neonatology Flashcards
(45 cards)
Hi there π«΅ ! Ψ³Ω ΩΩ Ψ§ΩΩΩ
Ψ¨Ψ³Ω Ψ§ΩΩΩ Ψ§ΩΨ±ΨΩ Ω Ψ§ΩΨ±ΨΩΩ π‘
π§ What clinical findings in a newborn suggest a diagnosis of subgaleal hematoma βοΈ
πΆ Rapidly increasing head circumference
𧽠Spongy , fluctuant scalp swelling that crosses sutures
π Tachycardia β suggests hypovolemia
π Pallor, lethargy, hypotonia
π©Ί Often follows vacuum-assisted delivery
π§ What is the pathophysiology of subgaleal hematoma in newborns βοΈ
π©Έ Rupture of emissary veins β blood collects between:
β’ Galea aponeurotica (above)
β’ Periosteum (below)
π§ This space can hold up to 40% of neonatal blood volume β π hemorrhagic shock risk
π¨ What is the most important initial management step in a newborn with suspected subgaleal hematoma βοΈ
π₯ Transfer to NICU for:
π Continuous monitoring of vitals & head size
π§ IV fluid resuscitation or π©Έ blood transfusion
π Phototherapy if jaundice develops
π§ͺ Check for coagulopathy
π§ What complications can arise from subgaleal hematoma in neonates βοΈ
π©Έ Hemorrhagic shock
π΄ Anemia β may need transfusion
π Hyperbilirubinemia (jaundice)
𧬠Consumptive coagulopathy (DIC)
β°οΈ Mortality risk up to 20%
β Why is CT scan not the first-line diagnostic tool for subgaleal hematoma βοΈ
π Diagnosis is clinical , based on exam & head growth
π§ CT is reserved only if thereβs suspicion of skull fracture or intracranial bleeding
π― Focus is on ICU monitoring and stabilization , not imaging
π οΈ What birth interventions increase the risk of subgaleal hematoma βοΈ
β’ πΌ Vacuum-assisted delivery (most common)
β’ π οΈ Forceps delivery
β’ β³ Prolonged labor
⒠𧬠Bleeding disorders (e.g. hemophilia)
π§ What are the classic risk factors for transient tachypnea of the newborn (TTN) βοΈ
πΌ C-section without labor
π― Twin gestation
π€° Gestational diabetes
π¬οΈ Maternal asthma
π Late preterm infants (34β37 weeks)
β‘ Rapid labor or precipitous delivery
π§ What is the pathophysiology behind TTN βοΈ
π§ Delayed clearance of fetal lung fluid β retained fluid in alveoli
π β Lung compliance β β Work of breathing
π« No surfactant deficiency β lungs are structurally mature
π§ What are the clinical features of TTN βοΈ
π¨ Tachypnea > 60/min (early onset)
π€ Mild retractions, nasal flaring, grunting
π¦ Possible cyanosis , improved with minimal Oβ
π Self-limited (resolves in 48β72 hrs )
π§ What is the chest X-ray finding in TTN βοΈ
πΈ Hyperinflated lungs
π«οΈ Prominent vascular markings
π¦ Fluid in interlobar fissures
##footnote
π No consolidation, no reticulogranular pattern
π§ What is the management of TTN βοΈ
π Supportive care only :
⒠𧴠Minimal Oβ via oxyhood or nasal cannula
β’ π©Ί Monitor for improvement
β’ π Resolves in 48β72 hrs
π§ What is the most likely cause of jaundice that appears within the first 24 hours of life and is mainly due to elevated unconjugated bilirubin in an otherwise healthy newborn βοΈ
β
Rh incompatibility
##footnote
π©Έ This occurs when an Rh-negative mother forms IgG antibodies against Rh-positive fetal red blood cells (typically in second or later pregnancies).
β οΈ Leads to hemolytic disease of the newborn with early-onset indirect hyperbilirubinemia , sometimes severe.
π Prevention includes anti-D immunoglobulin administration to Rh-negative mothers.
π§ What are the clinical clues that suggest Rh incompatibility as the cause of neonatal jaundice βοΈ
𧬠Rh-negative mother, Rh-positive baby
β οΈ Early-onset jaundice (<24 hrs)
π Rapidly rising bilirubin
π©Έ Often accompanied by anemia, positive direct Coombs test
π©Ί May require phototherapy or exchange transfusion
π§ Why is adrenal hemorrhage an unlikely cause of early jaundice in a term newborn βοΈ
π¨ Adrenal hemorrhage presents with signs such as:
π©Έ Shock or hypotension
π€ Abdominal mass
π§ Hypoglycemia or ambiguous genitalia
π‘ Jaundice is not a typical isolated early sign
π§ Why are gallbladder stones unlikely to cause jaundice in the first day of life in a full-term neonate βοΈ
πͺ¨ Gallstones in neonates are rare and usually related to chronic hemolysis or prolonged TPN
π Jaundice due to gallstones is typically late-onset
π§ͺ Direct hyperbilirubinemia may occur but not typically in the first day
π§ Why is biliary atresia an incorrect diagnosis in a term neonate with jaundice at 13 hours of life and indirect hyperbilirubinemia βοΈ
π« Biliary atresia presents with:
π
Jaundice after 2 weeks (not within first day)
π§ͺ Direct (conjugated) hyperbilirubinemia
πͺ Pale stools, dark urine, hepatomegaly
β Not consistent with early indirect hyperbilirubinemia
π§ What are the key risk factors for early severe hyperbilirubinemia in newborns βοΈ
𧬠Blood group incompatibility (Rh or ABO)
π€ Cephalohematoma or bruising
πΆ Prematurity
πΌ Exclusive breastfeeding
π₯ Delivery by cesarean without labor
π§ What is the most likely cause of a full-term newborn (3500g, 40 weeks) with jaundice in the first day of life and total bilirubin 7 mg/dL (direct 0.2), born to an O+ mother? βοΈ
β‘οΈ ABO incompatibility
##footnote
π§ A group O+ mother can have anti-A or anti-B IgG antibodies that cross the placenta and cause hemolysis even in first pregnancies.
** Why is Rh incompatibility ruled out in this newborn with early jaundice** ?
β‘οΈ β Rh incompatibility occurs when the mother is Rh-negative, but in this case, she is Rh-positive
##footnote
π‘ Rh disease usually causes anemia , worsens with each pregnancy, and is rare in the first pregnancy of Rh+ mothers.
Why is physiologic jaundice unlikely in a baby with jaundice during the first day of life ?
β‘οΈ β Physiologic jaundice typically appears after day 2 (usually day 3β5)
##footnote
π‘ Jaundice on day 1 suggests a pathological cause , such as hemolysis.
Why is congenital hypothyroidism unlikely in a newborn presenting only with early jaundice ?
β‘οΈ β Congenital hypothyroidism presents after the first week with prolonged jaundice and features like large fontanelles, umbilical hernia, and hypotonia
##footnote
π§ It does not cause isolated early jaundice.
Why is congenital CMV infection unlikely in an otherwise healthy newborn with jaundice ?
β‘οΈ β CMV typically causes systemic signs : low birth weight, microcephaly, rash, hepatosplenomegaly, and brain involvement
##footnote
π§ Not expected in a well-appearing newborn with only jaundice.
What mechanism allows ABO incompatibility to cause hemolysis even in a firstborn ?
β‘οΈ Group O mothers may produce anti-A or anti-B IgG antibodies β cross placenta β cause immune-mediated hemolysis
##footnote
π§ Most ABO antibodies are IgM (donβt cross placenta), but IgG does , especially in type O mothers.
