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come fly with me A Case DiscussionRyan Em C. DalmanMD MBA - 070070February 17, 2010

ObjectivesPresent a case of traumaHistory and Physical ExamDiagnostics DifferentialsDiscuss its basic concepts of management

Case PresentationPatient History

General DataMDG36-year-oldMaleBorn on Dec 29, 1974Roman CatholicLives in Antipolo CityInformant: Wife, 50% reliability

Chief ComplaintNahulog mula sa second floor the bahayFall

History of Present IllnessPatient was intoxicated and fell on the 2nd floor of their houseHit the head first on the pavement Lost consciousness and unresponsiveNo seizures, vomitingRushed to a nearby hospitalCT-scan: multiple cortical and subcortical contusion, subarachnoid and subdural hematoma, multiple skull fracturesPatient was deteriorating

1 day PTAConsult6Review of SystemsGeneral: no weight loss, no change in appetiteCutaneous: no lesions, no change in color, no pruritusHEENT: no headaches no rednessno aural/nasal dischargeno neck massesno sore throatCardiovascular: no easy fatigability, no fainting spells7Review of SystemsRespiratory: no cough, coldsGastrointestinal: no abdominal pain, no change in bowel movementsGenitourinary: no pain in urination or difficulty in urinatingEndocrine: no polyuria, polydypsia, no heat/cold intoleranceMuskuloskeletal: no weakness, numbness on all extremities Hematopoietic: no easy bruisability, or bleeding

Past Medical HistoryNo Hypertension, Diabetes, Asthma, PTBNo Cancer, Allergies to food or medications

No previous surgeries or hospitalizations

No maintenance medications

Family HistoryHypertension, maternalNo heart disease, cancer, stroke, diabetes, asthma, or allergiesPersonal and Social HistoryMarriedOFW at QatarLives with her family in a 2 story houseSmoking 10 pack yearsOccasional alcoholic beverage drinkerDenies substance abuseCase PresentationPhysical Exam

Physical ExamGeneral SurveyIntubated and unconscious Vital SignsFebrile at 38oC RR 20 bpmHR 150-160 bpmHeight:168cm weight:70kg BMI:24.8Physical ExamSkinMultiple abrasions on the extremitiesHeadsoft tissue swelling of the entire head (including the face)sutured lacerations on the temporo-occipital portion of the headEyesSwollen eyelids Physical ExamNeck with neck braceChestadynamic precordiumno heaves, thrills, or lifts, PMI at 5th ICS MCLDistinct S1 anf S2Tachycardic, normal rhythmno murmursLungssymmetrical chest expansion, no retractionswith bilateral cracklesPhysical ExamAbdomenflat, no lesionsnormoactive bowel soundstympanitic on all quadrantssoft, no guardingno masses, no organomegallyExtremitiesSemi-purposeful movement No signs of fractures or deformitiesMultiple abrasions noted on the arms and legsFull and equal pulses

Salient FeaturesHistory36 year old maleFell from a 2 story building, head firstCT scan showing multiple cortical and subcortical contusion, subarachnoid and subdural hematoma, multiple skull fracturesAlcohol intoxication Unconscious No seizures, no vomiting

Physical ExamSoft tissue swelling of the headsutured lacerations on the temporo-occipital areaBilateral lung crackles No signs of fractures (extremities)17Case DiscussionPrimary ImpressionTraumatic brain injury, severe cortical and subcortical contusionsSubarachnoid and subdural hematomaMultiple skull fractures Rule out pulmonary contusion History52 year old femaleFlank pain with dysuria of 5 daysWith radiation to the RLQNo history of traumaCT stono - NephrolithiasisPhysical ExamRLQ tendernessNo obturator, psoas, and rovsings signRight CVA tenderness19Head CT

TraumaDefinition

.Cellular disruption caused by an exchange with environmental energy that is beyond the bodys resilience

Schwartzs Principles of Surgery , 9th ed35TraumaMost common cause of death 1-44 years old3rd most common cause of death regardless of ageNumber 1 cause of years of productive life lostSchwartzs Principles of Surgery , 9th edTraumaTypes of TraumaBlunt forceful impact Blow, kick, strike with object, fall, motor vehicle collision, blastPenetrating breech of the skin by an object/projectileKnife, broken glassBullet, shrapnel from explosionOther injuriesThermal and chemical burns, toxic inhalations or ingestions, and radiation injuries

