Neonate and Reflexes Flashcards

Question

🧠 What are the main causes of pathologic unconjugated hyperbilirubinemia in neonates⁉️

Answer 1

✅ 🔹 **Hemolytic** causes: • Intrinsic: **G6PD deficiency, hereditary spherocytosis, thalassemia** • Extrinsic: **Drugs** , **isoimmune hemolysis** (ABO, Rh), **sepsis** 🔹 **Non-hemolytic** causes: • **Hypothyroidism, cephalohematoma, sepsis, Gilbert syndrome, Crigler-Najjar syndrome**

Answer 2

✅ • **Coombs test** (direct antiglobulin test) • **CBC with differential** • **Peripheral blood smear** • **Blood culture**

Answer 3

✅ **UDP-glucuronosyltransferase** ##footnote 🧬 Deficiency causes impaired conjugation → very high unconjugated bilirubin

Answer 4

✅ **Hepatitis** and **cholestasis** are the most common ##footnote 🧪 Requires urgent evaluation — conjugated bilirubin is always pathologic

Answer 5

✅ Rh incompatibility occurs when an **Rh-negative mother carries an Rh-positive fetus** , causing maternal immune sensitization against fetal RBCs.

Answer 6

✅ The **first Rh+ baby usually escapes hemolysis** because maternal sensitization typically happens **during delivery** , not during the first pregnancy.

Answer 7

✅ • **Incompatible blood transfusion** • **Abortion** • **Placental abruption/separation** • **Previous Rh+ pregnancy or delivery**

Answer 8

✅ The mother’s immune system **rapidly produces IgG antibodies** against Rh antigens, which **cross the placenta** and cause **hemolysis of fetal red blood cells** .

Answer 9

✅ **IgG antibodies** , which cross the placenta and destroy fetal Rh+ red blood cells.

Answer 10

✅ Leads to **hemolytic disease of the newborn (HDN)**, which can result in **fetal anemia, hydrops fetalis, or stillbirth** .

Answer 11

✅ Administer **anti-D immunoglobulin (Rho(D) immune globulin)** 🕒 Given at: • **28 weeks gestation** • **Within 72 hours** after delivery of an Rh+ baby

Answer 12

✅ It binds fetal Rh+ RBCs in the maternal circulation, preventing the **maternal immune system from recognizing and becoming sensitized** to Rh antigen.

Answer 13

✅ Due to the routine use of **anti-D prophylaxis** in Rh-negative mothers exposed to Rh-positive fetal blood.

Answer 14

✅ **Hydrops fetalis** , a life-threatening condition with **severe anemia, heart failure, and generalized edema (anasarca)** due to massive hemolysis.

Answer 15

✅ • **Severe abdominal swelling** • **Generalized edema (anasarca)** • **Heart failure** • **Massive hepatosplenomegaly** • May lead to **stillbirth or death shortly after birth**

Answer 16

✅ • **Anemia at birth** , worsening rapidly • **Moderate hepatosplenomegaly** • **Marked indirect hyperbilirubinemia (jaundice)** • May progress to kernicterus or heart failure if untreated

Answer 17

✅ • **Mild anemia** • **Mild hepatosplenomegaly** • **Indirect jaundice** (usually less severe) • No hydrops or heart failure

Answer 18

✅ Death occurs due to **heart failure** or **kernicterus** (bilirubin encephalopathy).

Answer 19

✅ **Hepatosplenomegaly** is enlargement of the liver and spleen due to **increased extramedullary hematopoiesis** in response to **severe fetal anemia**.

Answer 20

✅ • **Massive generalized swelling (anasarca)** • **Severe respiratory distress** • **Distended abdomen** • **Pale or hydropic appearance** • **Enlarged liver and spleen**

Answer 21

✅ **Kernicterus** is bilirubin-induced neurologic dysfunction caused by **unconjugated bilirubin crossing the blood-brain barrier** , commonly seen in severe untreated Rh hemolytic disease.

Answer 22

✅ **Ultrasound signs of hydrops fetalis** , such as: • **Ascites** • **Skin edema** • **Pericardial or pleural effusion** • **Placental thickening**

Answer 23

✅ It may lead to **stillbirth, neonatal death** , or **severe disability due to kernicterus or heart failure** .

Answer 24

✅ **Mother is type O** , and **fetus is type A, B, or AB** . Maternal anti-A or anti-B antibodies (especially IgG) may cross the placenta.

Answer 25

✅ Most maternal anti-A/B antibodies are **IgM** , which **do not cross the placenta** . Only some mothers (especially blood group O) have **IgG** antibodies that can cross and cause mild hemolysis.

Answer 26

✅ • **Mild jaundice** , often in the **first 24 hours** • **No anemia or mild anemia** • **Spherocytosis** on blood smear • **Positive or weakly positive direct Coombs test (DCT)**

Answer 27

✅ • **Observation** and **close follow-up** • **Phototherapy** if bilirubin is high • **Exchange transfusion** in rare severe cases

Answer 28

✅ • **Rh HDN** : **Usually severe** , affects **second pregnancy** or later • **ABO HDN** : **Usually mild** , can affect **first pregnancy**

Answer 29

✅ • **Rh disease** : **Erythroblastosis** (nucleated RBCs) • **ABO disease** : **Spherocytosis**

Answer 30

✅ **Jaundice lasting more than 2 weeks** in a **term infant** (or **>3 weeks** in a **preterm infant** )

Answer 31

✅ 1. **Breast milk jaundice** 2. **Infections** (especially **UTIs** ) 3. **Congenital hypothyroidism** 4. **Hemolysis** (e.g. **G6PD deficiency** ) 5. **High GI obstruction** (e.g. **pyloric stenosis** ) 6. **Crigler-Najjar syndrome**

Answer 32

✅ 1. **Biliary atresia** 2. **Choledochal cyst** 3. **Neonatal hepatitis** (e.g. **TORCH** , **galactosemia** , **tyrosinemia type I** , **cystic fibrosis** )

Answer 33

✅ When **direct (conjugated) bilirubin is >20% of total** or **>2 mg/dL**

Answer 34

✅ A **rare cause of severe unconjugated hyperbilirubinemia** due to **glucuronyl transferase deficiency** • **Type I** : **Autosomal recessive** , complete enzyme absence • **Type II** : **Autosomal dominant** , partial enzyme deficiency

Answer 35

✅ • **Type I** : Severe, causes **kernicterus** , unresponsive to phenobarbital, needs **exchange transfusion & phototherapy** • **Type II** : Less severe, responsive to phenobarbital

Answer 36

✅ • **Type I*. : **Phototherapy + Exchange transfusion** • **Type II** : **Phenobarbital trial**

