Trauma M

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Trauma MM

• Habeeba Park
• November 25, 2008

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MRN 01696149

• Ms. AR 77 yo F s/p fall down 12 steps
• CP
• PMH HTN, hyperlipid, migraines
• Meds HCTZ, Inderal
• Allergies compazine
• Soc hx no ETOH/smoking/illicit drugs
• PE
• VS 36.3, 67, 100/51, 17, 96 RA
• Primary survey ABCs intact, GCS 15
• Mild tend over sternum and ribs, contusion over
  midsternum
• RRR, CTAB
• Abd NTND, hypoact BS
• Bony tenderness on palpation of upper T spine
• b/l LE normal sensation, no movement, normal
  pulses
• Deformity of R wrist w/ hematoma/swelling
• Rectal tone normal

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Labs

• EKG no changes
• Troponins lt0.04
• BMP Na 142, K 3.9, Cl 107, HCO3 25, BUN/creat
  25/1.14, glucose 150
• CBC WBC 16, H/H 12/36, plat 209

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Imaging

• CT
• C spine nondisplaced C2 comminuted fx of
  vertebral body, fx posterior arch of C7, R 1st
  rib fx
• T spine T1 fx, T3/T4 fx of body and
  retropulsion, spinal stenosis
• Chest upper sternal fx
• Abd/pelvis no injury
• XR R wrist comminuted fx of distal radius

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A/P

• Multip spinal fx of C and T spine with
  retropulsion/spinal stenosis, T4 paraplegia, CP
  with sternal/rib fx
• Tx
• IVF
• Foley
• Morphine
• Neurosurg consult
• Miami J
• Steroid protocol (methylprednisolone)
• Bolus 30 mg/kg IV
• 5.4 mg x kg x 23h gtt
• Log roll precautions
• MRI C/T spine once pt stable
• Operative repair in future
• Ortho consult
• Reduction of displaced R intraarticular fx
• Splint
• Outpt operative repair in future

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Hospital Course

• Admit to ICU 11/6/08
• HR 50s, SBP 80-90 despite multiple fluid boluses
• No sharp/dull sensation/motor fxn in b/l LE
• Started Levophed for goal SBPgt110
• Flat in bed
• Contin steroid protocol x 24h
• Neck brace with T spine extension
• R wrist splint
• Dilaudid for pain
• ABG 7.23/46/57/19/-8 on 70 FM
• Placed on 100 NRB

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Hospital Course

• ICU day 2
• Neuro exam no motor fxn b/l LE, no sensory fxn
  below T4, no rectal tone
• Resp and metab acidosis, relative hypoxia
• Increased work of breathing
• Anesthesia called to intubate pt for resp
  distress
• Propofol, fent gtt
• ICU day 3
• Temp drop to 34
• HR drop to 40s? started on Dopamine gtt w/
  response to 60s
• 8L positive
• Afeb, no Abx WBC 19 (rising)

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Hospital Course

• Continuing hypotension (SBP 60s)
• Given more NS boluses? no response
• started neo, vasopressin? SBP 120s
• WBC dropped to 1.9, lactate up to 3.7
• Pan cxd? sputum grew heavy Enterobacter
  aerogenes, MRSA
• Started on vanc and zosyn for septic shock
• ICU day 4
• Desaturation to 80s on AC 65? PEEP increased to
  12, FIO2 to 100
• Worsening pulm edema
• contin desat to 60s? ? PE
• Started on heparin gtt
• pH dropping 7.08/58/41/17/-12
• Increased bicarb gtt given NS boluses
• Head CT neg? started lovenox
• Family reaffirmed desires to contin full resusc

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Hospital Course

• MOF
• BP contin drop70/30
• Creat increasing (peak _at_ 1.5) U/O decreased
• O2 sats dropping, tachypnea? resp failure
• Lactate risingpeaked _at_ 10.4
• Resp and metabol acidosis
• 6.90/76/37/15/-17
• ACLS initiated
• Asystole? death _at_ 1453 11/9/08

