1 / 50

Hypoxic Ischemic Encephalopathy (HIE) Case Studies

Hypoxic Ischemic Encephalopathy (HIE) Case Studies. Lisa Jorgenson, MSN, NNP-BC Angela Riley, MSN, NNP-BC Avera McKennan Hospital NICU. Objectives. Review incidence, timing, risk factors, and pathophysiology for HIE Review Sarnet Staging for Encephalopathy Briefly review Whole Body Cooling

keegan
Download Presentation

Hypoxic Ischemic Encephalopathy (HIE) Case Studies

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Hypoxic Ischemic Encephalopathy (HIE) Case Studies Lisa Jorgenson, MSN, NNP-BC Angela Riley, MSN, NNP-BC Avera McKennan Hospital NICU

  2. Objectives • Review incidence, timing, risk factors, and pathophysiology for HIE • Review Sarnet Staging for Encephalopathy • Briefly review Whole Body Cooling • Discuss HIE case studies

  3. Definition of HIE • Hypoxic= not enough oxygen to the tissues • Ischemic= a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissues alive) • Encephalopathy= disturbed neurological function

  4. Hypoxic Ischemic Encephalopathy (HIE) • Incidence • Affects 2-3/1000 full term live births, • With annual birth rate of 4 million it is expected 8000-12,000 will be diagnosed with this disorder each year in the USA. • The SD birth rate in 2013 was 11,894 so that would be about 24-36 babies each year in SD. • Accounts for 15-25% neonatal mortality • Accounts for 15-28% of children with cerebral palsy and 25% of all cases of developmental delay

  5. HIE – Timing • Timing of insult occurrence • Antepartum: 20% • Intrapartum: 30% • Antepartum-intrapartum: 35% • Postpartum: 10%

  6. HIE - Etiology • Antepartum • Socioeconomic status (SES) • Maternal thyroid disease • Fetal Growth Restriction • Post-dates • Faulty placental gas exchange • Diabetes • Preeclampsia or severe PIH • Acute • Acute hypotension • Placental separation with uterine hemorrhage

  7. HIE - Etiology • Intrapartum risk factors • Cord strangulation (i.e. Nuchal Cord, Knot in Cord, Prolapsed Cord) • Placental problems • Difficult delivery • Maternal fever • Persistent occiput posterior (OP) fetal position • Uterine abruption or rupture • Abnormal fetal heart rate pattern • Fresh meconium

  8. HIE Pathophysiology • Impaired cerebral blood flow is the principal pathogenetic mechanism underlying neuropathology of hypoxia-ischemia • Brain injury occurs in phases • Acute – During the initial insult • Recovery-After restoration of circulation (reperfusion injury) • Infant evolves from primary energy failure→ reperfusion period→latent phase→secondary energy failure

  9. Primary Energy Failure • Initial increased cerebral vasodilation (secondary to hypercapnia and hypoxemia) • Loss of cerebral autoregulation • Redistribution of organ blood flow • ↑CBF is quickly followed by impairment (bradycardia and hypotension) • Activation of cell death • Neuronal death vs. necrosis • Cell lysis • Excitotoxins • Calcium entry • ↓ATP & PCr • ↑ anaerobic glycolysis • Occurs in the first 30 minutes after insult

  10. Reperfusion Period • Return of CBF • Normal BP and pH • Transient improvement in cytotoxic edema • Absence of seizures (EEG depressed) • Rapidly transitions into the latent phase

  11. Latent Phase of Cerebral Injury • Occurs during hours 6 – 15. • Recovery of oxidative metabolism • Apoptotic cascade (ATP and PCr again ↓) • Secondary inflammation • Receptor hyperactivity • Unlike primary phase, intracellular pH and cardiorespiratory status are usually stable

  12. Secondary Phase of Cellular Injury • Occurs from 3 – 10 days • Failing oxidative metabolism • Seizures (↑ CBF) • Cytotoxic edema • Excitotoxins • Final cell death

  13. Sarnat Stage for HIE • Sarnat Stage 1 (mild encephalopathy) • Hyper alertness • Normal muscle tone, active suck, strong Moro reflex, normal/strong grasp, normal doll’s-eye reflex • Increased tendon reflexes • Myoclonus present • Hyper-responsiveness to stimulation • Tachycardia possible • Dilation of pupils, reactive • No convulsions (unless by other cause, i.e. hypoglycemia) • EEG within normal limits • Usually lasts <24 hours

