low platelet count
• PT/PTT and other coagulation factors are normal
• Elevated forms of immature platelets

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Thrombocytopenia

• Management
• Basic resuscitation and stabilization
• Control of bleeding and fluid resuscitation
• CBC with diff, PT, PTT, clotting factors,
  fibrinogen, FDP, blood cultures
• Administer blood products as necessary
• Thorough H P for risk factors and causes

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Thrombocytopenia

• Management (continued)
• Antenatal treatment with corticosteroids
• Postnatal steroid therapy
• Strict Is and Os
• Guiac stools, gastrocult gastric
  secretions,dipstick urine

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Thrombocytopenia

• Management (continued)
• Control and prevention of S/S-
• only necessary heelsticks
• constant assessment all PIV sites, umbilical line
  sites, puncture sites, drain sites, foley site,
  and wound sites
• minimal tape use

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Thrombocytopenia

• Management (continued)
• Control and prevention of S/S-
• treatment of anemia
• assess of S/S of intracranial hemorrhage,NEC, GI
  bleeding, hyperbilirubinemia
• administration of Vitamin K

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Thrombocytopenia

• Management (continued)
• Treatment of underlying pathophysiology
• Treatment of anemia
• Exchange transfusion using blood less than 2 days
  old
• Platelet transfusion-using single donor platelets
  when possible
• Administration of clotting factors
• FFP
• Specific clotting factors
• Cryoprecipitate

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Thrombocytopenia

• Long-term follow-up/prognosis
• Assess for recurrence of S/S
• Follow-up platelet counts and clotting factor
  levels
• Prognosis is dependent on the degree of
  thrombocytopenia, underlying disease, and
  existing syndromes

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Care of the Neonate with DIC
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Disseminated Intravascular Coagulation

• Definition-an acquired hemorrhagic disorder with
  an underlying disease manifested as an
  uncontrollable activation of coagulation and
  fibrinolysis. Consumption of clotting factors is
  thought to be initiated by the release of
  thromboplastic material from damaged or diseased
  tissue into circulation. Fibrinogen converts to
  fibrin to form microthrombi (Andrew, 1997
  Beardsley and Nathan, 1998 Fuse et al, 1996
  Hilgartner and Corrigan, 1995 Kuehl, 1997 Pugh,
  1997 ). DIC presents with depletion of
  platelets, PT, fibrinogen, and Factors V, VII,
  and VIII. PT and PTT are prolonged.

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DIC-Risk Factors

• PIH, pre-eclampsia, eclampsia
• Placental abruption
• Placental abnormalities
• Infection/sepsis

• Fetal distress
• Hypoxia and acidosis
• Obstetrical complications, traumatic delivery
• Dead fetal twin

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DIC-Risk Factors

• Severe Rh incompatibility
• Thrombocytopenia
• Respiratory distress
• Hypotension
• Persistent pulmonary hypertension

78
DIC

• Physiology
• results from a pre-existing disorder and does not
  develop independently the underlying problem
  must be identified and treated
• Lab values-
• PT/PTT are prolonged
• Fibrinogen is low
• FDP is high
• Platelet count is low
• D-dimer is greater than 1.0
• Abnormal red blood cell shape, cell
  fragmentation, and decreased number of platelets
  on peripheral smears

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DIC

• Clinical Findings
• S/S depend on the underlying disease
• Continued/prolonged bleeding or oozing from
  puncture sites, wound sites, and/or umbilicus
• Presence of petechiae, purpura, and ecchymosis
• Hemorrhage-often from every orifice
• Thrombosis of peripheral vessels resulting in
  localized necrosis and gangrene

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DIC

• Clinical Findings (continued)
• Generalized multiple site bleeding
• Organ and tissue ischemia secondary to
  microvascular occlusion by thrombi
• Septic shock
• Presence of anemia
• Blueberry muffin spots

81
DIC

• Management and Nursing Care
• Basic resuscitation and stabilization
• Remember the A, B, Cs
• Assess for areas of bleeding/hemorrhaging
  (internal and external) control of bleeding and
  decompensation
• Thorough H P
• Labs CBC w/ differential, PT, PTT, fibrinogen,
  FDP, D-Dimer, specific clotting factors, blood
  cultures
• Need to differentiate from other possible disease
  processes such as Vitamin K deficiency and
  hemophilia
• Treatment of underlying disease process

82
DIC

• Management Nursing Care (continued)
• Treatment of clinical symptoms
• Administration of applicable blood products
• Hemodynamic stabilization
• Strict Is and Os
• Assess for signs and symptoms of anaphylactic
  blood products
• Maintain fluid and electrolyte balance, adequate
  hydration
• Keep infant warm
• Minimal tape use

83
DIC

• Long-term follow-up/prognosis
• Prognosis is related to the expected outcome and
  successful management of the disease process,
  severity of DIC, and severity of complications
• Need to assess for
• Complications
• S/S of organ failure
• GI bleeding
• Intraventricular, parenchymal hemorrhage
• Severe depletion, hypovolemic shock
• Continue to assess for S/S of DIC

84
Care of the Neonate with ABO and Rh
Incompatibilities
85
ABO and Rh INCOMPATILITIES

• Definition
• ABO-RBC destruction or adverse clustering of
  RBCs as a result of exposure of antibodies or
  agglutinins of one blood type to another
• Rh-more severe occurs when an Rh negative
  mothers antibodies to Rh positive factor are
  exposed to the antigens of an Rh positive infant
  leading to the destruction of the infants RBCs

86
ABO Incompatibilities

• Risk factors-Exposure of mixing of fetal
  maternal circulation usually occurs via
  hemorrhage during labor, delivery, amniocentesis,
  abortion, and ectopic pregnancy

87
ABO

• Clinical findings
• jaundice within the first 24 hours of life
• evidence of hemolytic disease in CBC values and
  peripheral blood cells (smears)
• positive direct and indirect Coombs tests
• hepatosplenomegaly

88
Rh

• Clinical findings
• Jaundice/hyperbilirubinemia
• Hepatosplenomegaly
• Hydrops fetalis-
• Anemia
• Hypoxia
• Congestive heart failure
• Hypoalbuminemia
• Erythroblastosis Fetalis

89
ABO and Rh

• Management-(NICU)
• Basic resuscitation and stabilization
• Blood products
• RhoGam to Rh negative mothers after delivery
• Hydration, fluid and electrolyte balance
• Maternal and obstetrical H P
• Type Cross, Coombs testing, CBC with diff, Bili
  levels

90
ABO and Rh

• Management (continued)-(NICU)
• Phototherapy
• Exchange transfusion
• Parancentisis or thorancentesis
• Hemodynamic monitoring and support
• Strict Is and Os
• Double volume exchange transfusions