Without a left eyelid,she needseyedrops to retain her vision
Reginald Stephey was convicted on two counts ofintoxicated manslaughter. He completed twoconcurrent seven-year prison sentences . On May20, 2011 Saburido again appeared on the 4th tolast episode of The Oprah Winfrey Show
SURGICAL THERAPIES NEUROLOGIC DETERIORATION ? RADIOLOGY? CLOSED REDUCTION—SUCCESSFUL?. SPINAL STABILITY---LOST?Accepted Indications for SurgeryProgressive neurologic deterioration in an unstable spine,especially with spinal canal compromiseFailure of closed reduction and stabilization of dislocation withresidual canal narrowing of > 50%Unstable spine with dislocated bilateral "locked" facetsUnstable spine where nonunion is likelyUncooperative patient with unstable spine risking furtherneurologic injuryCompression of conus medullaris or cauda equina
Early Surgical TherapyExperimental studies…. Go for it!Clinical studies………..favourable outcomeMust occur <24 hrs, especially in incompleteinjuriesLate (>48hrs) only stabilizes spinal column andhelps rehabilitation
SURGICAL APPROACHESANTERIOR APPROACH Your Text herefor removal of disk material, bone, or ligamentous tissue compressingthe spinal cord anteriorlyto treat unstable compression-flexion and distractive-flexion injuries,often in conjunction with a decompressive corpectomy (removal ofvertebral body) if the cord is compressedPOSTERIOR APPROACHfor significant disruption of the posterior bony or ligamentous structuresof the cervical spine, particularly with minimal or no involvement of thevertebral bodyto treat occipitocervical and atlantoaxial instability and for spinalinstability causing flexion injuriesCOMBINED APPROACH [BOTH ANT & POST STRUCTURES]flexion teardrop fractures, vertical compression burst fractures withsignificant posterior ligamentous injury, and bilateral facet dislocation withdisk compression of the spinal cord.
NASCISNASCIS-I No neurologic benefit; ? Inadequatedose?NASCIS-II patients treated within 8 hours ofinjury showed significant improvement in motorand sensory function Vs30 mg/kg, followed by 5.4 mg/kg/hr Treatment 1:methylprednisolone, placebo…..PRACTICEfor 23 hoursTreatment 2:naloxone, 5.4 mg/kg fol-lowed by 4 mg/kg/hr for 23 hoursTreatment 3:placeboNASCIS-III MP 30 mg/kg within 824 hours Treatment 1: Methyprednisolone 5.4 mg/kg/hr for hrs f/b Treatment 2: Methyprednisolone 5.4 mg/kg/hr for 48 hours Treatment 3: Tirilizad mesylate 2.5 mg/kg every 6 hours for 48 hours
NASCIS-IIITreatment group 2 :especially among patientswhose therapy was initiated 3 to 8 hours afterinjury ‘showed’ greater motor recovery at 6 weeksand 6 months after injury than patients treated withthe same agent for 24 hours. [ post-hoc analysis;NOT Level 1/Level 2/Level 3 ]No functional benefit was demonstrated for the useof steroid therapy in the treatment of penetrating
REAL STORYNASCIS II flaws in study design and statisticalanalysis, NASCIS III concerns regarding thetiming of surgery, the process of neurologicassessment, and the fact that differences in motorscores and functional outcome were clinicallynegligible…no difference in the level of disabilityMP-48-hour infusionhigher incidence ofinfectionsSo STEROIDS ARE NOT STANDARD Rx IN A/CSCI; JUST A TREATMENT OPTION
HYPOTHERMIAEfficacy in mild to moderate traumatic SCI; not insevereCirculatory, pulmonary, metabolic, andimmunologic side effectsOnly experimental; no clinical evidenceHence this also is an option; not a standard Rx
HypertensionIn patients with hypo-perfusionMAP above 85 mm Hg for the first 7 days afterinjury is recommended to preserve neurologicfunction because autoregulation is impaired… [Nodefinitive data]more aggressive hypertensive therapy may haveadvantages, but risk of hemorrhage and edema.
