SHOULDER DYSTOCIA Incidence and Risk Factors 3000 g 0 3001 - 3500 0.3 3501 - 4000 1.0 4001 - 4500 5.4 > 4500 19.0 all weights 0.9 Fetal Macrosomia DiabetesObesity Post-term pregnancy Prior shoulder dystocia REPORTED INCIDENCE: 0.9 - 1.4 % (~ 0.6% require special maneuvers to deliver shoulders) (~ 0.6% require special maneuvers to deliver shoulders) INCIDENCE BY BIRTHWEIGHTRISK FACTORS INCIDENCE BY BIRTHWEIGHT RISK FACTORS %
PREVENTION OF SHOULDER DYSTOCIA and its consequences Awareness of risk factors Awareness of risk factors Prompt recognition of the shoulder dystocia shoulder dystocia “Retraction of the fetal head immediately on its delivery (the turtle sign) (the turtle sign) is an early warning that delivery of the shoulder will be difficult” Avoidance of excessive downward Avoidance of excessive downward traction of the fetal head traction of the fetal head “Now you see me... …Now you don’t”
SHOULDER DYSTOCIA Potential Neonatal Injuries/Morbidities Birth Asphyxia Birth Asphyxia Traumatic Injuries (~ 25%) Fracture of the humerus - 17%Fracture of the humerus - 17% Fracture of the clavicle - 38%Fracture of the clavicle - 38% Brachial plexus injury - 65%Brachial plexus injury - 65% Neonatal Death Neonatal Death
SHOULDER DISTOCIA CLAVICULAR FRACTURE Fracture of Clavicle Congenital Pseudarthrosis
SHOULDER DYSTOCIA BRACHIAL PLEXUS INJURY ETIOLOGY: downward lateral traction ETIOLOGY: downward lateral traction of the head and neck away from shoulder of the head and neck away from shoulder traumatic injury to cervical nerve roots traumatic injury to cervical nerve roots INJURIES: Least severe: Neuropraxic Intermediate: Neurotmesis Most severe: Avulsion Erb palsy CLINICAL FORMS: CLINICAL FORMS: Duchenne - Erb paralysis (upper arm) Duchenne - Erb paralysis (upper arm) C 5 - C 6 ~ 70 - 80% C 5 - C 6 ~ 70 - 80% Klumpke paralysis (lower arm) C 7 - T 1 ~ Rare (<5%) C 7 - T 1 ~ Rare (<5%) Entire arm paralysis C 5 - T 1 ~ 20 - 25% C 5 - T 1 ~ 20 - 25%
SHOULDER DISTOCIA BRACIAL PLEXUS INJURY PHRENIC NERVE INJURY: C 4 diaphragmatic paralysis diaphragmatic paralysis HORNER SYNDROME: Cervical sympathetic fibers of T 1 sympathetic fibers of T 1 (ptosis, miosis, enophthalmos) (ptosis, miosis, enophthalmos) PROGNOSIS: severity of injury The faster the recovery, the more complete the functional return 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 93% recovery by 18 - 24 months “waiter’s tip” position
FORCEPS DELIVERY Fracture base of the orbit Intraorbital hemorrhage (Traumatic hyphema) (Traumatic hyphema) Corneal laceration Break of Descemet’s membrane (Corneal opacification) (Corneal opacification) Injuries to the Orbit Intraorbital hemorrhage
FORCEPS DELIVERY AND OCULAR INJURIES Breaks 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 Amblyopia and astigmatism need to be recognized early There is always visual loss (severe)
FORCEPS DELIVERY Trauma to the nose FORCEPS DELIVERY Trauma to the nose Flattening Dislocated Septum & Fracture Nasal Bone
No. Of deliveries No. Of FacialPalsies Incidence Natural 159 10 6.3% Forceps** 716 46 6.4% *Adapted from Hepner. 68 ** Not further characterized re: low, mid, high. etc. Type of delivery Incidence of Facial Palsy by Delivery Route
FACIAL PALSY Relation of Side of Facial Paresis to Intrauterine Position No. Of Infants Type of Delivery Side of FacialParesis Intrauterine Position 6 Natural Left Occiput left transverse 6 Natural Left Occiput left transverse 4 Natural Right Occiput right transverse 4 Natural Right Occiput right transverse 34 Forceps Left Occiput left transverse or anterior or anterior 12 Forceps Right Occiput right anterior, transverse or posterior transverse or posterior Adapted from Hepner. 68
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
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
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.
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.
Subgaleal Hemorrhage Diagram of Subgaleal or Subaponeurotic Hemorrhage Clinical Appearance of Subgaleal or Subaponeurotic Hemorrhage Ref: Advances in Neonatal Care, Vol 1, No 1 (October), 2001: pp 22-27
SGH is almost always preceded by difficult extraction, prolonged traction and multiple attempts 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 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 With anticipation, early recognition and appropriate management most severe forms of SGH are likely to recover without neurodevelopment impairment VACUUM EXTRACTION AND SUBGALEAL HEMORRHAGE Important Facts
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.
Risks for Newborn Encephalopathy Abnormal placenta Family history of seizures, neurologic disease Viral illness Antepartum bleeding IUGR Intrapartum fever Infertility treatment Thyroid disease
Essential Criteria: Perinatal Asphyxia Metabolic acidemia in fetal UA; pH 12 mmol/L Early onset of neonatal encephalopathy Cerebral palsy of spastic quadriplegia or dyskinetic type Exclusion of other etiologies
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
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
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
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
HIE: Late Sequelae Cerebral palsy Seizure disorders Cognitive deficits
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
Asphyxia: Outcome Predictors Severity of hypoxic-ischemic encephalopathy Refractory seizures Markedly abnormal EEG Hypodense areas on CT scan Early diffusion weighted MRI
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
Staging of HIE VariableStage 1Stage 2Stage 3 LOCAlertLethargyComa ToneNormal or increased HypotoniaFlaccid DTR’sIncreased Depressed or absent MyoclonusPresent Absent SeizuresNoFrequent
Staging of HIE VariableStage 1Stage 2Stage 3 Complex reflexes SuckActiveWeakAbsent Moro Exaggerated IncompleteAbsent Grasp Normal or exaggerated Exaggerated Absent Doll’s eyesNormalOveractiveReduced or absent
Staging of HIE VariableStage 1Stage 2Stage 3 Autonomic function RRRegularIrregularApnea HRNormal or increased Bradycardia EEGNormal Low voltageBS pattern or isoelectric
Outcome Based on Sarnat Stages Stage 1: mild - no death or disability Stage 2: moderate - 6% die, 20% with neuro handicap, 35% with reading disabilities without other handicap Stage 3: severe - 100% of survivors with neurologic handicap, 75% mortality by 3.5 years of age
Your consent to our cookies if you continue to use this website.