Answer 37

✅ A condition caused by **deposition of unconjugated bilirubin** in the **basal ganglia and cerebellar nuclei** , leading to **neuronal necrosis** and **permanent brain damage**

Answer 38

✅ **Unconjugated bilirubin** is **lipid-soluble** and can **cross the blood-brain barrier (BBB)** , while **direct (conjugated) bilirubin is water-soluble** and **cannot cross the BBB**

Answer 39

✅ **Dyskinetic cerebral palsy** (due to basal ganglia damage)

Answer 40

✅ Primarily the **basal ganglia** , especially the **globus pallidus** , and **brainstem nuclei**

Answer 41

✅ * **Lethargy** * **High-pitched cry** * **Poor feeding** * **Hypotonia → hypertonia** * **Opisthotonus** * **Seizures** * **Permanent motor deficits** (e.g. dystonia, choreoathetosis)

Answer 42

✅ 1. **Prematurity** 2. **Low birth weight (LBW)** 3. **Sepsis** 4. **Acidosis** 5. **Hypoxia** 6. **Hypothermia**

Answer 43

✅ 1. **Drugs** (e.g. sulfonamides, aspirin, ampicillin) 2. **Hypoalbuminemia** 3. **Severe anemia**

Answer 44

✅ **Hemolytic disease of the newborn** — especially **ABO incompatibility** or **Rh incompatibility**

Answer 45

✅ Biliary atresia is a **progressive fibrosis and obliteration** of the **extrahepatic and intrahepatic bile ducts** , leading to **bile flow obstruction** , and if untreated, results in **chronic liver failure and death within 2 years**

Answer 46

✅ Direct (conjugated) hyperbilirubinemia, with **clay-colored stools** , **dark urine** , and **prolonged jaundice lasting >2 weeks**

Answer 47

✅ Suspect **biliary atresia** in any infant with ➡️**jaundice lasting >2 weeks** Especially if **stools are pale** and **urine is dark**

Answer 48

✅ The **Kasai operation (hepatoportoenterostomy)** ##footnote Connects the small intestine directly to the liver to allow bile drainage

Answer 49

✅ The **Kasai procedure** is most successful when **performed before 60 days of age**

Answer 50

✅ The **bile ducts are missing or fibrosed** , so **bile cannot exit the liver** , leading to **backflow, liver damage, and cholestasis**

Answer 51

✅ **Neonatal seizures** are due to **abnormal electrical activity in the neonatal brain** , often indicating **underlying neurological or metabolic dysfunction**

Answer 52

✅ **Hypoxic-Ischemic Encephalopathy (HIE)** is the **most common** cause of neonatal seizures

Answer 53

✅ CNS causes include: * **HIE** * **Infections** (e.g., meningitis, encephalitis, TORCH) * **Intracranial hemorrhage or stroke** * **Brain malformations** * **Kernicterus (bilirubin encephalopathy)**

Answer 54

✅ Common metabolic causes: * **Hypoglycemia** * **Hypocalcemia** * **Hypomagnesemia** * **Hyponatremia or hypernatremia** * **Inborn errors of metabolism** * **Pyridoxine (Vitamin B6) deficiency**

Answer 55

✅ **Pyridoxine** (Vitamin **B6**) deficiency can cause neonatal seizures

Answer 56

✅ Seizures can result from: * ↓ Glucose * ↓ Calcium * ↓ Magnesium * ↓ or ↑ Sodium

Answer 57

✅ Other causes include: * Maternal substance abuse * Neonatal abstinence syndrome * Benign familial neonatal seizures

Answer 58

✅ **Subtle seizures** are the most common. | subtle means غامض (difficult to analyse).

Answer 59

🔹 **Oculo-oro-facial signs:** ▪️ Eye rolling, ▪️ eye deviation, ▪️ staring, ▪️ sucking, ▪️lip smacking, ▪️ blinking 🔹 **Limb movements:** ▪️ Bicycling ▪️ pedaling movements 🔹 **Central/Autonomic signs:** ▪️ Apnea ▪️ Desaturation ▪️ Change in heart rate (HR)

Answer 60

✅ ABC approach: 🫁 **A** – Airway 🌬️ **B** – Breathing (O₂ via mask) 💉 **C** – Circulation (IV access + blood tests)

Answer 61

✅ Treat underlying metabolic causes: * Hypoglycemia ➤ Dextrose 10%, 2–5 mL/kg IV * Hypocalcemia ➤ IV Calcium gluconate * Consider Sepsis, Electrolytes, Pyridoxine deficiency

Answer 62

✅ **Phenobarbitalg** • Loading dose: 15–20 mg/kg IV • Maintenance: 5–8 mg/kg/day

Answer 63

✅ **Phenytoin** • Same dosing: 15–20 mg/kg IV loading, 5–8 mg/kg/day maintenance

Answer 64

✅ **Benzodiazepines** (Diazepam or Midazolam) ✅ Still uncontrolled? ➤ **Pyridoxine trial** (50–100 mg IV) ✅ If seizures persist → **General anesthesia + mechanical ventilation**

Answer 65

✅ **Jitteriness is stimulus-provoked** , while seizures occur spontaneously. ✅ **Jitteriness stops when you hold the limb** , seizures continue. ✅ **Seizures usually have eye deviation or blinking** , jitteriness does not. ✅ **Seizures often cause autonomic signs** like apnea, desaturation, and HR changes. ✅ EEG in seizures is **abnormal** , but normal in jitteriness.

Answer 66

✅ Preterm infants, especially those born **<32 weeks gestation** ##footnote Due to fragile germinal matrix vasculature. | premature baby🔸 <1500kg, or🔸 <32w

Answer 67

✅ **Within the first 72 hours of life** — early postnatal period is highest risk.

Answer 68

✅ **Perinatal asphyxia** ✅ **Severe RDS** (Respiratory Distress Syndrome) ✅ **Pneumothorax** ✅ **Very low birth weight**

Answer 69

✅ **Cranial ultrasound (head U/S)** is the best initial modality ##footnote 📍CT/MRI may be used for further evaluation.

