Spinal Cord Lesions

Jia Yan-jie M.D Ph.D 贾 延劼
Department of Neurology, the First Affiliated Hospital, Zhengzhou University

CNS Brain Spinal Cord

Brain Vascular Degenerative Inflammatory Trauma Infectious Spinal Cord Trauma or mechanical Tumor Inflammatory Infectious Vascular


Major cause of disability in spinal
cord due to effects on motor, sensory and autonomic pathways.

Most common causes are
compression due to trauma and metastatic cancer.



Anatomy and Physiology

Spinal cord Dorsal root ganglion Spinal nerve Vertebra

Meninges (protective coverings)

Intervertebral disk Sympathetic ganglion chain

Cervical cord

Cervical nerves


Thoracic cord

Thoracic nerves

Lumbar cord Sacral cord

Lumbar nerves Sacral nerves Coccygeal nerve Cauda equina

Anatomy and Physiology
C1—C4 C5-T4 T5—T8 T9—12 L1—5 12 +1 +2 +3 T10 、 11 、



S2 Medullary anaesthesia Spinal puncture

A region of the body surface innervated by sensory fibers from the dorsal roots of a single spinal cord segment is a dermatome.

Anatomy and Physiology

Anatomy and Physiology

Anatomy and Physiology

Anatomy and Physiology

Anatomy and Physiology

Corticospinal tract, anterior

Corticospinal tract, lateral

Anatomy and Physiology

Motoneuron in spinal cord

Anatomy and Physiology
Somatosensory modalities = bodily sensations of touch, pain, temperature, vibration, and proprioception The somatosensory pathways are 2 long sensory tracts 1. Posterior column – medial lemniscus system Proprioception, vibration, fine discriminative touch 2. Anterolateral system (including the spinothalamic tract) Pain, temperature, crude touch

Anatomy and Physiology

Dorsal root entry zone Posterior (dorsal) columns Posterior (dorsal) column nuclei Gracile fasciculus Cuneate fasciculus Nucleus gracilis Nucleus cuneatus Internal arcuate fibers Medial lemniscus Ventral posterior lateral nucleus of thalamus Posterior limb of internal capsule Thalamic radiations Primary somatosensory cortex

Trigeminal sensory fibers go to Dorsal column –posterior medial nucleus ventral medial lemniscus of thalamus system

Anatomy and Physiology

Dorsal root entry zone Some axons ascend/descend a few segments in Lissauer’s tract Lamina I and lamina 5 Spinal cord anterior commissure Ascend diagonally over 2-3 cord segments and enter the Contralateral spinothalamic tract Ventral posterior lateral nucleus of thalamus Primary somatosensory cortex Trigeminal fibers go to ventral posterior medial nucleus of thalamus Spinoreticular tract (old pain path) Spinomesencephalic tract (PAG) Anterolateral (spinothalamic) system

Anatomy and Physiology

Anatomy and Physiology


Acute infectious disease, in severe
form, affects the central nervous system with destruction of lower motor neurons in spinal cord resulting in flaccid paralysis.

 Associated with man since ancient times  Egyptian hieroglyph indicates presence since 1400 BC  1840 - Heinle characterizes poliomyelitis  Poliomyelitis – “grey marrow” in Greek  1954 - Salk vaccine  1960 - Sabin vaccine  1991 – Molla produces polio in vitro from virus RNA  2002 – completele synthetic production

History Summer of 1916:
epidemic struck New York City -27,000 people paralyzed -9,000 people dead

 Small; 28 – 30 nm in diameter  Structure is intersection of icosahedron and dodecahedron  3 external capsid proteins (VP1, VP2, and VP3) with conserved antiparallel beta barrel cores  Capsid structural stability extremely temperature sensitive  B – C loop of VP1 important for antigenic site  Sequence canyon formed between proteins important for immunological reasons and receptor binding


Cell Binding and Entry
 Binds only to poliovirus receptor (Pvr)  Pvr is a transmembrane glycoprotein with three extracellular immunoglobulin like domains  Pvr is involved with actin skeleton  Poor viral entry probability ( 0.1 - 1%)

Cell Binding and Entry

Poliovirus Genome
 Single RNA molecule ~7500 nucleotides  3 sub-regions with 10 protein products  IRES (internal ribozyme entry site)important for virulence

Anti-Host Activity
 Shuts off host transcription  2B, 2BC, and 3A interfere with apoptotic pathways  3A causes tumor necrosis receptor depletion, making cell resistant to TNFα necrosis  2BC, 3A interfere with antiviral cytokine secretion  Many transcription factors bound rather than proteolysed  Increases cell membrane lipid composition, leads to membrane rupture  5’ UTR determines if the virus will by lytic or nonlytic

