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TRAUMATIC DELIVERIES

TRAUMATIC DELIVERIES. Caring for the Newborn. Adam A. Rosenberg, MD Professor of Pediatrics UC Denver. Financial disclosure. I have no relevant financial disclosures to make regarding this presentation. Traumatic Deliveries. Traumatic injuries Hypoxic injuries. Traumatic Injuries.

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TRAUMATIC DELIVERIES

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  1. TRAUMATIC DELIVERIES Caring for the Newborn Adam A. Rosenberg, MD Professor of Pediatrics UC Denver

  2. Financial disclosure I have no relevant financial disclosures to make regarding this presentation

  3. Traumatic Deliveries • Traumatic injuries • Hypoxic injuries

  4. Traumatic Injuries

  5. SHOULDER DYSTOCIA Watch for the “turtle sign”!

  6.  3000 g 0 3001 - 3500 0.3 3501 - 4000 1.0 4001 - 4500 5.4 > 4500 19.0 all weights 0.9 Fetal Macrosomia Diabetes Obesity Post-term pregnancy Prior shoulder dystocia SHOULDER DYSTOCIAIncidence and Risk Factors • REPORTED INCIDENCE: 0.9 - 1.4 % • (~ 0.6% require special maneuvers to deliver shoulders) • INCIDENCE BY BIRTHWEIGHT RISK FACTORS %

  7. PREVENTION OF SHOULDER DYSTOCIA and its consequences “Now you see me... • Awareness of risk factors • Prompt recognition of the shoulder dystocia “Retraction of the fetal head immediately on its delivery (the turtle sign) is an early warning that delivery of the shoulder will be difficult” …Now you don’t” • Avoidance of excessive downward traction of the fetal head

  8. SHOULDER DYSTOCIAPotential Neonatal Injuries/Morbidities • Birth Asphyxia • Traumatic Injuries (~ 25%) • Fracture of the humerus - 17% • Fracture of the clavicle - 38% • Brachial plexus injury - 65% • Neonatal Death

  9. SHOULDER DISTOCIA SHOULDER DISTOCIA CLAVICULAR FRACTURE CLAVICULAR FRACTURE Fracture of Fracture of Congenital Congenital Clavicle Clavicle Pseudarthrosis Pseudarthrosis

  10. SHOULDER DYSTOCIABRACHIAL PLEXUS INJURY • ETIOLOGY: downward lateral traction of the head and neck away from shoulder  traumatic injury to cervical nerve roots • INJURIES: • Least severe: Neuropraxic • Intermediate: Neurotmesis • Most severe: Avulsion • CLINICAL FORMS: • Duchenne - Erb paralysis (upper arm) C5- C6 ~ 70 - 80% • Klumpke paralysis (lower arm) C7 - T1 ~ Rare (<5%) • Entire arm paralysis C5 - T1 ~ 20 - 25% Erb palsy

  11. SHOULDER DISTOCIABRACIAL PLEXUS INJURY • PHRENIC NERVE INJURY: C4 diaphragmatic paralysis • HORNER SYNDROME: Cervical sympathetic fibers of T1 (ptosis, miosis, enophthalmos) • PROGNOSIS: severity of injury • The faster the recovery, the more complete the functional return • More favorable in shoulder dystocia • Better for upper arm paralysis • Poor for lower arm paralysis • 80% recovery by 4 months 93% recovery by 18 - 24 months “waiter’s tip” position

  12. FORCEPS DELIVERY “The Mark of the Zorro”

  13. FORECPS DELIVERY Potential Injuries • Skull fractures • Cephalohematomas Subgaleal hemorrhage • Injuries to the orbit • Trauma to the nose • Fractures of facial bones • Facial palsy • Intracranial hemorrhages • Soft tissue injuries

  14. FORCEPS DELIVERYSkull fractures Linear Comminuted

  15. FORCEPS DELIVERYDepressed Skull Fracture Plain Skull X-ray CT Scan

  16. FORCEPS DELIVERY Injuries to the Orbit • Fracture base of the orbit • Intraorbital hemorrhage (Traumatic hyphema) • Corneal laceration • Break of Descemet’s membrane (Corneal opacification) Intraorbital hemorrhage

  17. FORCEPS DELIVERY ANDOCULAR INJURIESBreaks in Descemet’s Membrane • The most common cause of corneal trauma leading to partial or total CORNEAL OPACIFICATION • Slit lamp examination shows linear breaks, usually vertically • Breaks  stromal and epithelial edema central opacities • Amblyopia and astigmatism need to berecognized early • There is always visual loss (severe)

  18. FORCEPS DELIVERYTrauma to the nose Dislocated Septum & Fracture Nasal Bone Flattening

  19. FORCEPS DELIVERYFacial Palsy A B

  20. Incidence of Facial Palsy by Delivery Route No. Of Facial Palsies Type of delivery No. Of deliveries Incidence Natural 159 10 6.3% Forceps** 716 46 6.4% *Adapted from Hepner. 68 ** Not further characterized re: low, mid, high. etc.