  14. Sarnat Stage for HIE • Sarnat Stage 2 (moderate encephalopathy) • Hypotonia and lethargy • Increased tendon reflexes • Diminished brainstem reflexes - weak suck or gag, incomplete Moro reflex, sluggish pupil reaction, varying respiration • Possible clinical seizures • At this stage, the condition will either improve & the infant will get better or it will worsen & the infant will deteriorate • Results in ~40-70% death or disability with more cases of disability than death (cerebral palsy, cognitive deficits and seizures)

  15. Sarnat Stage for HIE • Sarnat Stage 2 (moderate encephalopathy) • Recovery • No further seizure activity • EEG returns to normal • Transient jitteriness • Improvement in level of consciousness

  16. Sarnat Stage for HIE • Sarnat Stage 3 (severe encephalopathy) • Clinical Features • Apnea/bradycardia • Mechanical ventilation required to sustain life • Level of consciousness deteriorates from obtunded to stuporous or coma • Seizures within the first 12 postnatal hours, usually multifocal clonic seizures; all display subtle seizures • Severe hypotonia & flaccidity; reflexes depressed or absent • Pupils often unequal; variable reactivity & poor light reflex

  17. Sarnat Stage for HIE • Sarnat Stage 3 (severe encephalopathy) • Deterioration • Occurs within 24 to 72 hours • Severely affected infants often worsen, sinking into deep stupor or coma • Death may ensue • Survivors • Often improve in the next several days to months • Feeding difficulties often develop • Generalized hypotonia is common; hypertonia is uncommon • Almost always result in death or disability with death > disability

  18. HIE - Outcomes • Factors associated with poor outcome: • Apgar score • If score is 0-3 for 20 minutes or more, approximately 60% die • If score is less than 3 at 1 minute & less than 5 at 5 minutes, with abnormal neurologic signs • About 20% die • About 40% are normal • About 40% suffer neurologic sequelae • Encephalopathy • Mild: No subsequent deficits • Severe: 75% die; 25% have sequelae • Disappearance of abnormal neurologic signs by 1 to 2 weeks: good chance of being normal

  19. HIE - Outcomes • Seizures early and/or difficult to control associated with poorer prognosis • Hyperactivity & attention difficulties seen in infants with less severe encephalopathy • Rapid initial improvement indicative of better outcomes • Long-term sequelae based on • Site • Extent of cerebral injury • Duration of abnormal clinical presentation

  20. Neuroimaging in HIE • MRI is the primary and most sensitive method for brain injury patterns, timing of injury, and diagnosis of HIE. • Injury to basal ganglia and thalamus is most strongly associated with poorest outcomes.

  21. Mechanism of Action forHypothermia Therapy • Better maintenance of the cerebral energy state • Attenuation of the release of exicitatory neurotransmitters • Decreased caspase -3 activation and morphologic evidence of apoptosis • Reduction in oxygen free radicals • Blockage of inflammatory mediators and inhibition of apoptotic pathways

  22. Whole Body Cooling • Actively works by cooling the head and body together by a water blanket composed of coils • Maintain an esophageal and skin temperature of 32.5°C – 34.5°C

  23. Outcomes in Hypothermia Therapy • Severe HIE – outcomes remain bleak despite cooling • One in 6 babies will garner some benefit • Studies have shown decrease in mortality from 39 -25% and reducing occurrence of cognitive impairments from 28 - 11% • More effective in milder encephalopathy • Either whole body cooling or selective head cooling protocols may be adopted to cool infants with HIE

  24. Avera Childrens’ Hypothermia Program • Established November 2010 • Infants undergo whole body cooling utilizing Blanketrol III system • Undergo 72 hours of active cooling with close monitoring of lab studies and esophageal temperature • Evaluation and follow up with pediatric neurologist and developmental follow up group

  25. Therapeutic Hypothermia – Inclusion Criteria • Before 6 hours of age (mandatory) • ≥35 weeks gestation (mandatory) • History of an acute perinatal event • Apgar score ≤ 5 at 10 minutes • Cord pH ≤ 7.0 or first postnatal blood gas pH ≤ 7.0 within 1 hour • Base deficit on cord gas ≥ 16 mEq/L or first postnatal blood gas ≥16 mEq/L within 1 hour • Continued need for ventilation initiated at birth and continued for at least 10 minutes

  26. Therapeutic Hypothermia – Inclusion Criteria • The attending physician or designee will perform a neurologic exam for infants who did not receive a ABG within one hour of delivery and does not have seizure activity. The infant must show signs of moderate or severe HIE in at least 3 of the 6 categories to be eligible for Therapeutic Hypothermia. • Infants who present with clinical seizures and meet the requirement of an acute perinatal event or have seizure activity with a qualifying blood gas will qualify for therapeutic hypothermia.