RNA Replication
 RNA polymerase (3D)  RNA is copied into –RNA template for further RNA replication; no free -RNA  50:1 ratio +RNA: -RNA  Vpg is used as primer for both + RNA synthesis and –RNA synthesis  Quality control proteins to maintain only intact RNA is used for replication  Mutation prone synthesis, ~1 mutation/ replication

 Specificity to receptor restricts mutation rate; slow genetic drift  Occur because of immunological reasons, vary at sequence canyon  Three serotypes with no cross immunity  Type 1 polio 90% Weakest, only 1% causes neuroparalysis  Type 2 polio 9% (Eliminated)  Type 3 polio 1% Greater temperature stability  Requires trivalent polio vaccine  Polioviruses can also vary in phenotype of virulence, host cell lysis, and ability to raise host defense triggers


 Symptoms of poliomyelitis always CNS specific  Neurological symptoms found in 1-2% of infected individuals  Three possible routes of entry into CNS  Retrograde axonal transport  Transport across blood – brain barrier  Transport via infected macrophages (Trojan Horse)  Specific to CD155 (Pvr) receptor  Tropic to lower spinal cord and alimentary tract  5’ NTR key to neurovirulence, especially IRES(

entry site)

internal ribozyme

 Virus with rhinovirus analogue IRES fails to propagate in neuronal cells  Provocation Poliomyelitis


 Salk or Inactivated Polio Vaccine (IPV) –1954
   

Formalin killed virus Balance between killing virus and antigenicity (Cutter Incident) Difficult to produce in mass quantities Does not work in tropical climates because of interference from other entric viruses Alters IRES function Reduces virus efficiency, replication rate, neuronal invasion Risk of reversion to more virulent form through mutation
1 in 1.2 million vaccinations produces neuronal effects

 Sabin or Oral Polio Vaccine (OPV) – 1960
  


 Historically, 0.5% of population became paralyzed by poliomyelitis  Easily transmissible, less than 1% clinically recognizable  1988 – World Health Assembly calls for global polio eradication by 2005

Decline in Poliomyelitis

World Polio Map

World Polio Map

World Polio Map

World Polio Map

The World Health Organization hopes to completely wipe out polio by


Subacute combined degeneration of the spine cord Vitamin B12 is needed for integrity of
myelin. In severe deficiency, insidious, diffuse, uneven demyelination – clinically manifested:
peripheral Spinal


cord degeneration affecting both posterior and lateral columns
Cerebral Optic

degeneration (dementia)


Subacute combined degeneration of the spine cord

Subacute combined degeneration of the spine cord
Vit B12 Deficiency Vit B12 Deficiency
Dietary - Vegans - Breastfed offspring of vegans Gastric disorders Pernicious anaemia Small Bowel disorders

Subacute combined degeneration of the spine cord Microscopically, spongy changes and foci of myelin and
axon destruction are seen in the white matter of the spinal cord. The most severely affected areas include the posterior and lateral columns of the cervical and upper thoracic spinal cord. In the peripheral nervous system, axonal degeneration, without significant demyelination, is seen. In some cases, involvement of the optic nerve and cerebral white matter can be seen.

Clinical features Neurologic manifestations
- proprioceptive and vibratory sensation, spinal ataxia - megaloblastic madness or psychosis symptoms of anemia gastrointestinal compraints - loss of appetite - glosstis (red, sore, smooth tongue) - diarrhea or constipation

•Vitamin B12 administration intramuscular in dose 1000 μg per day for a week , then 100 μg 2x per week for 2 weeks, 1 x per week 100μg for month •Reticulocytosis begins 2 or 3 days after therapy started and maximal number reached on day 5 to 8. •Serum iron monitoring, after 7-10 days of vit.B12 treatment, if Fe deficiency is diagnosed we should start iron substitution •100 ug vit.B12 i.m. every month, regimen that must be maintained for the rest on the patients life.

     A sensory level and motor dysfunction Abnormal sphinocteric function Spinal shock Myelitis Nerve Roots or Peripheral Nerves Distal symmetrical polyneuropathies cause bilateral sensory loss in a "glove and stocking" distribution in all modalities. Specific nerve or nerve root lesions cause sensory loss in specific territories. Associated deficits of lesions of the peripheral nerves or nerve roots often include LMN-type weakness.


 Transverse Cord Lesion All sensory and motor pathways are either partially or completely interrupted. There is often a sensory level.The pattern of weakness and reflex loss can also help determine the spinal cord level. Common causes of transverse cord lesions include trauma, tumors, multiple sclerosis, and transverse myelitis.

