(PDF) BIRTH TRAUMA - elearning.sumdu.edu.ua fileOxytocin during labor (50% of brachial plexus injuries) Large fetal size (>3,500 g in 50–75% of brachial plexus injuries) Low Apgar score

BIRTH_TRAUMA.docxОлена Костянтинівна Редько

2014

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BIRTH TRAUMA, INTRAABDOMINAL INJURIES, BIRTH TRAUMA: BRACHIAL PLEXUS INJURY, BIRTHTRAUMA: CEPHALOHEMATOMA, SUBGALEAL, BIRTH TRAUMA: INTRACRANIAL HEMORRHAGE,,HEMATOMA, Physical findings of brachial plexus injury distinctive, SKULL FRACTURES, follow-up,history & physical, managementBIRTH TRAUMA, INTRODUCTION

Caused by mechanical trauma to fetus during labor &/or delivery■ Incidence estimated 5–8/1,000 births■ Risk factors for injury➣ Prolonged labor➣ Precipitous delivery➣ Abnormal fetal presentation (e.g., face, breech)➣ Difficult fetal extraction (e.g., w/ shoulder dystocia)➣ Use of forceps or vacuum➣ Nuchal cord➣ Fetal size (very large or very small)➣ Fetal anomalies predisposing to injury (e.g., osteogenesis imperfecta,hepatosplenomegaly)BIRTH TRAUMA: BRACHIAL PLEXUS INJURY

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■ Oxytocin during labor (50% of brachial plexus injuries)■ Large fetal size (>3,500 g in 50–75% of brachial plexus injuries)■ Low Apgar score (<4 at 1 min in 39% of brachial plexus injuries)Physical■ Typical pattern: progressive, downward involvement; cephalic tocaudal■ Weak, hypotonic, hyperextended upper extremity; asymmetricMoro reflex■ Erb’s palsy: C5, C6, C7; shoulder internally rotated; elbow extended;wrist flexed; hand pronated■ Erb-Klumpke’s palsy: C5-T1; Erb’s palsy findings + weak handmovement; absent grasp■ Assoc findings➣ Diaphragmatic palsy (∼5%): involves C4, C5; paradoxicalbreathing pattern➣ Horner’s syndrome (30% in Klumpke’s palsy): involves T1; ptosis,miosis on affected side➣ Facial palsy, fractured clavicle, fractured humerus, subluxationof shoulder, cervical spine injury (5–20%)■ Extent, progress of lesion defined mainly by physical exam; persistentlesions should be monitored for recovery using standardizedtool (e.g., BritishMuscleMovement Scale)tests■ X-ray to r/o associated clavicular or humeral fracture, humeralepiphysealseparation

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■ EMG, nerve conduction velocity, MRI, myelography not helpful inearly mgt■ Fluoroscopy or US to confirmpresence of diaphragmatic paralysisdifferential diagnosis■ Physical findings of brachial plexus injury distinctive■ AsymmetricMoro reflex➣ Fracture of clavicleMay be assoc w/ brachial plexus palsyIncidence 5/1,000 live birthsRisk factors similar to those for brachial plexus injury, but halfw/ normal labor/deliveryMore common on right due to LOA fetal positionNormal muscle tone; abnl Moro reflex; pain on motion; localswelling, crepitus➣ Positive x-ray findings➣ Fractured humerus, shoulder subluxation – distinguished byphysical signs, x-ray➣ Septic arthritis; osteomyelitis of humerus■ Fractured humerus, subluxed shouldermanagement■ Gentle immobilization of armin 1st wk■ Physical therapy, wrist splints after 1–2 wk to prevent contracturesif persistentspecific therapy■ After partial recovery, tendon transfers can further improve shoulderexternal rotation & abduction■ Microsurgery (nerve transfer or nerve grafts) has successfullyrestored some function in selected pts w/ persistent paralysis (see“Complications and Prognosis”)follow-up■ Careful neurol exams to follow progress of recovery■ EMG, nerve conduction, myelography, CT-MRI may help definelesion at 1–4 mo of age, but physical exam remains the ultimateguide to assess recovery & decide on surgical interventions■ Physical therapycomplications and prognosis■ Full, spontaneous recovery in >90%of infants by 4–12mo of age■ Usually some improvement noted by 2 wk■ Patterns of damage & recovery➣ Neurapraxia: hemorrhage; edema between nerve sheath, axon:recovery➣ Neurotmesis: axon ruptures w/in intact nerve sheath: regenerationalong sheath, partial recovery➣ Complete avulsion, rupture at nerve or nerve root: poor recovery■ Non-recoverers➣ Nerve root avulsion will not recover spontaneously; in thesecases nerve transfer before 3 mo of age may limit motor endplateloss & maximize recovery➣ Ruptures have varying degrees of recovery; indications & timingof microsurgery controversial; most centers recommendtransection of the neuroma & sural nerve grafting in extraforaminalruptures btwn 3–9mo of age➣ Long-termprognosis: significant psychosocial disabilityBIRTH TRAUMA: CEPHALOHEMATOMA, SUBGALEALHEMATOMAHistory■ Vertex presentation, sometimes w/ forceps or vacuum assistance■ Prolonged, difficult labor; primigravidity■ Subgaleal hematoma assoc w/ vacuum extraction, coagulopathyPhysical■ Cephalohematoma