  27. Therapeutic Hypothermia – Exclusion Criteria • Inability to enroll within 6 hours • Gestational age <35 weeks • Presence of known chromosomal anomaly • Presence of major congenital anomalies • Severe intrauterine growth restriction (weight ≤ 1800g) • Infants in extremis; no additional intensive therapy planned

  28. Case Study #1 • Risk Factors: variable and prolonged decels, category 2 FHTs, induction at 40.6 weeks for post dates, meconium • Apgars 1 (for present HR) and 8 (-1 color and -1 tone) • Baby born with meconium stained fluid with no tone/resp effort, brought to warmer and immediately intubated for meconium. No meconium noted below cords. PPV initiated and baby improved so changed to CPAP. Blowby continued until 7 mins of age for sats. • Brought to NICU for further care

  29. Initial Lab Results • Cord blood gas: 7.26/40/24/18/-9 arterial and 7.30/35/26/17/-9 venous • Started on oxygen at 2 hours of age for desats. Blood gas 7.37/39/53/23/-2 on NC 1L 30%

  30. NO No NO

  31. Case Study #1 • At 7 hours of age, baby presented with seizure activity. He was loaded with phenobarbital. EEG showed several persistent subclinical seizures that would last up to 5 min. with short interval resolution between episodes. • Baby then loaded with Keppra. Seizures persisted so baby started on a versed drip. Intubated for his heavy sedation/seizure management.

  32. Healthcare Maintenance • Infection: Amp/Gent x 48 hour rule out, Acyclovir, BC negative, LP negative • Neurologic: • CT was essentially normal, no acute intracranial process • MRI- extensive cortical and subcortical signal hyperintensity and diffusion restriction in the left cerebral hemisphere, etiology uncertain. • PedsNeurologist consulted/following patient

  33. Healthcare Maintenance • Fluids, Electrolytes, Nutrition: Initially presented with hypoglycemia and was placed NPO. Started on gavage feedings at 3 days of life. Started feeding by mouth by 7 days of life and feeding ad lib by 11 days of life. • Respiratory: Extubated at 4 days of life. Attempts made to wean NC but still required it for discharge. • Discharge: Home at 14 days of age and 43 weeks gestation

  34. Case #2 • Risk Factors: decreased fetal movement for prior 24 hours, fetal heart tones nonreactive, occasional late decelerations during induction, vacuum assisted delivery • Apgars: 1(heart rate noted),4(2-HR, 1-RR, 1-color),5(2-HR, 1-tone, 1-reflex, 1-color), 6(2-HR, 1-RR, 1-tone, 1-reflex, 1-color) • Baby gave initial gasp, followed by no respiratory effort, infant noted to poor tone and very pale in color

  35. Case #2 • Baby was given PPV with good HR response but still minimal respiratory effort noted, so was electively intubated • No spontaneous movement noted until around 9 min. of age when she opened her eyes • Baby brought to NICU for further care

  36. Initial lab results • Cord arterial gas: 7.17/49/35/17/-10 • Cord venous gas: 7.17/75/39/18/-12 • Capillary gas upon immediate admission to NICU: 6.81/72/42/11.4/-23 • Follow-up arterial blood gas: 7.14/13.5/70/4.7/-24 • WBC-37.7, Hgb-3.2, Hct-11.4, Plt-142, Segs-30, Bands-19

  37. Healthcare Maintenance • Neurologic: Baby was electively cooled per policy • EEG obtained showing no seizure activity • MRI obtained after rewarming DOL 4 showing acute focal infarct on the right with no mass effect or associated hemorrhage • Hematologic: She received 3 rounds of PRBC that day • Respiratory: Extubated by 2 days of life. ENT consult done on day 5 of life for stridor and noted moderate bilateral vocal cord paresis • FEN: Gavage feeds started on day 6 of life and baby began orally feeding by day 10 of life • Discharge: home after spending 17 days in the NICU eating all feeds and thriving