KEY CLINICAL CONCEPTS SPINAL CORD LESIONS  Hemicord Lesions: Brown-Sequard Syndrome Damage to the LCST causes ipsilateral UMN-type weakness. Interruption of the posterior columns causes ipsilateral loss of vibration and joint position sense. Interruption of the ALS (anterolateral sclerosis) causes contralateral loss of pain and temperature sensation.

 Central Cord Syndrome
Spinothalamic fibers causes bilateral regions of suspended sensory loss to pain and temperature. Lesions of the cervical cord: the classic cape distribution; With larger lesions, the anterior horn cells are damaged, producing LMNS UMN when CST(corticospinal tract) are affected Spinal cord contusion, posttraumatic syringomyelia, and spinal cord tumors.


 Posterior Cord Syndrome loss of vibration and position sense below the level of the lesion. With larger lesions, there may also be encroachment on the LCST causing UMN-type weakness. Common causes include trauma, compression from posteriorly located tumors, multiple sclerosis vitamin B12 deficiency and tabes dorsalis.

KEY CLINICAL CONCEPTS SPINAL CORD LESIONS  Anterior Cord Syndrome Damage of: ALS(anterolateral sclerosis) pathways; loss of pain and temp. sensation below the level of the lesion;to the anterior horn cells produces LMNS at the level of the lesion; larger lesions, the LCST causing UMN signs. Incontinence is common Causes include trauma, multiple sclerosis, and anterior spinal artery infarct.

KEY CLINICAL CONCEPTS SPINAL CORD LESIONS  Bladder, Sexual Lubrication, Erectile and Ejaculatory Function  Acontractile (flaccid, atonic) or hyperreflexic (spastic) bladder include trauma, tumors, transverse myelitis, and multiple sclerosis.  Lesions of the peripheral nerves, or of the spinal cord at S2 to S4, usually cause a flaccid areflexic bladder; overflow incontinence.

Upper Motor Neuron Lesion

 Following a bilateral lesion of the entire spinal cord at C2 the detrussor initially becomes flaccid (like arm and leg muscles following a lesion of the LCST) resulting in urinary retention.  With time spasticity develops and the bladder contracts with small degrees of stretch: urinary frequency and urgency.  In acute lesions of the spinal cord rostral to the sacral cord (UMNL), two things occur. First there is a flaccid bladder (acute), then later there is a spastic bladder (chronic).

Lower Motor Neuron Lesion

 LMNL results in weakness, atrophy, and hyporeflexia. The bladder does not contract and, if the sensory afferents are affected, no sensation of a full bladder will be perceived.  Remember, lesions of the spinal cord rostral to the sacral cord result first in a flaccid (atonic; acute) bladder, followed by a spastic (chronic) bladder. Lesions from S1 down, and involving all of the various nerves, result in ONLY a flaccid bladder.

Term definition
 Paresis Weakness (partial paralysis) Hemiparesis Weakness of one side of body (face, arm, and leg)  -plegia No movement Hemiplegia No movement of one side of body (face, arm, and leg)  Paralysis No movement  Palsy Imprecise term for weakness or no movement  Facial palsy Weakness or paralysis of face muscles

Term definition
 HemiOne side of body (face, arm, and leg) Hemiparesis Weakness of one side of body (face, arm, and leg)  ParaBoth legs Paraparesis Weakness of both legs  MonoOne limb Monoparesis Weakness of one limb (arm or leg)  DiBoth sides of body equally affected Facial diplegia Symmetrical facial weakness  Quadri- or Tetra- All four limbs Quadriplegia (tetraplegia) Paralysis of all four limbs

Transverse Cord Lesion
all sensory and motor pathways partially or completely interrupted. Dermatomes affected will give localization

trauma, tumors, MS, transverse myelitis

Central Cord Syndrome

Central Cord Syndrome
 Small lesion gives sensory loss in cape distribution due to damage to anterior white commissure fibers.  Large lesions often include ventral horn neurons giving LMN symptoms.  Corticospinal tracts can be damaged giving UMN deficits.  Dorsal columns are also often damaged.  Sacral sparing can occur due to somatotopic organization of spinothalamic tract.

Causes include cord contusion, posttraumatic syringomyelia,
and intrinsic cord tumors.


Anterior cord syndrome

Compression of the ant. Cord, usually a flexion injury Sudden, complete motor paralysis at lesion and below; decreased sensation (including pain) and loss of temperature sensation below site. Touch, position, vibration and motion remain intact.

Posterior cord syndrome
 Assocciated with cervical hyperextension injuries  Dorsal area of cord is damaged resulting in loss of proprioception  Pain, temperature sensation and motor function remain intact.