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Spinal Cord Injury

• Definitions of complete and incomplete SCI are
  based on the above ASIA definition with
  sacral-sparing.
• Complete - Absence of sensory and motor functions
  in the lowest sacral segments
• Incomplete - Preservation of sensory or motor
  function below the level of injury, including the
  lowest sacral segments

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Spinal Cord Injury

• Central cord syndrome
• cervical region injury leading to greater
  weakness in the upper limbs than in the lower
  limbs with sacral sensory sparing
• Brown-Séquard syndrome
• hemisection lesion of the cord
• relatively greater ipsilateral proprioceptive and
  motor loss with contralateral loss of sensitivity
  to pain and temperature
• Anterior cord syndrome
• variable loss of motor function and sensitivity
  to pain and temperature
• proprioception preserved
• Conus medullaris syndrome
• injury to the sacral cord and lumbar nerve roots
• areflexic bladder, bowel, and lower limbs
• sacral segments occasionally may show preserved
  reflexes (eg, bulbocavernosus and micturition
  reflexes).
• Cauda equina syndrome
• injury to the lumbosacral nerve roots in the
  spinal canal
• areflexic bladder, bowel, and lower limbs

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Neurogenic Shock

• Neurogenic shock occurs as peripheral vascular
  tone decreases
• Sudden loss of the autonomic nervous system
  signals to the smooth muscle in vessel walls
• With the sudden loss of background sympathetic
  stimulation, the vessels suddenly relax resulting
  in a sudden vasodilation
• Sx
• Hypotension
• Autonomic dysreflexia
• Cardiac arrhythmias (persistent bradycardia)
• Major cardiovascular complications can occur up
  to 30 days following acute SCI

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Neurogenic Shock

• Management
• Monitoring of cardiac and hemodynamic parameters
  in the acute phase of SCI
• Maintenance of a minimum mean arterial blood
  pressure of 85 mm Hg during the hyperacute phase
  (1 week after SCI)
• Timely detection and appropriate treatment of
  neurogenic shock and cardiac arrhythmias
• Immediate and adequate treatment of episodes of
  acute autonomic dysreflexia
• High risk for DVT and PE due to loss of mobility,
  altered fibrinolytic activity, abnormal platelet
  function
• thromboprophylaxis using mechanical methods and
  anticoagulants during the acute stage up to 3
  months following SCI
• Low-molecular-weight heparin is the first choice
  for anticoagulant prophylaxis in patients with
  acute SCI

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Use of Steroids

• 3 studies done on the use of methylprednisolone
  in acute SCI
• Consistent beneficial results have not been
  confirmed by subsequent studies
• Arbitrary choices of steroid dose and time limits
  for onset of therapy
• Use of megadose steroids or for 48 hrs associated
  with higher incidence of complications
• Sepsis
• Pulmonary embolism
• Wound infection
• GI hemorrhage
• Acute corticosteroid myopathy

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Steroid Use in Acute SCI

• 70 of Canadian spinal surgeons administering
  steroids for acute SCI did so out of fear from
  being sued or from peer pressure
• 17 of prescribing surgeons did so because they
  felt steroids were clinically effective

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Sources

• Dawodu, S. et al. Spinal Cord Injury Definition,
  Epidemiology, Pathophysiology. Emedicine.
  Accessed November 21, 2008.
• Furlan, J. et al. Cardiovascular complications
  after acute spinal cord injury pathophysiology,
  diagnosis, and management. Neurosurg Focus.
  200825(5)E13
• Guly, H. et al. The incidence of neurogenic
  shock in patients with isolated spinal cord
  injury in the emergency department.
  Resuscitation. 2008 Jan76(1)57-62. Epub 2007
  Aug 3.
• Hurlbert, R. et al. Methylprednisolone for
  Acute Spinal Cord Injury 5-year Practice
  Reversal. Can J. Neurol. Sci. 2008 3541-45.
• Miller, S. Methylprednisolone in Acute Spinal
  Cord Injury A Tarnished Standard. Journal of
  Neurosurgical Anesthesiology. Volume 20(2), April
  2008, pp 140-142.