..

Intensive care of spinal trauma patients

..

Dr Unnikrishnan P,Neuroanaesthesia,

Sree Chitra Thirunal Institute for Medical

Sciences and Technology,Kerala,India

.

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

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

She was in the burning car for 45 seconds.

Following accident,she required 40 surgeries

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

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

Doctors are still working on her.

.Outline

• How to preserve what we have got and how to get the best out of it?

• System wise intensive care Rx

SPINAL CORD PROTECTIVE STRATEGIES

SURGICALPHARMACOLOGICAL

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

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

SURGICAL APPROACHES

Your Text hereANTERIOR APPROACH

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 injuriesCOMBINED 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.

PHARMACOLOGICAL STRATEGIES

CORTICOSTEROIDS

HYPOTHERMIA

HYPERTENSION

CORTICOSTEROIDS

.

stabilize membranes• prevent the release of lysosomes

and excessive Ca2+ ionic fluxes into cellsImprovement in blood flow

• Reduction in tissue edema,• direct vasodilative effects of steroids• antioxidant propertiesalter ionic-clearing mechanismsenhance Na+ K+-ATPase activity

inhibit lipid peroxidation formation

NASCIS

Your Text here• R

Ref :trauma.org

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 Vs placebo…..PRACTICE

NASCIS-III MP 30 mg/kg within 8 hrs f/b

Treatment 1:methylprednisolone, 30 mg/kg, followed by 5.4 mg/kg/hr for 23 hoursTreatment 2:naloxone, 5.4 mg/kg fol lowed by 4 mg/kg/hr for 23 hoursTreatment 3:placebo

Treatment 1: Methyprednisolone 5.4 mg/kg/hr for 24 hoursTreatment 2: Methyprednisolone 5.4 mg/kg/hr for 48 hoursTreatment 3: Tirilizad mesylate 2.5 mg/kg every 6 hours for 48 hours

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 SCI

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 disabilityMP-48-hour infusionhigher incidence of infections So STEROIDS ARE NOT STANDARD Rx IN A/C SCI; JUST A TREATMENT OPTION

HYPOTHERMIA

Efficacy in mild to moderate traumatic SCI; not in severeCirculatory, pulmonary, metabolic, and immunologic side effectsOnly experimental; no clinical evidenceHence this also is an option; not a standard Rx

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.

CONCLUSION

no clear benefit from any pharmacologic therapy has yet emerged

MEDICAL THERAPY

PULMONARY SYSTEMCARDIOVASCULAR SYSTEMGITGENITO URINARYTEMPERATURE CONTROLCOAGULATION

PULMONARY SYSTEM• The main key which we need

to keep the engine revving …. Never loose it in SCI

PULMONARY SYSTEMLEVEL VENT

FUN0=no fun+++= N/L

COUGH0=no fun+++= N/L

COMMENTS

ABOVE C3

0 0 Paralysis of diaphragm and accessory muscles, 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 Tx

++ ++ Partial paralysis of accessory muscles; reduction in lung volumes with ateiectasis1

increased incidence of pneumonia; possible need for mechanical ventilation

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 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.

↑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

Other pulmonary complications

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

(noncardiogenic, cardiogenic)

aspiration pneumonitis

coexisting blunt chest trauma (pulmonary contusions, hemothorax)

.

Protocol For Reduction of Pulmonary Complications in Patients with SCI

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 stayChest percussion every 4 hours

Assisted coughing exercises every 4 hours rs

Deep breathing exercises every 4 hours

Incentive spirometry every 4 hours

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 mlClose monitoring of respiratory mechanics in patients

receiving mechanical ventilation• with optimal use PEEP therapy and• limitation of plateau pressure to <30 cm Hg

Anticipation is important

. • significant declines in pulmonary reservefirst 1 to 3 days

• progressive cord edema• Ascending neurologic

injuryso what will happen?

first 2 days

@admission- diaphragm

functioning then respiratory

failure

• VC check Q6H if <2L;If <1L & symptomaticintubate

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 with clearing

secretions. In this setting, a tracheostomy

should be placed early

Suggested settings

ACMV / SIMV Ventilator settings should be selected that limit the occurrence of ventilator-associated lung injuryPEEP is added to recruit collapsed alveoli and prevent further atelectasisVt of 6 to 8 mL/kg

PEEP of 5 ; plateau pressure of <30 mm Hg

RR of 8 to 15 breaths/min

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.

