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Pedatrics morbidity and mortality nov 2021 aaron
- 1. PEDIATRICS MORTALITY AND MORBIDITY FORNOVEMBER 2021 PRESENTED BY: DR. KEMBOI K. A. MEDICAL OFFICER INTERN LONGISA COUNTY REFERRAL HOSPITAL 2ND DECEMBER, 2021
- 2. Pediatrics Medical ward •ADMISSIONS-88 • MORTALITIES -1 • REFERRALS - 3
- 3. • ADMISSION BYDIAGNOSIS • Pneumonia – 34 (39%) • Anemia -10 (11%) • GE – 9 (10%) • Meningitis- 6 (6%) • Opp poisoning-6 (6%) • Datura poisoning- 4 (4.5%) • Malnutrition – 3 (3.4%) • CHD- 3 (3.4%) • Ascariasis-3 (3.4%) • Convulsive disorder-3 (3.4%) • Cerebral palsy-2 (2.4%) • Sepsis-2 (2.4%) • Tonsilitis-2 (2.4%) • HIV-2 (2.4%) • PTB-2 (2.4%) • CCF-1 (1.1%)
- 4. REFERRALS- 3 (3.4%) •MC 4 Years old female Dx- S.anaemia/pancytopenia • DC 11years female Dx- S.anemia/lymphoproliferative disorder • IK 2 months old Dx- CHD/pneumonia
- 5. Mortality- 1 (1.1%) •IK, 7months, Male dx: Severe pneumonia passed on day 3 of admission to the ward in HDU. D.O.A: 15/11/2021
- 6. NBU • Admissions –81 • Mortalities – 15 • Referrals - 2
- 7. • Admission bydiagnosis • Birth Asphyxia – 29 (32%) • Prem/LBW – 34 (37%) • N. sepsis – 23 (28%) • N. Jaundice – 7 (8.6%) • RDS-6 (7.4%) • SGA – 1 (1.2%) • Meconium aspiration -1 (1.2%) • Disorders of breast and lactation- 1 (1.2%) • Hydrocephalus-1 (1.2%) • Club foot- 1 (1.2%) • Pyloric stenosis-1 (1.2%) • Urinary tract malformation-1 (1.2%)
- 8. REFERRALS- 2(2.5%) • SC14 days old female Dx- pyloric stenosis • JC 8days old female Dx- urinary tract malformations
- 9. Mortality cases NBU-15 (18.5%) 1. Severe birth asphyxia- 7(8.6%) 2. Prematurity/LBW-5(6.1%) 3. Neonatal sepsis- 3(3.7%)
- 10. Mortality • B`LC 2days old, Term Born via EMCS at longisa, BWT 2375grams hosp dx: neonatal sepsis/Hemolytic disease of newborn passed on day 2 of admission to the NBU. D.O.A: 9/11/2021. • B`GK 1 day old, Term Born SVD at peripheral facility, BWT 1050grams dx: birth asphyxia/prem/VLBW passed on the day of admission to the NBU. D.O.A:10/11/2021. • B`HTi 26 days old, Born EMCS at hosp, BWT 1235grams dx: Prem/VLBW/NNS passed on the day 26 of admission to the NBU. D.O.A:14/10/2021 • B`SY 2 days old, Born Preterm at 22/40GBD SVD at hosp, BWT 665grams dx: Prem/ELBW passed on the day 2of admission to the NBU. D.O.A:15/11/2021 • B`NC 1 day old, Born Preterm at 28/40GBD SVD at home,, BWT 912grams dx: Prem/ELBW passed on the day of admission to the NBU. D.O.A:17/11/2021
- 11. • B`SK 1day old, Born at term SVD at hosp, BWT 2312grams, apgar score of 4,5,6 dx: moderate birth asphyxia passed on the day of admission to the NBU. D.O.A:20/11/2021 • B`JC 1 day old, Born Preterm at 25/40GBD SVD at hosp,, BWT 822grams dx: Prem/ELBW passed on the day of admission to the NBU. D.O.A:20/11/2021 • B`CK 1 day old, Born at term SVD at hosp, BWT 2800grams, apgar score of 2,4,4 dx: severe birth asphyxia passed on the day of admission to the NBU. D.O.A:20/11/2021 • B`MC 12 days old, Born SVD at hosp, BWT 1335grams dx: Prem/VLBW/NNS passed on the day 12 of admission to the NBU. D.O.A:10/11/2021 • B`MC 1 day old, Born at term EMCS at hosp, BWT 3450grams, apgar score of 2,2,2 dx: severe birth asphyxia passed on the day of admission to the NBU. D.O.A:24/11/2021
- 12. • B`BC 1day old, Born at term SVD at hosp, BWT 3345grams, apgar score of 3,4,5 dx: severe birth asphyxia passed on the day of admission to the NBU. D.O.A:25/11/2021 • B`DL 1 day old, Born at term EMCS at hosp, BWT 3585grams, apgar score of 3,4,4 dx: severe birth asphyxia passed on the day of admission to the NBU. D.O.A:26/11/2021 • B`AK 2 days old, Born SVD at peripheral hosp, BWT 1390grams dx: Prem/VLBW/RDS passed on the day 2 of admission to the NBU. D.O.A:26/11/2021 • B`BK 2 days old, Born preterm SVD at hosp, BWT 1345grams dx: NNS/ Prem/VLBW passed on the day2 of admission to the NBU. D.O.A:26/11/2021 • B`MC 1 day old, Born at term SVD at hosp, BWT 3760grams, apgar score of 2,3,4 dx: severe birth asphyxia passed on the day of admission to the NBU. D.O.A:27/11/2021