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➣ Fluctuant, subperiosteal hemorrhage (does not cross suturelines)➣ Slow accumulation, hours-days➣ Lateralized to one or both parietal bones➣ Transillumination negative■ Subgaleal hematoma➣ Dependent, fluctuant mass➣ May expand rapidly, leading to tachycardia, poor peripheral perfusion,pallor, oliguria➣ Crosses suture lines➣ Transillumination negative➣ Cranial molding➣ Subconjunctival hemorrhage➣ Jaundicetests■ Transilluminationmay help differentiate an edema (caput succedaneum)from a hemorrhagic fluctuance■ Skull x-rays not usually indicated■ Hemoglobin, bilirubin w/ large-volume bleeds, clinical jaundice■ Platelet count, coagulation studies w/ subgaleal hemorrhagedifferential diagnosis➣ Edema, usually pitting not fluctuant➣ Present at delivery➣ Crosses suture lines➣ Transillumination usually +➣ Resolves quicklymanagement■ Supportive for jaundice, anemia, hypovolemiaspecific therapy■ Nonefollow-upN/Acomplications and prognosis■ Cephalohematoma➣ Resolves slowly (wks) w/o treatment➣ Linear skull fracture (incidence <5% if cephalohematoma isunilateral, 18% if bilateral)➣ Jaundice, anemia, thrombocytopenia, infection (rare)➣ Parental reassurance, documentation important■ Subgaleal hematoma➣ Jaundice, anemia, thrombocytopenia, hypovolemia, infection(rare)➣ Hypovolemia, shock➣ Resolves spontaneously w/ visible dependent ecchymosisBIRTH TRAUMA, INTRAABDOMINAL INJURIES■ Liver, spleen, adrenals: highly vascular organs susceptible to traumaticinjuryHistory■ Predisposing factors➣ Breech presentation➣ Organ enlargement➣ Coagulopathy■ Caput succedaneum➣ Asphyxia➣ Storage diseases

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Physical■ Enlarging RUQ or LUQmass■ Enlarging flank mass■ Signs of hypovolemic shock (see SHOCK)tests■ Abdominal US or CT scan■ Serial hematocrit/hemoglobin■ Serum electrolytes, glucose for adrenal hemorrhage (see ADRENALINSUFFICIENCY)■ Urinalysis for hematuriadifferential diagnosis■ Organomegaly w/ deteriorating clinical status may occur in:➣ Overwhelming bacterial or viral infection (e.g., congenital infection)➣ Acute congestive cardiac failure➣ Rh hemolytic disease➣ Inborn error ofmetabolism■ Hematuria: renal vein thrombosis – usually related to hypovolemia,hyperviscosity■ Calcifications after adrenal hemorrhage may be confused w/ neuroblastomamanagement■ Replace blood vol, clotting factors■ Emergency imaging to determine cause of organ enlargement, siteof hemorrhage■ Pediatric surgical consultationspecific therapy■ Surgical intervention usually reserved for rupture of hematoma■ Partial preferable to complete splenectomyfollow-up■ Neurodevelopmental w/ shockcomplications and prognosis■ Prognosis for full recovery excellent for infants who receive timelysupportivemeasures &/or surgery■ Antibacterial prophylaxis/pneumococcal vaccine after total splenectomyrequired■ Bilateral adrenal hemorrhage rarely results in adrenal insufficiencyBIRTH TRAUMA: INTRACRANIAL HEMORRHAGE,SKULL FRACTURES

History■ Same general risk factors as other birth injuries; in particular:➣ Difficult, traumatic cephalic delivery➣ Birth asphyxia➣ Forceps delivery➣ Premature birth, lethargy, hypotoniaPhysical exam■ Signs of trauma➣ Facial bruising, forceps marks➣ Caput, cephalohematoma➣ Extrememolding of skull➣ Facial nerve palsy, asymmetric crying face