Brown-Sequard syndrome
 Damage to one half of the cord on either side.  Caused by penetrating trauma or ruptured disk. ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis(MS) BSS may be caused by a spinal cord tumor, trauma (such as a puncture wound to the neck or back),.  a rare SCI syndrome which results in  weakness or paralysis (hemiparaplegia) on one side of the body and  a loss of sensation (hemianesthesia) on the opposite side.

acute (developing over hours to several days)

Acute myelitis

subacute (developing over 1 to 2 weeks).

Acute transverse impairments caused by demyelination or necrosis on white matter of the myeline. Such as: myelitis following infection, myelitis following vaccine inoculation, demyelinative myelitis, necrosis myelitis, para-tumor myelitis.

Myelinated nerve fibers in SC

• Similar to Myelinated nerve fibers in PNS;
• No neurolemma, no incisures of Schmidt-Lanterman;

Myelin sheath is formed by processes of oligodendrocytes.

Acute myelitis

• Researchers are uncertain of the exact causes of transverse

auto-immune reaction in association with a viral infection or vaccine inoculation 1~4 weeks ago. But there were no detective virus in nervous tissues, also no antibodies in CSF(cerebrospinal fluid) detected.

Acute myelitis
 Every segment may be involved, Range: T3~5, cervical or lumbar segment.Focal or transverse lesions,  Findings under naked eyes  Findings under microscope

Clinical features

 The youth & post adolescent,  No difference between the two sex.  Infection or vaccine inoculation history  Inducement of cold, overfatigue, trauma

Clinical features
Acute onset, gets to the peak after several hours or 2~3 days. The initial symptoms: Numbness and weakness Backache and girdle sensation The most frequent sites: T3-5,

Clinical features

• •

Dyskinesia: spinal shock 2~4weeks upper motor neuron paralysis Sensory disturbance Autonomic nerves dysfunction

Clinical features

From this wide array of symptoms, four classic features of transverse myelitis emerge: (1) weakness of the legs and arms, (2) pain, (3) sensory alteration, and (4) bowel and bladder dysfunction.

Clinical features

Pain is the primary presenting symptom of
transverse myelitis in approximately one-third to one-half of all patients. The pain may be localized in the lower back or may consist of sharp, shooting sensations that radiate down the legs or arms or around the torso.

Clinical features

Patients who experience sensory disturbances often
use terms such as numbness, tingling, coldness, or burning to describe their symptoms. Up to 80 percent of those with transverse myelitis report areas of heightened sensitivity to touch, such that clothing or a light touch with a finger causes significant discomfort or pain (a condition called allodynia). Many also experience heightened sensitivity to changes in temperature or to extreme heat or cold. .

Clinical features

Bladder and bowel problems may involve
increased frequency of the urge to urinate or have bowel movements, incontinence, difficulty voiding, the sensation of incomplete evacuation, and constipation. Over the course of the disease, the majority of people with transverse myelitis will experience one or several of these symptoms.

Clinical features
Acute ascending myelitis Demyelinative myelitis

1. Blood routine test Rule out various disorders such as systemic lupus erythematosus, HIV infection, and vitamin B12 deficiency. 2. Examination of the CSF: normal pressure, The cerebrospinal fluid that bathes the spinal cord normal or increased white cell count, and brain contains more protein than usual and an slightly increased protein concentration, increased number of leukocytes (white blood cells), indicating possible infection. normal glucose and chloride


3.Electro-physiologic examination: VEP(visual evoked potential) 、 SEP(sensory evoked potential) 、 MEP 。 4. Iconographic examination



Diagnosis Physicians diagnose transverse myelitis by taking a
medical history and performing a thorough neurological examination. If none of all tests suggests a specific cause, the patient is presumed to have idiopathic transverse myelitis.

• • • 

Acute onset The history of infection and vaccine inoculation The symptoms of cord transverse or focal impairment The examination of CSF \ Electro-physiologic examination\MRI (magnetic resonance imaging)

Differential diagnosis

Acute epidural abscess Spinal hemorrhage Carcinomatous metastases

Differential diagnosis

Neuromyelitis optica
A subtype of multiple sclerosis, neuritis optica: decline of eyesight signs reflecting multiple focus, such as: nystagmus, diplopia, ataxia.

Treatmment As
with many disorders of the spinal cord, effective cure currently exists for people with transverse myelitis.



are designed to manage and alleviate symptoms and largely depend upon the severity of neurological involvement.

Therapy generally begins when the patient first experiences symptoms. Physicians often prescribe corticosteroid therapy during the first few weeks of illness to decrease inflammation. Although no clinical trials have investigated whether corticosteroids alter the course of transverse myelitis, these drugs often are prescribed to reduce immune system activity because of the suspected autoimmune mechanisms involved in the disorder.