  21. FACIAL PALSY Relation of Side of Facial Paresis to Intrauterine Position Side of Facial Paresis No. Of Infants Type of Delivery Intrauterine Position 6 Natural Left Occiput left transverse 4 Natural Right Occiput right transverse 34 Forceps Left Occiput left transverse or anterior 12 Forceps Right Occiput right anterior, transverse or posterior Adapted from Hepner. 68

  22. FORCEPS DELIVERY Intracranial Hemorrhage Subdural Posterior fossa

  23. Venous Drainage of the Brain

  24. Subdural Bleeds • Posterior fossa hematoma due to tentorial laceration with rupture of vein of Galen, straight sinus or transverse sinuses • Falx laceration with inferior sagittal sinus rupture • Tear of bridging cerebral veins

  25. Subdural Bleeds: Clinical Signs • Posterior fossa bleeds lead to brainstem compression with lateral eye deviation, unequal pupils, apnea and bradycardia • Other sites present with seizures, irritability and focal neurologic signs

  26. VACUUM DELIVERY You’d better watch out!

  27. VACUUM DELIVERY Potential Head Injuries • Scalp marking (ecchymosis) • “Chignon” or artificial caput • Scalp abrasions/laceration • Hemorrhagic caput • Cephalohematoma • SUBGALEAL HEMMORRHAGE • Retinal hemorrhages • INTRACRANIAL BLEEDING

  28. VACUUM EXTRACTION Scalp trauma Soft tissue and bone deformity “Chignon”

  29. VACUUM EXTRACTION Scalp trauma Abrasion Laceration

  30. SUBGALEAL HEMORRHAGE (SGH) associated with VACUUM EXTRACTION

  31. Sites of Cranial Bleeding

  32. SUBGALEAL HEMORRHAGE The danger arises because the subaponeurotic space stretches over the whole of the cranial vault, and a large proportion of the baby’s blood volume may accumulate in this space from damage to emissary veins.

  33. SUBGALEAL HEMORRHAGE Hemorrhage into the subgaleal space may occur over several hours following delivery and unless careful observations are made, the bleeding may not become obvious until the hematoma is extensive.

  34. Subgaleal Hemorrhage Diagram of Subgaleal orSubaponeurotic Hemorrhage Clinical Appearance of Subgalealor Subaponeurotic Hemorrhage Ref: Advances in Neonatal Care, Vol 1, No 1 (October), 2001: pp 22-27

  35. VACUUM EXTRACTION AND SUBGALEAL HEMORRHAGE Important Facts • SGH is almost always preceded by difficult extraction, prolonged traction and multiple attempts • There is little doubt that the experience of the operator is a major determinant of the success or failure of VE • With anticipation, early recognition and appropriate management most severe forms of SGH are likely to recover without neurodevelopment impairment

  36. SUBGALEAL (SUBAPONEUROTIC) HEMMORRHAGE - SGH “ A potentially life-threatening condition”

  37. Management of Subgaleal Bleed • Immediate placement of central access (UAC, UVC) • Aggressive replacement of volume loss (NS, Blood, Clotting factors) • Anticipate 40 ml blood loss for each 1 cm increase in OFC • Monitor hct, coags, I&O, blood pressure • Supportive care: oxygenation, correct acidemia etc.

  38. Perinatal Asphyxia Neonatal encephalopathy

  39. Risks for Newborn Encephalopathy • Abnormal placenta • Family history of seizures, neurologic disease • Viral illness • Antepartum bleeding • IUGR • Intrapartum fever • Infertility treatment • Thyroid disease

  40. Essential Criteria: Perinatal Asphyxia • Metabolic acidemia in fetal UA; pH < 7.00 or BD > 12 mmol/L • Early onset of neonatal encephalopathy • Cerebral palsy of spastic quadriplegia or dyskinetic type • Exclusion of other etiologies

  41. Supporting Criteria: Perinatal Asphyxia • Sentinel event; eg: abruption • Sudden severe fetal bradycardia, absent variability, late decelerations • Apgar < 3 at 5 minutes • Multiorgan involvement • Nonfocal brain injury on scans

  42. Clinical Sequelae of Perinatal Asphyxia • Hypoxic/ischemic encephalopathy • Respiratory distress due to aspiration, surfactant deficiency and/or PPHN • Myocardial failure with hypotension • Acute tubular necrosis with anuria or oliguria • Feeding intolerance; NEC • Liver injury with elevated transaminases • Disseminated intravascular coagulation • Hypocalcemia; hypoglycemia

  43. Hypoxic Ischemic Encephalopathy • Incidence: 2-6/1000 live births • Clinical syndromes: • Mild: alterations in level of consciousness, hyperalert, hyperreflexic, jittery, dilated pupils • Moderate: lethargy, hypotonia, weak suck, poor Moro, seizures, miosis • Severe: stupor, hypotonia, absent suck and Moro, seizures, small midposition pupils

  44. HIE: Late Clinical Features • persistent, but diminished stupor • disturbed suck, swallow, gag and tongue movements • hypotonia • proximal limb weakness more prominent in the upper extemities

  45. HIE: Late Sequelae • Cerebral palsy • Seizure disorders • Cognitive deficits

  46. Cerebral Palsy • incidence: 2 per 1000 live births • 9-23% felt to be due to perinatal asphyxia • incidence is increased 25 fold at < 1500g • no change in incidence despite obstetric advances • antepartum factors without perinatal asphyxia can lead to cerebral palsy

  47. Asphyxia: Outcome Predictors • Severity of hypoxic-ischemic encephalopathy • Refractory seizures • Markedly abnormal EEG • Hypodense areas on CT scan • Early diffusion weighted MRI

  48. EEG in Perinatal Asphyxia • Decreased amplitude (suppression) and frequency • Periodic pattern and/or multifocal or focal sharp wave activity • Periodic pattern with fewer bursts and more voltage suppression (burst suppression) • Isoelectric • 1 lead integrated EEG (cfm) also can be used to identify high risk groups rapidly

  49. Staging of HIE

  50. Staging of HIE

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