- 13. CASE PRESENTATION • NAME:B`BC • SEX: M • AGE : 1 DOL • BWT: 3345g • DOA: 25/11/2021 • Presenting complain- did not cry immediately after birth
- 14. HPI • Baby BCborn at term to para 7+0 34 year old mother SVD at labor ward, birth weight of 3345grams. He did not cry immediately after birth Apgar score of 3 in 1 minute, 4 in 5 minutes and 5 in 10minutes. • FMSHx- 7th born to a 34 YEAR OLD MOTHER. Siblings alive and well. Father and mother live together, casual laborers. No hx of previous complications in pregnancy. • Birth hx – ANC- mother attended clinic 3 times starting at 14/40 GBD, Was started IFASS supplements and had no complication during pregnancy. ANC profile- blood group O, rhesus positive, VDRL- negative, HIV-non-reactive, urinalysis-nad.
- 15. Examination • GENERAL EXAM-sick looking, in respiratory distress with gasping respirations on oxygen via nasal prongs 2l/min, weak cry, no pallor, no jaundice, no dehydration, no cyanosis, no edema. • Vitals: RR-34, Temp- 36.9degrees celcius • Head to Toe examination:–Head normal shape, HC-35cm, ant & post fontanel not Bulging, ENT normal. Resp exam: RR-34, gasping, FAN++, lower chest wall in drawing, auscultation clear. CVS exam: S1, S2 heard, no murmur. Cord clean. Abdomen not distended. Reflexes: weak suck, weak grasp, no rooting reflex. Extremities and back normal No congenital anomaly found. • Other systems essentially normal.
- 16. • LAB WORKUPS •FHG: WBC- 12, neutrophilia- 76%, HB- 17.9 plt-210 • RBS-7.7mmol/l
- 17. • Further Investigationswe would have wanted to do: • CRP/PROCALCITONIN • Blood culture and sensitivity • Blood gas analysis Imp: Severe birth asphyxia
- 18. management • IV- Benzylpenicillin125000iu and Gentamicin 8mg • Kept NPO and IVF- D10 60mls/kg • Oxygen via nasal prongs • Aminophylline loading dose 6mg/kg and maintenance-3mg/kg. OUTCOME- • Baby`s condition deteriorated on day of admission and noted to have gasping respirations RR-16 breaths per minute with low heart rate of 50 beats per minute. Resuscitation started and continued for 30 minutes but was not successful. Mother was informed and counselled about the outcome.
- 19.
- 20. DEFINITION • The simpledefinition of asphyxia at the time of delivery is “failure to initiate breathing soon after birth and need for assistance to initiate breathing”. • In HIE, the brain injury is caused by a deficit in oxygen supply. This can occur by Hypoxemia - a decrease in oxygen saturation in the blood supply, or Ischaemia - a decrease in the amount of blood perfusing the brain or both processes. • It can occur prepartum, intrapartum or immediately postpartum; hence the terms ‘birth asphyxia’ or ‘perinatal asphyxia’ should be avoided. The terminology NE is preferred to Hypoxic Ischemic Encephalopathy (HIE). • Neonatal Encephalopathy (NE) is a clinical syndrome of disturbed neurological function, caused by failure to make a successful transition to extrauterine gas exchange • Other aetiologies such as CNS malformation, infection, multiple gestation, IUGR, maternal autoimmune disorders, metabolic disorders, drug exposure, and neonatal stroke as possible causes of the encephalopathy • Manifests in a difficulty in initiating and maintaining spontaneous respiration, depression of muscle tone and reflexes, depressed consciousness and often seizures.