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 indicators of fluid adequacy are unreliable

CARDIOVASCULAR SYSTEM• 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

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…

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 baselinemay be responsible for the noncardiogenic pulmonary edema

Aftermath…..

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

‘Shock’ing consequences

autonomic imbalance leads to….

inadequate cardiac contraction

loss of tonic vasoconstriction

hypotension, bradycardia, and hypothermia termed neurogenic shock

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

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

Lack of speed kills….

Beware of the bradycardia in SCIcomplete 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-weeksprofound degrees of bradycardia, even cardiac arrest, may occur during turning or tracheal suctioningsedation, 100% oxygen before suctioning, and limiting the 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 optimal preservation of neurologic function and reduction of 20 injuryNo autoregulation; so aggressive RxNeurogenic shock relative hypovolemia due to vasodilation so fill, but carefully [pulmonary edema][1]Blood : to maintain Hb>10g[2]Fluids : isotonic crystalloids / ?HYPERTONIC SALINE improve SCBF & preserve spinal cord function

DON’T ‘PRESS’ TOO MUCHvasopressor Vs inotropic agentspotent 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 perfusionInvasive hemodynamic monitoring is recommendedThere 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 period.

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

Arrhythmias continued

..

frequency of brady-dysrhythmias was maximal on day 4 after injuryall abnormalities resolved over a 14-day to 6-week period

TYPE persistent bradycardia

Primary cardiac arrest

severe cervical SCI 31/31 5/31

mild cervical SCI 6/17 -

thoracolumbar SCI 3/23 -

GASTROINTESTINAL SYSTEM

.Issues Comments

Gastric distentionGastric emptying delayed

Increased risk of aspirationAdversely affect ventilationRx : put N-G tube

peptic ulcer diseasegastritis,hemorrhage

One cause- high dose steroidsRx: PPI, Sucralfate [continued for 4 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

GENITO URINARY SYSTEM• .

GENITO URINARY SYSTEM

.

PERSISTANT URINARY PROBLEMS

RECURRENT UTI , STONESNEPHROCALCINOSIS,

RECURRENT BOUTS OF UROSEPSIS

LATER

BLADDER SPASTICITY

INITIAL PHASE

FLACCID BLADDER CATHETERISE

TEMPERATURE CONTROL• .

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

COAGULATION• .

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 patientsthird leading cause of deathmoreoften with complete SCI and thoracic miury

Diagnosis and Treatment

Diagnosis

Treatment

CLINICAL SUSPICION D-DIMER LEVELS,VENOGRAPHY,COLOR FLOW DUPLEX IMAGING CT ANGIOGRAPHY,PULMONARY ANGIOGRA-PHY

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 HYPERREFLEXIA• .

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 arising from the brainstem and hypothalamus

AUTONOMIC HYPERREFLEXIA

Vasoconstriction occurs below the lesion; reflex activity of carotid and aortic baroreceptors produces vasodilation above the lesionoften 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 effectiveHypertension Rxdirect-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),

OTHER ISSUES

• .

Infections

leading cause of death

pneumonia, urosepsis

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.

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.

LONG-TERM IMMOBILIZATION

altered calcium metabolismpainful heterotopic ossification calcification of muscles joint immobility osteoporosis with hypercalcemianephrocalcinosis and secondary renal failure. Late mobilization pathologic fractures.Early institution of active physical therapy is essential

THANK YOU

• LET’S TRY TO MAKE OUR ROLES MORE AND MORE JUSTIFIABLE IN THIS WORLD