nicu mortality. objectives emphasize the importance of adequate communication between medical teams,...
TRANSCRIPT
NICU MORTALITY
Objectives
• Emphasize the importance of adequate communication between medical teams, regular and proper evaluation of adequacy of resuscitation
• Present the Therapeutic Hypothermia Protocol according to the Journal of Clinical Neonatology
R.V.
• Term Baby Boy• NSD • 35 y.o. G2P2 (2002) • 39 3/7 weeks AOG• Anthropometrics:– BW 3120g, BL 53cm, HC 34cm, CC 31cm, AC 30cm– AGA
• Apgar score: 0, 0, 1, 1, 1
Maternal History
• Regular prenatal check-up• Regular intake of multivitamins• Ultrasound – unremarkable • Congenital anomaly scan – normal• Normal OGCT• No BP elevations• CBC and UA upon admission – normal
Past Medical History
• No hypertension, no DM
Family History• (+) hypertension, DM, heart disease, colon CA
Personal/Social History• Occasional alcoholic beverage drinker,
nonsmoker, no use of illicit drugs
OB History
• G1 – 2009 – NSD, full term male, no fetomaternal complications
• G2 – present pregnancy
Admitting CTG: 3hrs 30mins prior to delivery
Baseline 130 - 135bpm, with accelerations, no decelerations, good fetal movement, strong contractions every 8 mins
After CEA: 3hrs prior to delivery
Baseline 140 bpm, with accelerations, no decelerations, good fetal movement, strong contractions every 8 mins
After AROM: 2hrs 30mins prior to delivery
Baseline 135 to 140 bpm, moderate variability, with accelerations, with variable decelerations as low as 60 bpm with slow recovery, with moderate to strong uterine contractions every 3-4 minutes
1hr and 30mins prior to delivery
Baseline 135 to 140 bpm, moderate variability, with accelerations, with variable decelerations as low as 70 bpm with slow recovery, with moderate to strong uterine contractions every 2-3 minutes
Prior to transfer to DR: 1hr prior to delivery
Baseline 130-135 bpm, moderate variability, no accelerations, with variable decelerations as low as 60 bpm with slow recovery, with moderate to strong uterine contractions every 3-4 minutes
FHT tracing at DR (supine)
Change in baseline 120 bpm, moderate variability, no accelerations, with variable decelerations as low as 50 bpm with slow recovery
Tracing at DR (Left lateral decub): 40mins prior to delivery
Maternal heart tone
APGAR Score
0
00000
0
00
00
0
000
0
1
101
001
00
000
1 1
39 2/7
NICU Transfer
At the NICU
• Pale, unresponsive • BP not appreciated, HR 180, on bag-tube ventilation,
T 34C• No dysmorphic features• Pupils 8-9mm dilated, not reactive to light• No spontaneous breathing, Equal chest rise, good air
entry both lungs• Regular cardiac rhythm, no murmur appreciated• Soft abdomen• Poor pulses, CRT prolonged
Severe Hypoxic-Ischemic Encephalopathy, post cardiopulmonary arrest
Initial assessment
Problems• Asphyxia• Mixed Metabolic and Respiratory Acidosis, Intractable
15 mins of life VBG (Bag tube vent at 10lpm)
pH 6.604
C02 61.2
PO2 114.5
HCO3 6.1
BE -30
O2 sat 82.9%
Mixed metabolic and respiratory acidosis
Correction with NaHCO3Therapeutic Hypothermia
VBG (MV settings: Fi02 100, iT 0.5 FR 10 PIP 26 PEEP 50 RR 50)
6.52
95.6
79
7.8
-30
60%
Mixed met and resp acidosis
Hooked to MV
Lactate (4.5-19.82
mg/dL)
223.2 mg/dL
Problems• Shock prob cardiogenic• Severe anemia prob sec to hemorrhage
Hgb Hct WBC Band Neut Lymph Mono Plt
57 20 42.7 6 45 41 8 188 70 nRBC
Cranial UltrasoundNormal
PT Control 13.3 Patient 38.5 % activity 0.2 INR 3.78aPTT Control 29.3 Patient 138
2D Echo
PA pressure 50Right to left shunting (PDA)Underfilled left ventricleSevere tricuspid regurgitationPFO bidirectional
PNSS 20mL/kg bolus 2xDopamine and Dobutamine DripBlood transfusion ordered but refused
Problems
• InfectionHgb Hct WBC Band Neut Lymph Mono Plt
57 20 42.7 6 45 41 8 188 70 nRBC
Blood culure and sensitivity
No growth
CRP (NV 0-0.5mg/dL)
0.01mg/dL
Ampicillin 50mg/kg/doseGentamicin 4mg/kg/day
INTRACTABLE METABOLIC ACIDOSIS SECONDARY TO MULTIORGAN DYSFUNCTION SECONDARY TO PERINATAL ASPHYXIA
Final Diagnosis
Learning Points
• Adequate communication between teams• Regular and proper evaluation of adequacy of
resuscitation
THANK YOU!!!
