PEDIATRICS 2

BLOOD AND HEMOSTATIC MECHANISM

Dr. Alabastro
2nd shifting / Sept. 15, 2008
Trans group: Chubimbonbon

Blood and Hemostatic Mechanism:

• Hgb = 17–19 mg/dL Low Hgb

• Leucocytosis and elative neutrophilia in 1st 24 hours

• Relative lymphocytosis after 1st week Retic count
• RBC with relatively low levels of reduced Glutathione
• Deficient capacity of liver to conjugate Bilirubin
• Normal hemostatic mechanism depends upon
establishment of normal intestinal flora and LOW
NORMAL OR HIGH
elaboration of Vitamin K Congenital
Coombs Test
Hypoplastin
Anemia Anemia
Definition:
• Full term : Hct < 45%; Hgb < 14.0 g/dL
(+)
• Pre-term: Hct < 40%; Hgb < 13.5 g/dL Immunoe Hemolytic
• Acute hemorrhage at time of bit may not be reflected (-)
Anemia
in initial Hct MCV
ABO, Rh
• Capillary Hct is higher than central hematocrit due to Minor Blood Group
sludging
• If pH is low, central H”ct may be inaccurate (high)
because of vasoconstriction LOW NORMAL OR HIGH
Chronic IU Blood Loss Peripheral Blood
Causes: a-thalassemia Smear
• Blood Loss: pre-natal, intrapartum, post-natal
• Hemolysis: isoimmune hemolysis, congenital defects of
the erythrocytes, abnormalities of erythrocyte
membrane, disorders of hemoglobin synthesis, NORMAL
acquired defects of erythrocytes ABNORMAL
Infection ….
• Underproduction of erythrocytes: Damond-Blackfan Blood Loss
Syndrome, parvovirus, vitamin deficiencies Misc
Laboratory:
History Data: • Samples of work-up obtained before treating CBC with
• Hemorrhage: feto-fetal transfusion, internal/external peripheral smear, reticulocyte count, Coomb’s test,
hemorrhage, OB bleeding, post-natal bleeding blood type and cross-matching, coagulation studies if
• Obstruction to placental blood flow: tight nuchal cord indicated
• Accelerated RBC hemolysis: isoimmunohemolysis, • Serial Hbg/Hct necessary to detect anemia early before
signs of decompensation occur
infection, hemoglobinopathies, erythrocyte enzyme
defects, red cell membrane disorders, DIC
Management:
• Immediately transfusion in baby with pallor and/or
Clinical Manifestations:
respiratory distress in 1-3 hours
• Pallor
• Immediate plasma expanders or resuscitation in baby
• Tachycardia with or without hemic murmur
with hypotension or shcok
• Respiratory distress initially tachypnea
• Partial exchange with packed RBC in anemic hydrops
• Weak pulse baby
• Shock • Whole blood or packed RBC diluted with plasma may
• Combination of sign points to decompensation: be pushed IV in continuing hemorrhage
EMERGENCY
Features of Coagulation System
• Prothrombin time of full-term and pre-term infants is
only slightly outside the adult range of 10-12 sec
(14+/1.3)
• PTT longer in newborn than adults (51/57+/-10/10.5)
• Factors XI and XII low in preterm infants
• PTT is of little value in the sick newborn prolonged
even without evidence of hemorrhage

BLEEDING DISORDERS

MARY YVETTE ALLAIN TINA RALPH SHERYL BART HEINRICH PIPOY KC JAM CECILLE DENESSE VINCE HOOPS CES XTIAN LAINEY RIZ KIX EZRA GOLDIE BUFF MONA AM MAAN ADI KC
PENG KARLA ALPHE AARON KYTH ANNE EISA KRING CANDY ISAY MARCO JOSHUA FARS RAIN JASSIE MIKA SHAR ERIKA MACKY VIKI JOAN PREI KATE BAM AMS HANNAH MEMAY PAU
RACHE ESTHER JOEL GLENN TONI
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• Local cord, scalp, GIT, abdomen, lung, intraventricular
hemorrhage
• Generalized acquired hemorrhage: Hemorrhagic
disease of the newborn, DIC, liver Normal or Low Hct

BILIRUBIN PATHWAY
• Unconjugated bilirubin – nonpolar, insoluble, indirect
bilirubin (B1) causes kernicterus Red cell morphology & reticulocyte count

