Everything about Intensive care for Spinal Cord Injury Patients

1. .
.

2. An engg student from Venezuela; Was living with her father .
Then she moved to Texas
.

4. Car of Jacqueline.Hit by a 17yr
old boy driving in a drunken
state.

5. She was in the burning car for 45
seconds.

6. Following accident,she required 40
surgeries

8. Without a left eyelid,she needs
eyedrops to retain her vision

9. Reginald Stephey was convicted on two counts of
intoxicated manslaughter. He completed two
concurrent seven-year prison sentences . On May
20, 2011 Saburido again appeared on the 4th to
last episode of The Oprah Winfrey Show

10. Doctors are still working on her.

11. .Outline
• How to preserve what we have got
and how to get the best out of it?
• System wise intensive care Rx

12. SPINAL CORD
PROTECTIVE STRATEGIES
SURGICAL
PHARMACOLOGICAL

13. SURGICAL THERAPIES
NEUROLOGIC DETERIORATION ? RADIOLOGY?
CLOSED REDUCTION—SUCCESSFUL?
. SPINAL STABILITY---LOST?
Accepted Indications for Surgery
Progressive neurologic deterioration in an unstable spine,
especially with spinal canal compromise
Failure of closed reduction and stabilization of dislocation with
residual canal narrowing of > 50%
Unstable spine with dislocated bilateral "locked" facets
Unstable spine where nonunion is likely
Uncooperative patient with unstable spine risking further
neurologic injury
Compression of conus medullaris or cauda equina

14. Early Surgical Therapy
Experimental studies…. Go for it!
Clinical studies………..favourable outcome
Must occur <24 hrs, especially in incomplete
injuries
Late (>48hrs) only stabilizes spinal column and
helps rehabilitation

15. SURGICAL APPROACHES
ANTERIOR APPROACH
Your Text here
for removal of disk material, bone, or ligamentous tissue compressing
the spinal cord anteriorly
to treat unstable compression-flexion and distractive-flexion injuries,
often in conjunction with a decompressive corpectomy (removal of
vertebral body) if the cord is compressed
POSTERIOR APPROACH
for significant disruption of the posterior bony or ligamentous structures
of the cervical spine, particularly with minimal or no involvement of the
vertebral body
to treat occipitocervical and atlantoaxial instability and for spinal
instability causing flexion injuries
COMBINED APPROACH [BOTH ANT & POST STRUCTURES]
flexion teardrop fractures, vertical compression burst fractures with
significant posterior ligamentous injury, and bilateral facet dislocation with
disk compression of the spinal cord.

16. PHARMACOLOGICAL
STRATEGIES
CORTICOSTEROIDS
HYPOTHERMIA
HYPERTENSION

17. CORTICOSTEROIDS
stabilize membranes
• prevent the release of lysosomes and
. excessive Ca2+ ionic fluxes into cells
Improvement in blood flow
• Reduction in tissue edema,
• direct vasodilative effects of steroids
• antioxidant properties
alter ionic-clearing mechanisms
enhance Na+ K+-ATPase activity
inhibit lipid peroxidation formation

18. NASCIS
Your Text here
• R
Ref :trauma.org

19. NASCIS
NASCIS-I  No neurologic benefit; ? Inadequate
dose?
NASCIS-II patients treated within 8 hours of
injury showed significant improvement in motor
and sensory function Vs30 mg/kg, followed by 5.4 mg/kg/hr
Treatment 1:methylprednisolone,
placebo…..PRACTICE
for 23 hours
Treatment 2:naloxone, 5.4 mg/kg fol-lowed by 4 mg/kg/hr for 23 hours
Treatment 3:placebo
NASCIS-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

20. NASCIS-III
Treatment group 2 :especially among patients
whose therapy was initiated 3 to 8 hours after
injury ‘showed’ greater motor recovery at 6 weeks
and 6 months after injury than patients treated with
the same agent for 24 hours. [ post-hoc analysis;
NOT Level 1/Level 2/Level 3 ]
No functional benefit was demonstrated for the use
of steroid therapy in the treatment of penetrating

21. REAL STORY
NASCIS II flaws in study design and statistical
analysis, NASCIS III concerns regarding the
timing of surgery, the process of neurologic
assessment, and the fact that differences in motor
scores and functional outcome were clinically
negligible…no difference in the level of disability
MP-48-hour infusionhigher incidence of
infections
So STEROIDS ARE NOT STANDARD Rx IN A/C
SCI; JUST A TREATMENT OPTION