Answer 70

✅ **Grade I** – Bleeding limited to germinal matrix ✅ **Grade II** – Intraventricular hemorrhage without ventricular dilation ✅ **Grade III** – IVH with ventricular enlargement ✅ **Grade IV** – IVH with parenchymal involvement (worst prognosis)

Answer 71

✅ Can be **asymptomatic** (Grade 1&2) OR • **Pallor** • **Jaundice** • **Seizures** • **Bulging anterior fontanelle** • **Apnea** • **Sudden deterioration or death**

Answer 72

✅ **NICU supportive care** ✅ **Blood transfusion** (if anemic) ✅ **Anticonvulsants** (if seizures) ✅ Neurosurgical consult for **ventriculoperitoneal shunt** if hydrocephalus develops

Answer 73

✅ **Hydrocephalus** ✅ **Cerebral palsy** ✅ **Neurodevelopmental delay** ✅ **Seizures**

Answer 74

🧠**A form of white matter brain injury near the ventricles, seen in premature infants. 🔻 Caused by ischemia or inflammation affecting immature oligodendrocytes**. ➡️ Results in **necrosis of white matter**, especially around the ventricles. ➡️ Leads to ** motor dysfunction and a high risk of cerebral palsy** (especially spastic diplegia). In short: ▪️ PVL = periventricular white matter injury ▪️ Premature babies ▪️ ➡️ Motor defects + ↑ risk of CP ## Footnote Disease of pre-mature baby.

Answer 75

✅ **Cerebral hypoxia/ischemia** leading to **bilateral necrosis** of the periventricular white matter with cyst formation. ## Footnote 💡So IVH + RO ➡️ <32 w PVL. ➡️ <28 w White matter starts developing **after 28 weeks** and matures around **30–32 weeks** , explaining vulnerability in early preterms.

Answer 76

✅ **Spastic diplegic cerebral palsy** (in ~80–90% of cases), often with **cognitive impairment**

Answer 77

✅ ROP is **neovascularization of the immature retina** due to exposure to **high oxygen concentrations** in **preterm infants** .

Answer 78

✅ **Hyperoxia** causes disruption of normal vessel growth → **abnormal neovascularization** in the retina.

Answer 79

✅ **>95%** increases **ROP** risk, ✅ **<91%** increases **NEC and death** risk.

Answer 80

✅ May progress to **retinal detachment** , **fibrosis** , and eventual **blindness** .

Answer 81

✅ Infants with **<1500g birth weight** or **<32 weeks gestational age** should be screened by an **ophthalmologist** .

Answer 82

✅ **Laser therapy** ##footnote It reduces abnormal vessels and helps prevent visual impairment.

Answer 83

✅ Use **lowest effective oxygen concentration** , target **SpO₂ of 91–95%** , and **avoid hyperoxia** or **hypoxia** . | prevention is effective than treatment! الوقاية خير من العلاج

Answer 84

✅ Start with **21%–30% O₂** to avoid both **necrotizing enterocolitis** (NEC) from low saturation and **ROP** from high saturation.

Answer 85

✅ Hypoxia → **anaerobic glycolysis in brain** → accumulation of **lactic acid & toxins** → **neuronal damage + vasodilation** → **brain edema** → **worsening ischemia** → **encephalopathy** .

Answer 86

✅ • **Stage I** : Hyperalert, ↑ reflexes, no seizures • **Stage II** : Lethargy, hypotonia, frequent seizures • **Stage III** : Coma, flaccidity, apnea, absent reflexes, poor outcome

Answer 87

✅ • **Stage I** : Hyperalert • **Stage II** : Lethargic • **Stage III** : Comatose

Answer 88

✅ • **Stage I** : Normal tone • **Stage II** : Hypotonia • **Stage III** : Flaccid

Answer 89

✅ • **Stage I** : Hyperactive • **Stage II** : Hyperactive • **Stage III** : Absent

Answer 90

✅ • **Stage I** : Exaggerated • **Stage II**: Weak • **Stage III** : Absent

Answer 91

✅ • **Stage I** : Dilated • **Stage II** : Constricted • **Stage III** : Variable

Answer 92

✅ • **Stage I** : Regular • **Stage II** : Periodic • **Stage III** : Apneic

Answer 93

✅ • **Stage I** : No seizures • **Stage II** : Frequent seizures • **Stage II** I: Frequent, severe seizures

Answer 94

✅ • **Stage I** : Good prognosis • **Stage II** : Variable outcome • **Stage III** : High risk of **death or severe neurologic deficit**

Answer 95

✅ **Stage III** — up to **80% mortality** , and most survivors have severe cerebral palsy or neurologic sequelae.

Answer 96

✅ At birth: **14–24 g/dL** → Drops to **10–11 g/dL** by **8–12 weeks** of life.

Answer 97

✅ Due to **intrauterine hypoxia** , which stimulates **erythropoietin release** → increased red blood cell production.

Answer 98

✅ After birth, there’s **no hypoxia, suppression of erythropoietin** , and the **short lifespan of fetal RBCs (~60–90 days)** → leads to physiological anemia.

Answer 99

✅ • **Term infants** : ❌ **No treatment** required • **Preterm infants** : ✅ **Iron supplementation** is needed

Answer 100

✅ Because preterms have: • **Shorter RBC lifespan** • **Lower iron stores** • **Faster postnatal growth, increasing demand**

Answer 101

✅ • **Reduced erythropoietin production after birth** • **Short red cell lifespan** • **Expansion of blood volume due to rapid growth**

Answer 102

✅ True. | Even babies with good health should receive one time IM shot (1,2mg). ## Footnote 💡As breast feeding deficient in vitamin K&D.

Answer 103

🩸 A neonatal **bleeding disorder** due to **vitamin K deficiency** ➡️ Results in impaired synthesis of coagulation factors 🪄 **1972** : ▪️ Factor II (Prothrombin) ▪️ Factor VII ▪️ Factor IX ▪️ Factor X

Answer 104

✅ Because: • **Breast milk is low in vitamin K** • **Gut is sterile** (no flora to synthesize vitamin K) • **Liver immaturity** reduces clotting factor production • **Preterm infants** have lower stores • **Home births** often miss routine vitamin K prophylaxis

Answer 105

✅ **Anticonvulsants** like **phenytoin, phenobarbital, and warfarin** ##footnote They cross placenta → interfere with fetal vitamin K metabolism.

Answer 106

✅ **Routine Vitamin K injection (IM)** at birth — **1 mg IM once** is standard for prophylaxis.

Answer 107

✅ • **Vitamin K (Konakion)** : 1–5 mg IV for 3 days • **Fresh frozen plasma (FFP)** : 10 cc/kg for serious bleeding • **Whole blood transfusion** : in severe hemorrhage

Answer 108

✅ RDS is a **respiratory condition in preterm infants** caused by **surfactant deficiency** , leading to alveolar collapse, impaired gas exchange, and respiratory failure. It’s also called **Hyaline Membrane Disease** .