CAUSES OF INDIRECT HYPERBILIRUBINEMIA

• Overproduction of bilirubin: hemolysis, extravated
blood, polycythemia, increased enterohepatic Abnormal Normal
circulation
• Undersecretion of bilirubin: decreased hepatic uptake
of bilirubin, decreased conjugation, decreased
Sp Morpho Non Sp Morpho
transport of conjugated bile out of hepatocytes
Abnormalities Abnormalities
• Combined: perinatal infection, multisystem disorder Extravascular blood
Inc. Enterohepatic
NON-PHYSIOLOGIC JAUNDICE Circulation
Definition: -Breastfeeding
• Cord bilirubin > 3 mg/dL -Pyloric Stenosis
Spherocytosis ABO
Metab.-Endocrine
• Clinical jaundice in the 1st 24 hours Elliptocytosis incompatibility
-Galactosemia
Stomatocytosis G6PD deficiency
• Rate of rise of bilirubin > 5 mg/d/day -Hypothyroidism
pyknocytosis Pyruvate kinase
• Total serum bilirubin >12.9/mg/dL in term, >15 mg/dL def
Other
in preterm -IDM
Other enzyme def
• Direct bilirubin >1.5 mg/dL a-thalassemia
• Jaundice persisting > 1 week in term, > 2 weeks in
preterm FACTORS ASSOCIATED WITH AN INCREASE IN BILIRUBIN LEVELS:
• Race: Oriental, American, Indian, Greek

Jaundice • Maternal: diabetes, HPN, OCP, 1st trimester bleeding,

decreased plasma zinc
• Drugs: Diazepam, Oxytocin, epidural anesthesia
Measure total and direct • Labor and delivery: PROM, breech delivery
bilirubin • Infant: LBW, prematurity, breastfeeding, caloric
deprivation, infection, increase in weight loss, delayed
meconium passage and cord clamping, decrease fluid
Blood types, Rb, Coombs, Hct, Red cell intake, low Zinc and Mg, male sex
morphology, reticulocyte count
Management
• Surgical determination of serum bilirubin, Hgb, Hct
reticulocyte count if hemolytic
Inc Direct Inc indirect
• Do specific testing if non-hemolytic
• For indirect phototherapy, decrease enterohepatic
circulation, stop breastfeeding for 1-3 days, supportive,
Intrauterine Coomb’s (+) exchange transfusion, Phenobarbital
infection isoimmunizatio • For direct: depends upon case
Sepsis n • Manage underlying cause or refer to surgery
Biliary atresia
Bile plugs Coomb’s (-) SEPSIS AND MENINGITIS
Galactosemia Etiology: bacterial, viral, fungal, parasitic
Choledochal Predisposing factors:
cyst • Prolonged ROM
Tyrosinosis Hct Normal or
• PROM
Cystic fibrosis Low
A-1 antitrypsin • Foul smelling amniotic fluid and baby
High
def • Maternal fever
transfusion
Delayed • Prematuriy
clumping SGA • Unexplained fetal distress
• Previous septic infant
• Unsterile delivery
• Unsterile practices
• Contaminated equipments
• Infected personnel/caretakers