Merck Manual 2009Traumatic Brain InjuryAlso known as acquired brain injury, head injuryOccurs when a sudden trauma damages the brain and disrupts normal brain functionMerck Manual 2009Traumatic Brain InjuryAnnual statistics of TBI in the USAt least 1.4 M50,000 mortality475,000 occur among 0-14yo80-90k people experience the onset of a long-term disability Medscape, EmedicineTraumatic Brain InjuryLeading causes of TBIFalls 28%MVA 20%Being struck by or against objects - 19%Assaults - 11%Medscape, EmedicineClassificationGlasgow coma scaleMild: 13-15Moderate: 9-12Severe: 3-8

Medscape, EmedicineClassificationLoss of consciousness

Medscape, EmedicinePathophysiologyPrimary InjuryInduced by mechanical force and occurs at the moment of injurySecondary InjuryOccurs hours or days after the inciting traumaMedscape, Emedicine43PathophysiologyPrimary InjuryContactScalp injurySkull fractureSurface contusionAcceleration-deceleration Shear, tensile, compressive strainsCoup and countercoupMedscape, Emedicine/ Merck Manual 2009Primary injury due to acceleration-deceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains44PathophysiologyPrimary InjuryContusion distinct areas of swollen brain tissuepoles and inferior aspects of the Frontal lobesCortex above and below the operculum of the sylvian fissuresLateral and inferior aspects of the temporal lobesMedscape, Emedicine/ Merck Manual 2009Primary injury due to acceleration-deceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains45PathophysiologyPrimary InjuryIntracranial hematoma most common cause of death and deterioration after TBIEpidural temporal bone fracture and MMA rupture Subdural rupture of bridging veins in the subdural spaceSub arachnoid damage to blood vessels in the posterior fossa stalkMedscape, Emedicine/ Merck Manual 2009Epidural hematomas - These are usually caused by fracture of the temporal bone and rupture of the middle meningeal artery. With epidural hematomas, clotted blood collects between the bone and the dura. Because the source of bleeding is arterial, this type of hematoma can grow quickly and create pressure against the brain tissue.

Subdural hematomas - Such hematomas are usually caused by rupture of the bridging veins in the subdural space. They can grow large enough to act as mass lesions, and they are associated with high morbidity and mortality rates.

Subarachnoid hematomas - These result from damage to blood vessels in the posterior fossa stalk.

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PathophysiologyPrimary InjuryIntracranial hematoma most common cause of death and deterioration after TBIDiffuse axonal injury rotational acceleration of the brainDefined clinically as LOC lasting > 6 hours in the absence of a specific focal lesionMedscape, Emedicine/ Merck Manual 2009Diffuse axonal injury (DAI) is one of the most common and important pathologic features of TBI. It constitutes mostly microscopic damage, and it is often not visible on imaging studies. The main mechanical force that causes DAI is rotational acceleration of the brain, resulting in unrestricted head movement. Rotational acceleration produces shearing and tensile forces, and axons can be pulled apart at the microscopic level. Microscopic evaluation of the brain tissue often shows numerous swollen and disconnected axons. Rapid stretching of axons is thought to damage the axonal cytoskeleton and, therefore, disrupt normal neuron function.8 48PathophysiologySecondary Injuryimpairment or local declines in cerebral blood flow Local edemahemorrhageIncreased ICPFailure of ion pumpsIntracellular Ca and Na overloadCellular destruction!Medscape, Emedicine/ Merck Manual 2009Secondary injury may occur hours or even days after the inciting traumatic event. Injury may result from impairment or local declines in cerebral blood flow (CBF) after a TBI. Decreases in CBF are the result of local edema, hemorrhage, or increased intracranial pressure (ICP). As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium and sodium. Resultant calcium and sodium overload may contribute to cellular destruction. 49PathophysiologySecondary Injuryimpairment or local declines in cerebral blood flow Release of excitatory amino acidsCells DieFree radical formationProteolysisLipid peroxidationNeuronal death!!!Medscape, Emedicine/ Merck Manual 2009Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of the ion pumps. As the cascade continues, cells die, causing free radical formation, proteolysis, and lipid peroxidation. These factors can ultimately cause neuronal death.9 50Signs and SymptomsEpidural hematomaIncreasing headacheDecreased level of consciousnessFocal neurologic deficitsPupillary dilation with loss of reactivity to light herniationGradual neurologic deteriorationSubdural hematomaImmediate loss of consciousness