  38. Case Study #3 • 3.5 kg 39 5/7 weeks CGA, G3 P23, vag delivery, nuchal cord x2, meconium stained fluid • Delivery: no respiratory effort, no heart rate, and pale so PPV and chest compressions required. Electively intubated with slow improvement. • Initial blood gas pH 6.9, pCO2 90, HCO3 -15

  39. Healthcare Maintenance • Neurologic: Whole body cooling initiated per protocol • EEG was normal • Head US normal • MRI showed left periatrial white matter ischemic changes • Respiratory: Severe pulmonary hypertension, intubated x 16 days, HFOV x 7 days • Cardiovascular: PPHN, hypotension upon rewarming requiring dopamine and dobutamine along with hydrocortisone

  40. Healthcare Maintenance • Infectious: Amp/Gent x 5 days for clinical sepsis and Acyclovir x 48 hours until HSV culture came back negative • Hematologic: Developed DIC, thrombocytopenia, anemia • Renal: mild renal failure with decreased urine output • Discharged at 33 days and 44 3/7 weeks feeding ad lib on demand

  41. Case study #4 • Risk factors: Unplanned pregnancy with no prenatal care, mother admitted to drinking alcohol, delivered at home, • Apgars: Unable to obtain due to delivery at home without medical supervision. • It was noted that infant was delivered into the toilet and had a loose nuchal cord. Nearby person delivered a finger sweep and gave two rescue breaths prior to calling EMS. • He was delivered resuscitation in the ambulance back to the hospital.

  42. Initial lab results • Venous gas at 0920: 7.05/32.5/134/8.8/-20.6 • Extubated to NC and received NS bolus • Follow up gas upon arrival of transport team: 7.14/62/36/22/-7 • WBC 16.9, Hgb 19.7, Hct 56.5, plt 135,000, segs 36, bands 24

  43. Healthcare Maintenance • Neurologic: Baby was electively cooled per policy • Baby was noted to have seizure-like activity - lip smacking, apnea, intermittent tonic posturing of UE>LE, lateral eye deviation, periodic breathing so baby was loaded with phenobarbital • Skull x-ray, Head US and MRI all obtained with all reported within normal limits • Cardiac: Pulmonary hypertension suspected and started on INO 20ppm with good response noted upon initiation

  44. Healthcare Maintenance • Infectious: Treated for with ampicillin/claforan until a positive culture was reported from outlying facility as coag neg staph. Antibiotics were switched to vancomycin and a blood culture was redrawn. Antibiotics were stopped after repeat culture was negative. • FEN: Baby was kept NPO initially with IV fluids of 60ml/kg/day. Gavage feeds started on DOL 5, began oral feeds on DOL 7 and ad lib by 10 days • Discharged home on DOL 12

  45. Avera McKennan’sSummary of TBC infants • Total of 14 patients have received total body cooling since the start in 2011 • 5 Had EEG confirmed seizures • 6 were placed on anti-seizure medications • MRI findings- 4 Showed evidence of HIE • 7 had no signs of HIE • Neurologic assessment upon discharge • 8 had normal exams • 4 had abnormal exams • ***2 infants were electively taken off life support, given the grim outcome**

  46. References • Department of Health, NSW. Whole Body Cooling – Neonates-Suspected Moderate or Severe Hypoxic Ischaemic Encephalopathy. Policy Directive, 28-July 2009. • Fatemi, A., Wilson, M., and Johnston, M. Hypoxic-Ischemic encephalopathy in the term infant. Clinics in Perinatology, 2009; 36: 835-858. • Rajadurai, VS. Therapeutic hypothermia for neonatal hypoxic-ischaemic encephalopathy. Annals Academy of Medicine. 2006; v35, 1: 3-5. • Sahni, R., and Sanocka, U. Hypothermia for hypoxic-ischemic encephalopathy. Clinics in Perinatology; 2008; 35: 717-734. • Schulzke, S., Rao, S., and Patole, SK. A systematic review of cooling for neuroprotection in neonates with hypoxic ischemic encephalopathy-are we there yet? BMC Pediatrics. 2007; 1-10. • Wachtel, E., and Hendricks-Munoz, K. Current Management of the Infant Who presents with Neonatal Encephalopathy. Current Problems in Pediatric Adolescent Health Care. 2011; 41: 132-153.

More Related