- 21. • Occurs in3.5 - 6/1000 live births; usually affects full term infants. • Causes of Neonatal Mortality Infection 32% Birth Asphyxia 29% Complications of Prematurity 24% Congenital Anomalies 10% Other 5% ESSENTIAL CHARACTERISTICS TO MAKE A DIAGNOSIS OF INTRAPARTUM ASPHYXIA defined jointly by the AAP and the ACOG include 1. Umbilical arterial cord pH <7.0 or base deficit >12 mmol/L or both. 2. Apgar score <5 for more than 5 minutes 3. Neuroimaging evidence of brain injury: Brain injury seen on MRI consistent with acute hypoxic ischemia. 4. Evidence of multi organ dysfunction (e.g. CNS, renal)
- 22. Etiology • Risk factorsfor neonatal encephalopathy were mainly seen in the antenatal period (69%) as compared to the intrapartum period (25%) in a large Western Australian study. Only 4% were due to intrapartum hypoxia. • Etiology is divided into maternal , placental , umbilical ,fetal and neonatal factors. • Maternal factors - chronic hypertension ; pulmonary disorder causing hypoxia eg hypoventilation during anesthesia , respiratory failure or carbon monoxide poisoning ; low maternal blood pressure from acute blood loss , spinal anesthesia or compression of the vena cava and aorta by the gravid uterus ;uterine tetany causing inadequate relaxation of the uterus to allow placental filling as in oxytocin overdose. 12/5/2021 Steven Akach_Med VI
- 23. Etiology (Causes) • Placentalfactors - abruption , infection , placental insufficiency from toxiemia or postmaturity. • Umbilical cord accidents – cord around the neck , compression , knotting. • Fetal factors – infection, severe anemia , cardiac abnormalities. • Neonatal factors(occur after birth) – congenital heart disease , septicemia with shock ,severe anemia from hemorrhage or hemolysis ,severe pulmonary disease. 12/5/2021 Steven Akach_Med VI
- 24. Neonatal Evaluation ASSESSING ENCEPHALOPATHY •The Thompson scoring system is used to classify the severity of the encephalopathy. • The Sarnat and Sarnat Staging system • APGAR Scoring- AAppearance P Pulse G Grimace AActivity R Respirations Take the APGAR score at one minute and five minutes. • APGAR Score of 7-10 points - The newborn should be active and vigorous. Provide routine care. 4-6 points - The newborn is moderately depressed. Provide stimulation and oxygen. 0-3 points - The newborn is severely depressed and requires extensive resuscitation. • Apgar Score- Total Score = 10 score 7-10 normal score 5-6 mild birth asphyxia score 3-4 moderate birth asphyxia score 0-2 severe birth asphyxia
- 25. Document the Thompsonscore at admission and daily until discharge from the unit. A Thompson score ≥ 7 is useful in predicting moderate to severe HIE thereby facilitating decision making for TH. A score ≥ 11 is an indication for possibly initiating TH. The time at which neurological findings have normalised, and normal newborn reflexes are obtained, determine long-term prognosis and need to be well-documented.
- 26. Clinical Presentation (NationalGuidelines) Steven Akach_Med VI 12/5/2021
- 27. INVESTIGATIONS • FBC andblood culture at birth to exclude infection. • U&E, Cr around 24 hours of life to check for renal function and electrolyte abnormalities, mainly hyponatraemia. • Serum glucose, calcium, magnesium and phosphate if having seizures (hypomagnesaemia tends to occur on the first day, whereas hypocalcaemia tends to occur on day 2-3 of life). • Lumbar puncture in infants with moderate or severe encephalopathy.. • LFTs (in those with jaundice) and cardiac enzymes (in those with hypotension/ tachycardia) may be required. Discuss the need for these with a consultant first. • Cranial Ultrasound To exclude haemorrhage and other intracerebral abnormalities. • Brain CT scan To exclude haemorrhage, cerebral oedema and other intracerebral abnormalities. May assist with prognosis. Extensive areas of low attenuation with apparent brightness of basal ganglia are associated with very poor prognosis (done after 1st week of life). • Brain MRI -MRI may provide prognostic information. Thalamic, basal ganglia abnormalities are associated with a risk of abnormal neuro-developmental outcome. Superior to CT scans. • Amplitude intergrated Electroencephalogram (aEEG) Overall risks for death or disability were 95% for a severely abnormal aEEG, 64% for a moderately abnormal aEEG and 3 % for a normal or mildly abnormal aEEG.