DISCUSSION
Perinatal Asphyxia
• Condition of impaired gas exchange that leads to fetal hypoxemia and hypercarbia
• Occurs during the 1st and 2nd stage of labor• In term infants, 90% occur in antepartum or
intrapartum period as a result of impaired gas exchange across the pacenta
• Postpartum – secondary to pulmonary, cardiovascular, neurologic abnormalities
Cloherty J. Manual of Neonatal care, 6th ed
Hypoxic-Ischemic Encephalopathy
• Abnormal neurobehavioral state in which the predominant pathogenic mechanism is impaired cerebral blood flow
• Suspected if:– AS <=3 at >5minutes– FHR <60 bpm– Prolonged (>1hr) acidosis– Seizures within the first 24-48hrs after birth– Burst-suppression patten EEG
• 20-30% of infants die in the neonatal periodCloherty J. Manual of Neonatal care, Lippincott Williams and Wilkins, 6th ed. 2008 p89
Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Sarnat and Sarnat Staging for HIE
Diagnostic Imaging
• Diffusion-weighted MRI
Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Treatment
• Therapeutic hypothermia– decreases the rate of apoptosis and suppresses
production of mediators known to be neurotoxic, including extracellular glutamate, free radicals, nitric oxide, and lactate.
Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Therapeutic Hypothermia
• >= 36 weeks AOG– Physiological criteria• Evidence of intrapartum hypoxia, including at least two
of the following: – 1.Apgar score 5 or less at 10 min – 2. Needing mechanical ventilation and/or
ongoingresuscitation at 10 min – 3. Metabolic or mixed acidosis defined as arterial cord gas, or
any blood gas within the first hour of life showing pH of 7 or less, or base deficit of ≥12 mmol/l
Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J Clin Neonatol 2012;1:101-6.
• Neurological criteria– One of the following: • Seizures is an automatic inclusion• Evidence of encephalopathy suggested a-EEG• Physical examination consistent with moderate to
severe encephalopathy
Therapeutic Hypothermia
Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J Clin Neonatol 2012;1:101-6.
Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J Clin Neonatol 2012;1:101-6.
Infants not Eligible for Cooling
• Birth weight less than 2000 g • Gestational age less than 36 weeks• Inability to initiate cooling by 6 h of age• Clinical coagulopathy• Life-threatening abnormalities of the cardiovascular or
respiratory systems such as complex congenital heart disease and PPHN
• Major congenital malformations, imperforate anus, suspected neuromuscular disorders, or presence of known lethal chromosomal anomaly
• Death appears inevitable
Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J Clin Neonatol 2012;1:101-6.
PROTOCOL
PROTOCOL
Specific Supportive Treatment during Hypothermia
• Respiratory support – assisted ventilation, keep 02 at 92-98%
• Cardiovascular support– asymptomatic sinus bradycardia without cardiac
dysfunction– At 33.5°C, the average HR is 80–100 beats per minute
bpm– If inotropic support is required, the following regime is
suggested:• Dopamine up to 10 mg/kg/min • If still hypotensive add dobutamine up to10 mg/kg/min
• Fluids– Start with 50–60 ml/kg/day– insert urinary catheter to measure urine output
• Electrolytes– Na and Cl levels could fall duet o increased renal
loss in hypothermia• Coagulation– mild derangement of blood viscosity and
coagulation
Specific Supportive Treatment during Hypothermia
Rewarming Procedure
• increase the rectal temperature to 36.5–37°C at a rate not to exceed 0.5°C per hour.
• final temperature goal is 36.5°C and should take about 7 hrs to achieve.
Prognosis
• Infants with initial cord or initial blood pH <6.7 – 90% risk for death or severe neurodevelopmental
impairment at 18 mo of age. • Apgar scores of 0-3 at 5 min, high base deficit
(>20-25 mmol/L), decerebrate posture, and lack of spontaneous activity are also at increased risk for death or impairment.
Thank you!