Manifestations
• Lethargy
• Poor feeding
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• Apnea - pH 7.5 or less at 5 min
• Tachypnea - pH 7.2 or less at 10 min
• Cyanosis - base deficit of 10 at 10 min
• Diarrhea
RESUSCITATION
• Metabolic acidosis
1. Drying, warming, positioning, suction
• Temperature instability 2. Tactile stimulation
• Abdominal distention 3. Oxygen
• Petechiae/purpura 4. Bag and mask ventilation
• Hepatospenomegaly 5. Chest compression
• Seizures 6. Medications
• Tense fontanelle ITEMS READILY ACCESSIBLE FOR RESUSCITATION
1. Ambu bag
Laboratory 2. Respiratory mask
- Sepsis work-up 3. Endotracheal tube
4. Laryngoscope
• CBC (WBC and differential)
5. Suction apparatus
• Urinalysis
• CSF analysis (WBC and differential, glucose, OXYGEN
protein) - Blow by oxygen for cyanosis with spontaneous respiration and
• Chest and abdominal X-ray a heart rate >100 bpm
• Cultures (blood, CSF, urine) - initial oxygen concentration close at 100%
- Other work up as appropriate: ABG, coagulation - Nasal cannula or facial mask
- The closer the distance to the nostril, the higher concentration
studies, stool culture and sensitivity ang gram stain,
of O2 delivered
CRP
- Cranial UTZ / CT Scan
BIG VALVE MASK
- use of apnea and HR < 100 bpm
Management
- appropriate for baby’s size and gestation not to exceed 750ml
- Do sepsis word-up on all babies considered as septic
- arte at 40-60 mins
- Antibiotic coverage, penicillin derivative and amino
- CI: thick meconium stain and diaphragmatic hernia
glycoside
- Supportive management as needed: transfusion,
ENDOTRACHEAL INTUBATION
thermoregulation, glucose, seizures, vital signs
Indications:
- Anticipate complications
1. Need for prolonged positive pressure ventilation
• DIC
2. Ineffective bag and mask ventilation
• NEC 3. Suspected diaphragmatic hernia
• Feeding problems
• Complications of meningitis (SIADH, UMBILICAL CANNULATION
ventricular obstruction, seizures, subdural Medications used in resuscitation
effusion, relapse) 1. Epinephrine 0.1-0.3 ml/kg of 1:10,000 rapid IV bolus
2. NaHCO3 2 mEq/kg slow IV
3. Glucose 10% 2ml/kg IV then infusion of 8-10mg/kg/min
BASIC REQUIREMENTS IN CARE OF NEWBORN 4. Naloxone HCl 0.01mg/kg rapid IV bolus
1. Immediate resuscitation 5. Ca gluconate 100mg/kg slow IV
2. Establishment of respiration 6. Atropine 0.01 mg/kg slow IV or IM
3. Adequate nutrition
4. Normal body temperature NECROTIZING ENTEROCOLITIS (NEC)
5. Avoidance of contact with infection • Most common life threatening emergency of the GIT in
the newborn period
ASPHYXIA • Necrosis – final common pathway of response to in the
Imbalance in oxygenation newborn gut
Causes:
Fetal • Onset usually occurs in the 1st 2 weeks or as late as 3
1. Placental separation month of age in VLBW infants
2. Inadequate perfusion of maternal side of • Most frequent site: distal ileum and proximal colon
placenta • Triad: intestinal ischemia, oral feedings,(metabolic
3. Interruption of umbilical blood flow substrate) and pathological organisms
Neonal • Greatest risk factor: prematurity
1. Airway obstruction • Complications: perforation, adhesion, diarrhea and
2. Excessive fluid in lungs malabsorption
3. Weak respiratory effort
4. Sequel to fetal hypoxia Pathogenic/Predisposing Factors
• Bowel immaturity and bowel injury
CRITERIA FOR ASPHYXIA
• Perinatal asphyxia
1. Historical factors (relative)
-Fetal distress fetal scalp acidosis • Infection: E. coli, Klebsiella, Pseudomonas, Salmonella,
2. Physical exam (relative) Clostridium, Staphylococcus epidermidis, and rotavirus
1 min APGAR score of 2 or less • Hypertonic substances in gut
5 min APGAR score of 5 or less • Indwelling umbilical catheter
3. Blood gas pH (absolute) • Exchange transfusion
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• Placement of NGT transfused cells (extravasated blood),
• Polycythemia increased enterohepatic circulation, infection
• Oral feeding 2. Damaged or reduced activity of transferase enzymes
• Genetic deficiency, hypoxia, infection,
Clinical Manifestation hypothermia and thyroid deficiency
3. Transferase enzyme block
• Significant residual  • Drugs and other substances requiring
• Gastric aspirate or vomiting  3 early signs of glucoronic acid conjugation for excretion
EC 4. Absence or reduced amounts of the enzymes or
reduced bilirubin uptake by the liver cells
• Abdominal distention 
• Genetic defect, prematurity
• Signs of sepsis: temp instability, lethargy
• Massive GI hemorrhage Factors increasing toxic effects of elevated of unconjugated
• Shock and DIC bilirubin

