Neonatal case presentation on hypoxic ischemic encephalopathy


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hypoxic ischemic encephalopathy

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Neonatal case presentation on hypoxic ischemic encephalopathy

  2. 2. HISTORY 15 days old female baby Mariyam, weighing 2.9kg and K/C of birth asphyxia delievered via LSCS due to breech presentation at 38 weeks of gestation was admitted on 15-9-2013 with C/O  Fits for 1 day  reluctant to feed for 1 day
  3. 3. HISTORY OF PRESENTING COMPLAIN: According to attendent, baby was in usual state of health 1 day back when she started having fits in the morning. Fits were focal and involved either one limb at one time with flickering of eyes and lasting 5-10 secs occuring every 2 to 3 hrs. There was no loss of consciousness, fecal or urinary incontinence and uprolling of eyeballs.There is no history of fever and vomiting .Baby is also reluctant to feed since then.
  4. 4. BIRTH HISTORY     ANTENATAL: It was a fullterm pregnancy and a booked case at some private hospital U/S scan was done twice at 8th and 9th mth Mother had no c/o gestational DM, hypertension,fever,rash or anemia during pregnancy  She took multivitamins and got tetanus toxoid.  NATAL:  Mother underwent LSCS due to breech presentation of baby at 38 wks of gestation.  There is no H/O PROM, preeclampsia or any other maternal complication at birth of baby.     POSTNATAL: Baby had delayed and weak cry. There was peripheral cyanosis.There was no jaundice. Baby had episode of fits half hr after birth.They took the baby to Jinnah hospital and upon their refusal to admit due to lack of incubators, they took the babyto Naseem centre.The baby was admitted there as a case of perinatal asphyxia for 9 days.No fits were observed during this period.Platelets and FFPs were tranfused.Baby was on tanzo and vancomycin and was discharged on 9-9-2013.
  5. 5.  VACCINATION HISTORY: No BCG vaccination done.  FEEDING HISTORY: Baby was kept NPO after birth.Breast feeding was started at 8th day of life and she was taking feed normally. She is reluctant to feed for 1 day.  FAMILY HISTORY: Baby is 5th product of cosanginuous marriage.She has 3 normal siblings.There is no significant family history of any illness.  SOCIOECONOMIC HISTORY:  Their socioeconomic status is average.  They use unboiled water for drinking.
  6. 6. EXAMINATION GENERAL PHYSICAL EXAMINATION  VITALS Heart rate: 142/min Respiratory rate: 48/min Temprature: 98.6F Capillary refill time: <2 sec O2 saturation: 92% RBS: 86mg/dl Anemia: -ve Cyanosis: -ve Jaudice: -ve Dehydration: -ve Edema: -ve  ANTHROPOMETRIC MEASUREMENTS Length: 53.5cm Weight: 2.9 kg FOC: 37.5cm
  7. 7. HEAD TO TOE EXAMINATION  HEAD:       Anterior fontanelle was wide open EYES normal NOSE MOUTH AND PALATE no cleft lip and palate EARS normally placed,no deformity LIMBS normal BACK normal
  8. 8. Systemic examination  RESPIRATORY SYSTEM NVB,equal bilateral air entry  CVS: s1+s2+0  ABDOMEN: soft, nontender, no liver or spleen palpable, gut sounds audible  CNS: Tone increased REFLEXES brisk Moro incomplete Suckig fair Rooting fair Grasping poor
  10. 10. DIFFERENTIAL DIAGNOSIS  Hypoxic ischemic encephalopathy  Meningitis  Sepsis
  11. 11. INVESTIGATIONS CBC 16-9 Hb 19-9 13.3 12.60 MCV 103.8 101.5 MCH 36.4 36.8 MCHC 35,1 35.2 HCT 37,9 38.9 TLC 9400 6200 Neutrophils 47 45 Lymphocytes 33 32 Basophils 0 0 Eosinophils 15 11 298000 371000 Platelets
  12. 12. 16-9 19-9 ELECTROLYTES Na 137 140 K 4.8 4.1 Cl 103 104 11 2 0.5 0.3 BUN Creatinine Total bilirubin 0.31 Direct bilirubin ALP 173 SGPT 150 51 PT control 10.5 test 9.7 INR 0.92 APTT 26.9 Calcium 14.4 CRP 0.30 9.8
  13. 13. CSF DR         AMOUNT: 1.5ml APPEARANCE: clear Ph: 7.3 PROTEIN: 5.3mg% GLUCOSE: 34mg/dl RBCS: 1-2/HPF WBCS: 5/CMM GRAM STAIN: no organism seen CSF CS  No bacterial growth BLOOD CS  no bacterial growth seen
  14. 14.  X-RAY SKULL:  Widening of sutures and anterior fontanelle suggestive of raised ICP      U/S brain: no solid or cystic lesion seen mild hydrocephalus with dilated all 4 ventricles brain edema grade 2 parenchymal and IVH including germinal matrix IMPRESSION:  Grade 2 intracranial hemorrhage  CT SCAN brain:  Extensive white matter edema invlving the subcortical regions of frontal,parietal and temporal lobes causing effacement of  right lateral ventricle.  No hemorrhagic density identified IMPRESSION:  Ischemic encephalopathy involving frontal,parietal and temporal regions.