Merck Manual 2009Signs and SymptomsIncreased ICPProjectile vomitingCushings Triad (increased pulse pressure, bradycardia, respiratory depression)Diffuse Brain Injury, markedly increased ICPDecorticate/ decerebrate posturingTranstentorial herniationComaUni/bilaterally dilated and unreactive pupilsHemiplegiaCushings triadMerck Manual 2009Signs and SymptomsBasilar skull fractureRhinorrhea, ottorhea, hemotympanumBattles sign (ecchymosis behind the ear)Raccoon eyes (ecchymosis in the periorbital area)

Merck Manual 2009Approach to a Trauma PatientInitial SurveyAirwayBreathingCirculationDisability Exposure/ Environmental ControlSecondary SurveyAllergiesMedicationsPast Medical HxLast mealEvents of injuryAirway with Cervical spine Control54Approach to a Trauma Patient

Approach to a Trauma PatientDefinitive CareEarly Total CareDamage Central SurgeryTertiary CareMissed Injuries

Diagnostics/ workupImaging tests are the cornerstoneLaboratory tests are generally ancillary Merck Manual 2009

Diagnostics/ workupPenetrating traumaHas focal unjuries, limit imaging to the involved regionsBlunt traumaIn significant deceleration (fall, MVA) used more liberallyChest, cervical, LS, and Pelvic X-rayAbdominal Ultrasound/ CTsuspected intra-abdominal injuryHead CTAltered mental status or loss of consciousnessPlain x-rayAny suspected fracturesMerck Manual 2009Diagnostics/ workupECGFor blunt chest injuryABGUrinalysisCBC with BTLactate

Merck Manual 2009Principles of ManagementMaintenance of:Adequate ventilationOxygenationBrain perfusion

Aggressive early management of:HypoxiaHypercapneaHypotensionIncreased ICPMerck Manual 2009Principles of ManagementControl of bleeding and replacement of intravascular volumeHypotonic fluids are contraindicated excess free water can increase brain edema ~ ICPMerck Manual 2009Principles of ManagementFor multiple injuries, simultaneous treatment is warrantedFor Traumatic Brain Injury

SeverityGCS scoreManagement Mild14-15Observation at homeModerate 9-13Observation in hospitalSevere3-8-Rapid sequence intubation-Intensive supportive care-Monitoring and treatment of ICP as indicatedMerck Manual 2009Principles of ManagementMild InjuryObservation at homeIf no LOC, stable VS, normal head CT, normal mental and neurologic functionWatch out for:Decreased level of consciousnessFocal neurologic deficitsWorsening headacheVomitingDeterioration of mental function Merck Manual 2009Principles of ManagementModerate and Severe InjuryThey often do not require intubation or mechanical ventilation or ICP monitoringBut deterioration is possible, thus admitted even if head CT is normalClose monitoring of GCS and pupillary responseMerck Manual 2009Principles of ManagementIncreased Intracranial PressureRapid sequence orotracheal intubationMechanical ventilationMonitoring of ICPOngoing sedation as neededMaintaining euvolemia and serum osmolality of 295-320 mOsm/kgIf unresponsive to treatment, consider CSF drainage, decompressive craniotomy, or pentobarbital comaMerck Manual 2009Principles of ManagementSkull FracturesNo treatment for aligned closed fracturesDepressed fractures surgeryOpen fractures debridementAntibiotic prophylaxis is controversialMerck Manual 2009Principles of ManagementSurgeryIntracranial hematomas surgical evacuationSmall intracerebral hematomas rarely require surgeryIndications for surgeryMidline brain shift of >5mmCompression of the basal cisternsWorsening neurologic examination findingsMerck Manual 2009Principles of ManagementRehabilitationPersistence of neurologic deficits Patients whose coma exceeds 24 hours prolonged rehab is advisedMerck Manual 2009Public HealthBurden of Trauma in the Philippines (1960-1995)Injury fatality rates increased by 196%1 in 11 deaths caused by traumaIntentional injuries: 48% of deaths 2o traumaMVA: 15%Public HealthBurden of Trauma in the Philippines (1960-1995)15-44yo males:42% of deaths (67% of which are intentional)Intentional injuries increased by 925%MVA by 600%Public Health

PrognosisUS dataAdults with severe TBI mortality 33%Mortality is lower with higher GCSChildren have better prognosis than adultsComa > 24h, 50% persistent neurologic sequelae, 2-6% remain persistent veg. stateTBI rapid recovery in the initial 6 mos. PrognosisGlasgow Outcome ScaleOutcomeDescriptionGood recovery return to previous functionModerate disability capable of self-careSevere disability incapable of self-careVegetativeno cognitive functionDeathcome fly with me A Case DiscussionRyan Em C. DalmanMD MBA - 070070February 17, 2010