22. HYPOTHERMIA
Efficacy in mild to moderate traumatic SCI; not in
severe
Circulatory, pulmonary, metabolic, and
immunologic side effects
Only experimental; no clinical evidence
Hence this also is an option; not a standard Rx

23. Hypertension
In patients with hypo-perfusion
MAP above 85 mm Hg for the first 7 days after
injury is recommended to preserve neurologic
function because autoregulation is impaired… [No
definitive data]
more aggressive hypertensive therapy may have
advantages, but risk of hemorrhage and edema.

24. CONCLUSION
no clear benefit from any pharmacologic
therapy has yet emerged

25. MEDICAL THERAPY
PULMONARY SYSTEM
CARDIOVASCULAR SYSTEM
GIT
GENITO URINARY
TEMPERATURE CONTROL
COAGULATION

26. PULMONARY
SYSTEM
• The main key which we need to
keep the engine revving …. Never
loose it in SCI

27. PULMONARY SYSTEM
LEVEL VENT COUGH COMMENTS
FUN 0=no
0=no fun fun
+++= N/L +++=
N/L
ABOVE 0 0 Paralysis of diaphragm and accessory muscles,
C3 resulting in apnea; lifelong ventilator dependence
C3-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 ventilation
C5-C7 + to ++ +to ++ Paralysis of accessory muscles; marked reduction
in volumes with hypoxemia-recurrent atelectasis
and pneumonia; many patients need mechanical
ventilation; possible tracheostomy
HIGH ++ ++ Partial paralysis of accessory muscles; reduction in
Tx lung volumes with ateiectasis1 increased incidence
of pneumonia; possible need for mechanical

28. 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

29. 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

30. Lungs get drowned!
Pulmonary complications -- leading causes of
morbidity and early mortality -- seen in as many as
75% of patients.
The reduction of lung volumes and the inability to
generate an effective cough  progressive
retention of pulmonary secretions  gradual
microatelectasis and lobar atelectasis 
incremental hypoxemia and CO2 retention.

31. ↑WOB ALSO TROUBLES
Vital capacity improve in supine position! [↓RV]*
↓ed lung compliance, ↑ed WOB
Gastric atony ↔ pulmonary mechanics
In 2-5 wks , spinal shock state resolves
progressive spasticity of chest wall + abdomen
improve pulmonary function

32. Other pulmonary
complications
Ventilatory failure and aspiration were the earliest
to occur: at 4.5 days [Jackson and Groomes et al]

33. .
Protocol For Reduction of
Pulmonary Complications
in Patients with SCI

34. Aggressive pulmonary
hygiene
.
Frequent nasotracheal suctioning
• to remove secretions
Positional changes every 2 hours [KINETIC Rx- Start early]
• best achieved with rotational or circle beds
• effectively ↓es complications & Ventilator duration- ICU stay
Chest percussion every 4 hours
Assisted coughing exercises every 4 hours rs
Deep breathing exercises every 4 hours
Incentive spirometry every 4 hours

35. PROTOCOL…continued
.
Bronchodilator therapy for assisting secretion clearance and bronchodilator
effects [relative parasympathetic overactivity in tetraplegics-↑secretions]
Early use FOB in cases of lobar atelectasis secondary to retained
secretions
Early institution of mechanical ventilation
• in those with progressive labored breathing,
• increasing respiratory failure (hypoxia or hypercapnia)
• and vital capacities <1000 ml
Close monitoring of respiratory mechanics in patients receiving mechanical
ventilation
• with optimal use PEEP therapy and
• limitation of plateau pressure to <30 cm Hg

36. Anticipation is important
. • significant declines in
first 1 to 3 days pulmonary reserve
• progressive cord edema
first 2 days • Ascending neurologic
injuryso what will happen?
@admission-
diaphragm •VC check Q6H if <2L;
functioning  then If <1L &
respiratory failure symptomaticintubate

37. Start seeing through a
binocular into the long term
plans……
cervical SCI below C4 when spinal shock
resolves (2-3 weeks)  muscles develop spasticity
 improvement in lung volumes and overall
ventilatory ability eventual weaning from
mechanical ventilation
Nearly all patients with complete cervical SCI
above C6 will require a tracheostomy because of
the length of time on the ventilator and the difficulty

38. Suggested settings
ACMV / SIMV
Ventilator settings should be selected that limit the
occurrence of ventilator-associated lung injury
PEEP is added to recruit collapsed alveoli and
prevent further atelectasis

39. Shift gears accordingly…
Chest trauma is associated with SCI
pulmonary contusions, rib fractures,
pneumothorax, hemothorax, and ARDS.
May result in prolonged mechanical ventilation with
difficult weaning and delayed operative spinal
intervention.