CONCLUSIONno clear benefit from any pharmacologictherapy has yet emerged
MEDICAL THERAPYPULMONARY SYSTEMCARDIOVASCULAR SYSTEMGITGENITO URINARYTEMPERATURE CONTROLCOAGULATION
PULMONARYSYSTEM• The main key which we need to keep the engine revving …. Never loose it in SCI
PULMONARY SYSTEMLEVEL VENT COUGH COMMENTS FUN 0=no 0=no fun fun +++= N/L +++= N/LABOVE 0 0 Paralysis of diaphragm and accessory muscles,C3 resulting in apnea; lifelong ventilator dependenceC3-C5 0 to + 0 Partial to complete diaphragmatic paralysis; paralysis of accessory muscles-marked reduction in lung volumes with hypoxemia; recurrent atelectasis and pneumonia; prolonged mechanical ventilator dependence; probabl° tracheostomy; most patients will be weaned from mechanical ventilationC5-C7 + to ++ +to ++ Paralysis of accessory muscles; marked reduction in volumes with hypoxemia-recurrent atelectasis and pneumonia; many patients need mechanical ventilation; possible tracheostomyHIGH ++ ++ Partial paralysis of accessory muscles; reduction inTx lung volumes with ateiectasis1 increased incidence of pneumonia; possible need for mechanical
Anatomy »Diaphragm– Phrenic nerve– C3-C4-C5– Contributes to 65% of Vital Capacity-- injury >C3 = cough tidal breath-- ↓in all lung volumes except RV in Cx spine injury improve over next 4-5 ms
Anatomy »Intercostal muscles– Intercostal nerves– T1-T11 • Both layers act as inspirators at low volumes, and expirators at large volumes • Below C3 ↑ing function of diaphragm;but cough is extremely limited, since expiratory assistance of i.c. muscles are not there
Lungs get drowned!Pulmonary complications -- leading causes ofmorbidity and early mortality -- seen in as many as75% of patients.The reduction of lung volumes and the inability togenerate an effective cough progressiveretention of pulmonary secretions gradualmicroatelectasis and lobar atelectasis incremental hypoxemia and CO2 retention.
↑WOB ALSO TROUBLESVital capacity improve in supine position! [↓RV]*↓ed lung compliance, ↑ed WOBGastric atony ↔ pulmonary mechanicsIn 2-5 wks , spinal shock state resolvesprogressive spasticity of chest wall + abdomenimprove pulmonary function
Other pulmonary complicationsVentilatory failure and aspiration were the earliestto occur: at 4.5 days [Jackson and Groomes et al]
. Protocol For Reduction ofPulmonary Complicationsin Patients with SCI
Aggressive pulmonary hygiene .Frequent nasotracheal suctioning • to remove secretionsPositional changes every 2 hours [KINETIC Rx- Start early] • best achieved with rotational or circle beds • effectively ↓es complications & Ventilator duration- ICU stayChest percussion every 4 hoursAssisted coughing exercises every 4 hours rsDeep breathing exercises every 4 hoursIncentive spirometry every 4 hours
PROTOCOL…continued .Bronchodilator therapy for assisting secretion clearance and bronchodilatoreffects [relative parasympathetic overactivity in tetraplegics-↑secretions]Early use FOB in cases of lobar atelectasis secondary to retainedsecretionsEarly institution of mechanical ventilation • in those with progressive labored breathing, • increasing respiratory failure (hypoxia or hypercapnia) • and vital capacities <1000 mlClose monitoring of respiratory mechanics in patients receiving mechanicalventilation • with optimal use PEEP therapy and • limitation of plateau pressure to <30 cm Hg
Anticipation is important. • significant declines in first 1 to 3 days pulmonary reserve • progressive cord edema first 2 days • Ascending neurologic injuryso what will happen? @admission- diaphragm •VC check Q6H if <2L;functioning then If <1L & respiratory failure symptomaticintubate
Start seeing through a binocular into the long term plans……cervical SCI below C4 when spinal shockresolves (2-3 weeks) muscles develop spasticity improvement in lung volumes and overallventilatory ability eventual weaning frommechanical ventilationNearly all patients with complete cervical SCIabove C6 will require a tracheostomy because ofthe length of time on the ventilator and the difficulty
Suggested settingsACMV / SIMVVentilator settings should be selected that limit theoccurrence of ventilator-associated lung injuryPEEP is added to recruit collapsed alveoli andprevent further atelectasis
Shift gears accordingly…Chest trauma is associated with SCIpulmonary contusions, rib fractures,pneumothorax, hemothorax, and ARDS.May result in prolonged mechanical ventilation withdifficult weaning and delayed operative spinalintervention.