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■ Bulging fontanels■ Altered in alertness, responsiveness, muscle tone (often dynamic,not static)➣ Hyperalertnessmay progress to coma➣ Hyperreflexia, clonusmay progress to hypotonia■ Abnl pupillary responses, abnl eye movements, depressed suck/swallowing■ Seizures (usually multifocal)■ Apnea, bradycardia, obtundation, shock■ Skull fractures➣ Linear fractures: +/− molding, superficial scalp trauma, orcephalohematoma➣ Depressed skull fracture: palpable “ping-pong ball” depressiontests■ Brain imagingHead CT or MRI useful for depressed skull fractures, subdural,subarachnoid, infratentorial hemorrhage, edema/infarction,structural malformationsnote: In the presence of head trauma, altered or deterioratingneurol condition, CT/MR scan is the only reliable way to determinepresence, location of bleed that may need immediate neurosurgicalattn➣ Cranial US useful to detect intraventricular hemorrhage, ventriculardilatation■ LP to r/o infectious etiology for abnl neurol status (defer w/ cardiorespinstability or signs of increased intracranial pressure)■ Acid-base status, electrolytes, Ca, Mg, glucose, NH3 to eval formetabolic etiology for abnl neurol status (Note: These are screeningtests, not diagnostic tests.)differential diagnosisDDx of signs■ Intracranial hemorrhage, asphyxia may coexist; signs, symptomsmay overlap■ Metabolic diseases (e.g., urea cycle defects, branched-chain aminoacidopathies,cytochrome C oxidase deficiency)■ Sepsis/meningitis■ Inherited neuromuscular disorder (e.g., congenital myasthenia ormyotonic dystrophy)■ Drug withdrawal (e.g., from opiates, methadone)DDx of intracranial hemorrhage■ Epidural hemorrhage➣ Usually assoc w/ linear skull fracture➣ Usually silent butmay cause neurol deterioration if large■ Subdural hemorrhage➣ Severe cranial distortion may lacerate internal dura (tentorium,falx) & rupture adjacent venous structures (eg venous sinuses,vein of Galen, infratentorial vein)➣ Acute neurol deterioration w/ seizures, coma if hemorrhagelarge➣ Posterior fossa bleeds: Danger! Possible brain stem compression,rapid deterioration & death➣ Subdural hemorrhage over convexity of brainmay have silent orchronic presentation■ Intraventricular, periventricular, subarachnoid hemorrhage➣ VLBW infants: germinal matrix hemorrhage due to hypoxicischemicevent➣ Term infants: choroid plexus hemorrhage due to hypoxicischemic-traumatic eventmanagement■ Serial brain imaging■ Serial neurologic exams to detect changes in status■ Cardiorespir stabilization, supportive care (mechanical ventilation,treatment of shock, electrolyte abnormalities, hypoglycemia, etc.)■ Anticonvulsants for seizures

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■ Fluid restriction for CNS edema■ Antibiotics for possible sepsis/meningitis➣ Treat immediately but defer LP in presence of cardiorespir instabilityor signs of increased intracranial pressure■ Neurosurgical consultation for:➣ Posterior fossa hemorrhage➣ Any significant subdural or epidural hemorrhage assoc w/altered/deteriorating neurologic status➣ Depressed skull fracturespecific therapyN/Afollow-up■ Neurodevelopmentalcomplications and prognosis■ Epidural hemorrhages: good prognosis for survivors cortical injury■ Subdural hemorrhages➣ Large hemorrhage due to laceration of tentorium or falx – fewsurvivors➣ Smaller subtentorial hemorrhageHydrocephalus, 15%Major sequelae, 5–10%➣ May evolve into chronic subdural effusion (w/ lethargy, vomiting,failure to thrive) when over convexity of brain & requiredrainage■ Intraventricular, periventricular hemorrhage➣ TerminfantsMost require VP shunt for hydrocephalus50% have major neurol deficit;most needing VP shunt➣ Preterminfants (see INTRAVENTRICULAR HEMORRHAGE)■ Skull fractures➣ Linear fractures usually heal w/o treatment; exception: “growing”skull fracture caused by arachnoid (“leptomeningeal”) cystprotruding through tear in dura into fracture line, requires repair■ Depressed fracture➣ May elevate spontaneously➣ Persistent depressions & those w/ bone fragments require neurosurgicalattn➣ Prognosis excellent w/o damage of underlying cortex

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(PDF) BIRTH TRAUMA - elearning.sumdu.edu.ua fileOxytocin during labor (50% of brachial plexus injuries) Large fetal size (>3,500 g in 50–75% of brachial plexus injuries) Low Apgar score - DOKUMEN.TIPS (2024)

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