40. Fluid plays… Don’t SLIP
Neurogenic Pulmonary oedema : Neurogenic
increases in extravascular water  pulmonary
edema [both in head injury and in SCI; ?related to
the initial sympathetic discharge]
Cardiogenic pulmonary edema : reduced
myocardial inotropy [in high SCI] , overzealous
fluid administration.
Because of the hemodynamic alterations observed
in SCI (hypotension, bradycardia), the usual

41. CARDIOVASCULAR
SYSTEM
• Body systems also crash like a
vehicle after the impact

42. Spinal cord…. Does it belong to CNS or
CVS!!!!
complete cervical SCI has the most pronounced
physiologic effects, consisting of cardiovascular
instability, cardiac dysrhythmias, and ventricular
dysfunction
SCI below T5 results in varying degrees of
hypotension caused by the functional
sympathectomy below the level of injury
DISTINCTLY DIFFERENT MECHANISMS…

43. The Sympathetic BOMB
BLAST
A transient severe increase in blood pressure
caused by an extensive sympathetic discharge at
the time of injury
The systolic blood pressure may be as high as 300
mm Hg, lasting 2 to 5 minutes, with a gradual
decline to values less than baseline
may be responsible for the noncardiogenic
pulmonary edema

44. Aftermath…..
After this HYPOTENSION predominates [ in all
patients with complete cervical SCI ]
Due to vasodilatation 20 to withdrawal of
sympathetic neural outflow
Its a functional sympathetic blockade [sympathetic
receptors lose their normal input and regulation]
Parasympathetic system remains intact since… the
vagus nerve exits from the brainstem.

45. ‘Shock’ing consequences
autonomic imbalance leads to….

46. SPINAL SHOCK
seen with physiologic or anatomic transection, or
near transection, of the spinal cord
consists of the loss of somatic motor and sensory
function below the level of injury, loss of voluntary
rectal contraction, and loss of sympathetic
autonomic function

47. SPINAL SHOCK continued
The more severe the functional spinal cord
transection and the higher the level of injury, the
greater the severity and duration of spinal shock.
If the loss lasts longer than 1 hour, pathologic
injuries to the spinal cord, as opposed to a
transient concussive injury are assumed to exist

48. Lack of speed kills….
Beware of the bradycardia in SCI
complete cervical SCI +++; thoracic and lumbar
injuries +/-
interruption of the cardiac accelerator nerves (Tl to T4)
First 2 wks-most dangerous ; resolves over 3- to 5-
weeks
profound degrees of bradycardia, even cardiac arrest,
may occur during turning or tracheal suctioning
sedation, 100% oxygen before suctioning, and limiting
the time allowed for suctioning
Rx: Atropine, Temporary pacemaker

49. What has fallen there…?
SBP < 90 mm of Hg / 30% below baseline
goal : ? MAP > 85 mm of Hg for first 7 days
correction of hypotension is crucial for optimal
preservation of neurologic function and reduction of
20 injury
No autoregulation; so aggressive Rx
Neurogenic shock relative hypovolemia due to
vasodilation  so fill, but carefully [pulmonary
edema]
[1]Blood : to maintain Hb>10g
[2]Fluids : isotonic crystalloids / ?HYPERTONIC

50. DON’T ‘PRESS’ TOO MUCH
vasopressor Vs inotropic
agents
potent ά-agonist substantial increases in
afterload  impair cardiac O/P can precipitate
LVF inotropic agent is often the drug of choice
for maintaining spinal cord perfusion
Invasive hemodynamic monitoring is
recommended
There is evidence to support improvement in
neurologic outcome in whom hemodynamics are
managed aggressively.
SC edema is maximal at 3 to 6 days after injury,
blood pressure support should continue during this