Laboratory Examination • Reduced retention of bilirubin in the circulation

• CBC, Hgb, Hct, WBC differential, platelet evidence of o Hypoproteinemia
sepsis o Displacement of bilirubin from its binding sites
o Immature to total neutrophil ratio > 0.2-0.5 on albumin by competitive binding of drugs
• ABG: hypoxiametabolic acidosis such as sulfisoxazole and moxalactam
• Abdominal x-ray: o Chuen-Lin herbal tea
o Mucosal damage o Acidosis
o Pneumatosis intestinalis (intramural air) – o Increased free fatty acid concentration
bubbly appearance (pathognomonic of NEC) secondary to hypoglycemia
o Portal vein gas – sign of severe o Starvation
disease(pathognomonic of NEC) o Hypothermia
o Pneumoperitoneum – indicates perforation • Increased permeability of blood brain barrier or nerve
• Blood culture cell membranes to bilirubin
• Increased susceptibility of brain cells to its toxicity
Management o Asphyxia, prematurity, hyperosmolarity,
• OGT and intermittent suction infection
• Septic workup Non-Pharmacologic Jaundice Definition
• Start antibiotics – 2ndary infection • Cord bilirubin > 3mg/dl
• Monitor w/ lab exams • Vlinical jaundice in 1st 24-26 hours
• Blood component replacement • Rate of rise of serum bilirubin
• Adequate metabolic balance • >5mg/dl/24 hr
• Monitor abnormal girth • Jaundice persisting after 10-14 days
• NPO for 7-10 days, reintroduce with formula/breast
milk Management
• IV fluids Indirect – phototherapy, dec. enterohepatic circulation, stop
• Refer to surgery: consider barium enema if with signs feeding for 1-3 days, supportive, exchange transfusion,
of obstruction Phenobarbital
• Respiratory status support: ventilation Direct – depends on cause

Thermoregulation
• Mechanism of heat production primarily by metabolism
of brown fat
• Mechanism of heat loss: convection, conduction, From Nelson:
evaporation (Magbasa pa rin po kayo ng Nelson. Baka hindi ito
• NTE: axillary temp at 36.4-37.2 deg enough. Hindi kasi nagbibigay si Dra. ng powerpoint.)
• Keep warm immediately in delivery room and nursery
Hypocalcemia
Avoidance of Contact with Infection • Hypocalcemia is common in sick and premature
• Hand washing newborns.
• Attire • Most infants are born with calcium levels that are
higher in cord blood than in maternal blood because of
• Asepsis for procedures
active placental transfer of calcium to the fetus.
• Recognize infection early
• Fetal calcium accretion in the third trimester
• Blood precaution approaches 150 mg/kg/24 hr, and fetal bone mineral
content doubles between 30 and 40 weeks of
JAUNDICE AND HYPERBILIRUBINEMIA gestation.
Biliverdin  Bilirubin (enzyme: biliverdin reductase) • All infants show a slight decline of serum calcium
levels after birth; the decline reaches trough levels at
Etiology of Indirect Hyperbilirubinemia 24 to 48 hours, the point at which hypocalcemia
Indirect –B1; Direct – B2 usually occurs.
1. Overproduction of bilirubin (increased load of bilirubin
• Total serum calcium levels of less than 7 mg/dL and
to be metabolized by the liver)
ionized calcium levels of less than 3 to 3.5 mg/dL are
• Hemolytic anemia, polycthemia, shortened
considered hypocalcemic.
red celllife as a result of immaturity or