Answer 109

✅ **Preterm infants** (especially <35 weeks), particularly: • **Male neonates** • **Infants of diabetic mothers** • **The smaller twin** • **Infants with erythroblastosis fetalis**

Answer 110

✅ • **Antenatal corticosteroids** (e.g., betamethasone) • **Thyroxine exposure** • **Prolonged PROM (>48 hrs)** • **Mild intrauterine stress** (e.g., preeclampsia)

Answer 111

🔹Substance Produced by: **Type II pneumocytes** 🔹Composition of surfactant: 🔻 **Lipids (90%)**: ▪️ **Phosphatidylcholine (Lecithin)** ~80% ▪️ **Phosphatidylglycerol** ~10% 💡 (Start at 20th weeks mature at 35 -36w).

Answer 112

✅ • **Reduces surface tension in alveoli** • **Prevents alveolar collapse during expiration** • **Improves lung compliance and reduces work of breathing**

Answer 113

📍 Lecithin/Sphingomyelin (L/S) ratio from amniotic fluid: ▪️ >2.5 ➡️ mature lungs ▪️ 1.5–2 ➡️ transitional ▪️ <1.5 ➡️ immature lungs

Answer 114

✅ If the **infant fails to maintain SpO₂ >90%** despite **CPAP and FiO₂ 40–70%** , give **exogenous surfactant** via endotracheal tube.

Answer 115

▪️ **Early** ➡️ **ground-glass opacity + air bronchogram** ▪️ **Late** ➡️ **bilateral opacification**

Answer 116

💊 Management of RDS 1️⃣ Respiratory Support ▪️ Supplemental O2 ▪️ CPAP / high-flow nasal cannula ▪️ Mechanical ventilation if needed 2️⃣ Surfactant therapy ➡️ Indicated if SpO2 <90% despite 40–70% O2 on CPAP ## Footnote Surfacternt indicated for infants with RDS who cannot keep oxygen saturation >90% while breathing 40-70% oxygen and receiving nasal CPAP).

Answer 117

✅ A **self-limited respiratory distress in **term or near-term newborns** ➡️ Caused by **delayed clearance of fetal lung fluid** ➡️ Leads to ▪️tachypnea, ▪️mild retractions, ▪️ grunting within hours of birth

Answer 118

✅ After birth, **lung fluid is normally absorbed** by the **lymphatics and pulmonary capillaries** . In TTN, **this process is delayed** , causing **fluid retention** → **decreased compliance** → **tachypnea** .

Answer 119

**24-48 h**

Answer 120

Tachypnea (rapid breathing) | mild RD within few hours after birth.

Answer 121

🩺 **Management: ✅ Supportive (oxygen + monitoring by RR and pulse oximeter.) ⏳ Resolves in 24–72 hours** 💡 o2 by head box.

Answer 122

🩻 Chest X-ray findings: ▪️ Prominent pulmonary vasculature ▪️ Fluid in interlobar fissures ▪️ Hyperinflated lungs with flat diaphragms ## Footnote TTN called wet lung disease. Key in MCQ.

Answer 123

🔶MAS = **serious respiratory disorder** in **term or post-term neonates** caused by **aspiration of meconium-stained amniotic fluid** , often due to **intrauterine asphyxia** .

Answer 124

🧠 **Risk Factors: ~Meconium OPC:**🙀‼️ 🚩 M ➡️ Meconium-stained fluid 🚩 O ➡️ Oligohydramnios 🚩 P ➡️ **Perinatal asphyxia** 🚩 C ➡️ Chorioamnionitis / maternal infection ## Footnot 💡More clarification of risk factors! • M ➡️ Meconium-stained fluid — already present in amniotic fluid • O ➡️ Oligohydramnios — less fluid = more concentrated meconium • P ➡️ Perinatal asphyxia — fetal stress → meconium passed • C ➡️ Chorioamnionitis — infection → fetal distress → meconium release

Answer 125

🚨 **Severe respiratory distress: grunting, cyanosis➕ Meconium staining of skin & umbilical cord** 🔹 **Vary by severity of asphyxia: ▪️ Complete airway obstruction → lung collapse ▪️ Partial obstruction → air trapping** ⚠️ Chemical pneumonitis → secondary infection 🧪 **Investigation of choice: Chest X-ray**

Answer 126

✅ **Hyperinflated lungs** 💡• Partial airway obstruction acts like a one-way valve • Air gets in but can’t fully escape → lungs overinflate ✅ **Patchy consolidation & collapse** 💡• Meconium blocks some airways completely → alveolar collapse • Inflammation from chemical pneumonitis → areas of fluid/infiltrates (consolidation) ✅ **May show pneumothorax or pneumomediastinum** 💡alveolar rupture from overpressure

Answer 127

👉🏼 **If baby is vigorous**: 🔹 Drying 🔹 Suctioning of mouth & nose 👉🏼 **If baby is non-vigorous:** 🔹 Direct suction of mouth, nose, and trachea 🔹 Do before respiratory support or stimulants 🔶 Prognosis depends on asphyxia severity & clinical condition ## Footnote 💡 vigorous (crying, breathing well, good tone) 💡non-vigorous (poor tone, not crying, not breathing) 💡 This approach prevents pushing meconium deeper into the lungs during ventilation.

Answer 128

🔻**Apnea is defined as a pause in breathing ⏰ lasting >20 seconds, or a shorter pause accompanied by ▪️bradycardia and/or ▪️oxygen desaturation (cyanosis) in a neonate**.

Answer 129

✅ • **Central apnea (40%)** – due to immaturity of the brainstem respiratory centers • **Obstructive apnea (10%)** – due to upper airway obstruction • **Mixed apnea (50%)** – has both central and obstructive components 👉 **Mixed apnea is the most common type** in premature infants.

Answer 130

**🧠🪄Mnemonic: “STOP HIM”** (Baby “stops” breathing — think “STOP HIM”!) ⸻ 🔶 **S – Sepsis** ▪️ Infection (sepsis, meningitis) 🔶 **T – Temperature** ▪️ Hypothermia 🔶 **O – Oxygen low (asphyxia)** ▪️ Perinatal asphyxia 🔶 **P – Prematurity** ▪️ Apnea of prematurity (immature respiratory centers) 🔶 **H – Hypo states** ▪️ Hypoglycemia ▪️ Hypocalcemia 🔶 **I – IVH / Intracranial causes** ▪️ Intraventricular hemorrhage ▪️ Seizures 🔶 **M – Medications** ▪️ Maternal narcotics ▪️ Magnesium sulfate ▪️ Sedatives ▪️ Anticoagulants Add 🫁 ♥️ 🥘 🩸 🔶**Respiratory:** ▪️ Respiratory Distress Syndrome (RDS) ▪️ Meconium Aspiration Syndrome (MAS) 🔶**Cardiovascular:** ▪️ Patent Ductus Arteriosus (PDA) ▪️ Congestive heart failure 🔶**Gastrointestinal:** ▪️ Necrotizing enterocolitis (NEC) ▪️ Gastroesophageal reflux 🔶**Hematologic / Metabolic:** ▪️ Anemia, polycythemia ▪️ Hypoglycemia, hypocalcemia, hypothermia

Answer 131

✅ Apnea of prematurity is typically due to **immature respiratory control** and is seen in **preterm infants** . In contrast, **secondary apnea** occurs in both term and preterm infants due to **underlying pathology** like infection, CNS insult, or metabolic issues.