Fluid plays… Don’t SLIPNeurogenic Pulmonary oedema : Neurogenicincreases in extravascular water pulmonaryedema [both in head injury and in SCI; ?related tothe initial sympathetic discharge]Cardiogenic pulmonary edema : reducedmyocardial inotropy [in high SCI] , overzealousfluid administration.Because of the hemodynamic alterations observedin SCI (hypotension, bradycardia), the usual
CARDIOVASCULARSYSTEM• Body systems also crash like a vehicle after the impact
Spinal cord…. Does it belong to CNS or CVS!!!!complete cervical SCI has the most pronouncedphysiologic effects, consisting of cardiovascularinstability, cardiac dysrhythmias, and ventriculardysfunctionSCI below T5 results in varying degrees ofhypotension caused by the functionalsympathectomy below the level of injuryDISTINCTLY DIFFERENT MECHANISMS…
The Sympathetic BOMB BLASTA transient severe increase in blood pressurecaused by an extensive sympathetic discharge atthe time of injuryThe systolic blood pressure may be as high as 300mm Hg, lasting 2 to 5 minutes, with a gradualdecline to values less than baselinemay be responsible for the noncardiogenicpulmonary edema
Aftermath…..After this HYPOTENSION predominates [ in allpatients with complete cervical SCI ]Due to vasodilatation 20 to withdrawal ofsympathetic neural outflowIts a functional sympathetic blockade [sympatheticreceptors lose their normal input and regulation]Parasympathetic system remains intact since… thevagus nerve exits from the brainstem.
SPINAL SHOCKseen with physiologic or anatomic transection, ornear transection, of the spinal cordconsists of the loss of somatic motor and sensoryfunction below the level of injury, loss of voluntaryrectal contraction, and loss of sympatheticautonomic function
SPINAL SHOCK continuedThe more severe the functional spinal cordtransection and the higher the level of injury, thegreater the severity and duration of spinal shock.If the loss lasts longer than 1 hour, pathologicinjuries to the spinal cord, as opposed to atransient concussive injury are assumed to exist
Lack of speed kills….Beware of the bradycardia in SCIcomplete cervical SCI +++; thoracic and lumbarinjuries +/-interruption of the cardiac accelerator nerves (Tl to T4)First 2 wks-most dangerous ; resolves over 3- to 5-weeksprofound degrees of bradycardia, even cardiac arrest,may occur during turning or tracheal suctioningsedation, 100% oxygen before suctioning, and limitingthe time allowed for suctioningRx: Atropine, Temporary pacemaker
What has fallen there…?SBP < 90 mm of Hg / 30% below baselinegoal : ? MAP > 85 mm of Hg for first 7 dayscorrection of hypotension is crucial for optimalpreservation of neurologic function and reduction of20 injuryNo autoregulation; so aggressive RxNeurogenic shock relative hypovolemia due tovasodilation so fill, but carefully [pulmonaryedema]Blood : to maintain Hb>10gFluids : isotonic crystalloids / ?HYPERTONIC
DON’T ‘PRESS’ TOO MUCH vasopressor Vs inotropic agentspotent ά-agonist substantial increases inafterload impair cardiac O/P can precipitateLVF inotropic agent is often the drug of choicefor maintaining spinal cord perfusionInvasive hemodynamic monitoring isrecommendedThere is evidence to support improvement inneurologic outcome in whom hemodynamics aremanaged aggressively.SC edema is maximal at 3 to 6 days after injury,blood pressure support should continue during this