• Early neonatal hypocalcemia occurs in the first 3
days of life and is often asymptomatic.
• Transient hypoparathyroidism and a reduced
parathyroid response to the usual postnatal decline of
serum calcium levels may be responsible for
hypocalcemia in premature infants and infants of
diabetic mothers.
• Congenital absences of the parathyroid gland and
DiGeorge syndrome also have been associated with
hypocalcemia.
• Treatment with calcium alone does not relieve
symptoms or increase serum calcium levels; for this to
occur, the hypomagnesemia also must be treated.
• Sodium bicarbonate therapy, phosphate release from
cell necrosis, transient hypoparathyroidism, and
hypercalcitoninemia may be responsible for early
neonatal hypocalcemia associated with asphyxia.
• Early-onset hypocalcemia associated with asphyxia
often occurs with seizures as a result of hypoxic-
ischemic encephalopathy or hypocalcemia.
• Late neonatal hypocalcemia, or neonatal tetany,
often is the result of ingestion of high phosphate-
containing milk or of the inability to excrete the usual
phosphorus in commercial infant formula.
• Neonatal hypocalcemia may be prevented by
administration of IV or oral calcium supplementation at
a rate of 25 to 75 mg/kg/24 hr.
• Early asymptomatic hypo-calcemia of preterm infants
and infants of diabetic mothers often resolves
spontaneously.
• Symptomatic hypocalcemia should be treated with 2 to
4 mL/kg of 10% calcium gluconate given intravenously
and slowly over 10 to 15 minutes, followed by a
continuous infusion of 75 mg/kg/24 hr of elemental
calcium.
• If hypo-magnesemia is associated with hypocalcemia,
50% magnesium sulfate, 0.1 mL/kg, should be given by
IM injection and repeated every 8 to 12 hours.
• The treatment of late hypocalcemia includes
immediate management, as in early hypocalcemia,
plus the initiation of feedings with formula containing
low phosphate levels.
• Subcutaneous infiltration of IV calcium salts can cause
tissue necrosis; oral supplements are hypertonic and
may irritate the intestinal mucosa.
Hypomagnesemia
• (<1.5 mg/dL) may be seen simultaneously with
hypocalcemia, especially in infants of diabetic
mothers.
• During exchange transfusion with citrated blood,
magnesium decreases 0.5 mg/dl; approximately 10
days is required for it to return to normal.
• Treatment consists of IM injection of Magnesium
sulfate.
Hypermagnesemia
• May occur in newborn infants of mother treated with
MgSO4 during labor.
• At high serum level, CNS is depressed and infants have
depressed and infants have profound respiratory
depression requiring mechanical ventilation.
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•
May be associated with failure to pass meconium
(Meconium plug syndrome).
• Occurs when serum magnesium value is >2.8 mg/dL
but symptoms rarely occur at levels below 5 mg/dl.
• IV calcium and diuresis can reduce magnesium levels.
Hyperphosphatemia
• (>8 mg/dL) usually occurs in infants with hypocalcemia
after the first week of life. Vitamin D deficiency states
and malabsorption also have been associated with
late-onset hypocalcemia.
The clinical manifestations of hypocalcemia and hypo-
magnesemia include apnea, muscle twitching, seizures,
laryngospasm, Chvostek sign (facial muscle spasm when the
side of the face over the seventh nerve is tapped), and
Trousseau sign (carpopedal spasm induced by partial inflation
of a blood pressure cuff). The latter two signs are rare in the
immediate newborn period. Occasionally, heart failure has been
associated with hypocalcemia.
Neonatal Drug Addiction and Withdrawal
• Infants may become passively and physiologically
addicted to medications or to drugs of abuse (heroin,
methadone, barbiturates, tranquilizers, amphetamines)
taken chronically by the mother during pregnancy;
these infants subsequently may have signs and
symptoms of drug withdrawal.
• Many of these pregnancies are at high risk for other
complications related to IV drug abuse, such as
hepatitis, AIDS, and syphilis.
• In addition, the LBW rate and the long-term risk for
sudden infant death syndrome are higher in the infants
of these high-risk women.
Opiates
• Neonatal withdrawal signs and symptoms usually
begin at 1 to 5 days of life with maternal heroin use
and at 1 to 4 weeks with maternal methadone
addiction.
• Clinical manifestations of withdrawal include sneezing,
yawning, ravenous appetite, emesis, diarrhea, fever,
diaphoresis, tachypnea, high-pitched cry, tremors,
jitteriness, poor sleep, poor feeding, and seizures.
• The illness tends to be more severe during methadone
withdrawal. The initial treatment includes swaddling in
blankets in a quiet, dark room.
• When hyperactivity is constant, and irritability
interferes with sleeping and feeding, or when diarrhea
or seizures are present, pharmacologic treatment is
indicated.
• Seizures usually are treated with phenobarbital.
• The other symptoms may be managed with
replacement doses of a narcotic (usually tincture of
opium) to calm the infant; weaning from narcotics may
be prolonged over 1 to 2 months.
Cocaine
• Cocaine use during pregnancy is associated with
preterm labor, abruptio placentae, neonatal irritability,
and decreased attentiveness. Infants may be SGA and
have small head circumferences. Usually no treatment
is needed.
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Hi 3B.
Aral lang ng mabuti.
Konti na lang and Clerkship here we come.