Answer 132

✅ Management Steps for Apneic Neonate: 🔹 **1. Position & Airway Check** ➡️ Reposition to open airway (check for obstructive apnea) 🔹 **2. Gentle Stimulation** ➡️ Tactile stimulation (e.g. rub back, flick sole) ➡️ Gentle pharyngeal suctioning if needed 🔹 **3. Oxygenation** ➡️ Supplemental O₂ (blow-by or nasal cannula) ➡️ Bag & mask ventilation if no spontaneous breathing **🔹 4. Respiratory Stimulants (for preterm)** ➡️ Caffeine citrate or theophylline 💡 Caffeine is most effective! **🔹 5. Escalation: Intubation if needed** ➡️ Endotracheal tube (ETT) + mechanical ventilation (MV) **🔹 6. Monitor & Treat Underlying Cause** ➡️ Continuous monitoring (SpO₂, HR) ➡️ Address sepsis, hypoglycemia, temp, etc. ## Footnote 💡Tactile stimulation and 💡Caffeine citrate is most effective!

Answer 133

✅ **Caffeine** citrate is a **central respiratory stimulant** used to treat **apnea of prematurity** , as it increases respiratory drive and reduces the frequency of apneic episodes.

Answer 134

✅ • **Apnea of prematurity** : **no abnormal movements** , may **respond to stimulation** , occurs in **preterm** • **Seizure-related apnea** : often with **eye deviation** , **twitching** , **no response to stimulation** , may occur in **term or preterm infants**

Answer 135

✅ A full workup is needed **if the infant is term, if apnea is severe, prolonged, or recurrent, or if associated with abnormal physical findings** , to rule out infection, CNS pathology, or metabolic disease.

Answer 136

🚩A **congenital defect of the diaphragm allowing herniation of abdominal contents into the thoracic cavity** ##footnote That’s leading to ➡️▪️lung compression ▪️ respiratory distress.

Answer 137

✅ • **Severe respiratory distress immediately after birth** • **Scaphoid (sunken) abdomen** due to abdominal contents being in chest • **Heart sounds shifted to the right** (mediastinal shift) • **Decreased air entry on the left side** of the chest • **Bowel sounds heard in chest**

Answer 138

✅ • **Chest X-ray** : diagnostic ➡️Shows **bowel loops in the thoracic cavity, displaced heart, and mediastinal shift** • **ABG** : may show **respiratory acidosis and hypoxia**

Answer 139

📍 **Acute Stabilization:** • Endotracheal intubation (ETT) ➕ mechanical ventilation ⛔ Avoid bag-mask ventilation 📍 **Supportive Measures:** • NGT for gastric decompression • NPO (nil per os), IV fluids 📍 **Definitive Treatment:** • ⚠️ **Urgent surgical repair** ## Footnote Abbreviations: ETT = Endotracheal Tube NGT = Nasogastric Tube NPO = Nothing by mouth .

Answer 140

✅ **Bag-mask ventilation** can lead to **gas insufflation of the stomach and intestines** , worsening **respiratory distress** by increasing pressure in the chest → **further lung compression**.

Answer 141

✅ Because the **herniated abdominal contents compress the lungs** , causing **pulmonary hypoplasia** , which leads to **severe respiratory distress** and **hypoxemia** shortly after birth.

Answer 142

✅ Depends on the severity of **lung hypoplasia** and **pulmonary hypertension** . Even after surgery, many infants require **long-term respiratory support and follow-up**

Answer 143

🔻**A syndrome of **acute intestinal necrosis** of unknown cause, primarily affecting 🚩 **preterm** and **very low birth weight (VLBW) neonates.**

Answer 144

🚩 **Risk Factors:** 1. **Prematurity ✅ (most common)** 2. **Perinatal asphyxia 3. Polycythemia 4. Aggressive enteral feeding, bottle feeds, hyperosmolar milk 5. Umbilical venous catheter (UVC), ibuprofen use** 🕒 Usually occurs in **1–2 weeks of life** due to feeding and hemodynamic changes. ## Footnote How‼️⁉️ ✅ Prematurity ➡️ Immature gut barrier + weak immunity → ↑ bacterial invasion & inflammation ✅ Perinatal asphyxia ➡️ Hypoxia → gut ischemia → mucosal necrosis & bacterial translocation ✅ Polycythemia ➡️ ↑ Blood viscosity → ↓ mesenteric perfusion → intestinal injury ✅ Aggressive feeding / hyperosmolar milk / bottle feeds ➡️ Stretches immature gut → distension & delayed emptying ➡️ Bacterial overgrowth → mucosal injury → ↑ NEC risk ✅ Formula feeding ➡️ Lack of protective factors found in breast milk → altered microbiota and gut injury ✅ Umbilical venous catheter (UVC), ibuprofen ➡️ UVC may reduce mesenteric flow ➡️ Ibuprofen (for PDA) decreases splanchnic circulation → ischemia ✅ Sepsis / systemic infection ➡️ Inflammatory state compromises gut perfusion and immunity

Answer 145

✅ Usually **between days 5–14 of life** (1–2 weeks), especially in **sick preterm neonates**

Answer 146

✅ ♦️ **Temperature instability** ♦️ **Lethargy, apnea, bradycardia** ♦️ **Erythematous abdominal wall** (cellulitis sign) ♦️ **Signs of sepsis and shock**

Answer 147

⏳**Early signs:** ♦️ **Vomiting (bilious)**, ♦️ **feeding intolerance** ♦️ **Abdominal distension** ♦️ **bloody stool** | أخضر من فوق، دم من تحت، وبطنه نافخ

Answer 148

🔬 **X-ray Abdomen findings:** 1. **Pneumatosis intestinalis**(intramural air) ✅ 2. Dilated bowel loops, **gas in portal venous system** 3. **Free air under diaphragm**if perforated

Answer 149

✅ **Yes, partially preventable.** ♦️ Exclusive breastfeeding (protective) ♦️ Slow and cautious feeding advancement ♦️ Antenatal steroids (for fetal gut maturity) ♦️ Early recognition and treatment of sepsis ♦️ Avoid hyperosmolar formula