ArrhythmiasExperimental models & clinical reports shown --Cardiac dysrhythmias [suppressed by atropine]tachycardia, and ST T wave changes [suppressedby propranolol]The initial response to spinal cord compression--sympathetic discharge elicited a secondary,compensatory, parasympathetic dischargeautonomic imbalance responsible for the cardiacdysrhythmias
Arrhythmias continued ..TYPE persistent bradycardia Primary cardiac arrestsevere cervical SCI 31/31 5/31mild cervical SCI 6/17 -thoracolumbar SCI 3/23 - frequency of brady-dysrhythmias was maximal on day 4 after injury all abnormalities resolved over a 14-day to 6-week period
GASTROINTESTINAL SYSTEMIssues Comments .Gastric distention Increased risk of aspirationGastric emptying delayed Adversely affect ventilation Rx : put N-G tubepeptic ulcer disease One cause- high dose steroidsgastritis, Rx: PPI, Sucralfate [continued for 4hemorrhage weeks] Enteral feedingIleusacalculous cholecystitisoccult acute abdomen patients with SCI may not demonstrate the usual signs and symptomselevated metabolic rates early nutritional supplementation
DEEP VEIN THROMBOSIS 40-100% ↑ed age, a concomitant lower extremity fracture, and lack of or delay in thromboprophylaxis ↑es risk PULMONARY EMBOLISM In 0.5% to 4.6% of patients third leading cause of death moreoften with complete SCI and thoracicmiury
Diagnosis and TreatmentDiagnosis CLINICAL SUSPICION D-DIMER LEVELS, VENOGRAPHY, COLOR FLOW DUPLEX IMAGING CT ANGIOGRAPHY, PULMONARY ANGIOGRA-PHYTreatment PROPHYLACTIC TREATMENT AS SOON AFTER INJURY AS IS POSSIBLE (I.E., 72 HOURS) CONTINUED FOR A MINIMUM OF 3 MONTHS. EFFECTIVE TREATMENT THE OCCURRENCE OF DVT DECREASES TO 5%.
AUTONOMIC HYPERREFLEXIAoccurs in 85% of patients with spinal cordtransections above T5is secondary to autonomic vascular reflexes, whichusually begin to appear about 2 to 3 weeks afterinjuryAfferent impulses from bladder or bowel distention,manipulations of the urinary tract, or surgicalstimulation the pelvic, pudendal, or hypogastricnerves to the isolated spinal cord a massivesympathetic response from the adrenal medullaand sympathetic nervous system, which is nolonger modulated by the normal inhibitory impulses
AUTONOMIC HYPERREFLEXIAVasoconstriction occurs below the lesion;reflex activity of carotid and aortic baroreceptorsproduces vasodilation above the lesionoften accompanied by bradycardia, ven-triculardysrhythmias, and even heart block.Sedation or topical anesthesia does not appear toattenuate the hypertensive response, but deepgeneral, epidural, or spinal anesthesia is effectiveHypertension Rxdirect-acting vasodilators (e.g., sodium nitroprusside)beta blocking agents (e.g., esmolol),combination beta blockers (e.g., labetalol), organglionic blocking agents e.g.,trimethaphanCCBs (nicardipine),
Infectionsleading cause of deathpneumonia, urosepsis
HYPERREFLEXIC SYNDROMESmuscle spasms caused by hyper-active spinalreflexes without the tempering effect of modulatingcortical, brainstem, and cerebellar influences.This "mass reflex" may make the management ofthe unanesthetized patient difficult.
PRESSURE ULCERSdirect pressure effects, reduced tissue perfusion,and limited mobility.The use of rotational beds, frequent patient turning,good skin care, foam padding of bonyprominences, or air floatation beds can helpprevent pressure ulcers.
LONG-TERM IMMOBILIZATIONaltered calcium metabolismpainful heterotopic ossificationcalcification of musclesjoint immobilityosteoporosis with hypercalcemianephrocalcinosis and secondary renal failure.Late mobilization pathologic fractures.Early institution of active physical therapy isessential
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