  16. 16. TREATMENT  Pt was kept NPO initially ,then mother feed was given 2cc 2hrly via        N/G Inj 1/5th in 10% D/S 150cc/kg/day i.e 450cc in 24 hrs Inj cefotaxime 150mg/kg/day i.e 225 mg iv B.D Inj amikacin 15mg/kg/day i.e 22 mg iv B.D Tab phenobarbitone 30 mg ¼+¼ Inj diazepam 0.3mg/kg iv sos Inj Phenytoin 20 mg/kg loading dose i.e 60mg iv stat,then 10mg iv BD in infusion Neb with N/S 6hrly
  17. 17. HYPOXIC ISCHEMIC ENCEPHALOPATHY Hypoxic-ischemic encephalopathy, is characterized by clinical and laboratory evidence of acute or subacute brain injury due to asphyxia. The primary causes of this condition are systemic hypoxemia and/or reduced cerebral blood flow (CBF).
  18. 18. RISK FACTORS
  19. 19. PATHOPHYSIOLOGY  The cerebral blood flow (CBF) of adults is typically maintained at constant levels despite fluctuations in the systemic blood pressure.  In the infant, CBF autoregulation is not as responsive; therefore, when hypoxia occurs, the infant's initial systemic response is to maintain perfusion to the brain and end organs with increased heart rate and the endogenous release of epinephrine.  These measures can only maintain CBF for a short time (minutes), and when the hypoxic state persists, the systemic blood pressure falls and neuronal cells are damaged through progressive intracellular energy failure and eventual cell death via apoptosis.  THIS IS THE FIRST PHASE OF HYPOXIA.
  20. 20.  The second or latent stage of this process, which occurs 6 to 24 hours after the initial insult, is the recovery of cerebral circulation and oxygenation leading to a progression of inflammatory response and significant cerebral edema, onset of seizures, secondary cytotoxic edema, and additional cell death.
  21. 21. INCIDENCE  In the United States and in most developed countries, the incidence of hypoxic-ischemic encephalopathy is 18 cases per 1000 births.  The incidence of hypoxic-ischemic encephalopathy is reportedly high in developing countries.
  22. 22. SIGNS AND SYMPTOMS CNS MANIFESTATIONS  Clinical manifestations and course vary depending on hypoxic-ischemic encephalopathy severity. Mild hypoxic-ischemic encephalopathy  Muscle tone may be slightly increased and deep tendon reflexes may be brisk during the first few days.  Transient behavioral abnormalities, such as poor feeding, irritability, or excessive crying or sleepiness.  The neurologic examination findings normalize by 3-4 days of life.
  23. 23. Moderately severe hypoxic-ischemic encephalopathy  The infant is lethargic, with significant hypotonia and diminished deep tendon reflexes.  The grasping, Moro, and sucking reflexes may be sluggish or absent.  The infant may experience occasional periods of apnea.  Seizures may occur within the first 24 hours of life.  Full recovery within 1-2 weeks is possible and is associated with a better long-term outcome.
  24. 24. Severe hypoxic-ischemic encephalopathy  Stupor or coma is typical. The infant may not respond to any physical stimulus.  Breathing may be irregular, and the infant often requires ventilatory support.  Generalized hypotonia and depressed deep tendon reflexes are common.  Neonatal reflexes (eg, sucking, swallowing, grasping, Moro) are absent.  Pupils may be dilated, fixed, or poorly reactive to light.  Seizures occur early and often and may be initially resistant to conventional treatments. They are usually generalized.  Irregularities of heart rate and blood pressure (BP) are common during the period of reperfusion injury, as is death from cardiorespiratory failure.  Infants who survive severe hypoxic-ischemic encephalopathy;  The level of alertness improves by days 4-5 of life.  Hypotonia and feeding difficulties persist, requiring tube feeding for weeks to months.
  25. 25. DIAGNOSIS  Serum electrolyte levels  Renal function studies  Cardiac and liver enzymes - These values are an adjunct to assess the degree of hypoxic-ischemic injury to the heart and liver  Coagulation system - Includes prothrombin time, partial thromboplastin time, and fibrinogen levels  Arterial blood gas - Blood gas monitoring is used to assess acid-base status and to avoid hyperoxia and hypoxia, as well as hypercapnia and hypocapnia
  26. 26.  Cranial ultrasonography Findings include global increase in cerebral echogenicity and obliteration of cerebrospinal fluid (CSF) containing spaces suggestive of cerebral edema.  Head CT scanning A CT scan of the head shows cerebral edema, manifested as narrowness of the lateral ventricles and flattening of gyri. Areas of reduced density that indicate evolving zones of infarction may be present. Evidence of hemorrhage in the ventricles or in the cerebral parenchyma may also be seen.