Answer 150

1. **NPO**, NG tube on free drainage 2. 💉 **IV fluids + broad-spectrum antibiotics** (e.g., 3rd-gen cephalosporin + metronidazole) 3. 🫁 Respiratory and circulatory support 4. 🛠️ **Surgical consultation if: • GI perforation** (air under diaphragm) • Failure of medical treatment ##footnote Abbreviations: NPO = Nothing by mouth, NG = Nasogastric, IV = Intravenous, GI = Gastrointestinal

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✅ ♦️ **Intestinal perforation** ♦️ **Sepsis and shock** ♦️ **Strictures or short bowel syndrome** ♦️ **Death**

Answer 152

🔶**Any newborn born to a mother with pre-existing (type 1 or type 2 diabetes) or gestational diabetes**

Answer 153

🧠🪄**Mnemonic: “Big Babies Have Problems CRaMPed”** B ➡️ **Big baby (Macrosomia) B ➡️ Blood sugar low (Hypoglycemia) H ➡️ Hypocalcemia P ➡️ Polycythemia C ➡️ Congenital anomalies R ➡️ Respiratory distress (RDS, TTN, MAS) M ➡️ Myocardium thickened (Hypertrophic cardiomyopathy) H ➡️ Hyperbilirubinemia** ⸻ 💡 “Big Babies Have Problems CRaMPed” — because IDM babies are big and packed with complications!

Answer 154

✅ **Maternal hyperglycemia** → fetal **hyperglycemia** → increased **fetal insulin** → acts as a **growth hormone** → **macrosomia** (birth weight > 4.5 kg)

Answer 155

✅ **Hypoglycemia** (BG < 45 mg/dL) ##footnote 🧠 **Pathophysiology** : • High maternal glucose crosses placenta → ↑ fetal insulin • After delivery → maternal glucose stops, but insulin remains high → **hypoglycemia**

Answer 156

➡️ **Maternal hyperglycemia** → **fetal hyperinsulinemia** ➡️ At **birth** , **glucose** supply **stops** but **insulin remains high** ➡️ Result: glucose < 45 mg/dL → **hypoglycemia**

Answer 157

🚩 **Clinical Picture:** ▪️ **Asymptomatic ▪️ jitteriness ▪️ poor feeding ▪️ apnea, ▪️convulsions** How ⁉️ Jitteriness & convulsions ➡️ Brain relies heavily on glucose → ↓ glucose → neural irritability → tremors, seizures Poor feeding & apnea ➡️ Low energy from hypoglycemia → weak suck reflex, lethargy, respiratory pauses 🔬 **Diagnosis: ▪️ Glucose < 45 mg/dL** 💊 **Treatment:** ▪️ Feed & oral dextrose (asymptomatic) ▪️ **IV D10% bolus** + infusion (symptomatic) ✅ **Prevention: ▪️ Early feeding, ▪️especially breastfeeding** 💡 Always check glucose even if no symptoms — many IDM infants are asymptomatic.

Answer 158

✅ ♦️ **Polycythemia** ♦️ **Short RBC lifespan** ♦️ **Prematurity** → all contribute to **increased indirect bilirubin**

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✅ Due to **transient hypoparathyroidism** 📌 Symptoms: **Jitteriness and convulsions** 💊 Rx: **IV calcium gluconate**

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• **Fetal hypoxia** → ↑ erythropoiesis → **Hct > 65%** • May cause **hyperviscosity syndrome** → **renal vein thrombosis** 💊 Rx: **Partial exchange transfusion**

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✅ **Hypertrophic cardiomyopathy** • Especially **interventricular septal hypertrophy** • Usually **asymptomatic** , but 5–10% develop signs of **heart failure or RD** • Often **resolves spontaneously**

Answer 162

• ❤️ **Cardiac** : **TGA, VSD, ASD** • 🧠 **Neurologic** : **Spina bifida** • 🩻 **Skeletal** : **Sacral agenesis** • 🧫 **Renal** : **Renal agenesis** • 🧬 **GIT** : **Small left colon syndrome** ##footnote 💡Abbreviations • TGA = Transposition of the Great Arteries • VSD = Ventricular Septal Defect • ASD = Atrial Septal Defect

Answer 163

➡️ **Due to macrosomia (> 4.5 kg): ▪️ Brachial plexus injury ▪️ Shoulder dystocia ▪️ Head trauma**

Answer 164

✅ **Most common** : **Cardiac** anomalies (e.g., TGA, VSD, ASD) ✅ **Most specific** : **Sacral agenesis** (caudal regression syndrome)** ##footnote Abbreviations: TGA = Transposition of the Great Arteries VSD = Ventricular Septal Defect ASD = Atrial Septal Defect IDM = Infant of a Diabetic Mother

Answer 165

🧠Mnemonic:**“Caput is Soft and Spreads, CeF(ph)alo is Firm and Fixed”** ✅ **Caput succedaneum** C ➡️ Crosses sutures A ➡️ Appears at birth P ➡️ Pliable (soft) U ➡️ Under skin (subcutaneous) T ➡️ Trauma (may show ecchymosis) 💡 **Think: Caput = Crosses + Compressible + Comes at birth+ S.C + Coft (s) + eCCymosis** ⸻ ✅ **Cephalohematoma** C ➡️ Contained (does NOT cross sutures) E ➡️ Emerges hours later P ➡️ Periosteal (subperiosteal) H ➡️ Hard (firm) A ➡️ Anemia / jaundice risk L ➡️ Linked to skull fracture 💡 **Think: CeF(p)halo = Confined + Calcifies + Comes later+Firm + subPeriosteal** ## Footnote 💡**Note: • Caput may show ecchymosis • Cephalohematoma may be associated with jaundice, anemia, or skull fracture** ⸻

Answer 166

✅ **Reassurance only** 🔹 Both resolve spontaneously ▪️ **Caput: within a few days** ▪️ **Cephalohematoma: within weeks** No treatment needed unless complicated

Answer 167

1. **Caput succedaneum** 2. **Cephalohematoma** 3. **Subgaleal hematoma**

Answer 168

🔻 **Blood in subgaleal space (between periosteum & aponeurosis) 🔻 Diffuse, soft, boggy swelling 🔻 extend anterior to posterior** ⚠️ **It can cause hypovolemic shock or DIC if severe**

Answer 169

✅ **Subgaleal hematoma** because of its potential for **massive blood loss** and **shock** ; prompt stabilization and serial head‑circumference monitoring are essential.

Answer 170

upper ( Duchenne) lower ( Klumpke’s palsy). | Duchenne= Erb’s palsy.