51. Arrhythmias
Experimental models & clinical reports shown --
Cardiac dysrhythmias [suppressed by atropine]
tachycardia, and ST T wave changes [suppressed
by propranolol]
The initial response to spinal cord compression--
sympathetic discharge  elicited a secondary,
compensatory, parasympathetic discharge
autonomic imbalance responsible for the cardiac
dysrhythmias

52. Arrhythmias continued
..
TYPE persistent bradycardia Primary cardiac arrest
severe cervical SCI 31/31 5/31
mild 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

53. GASTROINTESTINAL
SYSTEM
Issues Comments
.
Gastric distention Increased risk of aspiration
Gastric emptying delayed Adversely affect ventilation
Rx : put N-G tube
peptic ulcer disease One cause- high dose steroids
gastritis, Rx: PPI, Sucralfate [continued for 4
hemorrhage weeks] Enteral feeding
Ileus
acalculous cholecystitis
occult acute abdomen patients with SCI may not
demonstrate the usual signs and
symptoms
elevated metabolic rates early nutritional supplementation

54. GENITO URINARY
SYSTEM
• .

55. GENITO URINARY SYSTEM
. INITIAL PHASE
FLACCID BLADDER CATHETERISE
LATER
BLADDER SPASTICITY
PERSISTANT URINARY PROBLEMS
NEPHROCALCINOSIS,
RECURRENT UTI , STONES
RECURRENT BOUTS OF UROSEPSIS

56. TEMPERATURE
CONTROL
• .

57. TEMPERATURE CONTROL
The body temperatures of patients with complete
SCI tend to approach that of the environment
No regulatory mechanisms like vasoconstriction/
sweating
prone to hypothermia

58. COAGULATION
• .

59. 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 thoracic
miury

60. Diagnosis and Treatment
Diagnosis
CLINICAL SUSPICION
D-DIMER LEVELS,
VENOGRAPHY,
COLOR FLOW DUPLEX IMAGING
CT ANGIOGRAPHY,
PULMONARY ANGIOGRA-PHY
Treatment
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%.

61. AUTONOMIC
HYPERREFLEXIA
• .

63. AUTONOMIC
HYPERREFLEXIA
occurs in 85% of patients with spinal cord
transections above T5
is secondary to autonomic vascular reflexes, which
usually begin to appear about 2 to 3 weeks after
injury
Afferent impulses from bladder or bowel distention,
manipulations of the urinary tract, or surgical
stimulation  the pelvic, pudendal, or hypogastric
nerves to the isolated spinal cord  a massive
sympathetic response from the adrenal medulla
and sympathetic nervous system, which is no
longer modulated by the normal inhibitory impulses

64. AUTONOMIC
HYPERREFLEXIA
Vasoconstriction occurs below the lesion;
reflex activity of carotid and aortic baroreceptors
produces vasodilation above the lesion
often accompanied by bradycardia, ven-tricular
dysrhythmias, and even heart block.
Sedation or topical anesthesia does not appear to
attenuate the hypertensive response, but deep
general, epidural, or spinal anesthesia is effective
Hypertension Rx
direct-acting vasodilators (e.g., sodium nitroprusside)
beta blocking agents (e.g., esmolol),
combination beta blockers (e.g., labetalol), or
ganglionic blocking agents e.g.,trimethaphan
CCBs (nicardipine),

66. OTHER ISSUES
• .

67. Infections
leading cause of death
pneumonia, urosepsis

68. HYPERREFLEXIC SYNDROMES
muscle spasms caused by hyper-active spinal
reflexes without the tempering effect of modulating
cortical, brainstem, and cerebellar influences.
This "mass reflex" may make the management of
the unanesthetized patient difficult.

69. PRESSURE ULCERS
direct pressure effects, reduced tissue perfusion,
and limited mobility.
The use of rotational beds, frequent patient turning,
good skin care, foam padding of bony
prominences, or air floatation beds can help
prevent pressure ulcers.

70. LONG-TERM IMMOBILIZATION
altered calcium metabolism
painful heterotopic ossification
calcification of muscles
joint immobility
osteoporosis with hypercalcemia
nephrocalcinosis and secondary renal failure.
Late mobilization  pathologic fractures.
Early institution of active physical therapy is
essential

71. THANK YOU
• LET’S TRY TO MAKE OUR ROLES
MORE AND MORE JUSTIFIABLE IN
THIS WORLD