  27. 27.  Brain MRI MRI is the imaging modality of choice for the diagnosis and follow-up of infants with moderate-tosevere hypoxic-ischemic encephalopathy (HIE). Demonstrates the injury pattern as area of hyperintensity  Amplitude-integrated electroencephalography (aEEG) aEEG performed within a few hours of birth can help evaluate the severity of brain injury in the infant with hypoxic-ischemic encephalopathy.
  28. 28. MANAGEMENT Initial management  1. Transfer the baby to special care newborn unit. A baby who fails to initiate and sustain respiration at birth is at risk of hypoxic brain injury and needs regular monitoring. All these babies should have a cord gas analysis performed. Infants with moderate asphyxia (Apgar score 4-6 at 1 minute of age) may be transferred to the mother. However, these infants should also be monitored frequently in the first 48-72 hours for features suggestive of HIE. Infants with severe asphyxia (Apgar score 0-3 at 1minute or need for prolonged bag and mask ventilation >5 minutes) should be transferred to a special care newborn unit for observation and treatment.  2. Maintain temperature Place the baby under the radiant warmer after drying the baby.
  29. 29.  3. Check vital signs Immediate clinical assessment should be made by recording respiration, heart rate, blood pressure, capillary refill time, temperature and oxygen saturation. Urine output monitoring should be done.  4. Start intravenous fluids  5. Check blood sugar, hematocrit and blood gases. Check blood sugar (to detect hypoglycemia or hyperglycemia), hematocrit (to detect anemia and polycythemia) and blood gases (to detect metabolic acidosis, hypoxia,hyperoxia and respiratory failure).  6. Consider infusion of volume expander If the capillary refill time is more than 3 seconds or if there is metabolic acidosis, volume expansion with normal saline (or Ringer’s lactate) 10 ml/kg over 5-10 min should be instituted. This may be repeated.Maintain the mean BP above 35 mm Hg (for term infants). Dopamine or dobutamine can be used to maintain adequate cardiac output.
  30. 30. SUBSEQUENT TREATMENT a) Maintain oxygenation and ventilation. b) Maintain adequate perfusion: Use saline, Ringer’s lactate and blood to maintain intravascular volume. c) Vasopressors: Dopamine and dobutamine are the drugs of choice. d) Maintain normal blood glucose e) Treat seizures: The anticonvulsant of choice for controlling seizures is phenobarbitone.The initial dose is 20 mg/kg, intravenously slowly over 20 minutes.Two additional doses of 10 mg/kg can be given every 15 minutes. The maximum loading dose is thus 40 mg/kg. If convulsions are still uncontrolled, phenytoin sodium should be added in a dose of 20 mg/kg intravenously slowly over 20 minutes. Maintenance therapy of both phenobarbitone and phenytoin is started 12 hours later in a dose of 5 mg/kg/day in a single dose. For intractable seizures Clonazepam, Midazolam, Paraldehyde, and Valproate may be tried. f)One promising modality on the horizon is cerebral hypothermia.Mil dreductions in temperature of the body as a whole or of the head (brain) has been shown to minimize the effects of hypoxic ischemic encephalopathy.
  31. 31. DIET In most cases (particularly in moderately severe and severe hypoxic-ischemic encephalopathy), the infant is restricted to nothing by mouth (NPO) during the first 3 days of life or until the general level of alertness and consciousness improves. In addition, infants undergoing hypothermia therapy should remain NPO until rewarmed. Enteral feeds should be carefully initiated about 5 mL every 3-4 h.
  32. 32. PROGNOSIS  In severe hypoxic-ischemic encephalopathy, the mortality rate is 25-50%. Most deaths occur in the first week of life due to multiple organ failure or . Some infants with severe neurologic disabilities die in their infancy from aspiration pneumonia or systemic infections.  The incidence of long-term complications depends on the severity of hypoxicischemic encephalopathy.  80% of infants who survive severe hypoxic-ischemic encephalopathy develop serious complications, 10-20% develop moderately serious disabilities, and 10% are healthy.  Among the infants who survive moderately severe hypoxic-ischemic encephalopathy, 30-50% may have serious long-term complications, and 1020% have minor neurological morbidities.  Infants with mild hypoxic-ischemic encephalopathy tend to be free from serious CNS complications  Complications include • Cerebral palsy - 30% • Epilepsy - 16% • Blindness - 14-17% • Severe hearing impairment - 6
  33. 33. THANK YOU