Answer 171

✅ **Erb’s palsy (C5–C6):** • **Arm adducted, internally rotated , pronated with flexed finger** • **Waiter tip” posture** • **Absent Moro** reflex, **intact grasp** ✅ **Klumpke’s palsy (C8–T1):** • **Claw hand posture** • **Elbow extended, wrist flexed , supination** • **Absent grasp** , **intact Moro** • May have Horner syndrome ## Footnote Both need Physiotherapy. 🛠️

Answer 172

🔹 **Erb’s: C5–C6 🔹 Klumpke’s: C8–T1** 💡 **Erb’s may affect phrenic nerve (C4); 💡Klumpke’s may associated with Horner syndrome** ## Footnote Erb’s may associated with phrenic nerve palsy (C4,C5) Klumpke’s may with Horner syndrome ( T1).

Answer 173

✅ **Good prognosis:** • **>90%** recover by **3 months** with **physiotherapy** ## Footnote ⚠️ If **no** improvement by **2–3 months**➡️ refer to **ortho/plastic surgeon** Most recover by 2 years

Answer 174

✅ Clavicle fracture ## Footnote Due to shoulder dystocia

Answer 175

➡️ Cause: **Shoulder dystocia** ➡️ Management: • **Immobilization of arm** • No specific treatment needed • **Heals spontaneously**

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✅ **Clinical** signs: • **Pseudoparalysis** of the affected limb • **Asymmetrical Moro reflex** • **Crepitus and callus formation over the clavicle** ✅ **Radiological** confirmation: • **X-ray of the clavicle**

Answer 177

🚩 **EOS** = **Early-Onset Sepsis** 🚩 **LOS** = **Late-Onset Sepsis** | 🧪 Neonatal sepsis is a clinical syndrome of systemic signs of infection and bacteremia in the first 28 days of life. ➡️ It includes both Early-Onset Sepsis (EOS) and Late-Onset Sepsis (LOS) depending on timing.

Answer 178

✅ **EOS: within the first week, often during/before delivery (via birth canal)** ✅ **LOS: after the first week, often postnatal (NICU/community-acquired)**

Answer 179

🧠🪄**Mnemonic: “PRE-GROUP M”** (Think: “PREgnant mothers with GBS risk pass it to GROUP M (Male, Minority, and preterm) babies via vertical transmission.”) ⸻ 🔻 **P** – Preterm delivery 🔻 **R** – ROM > 18 hrs (PROM) 🔻 **E** – Existing maternal infection (UTI, chorioamnionitis) 🔻 **G** – GBS in previous baby 🔻 **R** – Race: Black 🔻 **O** – Organism in maternal blood (bacteremia) 🔻 **U** – UTI during pregnancy 🔻 **P** – Positive male sex (male neonates)** 🧠 ➡️ All transmitted vertically to the neonate | Mainly factors related to mother ( vertical transmission).

Answer 180

🔻 **Preterm** 🔻 **Hospitalization** 🔻 **Invasive procedures (ETT, UVC)** 🔻 **Male and Black neonates** ➡️ Nosocomial or community-acquired

Answer 181

✅ Respiratory Distress, ✅ Meningitis. ## Footnote 🧠Mnemonic: “**Early Resp, Late Meningitis”** ➡️ ERLM ⸻ **✅ EOS (Early Onset Sepsis) ➡️ R = Respiratory Distress** • Infection during delivery • Head presents first → lungs exposed → RD develops **✅ LOS (Late Onset Sepsis) ➡️ M = Meningitis** • Infection after birth • Septicemia → crosses BBB → meningitis Or 🧠 “**Head breathes, Blood spreads”**

Answer 182

🚩 **EOS Pathogens:** 🧠🪄Mnemonic: “**Great Early Kills Little Ones”** 🔻 **G – GBS (Group B Streptococcus) 🔻 E – E. coli 🔻 K – Klebsiella 🔻 L – Listeria monocytogenes** 💊 **Treatment: Ampicillin ➕ Gentamicin or Ampicillin ➕ 3rd-gen cephalosporin** 🚩 **LOS Pathogens: 🧠Mnemonic: **“Late Sepsis Gives High Killer Pathogens”** 🔻 **S – Staph aureus 🔻 G – GBS (Group B Streptococcus) 🔻 H – H. influenzae 🔻 K – Klebsiella 🔻 P – Pseudomonas** 💊 **Treatment: Flucloxacillin ➕ Gentamicin ➡️ consider Vancomycin/Meropenem if no improvement** ## Footnote Treatment is IV and lasts 10-14 days. if meningitis> 14-21 days.

Answer 183

✅ 1. **CBC** (↑ or ↓ WBC, ↓ platelets) 2. **CRP** or Procalcitonin (elevated) 3. **Blood culture** 4. **Urine culture** 5. **Chest X-ray** (if respiratory signs) 6. **CSF analysis** (if signs of meningitis) 7. **Surface swabs** if applicable

Answer 184

✅ • **10–14** days for sepsis • 14–21 days if meningitis is confirmed

Answer 185

**To** : Toxoplasmosis **R** : Rubella **C** : CMV **H** : Herpes Simplex**

Answer 186

✅ • Recurrent **abortion** • **Fever or rash** during pregnancy • Known exposure to infections

Answer 187

♦️ **LBW** (IUGR, prematurity) ♦️ **Hepatosplenomegaly** — Lymphadenopathy ♦️ **Anemia or Thrombocytopenia, Neutropenia, petechial rash** ♦️ **Hepatitis** (Direct Jaundice). ♦️ **Convulsions** — microcephaly — chorioretinitis * **Neurodevelopmental delay, MR**

Answer 188

✅ • **Chorioretinitis** • **Intracranial calcifications (diffuse)** • **Hydrocephalus**

Answer 189

✅ • **Periventricular calcifications** • **Sensorineural hearing loss** • **Petechiae** (“blueberry muffin rash”) • **Seizures** , microcephaly, hepatosplenomegaly

Answer 190

✅ • **Localized skin, eye, mouth lesions** • **CNS disease** (encephalitis) • **Disseminated disease** involving liver, lungs, and brain

Answer 191

✅ **Cytomegalovirus (CMV)**

Answer 192

✅ • **Cataracts** • **Sensorineural deafness** • **Cardiac defects** (PDA) • **Blueberry muffin** ash • **IUGR**

Answer 193

Neonatal Syphilis. ## Footnote Hutchinson’s incisors. Interstatial keratitis. Olympian brow. Clutton Joint.

