CASE PRESENTATION ON LATE PRETERM, HYPERBILIRUBINEMIA, ECLAMPSIA
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CASE PRESENTATION ON LATE PRETERM, HYPERBILIRUBINEMIA, RESPIRATORY DISTRESS , ANTENATAL HISTORY OF ECLAMPSIA Presented by: Chandana C 2 nd Pharm.D
LATE PRETERM GESTATION PERIOD: fetal development period from time of conception until birth. Normal duration of pregnancy: 37- 42 weeks of gestation Preterm: < 37 weeks of gestation during birth. Late preterm: born between 34- 37 weeks of gestation Very late preterm: born between 33- 28 weeks of gestation Extremely preterm: born at less than 28 weeks of gestation Post term: 42 weeks completed during birth. Antenatal/ prenatal period: period before child birth Postnatal period: period after child birth
ETIOLOGY: The exact cause of preterm birth is not known in many cases. But it can be due to following cases; Multiple pregnancies Infections Diabetes mellitus Hypertension Conception by in vitro fertilization Preterm birth is a worldwide epidemic with global incidence of 15 million cases per year. It accounts for 47% of all neonatal deaths.
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) Neonatal ARDS occurring in newborn begins with dyspnea within a few hours after birth with tachypnea, hypoxia and cyanosis; in severe cases death may occur within few hours. ARDS has a morphological feature of formation of hyaline membrane in the alveoli hence it is also called as hyaline membrane disease .
ETIOLOGY Many cases of neonatal ARDS remain idiopathic; but following reasons can lead to ARDS Preterm infants Infants born to diabetic mothers Delivery by caesarean section Infants born to mothers with previous premature infants Excessive sedation of mother causing depression in respiration of infant Birth asphyxia
PATHOGENISIS: The basic defect in neonatal ARDS is a deficiency of pulmonary surfactant, its deficiency leads to increased alveolar surface tension which causes atelectasis. Atelectasis results in hypoventilation, pulmonary hypo perfusion and ischemic damage to capillary endothelium. This results in ischemic necrosis of alveolocapillary wall, exudation of plasma protein into alveoli and hyaline membrane is formed.
HYPERBILIRUBINEMIA It is a condition in which there is increased level of bilirubin in blood. Bilirubin is a bile pigment, yellowish-orange in color. It is product of hemoglobin metabolism. SYMPTOMS: Yellow coloring of baby's skin and eyes. Poor feeding
ETIOLOGY PHYSIOLOGIC JAUNDICE: it is a normal response. BREAST MILK JAUNDICE: caused by a substance in breast milk that increases reabsorption of bilirubin from intestine JAUNDICE FRM HEMOLYSIS: excess breakdown of RBC JAUNDICE RELATED TO INADEQUATE LIVER FUNCTION DIAGNOSIS BILIRUBIN LEVELS: direct and indirect bilirubin levels are examined
EPIDEMIOLOGY 80% of premature babies develop hyperbilirubinemia 60% of new born develop hyperbilirubinemia Neonates of diabetic mothers are more prone to develop it.
PATHOGENESIS Excess catabolism of hemoglobin leads to hyperbilirubinemia HEMOGLOBIN HEME VERDO HEME BILIVERDIN BILIRUBIN
ECLAMPSIA It is a severe complication in pregnancy characterized by hypertension, proteinuria and seizures. It usually follows preeclampsia. Eclampsia affects about 1 in every 200 women with preeclampsia If the patient doesn’t have a history of seizures also eclampsia will be developed.
SYMPTOMS: Seizures Elevated BP Loss of consciousness Agitation Swelling in face and limbs Excessive weight gain Blurred vision Difficulty in urinating
RISK FACTORS: Chronic gestational hypertension Being older than 35 years or younger than 20 years Pregnancy with twins or triplets First time pregnancy Diabetes mellitus Kidney diseases
PATIENT DEMOGRAPHIC DETAILS: Name: B/O h…. Age: NB Gender: male Weight: 2.9 Kg IP no: 18/20004 Unit: NICU DOA: 01/12/18 DOD: 07/12/18
CHIEF COMPLAINTS ON ADMISSION: Preterm baby of 34+ weeks
ANTENATAL HISTORY: Eclampsia Brief history of mother: primigravida with 34+ weeks of gestation
BIRTH HISTORY Mode of delivery: LSCS APGAR score: 1 min:7 5 min: 8 Post natal history: no spontaneous breath at birth, baby did not cry immediately, after doing touch stimulation weak cry.
EXAMINATION OF NEW BORN GENERAL PHYSICAL EXAMINATION VITALS CVS: Heart sounds- S1 S2 No murmurs HR: 160 bpm RS: Bilateral air entry RR: 62 bpm Per abdomen: shape of abdomen, posture umbilicus NAD SPO2: 88% on room air
PROVISIONAL DIAGNOSIS Late preterm with respiratory distress
TREATMENT GIVEN DRUG NAME DOSE FREQUENCY ROA 1 2 3 4 5 6 7 Inj. cefotaxime 145mg BD IV Inj. amikacin 22mg BD IV Inj. 10% dextrose 60ml/Kg IV Inj. Vitamin K 1mg IV
DAY:2 Baby color is good. Baby cried Vitals were normal Advice: CST DAY:3 GC- stable Advice: direct breast feed, CST
DAY: 4 Baby skin color changed to yellow Vitals are normal Advice: test for bilirubin, TSH, stop antibiotics DAY:5 DSPT – double surface photo therapy is advised Vitals are normal Shifted from NICU to OBG semi-private ward
DAY:6 Single surface photo therapy was advised Skin color was good Vitals are normal DAY:7 Stop photo therapy Baby hemodynamically stable Prepare for discharge
PHARMACEUTICAL CARE PLAN SUBJECTIVE EVIDENCE OBJECTIVE EVIDENCE FINAL DIAGNOSIS Apnea Yellow coloration of skin SPO2: 88% Bilirubin: total- 11.7 mg/dl direct- 0.7 mg/dl indirect- 11.0 mg/dl Normal value: > 10 mg/dl Respiratory distress, hyperbilirubinemia
TREATMENT GOAL To improve breathing. To decrease the bilirubin concentration. To decrease the yellowish color of skin and eyes .