- 28. MANAGEMENT Principles of Management •Resuscitation • Supportive therapy • Anticonvulsants • Neuroprotective interventions • Monitoring
- 29. RESUSCITATION • For resuscitationto be effective, there must be availability of well trained personnel, good communication between paediatricians and obstetricians for early identification of high risk babies and readiness for resuscitation as the need arises. • The ABCD of resuscitation is : Establish patent airway, Initiate breathing, Maintain circulation, Drugs. • Ensure effective airway and ventilation. • Ensure good circulation, offer circulatory support if needed.
- 30. Supportive therapy • Avoidhyperthermia that may be associated with adverse outcome • Vital sign monitoring. Monitoring of blood gases, urine output, blood sugar and electrolytes. • Maintain normoglycaemia, both hypo- and hyperglycemia can be harmful. • Maintain normal Blood Pressure. If necessary, consider use of inotrope infusion rather volume expander unless there is hypovolaemia. • Review infection risk and cover with antibiotics if necessary • Maintain adequate hydration (do not dehydrate or over hydrate). • Mechanical ventilation to maintain normocarbia
- 31. Anticonvulsants • Monitor forthe development of seizures and treat convulsions promptly if they develop. • If the infant starts fitting give Phenobarbital 20mg/kg as a loading dose, followed by a second and third dose of 10 mg/kg if no response. Start maintenance Phenobarbital if the infant has more than one episode of convulsions • If convulsions continue, give one of the following drugs, one at a time and reassess:Keppra, Phenytoin, Lorazepam (Ativan), Midazolam (Dormicum) or Rivotril (Clonazepam). Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for refractory seizures. • seizures may be caused by hypoglycaemia or hypocalcaemia. • seizures, including asymptomatic electrographic seizures, may contribute to brain injury and increase the risk of subsequent epilepsy
- 32. NEUROPROTECTIVE INTERVENTIONS • HYPOTHERMIA-Therapeutic hypothermia attenuates secondary energy failure by decreasing the following: Cerebral metabolism, Inflammation, Excitotoxicity, Oxidative damage and Cellular apoptosis. • Free radical inhibitors such as allopurinol. • Prophylactic use of calcium channel blockers • Magnesium an N-methyl-D-aspartate (NMDA) glutamate receptor antagonist • Erythropoietin. • There is some clinical evidence that high-dose prophylactic phenobarbital may decrease neurodevelopmental impairment in infants with HIE but it’s role remains unclear.
- 33. Treat other systemiccomplications that arise • Renal. Acute tubular necrosis. If oliguria with urine output < 1ml/kg/hr, check for prerenal cause and treat accordingly. If in established renal failure, restrict fluid and maintain normal electrolyte levels. • Cardiac. Hypoxic damage to myocardium with cardiogenic shock and failure. Use of inotropes and careful fluid balance. • Lungs. Persistent Pulmonary Hypertension (PPHN). See relevant chapter on PPHN • Gastrointestinal. Stress ulcers, feed intolerance, necrotizing enterocolitis. Enteral feeding is preferable to parenteral but avoid rapid increase in volume of feeds to decrease risk of necrotizing enterocolitis. • Haematology. Disseminated Intravascular Coagulation. Correct coagulopathy as indicated. • Others. SIADH, hypoglycaemia, hypocalcaemia, and hypomagnesaemia. Restrict fluids in SIADH. Correct hypoglycaemia and electrolyte imbalances
- 34. Follow up • Counselparents: Start early and involve them in care as much as possible. Teach them how to recognize a convulsion. As the baby recovers plan for discharge and long term follow up according to complications • All infants with NE should be followed up to look for development and neurological problems. • Consult allied health workers (speech therapists, physiotherapists and occupational therapists) so that they can be involved early in management. • LONG TERM HANDICAPS: developmental delay, cerebral palsy, microcephaly, seizures, blindness, deafness, problems with cognition, memory, fine motor skills, and behaviour.
- 35. Prognosis Depends on severityof hypoxia and timing of intervention • Mild (7-10) • 98-100% normal neurological outcome • Moderate(11-14) • 20-40% die/abnormal neuro outcome • Signs >7 days have poorer outcome • Severe(15-22) 40-50% die – All survivors have major neurodevelopment impairment. • Cardiac, GIT, pulmonary, hepatic & hematological problems usually resolve if the infant survives except the KIDNEY 12/5/2021 Steven Akach_Med VI
- 36. PREVENTION • Recognition ofhigh risk pregnancies. • Adequate antenatal monitoring during pregnancy and labour (CT, fetal scalp pH). • Good communication between the Obstetrician and Paediatrician at the peripartum period. • Efficient resuscitation at birth. • Institution of therapeutic hypothermia within 6 hours of birth.
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