Answer 194

→ 1. **Symmetrical IUGR** (proportional) → 2. **Asymmetrical IUGR** (disproportional)

Answer 195

→ 1. **Chromosomal abnormalities** (e.g. Trisomy 13, 21, 18) → 2. **Congenital malformations** → 3. **Intrauterine infections (TORCH)**

Answer 196

→ 1. **Maternal diseases** : malnutrition, diabetes, preeclampsia, smoking, alcohol → 2. **Placental insufficiency** : e.g. preeclampsia, multiple gestations

Answer 197

➡️ The Moro reflex is elicited by **suddenly dropping the infant’s head** backward while they are lying supine, or by producing a sudden loud noise.

Answer 198

→ The infant **arches the back, extends the arms and legs** , then **brings the arms toward the body** in an “embracing” motion. .

Answer 199

→ **By 6 months** of age.

Answer 200

→ Possible causes: 1. **Severe prematurity** 2. **Cerebral injury (brainstem or cortex damage)** 3. **Bilateral brachial plexus injury**

Answer 201

→ Possible causes: 1. **Clavicle fracture** 2. **Brachial plexus injury (e.g., Erb’s palsy)** 3. **Hemiplegia**

Answer 202

→ By **placing an object or finger beneath the infant’s toes** (light pressure on the sole near the base of the toes).

Answer 203

→ **Curling (flexion) of the toes** around the object or finger.

Answer 204

→ Disappears by **5-6 months of life** .

Answer 205

→ **Neurological dysfunction** (e.g., cerebral palsy, spasticity).

Answer 206

→ By **holding the baby upright with bare feet touching a surface** and moving them slightly forward.

Answer 207

→ The baby makes **stepping motions** as if attempting to walk.

Answer 208

→ Disappears by around **3 months of age** . ##footnote 🧠 Clinical Insight: → Persistence or absence beyond the expected age may signal **neurological issues** such as **hypotonia or brainstem dysfunction** .

Answer 209

→ By **gently turning the baby’s head to one side** while the infant is lying awake on their back.

Answer 210

→ The infant assumes a **“fencing position”** : • **Arm on the side the head is turned toward is extended** • **Opposite arm is flexed**

Answer 211

→ By **4 to 6 months of age** ##footnote 🚨 Clinical Note: → **Persistence beyond 6 months** may suggest **cerebral palsy** or **other upper motor neuron dysfunction** .

Answer 212

→ **Stroke the sole of the foot** from **heel to toe** (lateral side then across the ball of the foot).

Answer 213

→ **Toes fan out and big toe dorsiflexes (extends upward)** — this is called an **extensor plantar response** .

Answer 214

→ By **8–12 months of age** (typically disappears when myelination of the corticospinal tract matures).

Answer 215

→ Suggests **upper motor neuron lesion** if seen **after 2 years of age** .

Answer 216

→ **Suspend the baby in a prone (horizontal) position** with one hand under the abdomen.

Answer 217

→ The infant will **extend the head, trunk, and hips** — resembling a **“superman” posture** .

Answer 218

→ **Appears at ~3 months** → **Disappears between 12–24 months** of age.

Answer 219

→ May indicate **hypotonia, hypertonia** , or **neurodevelopmental delay** (e.g., cerebral palsy or intellectual disability).

Answer 220

→ Hold the infant in **ventral suspension** and **rapidly lower them head-first** toward a surface (e.g., couch).

Answer 221

→ The infant **extends arms forward** as if trying to **break a fall** — a **defensive extension response** . .

Answer 222

→ **Appears at 6–9 months** of age, → **Disappeared approx. 9-10 month** of age

Answer 223

→ Suggests **upper motor neuron lesion** or **neurological dysfunction** , as seen in **cerebral palsy** .

Answer 224

→ **Place a finger or nipple in the infant’s mouth**

Answer 225

→ The infant **sucks rhythmically** .

Answer 226

→ Around **4 months** , replaced by **voluntary sucking** .

Answer 227

→ **Permits effective feeding** in early infancy.

Answer 228

→ **Stroke near the corner of the infant’s mouth**

Answer 229

→ The infant **turns their head toward the stimulus** .

Answer 230

→ **Dry the infant** , **clear airway secretions** , and **provide warmth** under a radiant warmer.

Answer 231

♦️ **Apnea** or **poor respiratory effort** ♦️ **Cyanosis** ♦️ **Bradycardia** ♦️ **Poor muscle tone**

Answer 232

→ If the baby is **apneic, gasping** , or has a **heart rate < 100 bpm** .

Answer 233

**PPV** | By bag-mask ventillation ## Footnote Initiated at rate of 40 -60 breaths /min.

Answer 234

**30 sec**

Answer 235

→ If **heart rate remains < 60 bpm after 30 seconds** of effective PPV with **100% oxygen** .

Answer 236

→ If **PPV is ineffective, prolonged** , or **chest compressions are needed** .

Answer 237

→ If **heart rate remains < 60 bpm despite adequate ventilation and chest compressions** .

Answer 238

A: Appearance. P: pulse. G: Grimace. A: Activity. R: Resoiration.

Answer 239

→ Initial adaptation to extrauterine life. • **7–10** = Normal • **4–6** = Moderately depressed • **0–3** = Severely depressed (needs resuscitation)

Answer 240

→ **Correlates with long-term neurological outcomes** . ##footnote **Persistent low score = increased risk of morbidity** .

Answer 241

→ At **1 minute** and **5 minutes** after birth. ##footnote (And at **10 minutes if score <7** )

Answer 242

An APGAR score of **4–6** indicates moderate depression.

Answer 243

A score of **0–3** at **1️⃣minute** suggests **severe depression** and **urgent resuscitation** .

Answer 244

0️⃣ : **Absent pulse** 1️⃣ : **<100 bpm** 2️⃣ : **>100 bpm**

Answer 245

0️⃣ : **Blue or pale all over** 1️⃣ : **Pink body, blue limbs** 2️⃣ : **Completely pink**

Answer 246

0️⃣ : **No response to stimulation** 1️⃣ : **Grimace or weak cry** 2️⃣ : **Vigorous cry or active withdrawal**

Answer 247

0️⃣ : **Flaccid** 1️⃣ : **Some flexion of limbs** 2️⃣ : **Active motion**

Answer 248

0️⃣ : **No breathing** 1️⃣ : **Slow, irregular breathing** 2️⃣ : **Good cry and regular breathing**

Answer 249

❗️ Reflects **neonatal adaptation and prognosis** ##footnote 🚨 A low 5-minute score (<7) suggests increased risk of **neurologic complications** and requires reassessment at **10 minutes** .

Answer 250

إلى هُنا تنتهي رحلتنا لهذا الشابتر 😵‍💫 والسّلام عليكم ورحمة الله🔻

Neonate and Reflexes Flashcards

(274 cards)