The principle of treatment in the acute stage:

Corticosteroids are often prescribed
• • •

Proper antibiotics to prevent infection Emphasis of nutrition, Emphasis of nursing, prevent complications.

Following initial therapy, the most critical part of the treatment for this disorder consists of keeping the patient’s body functioning while hoping for either complete or partial spontaneous recovery of the nervous system.

Treatment in recovery phase
Physical Therapy Occupational Therapy Vocational Therap

 Recovery from transverse myelitis usually begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years  About one-third of people affected with transverse myelitis experience good or full recovery from their symptoms

 Another one-third show only fair recovery and are left with significant deficits such as spastic gait, sensory dysfunction, and prominent urinary urgency or incontinence  The remaining one-third show no recovery at all, remaining wheelchair-bound or bedridden with marked dependence on others for basic functions of daily living.

 The majority of people with this disorder experience only one episode although in rare cases recurrent or relapsing transverse myelitis does occur.  In all cases of relapse, physicians will likely investigate possible underlying causes such as MS or systemic lupus erythematosus

Compression myelopathies
 The symptoms and signs of spinal cord compression consists of sensory (pain, numbness and paresthesia), motor and autonomic disturbances, the nature and extend of which is related to:  The level that is compressed  The direction from which the compression originates  The speed with which the compression is accomplished

Compression myelopathies
 Extra-medullary tumors The loss of pain and temperature appears first, and is most complete, in the sacral dermatomes. As the tumor expands, the sensory loss


Compression myelopathies

Intra-medullary tumors

Compression myelopathies
 The pain and temperature loss starts near the level of the tumor  As the tumor grows laterally within the ALS(anterolateral sclerosis),deficit DESCENDS LOWER to the location of the lesion,(sacral sparing) before the sensory loss is complete.  Lesions within the center of the spinal cord cause a symmetrical loss of pain and temperature, usually with sparing of other sensory modalities,ex. Syringomyelia.

Lesions within the spinal cord

The dorsal columns
 Dorsally situated tumors compress the dorsal or posterior column first, and cause paresthesia (funny sensations), numbness and impairment of 2-point discrimination, vibration and conscious proprioception on the side of the tumor.  The "Lhermitte sign." an electric shock like sensation running through the back and limbs upon flexion of the neck.  Lesions in the cervical cord (compression, multiple sclerosis, subacute combined degeneration from B12 deficiency).

Figure: The dorsal (posterior) columns





Spinal Cord Injuries
Incidence –40/million –10,000 new cases per year –Does not include those who die at scene 4/million or 1,000 per year Prevalence –200,000 – 400,000 in US

Spinal Cord Injuries
Life expectancy greatly increased since WW II. –Intermittent catheterization –Medications, equipment, etc Cause of premature death is usually related to COMPROMISED RESPIRATORY FUNCTION

Spinal Cord Injuries
 Age at injury increasing
 

Mean 32 years More people 60 years+ at time of injury

 80% male  Neurologic level and completeness (ASIA)
  

Cervical 50.7% Thoracic35.1% Lumbosacral 11%

 C5 > C4 > C6 > T12 > C7 > L1

Spinal Cord Injuries
 Causes (in order of frequency)
   

MVA Gunshot wounds/acts of violence Falls Sports injuries

Spinal and Neurogenic Shock
 Below site of injury:
 

 

Total lack of function Decreased or absent reflexes and flaccid paralysis Lasts from a week to several months after onset. End of spinal shock signaled by muscular spasticity, reflex bladder emptying, hyperreflexia

Spinal and Neurogenic Shock
In acute trauma of spinal cord there is often initially a period of spinal shock characterized by flaccid paralysis below the level of the lesion, loss of tendon reflexes, decreased sympathetic activity to vascular smooth muscle causing reduced blood pressure, and absent sphincter reflexes and tone. Over several weeks or months spasticity and other upper motor neuron signs typically develop.Some sphincter and erectile reflexes may return, although often w/o voluntary control. Acute spinal cord trauma patients may have improved outcome if treated in the first 8 hrs with high doses of steroids. New experimental drugs are being tested that will block the effects of glutamate release following injury.

Classification of SCI
 Mechanism of injury
   

Flexion (bending forward) Hyperextension (backward) Rotation (either flexion- or extension-rotation) Compression (downward motion)

Pathophysiology of SCI
 Insert stuff here  Insert picture here

Classification of SCI
 Level or Injury
  

Cervical (C-1 through ??) Thoracic (T-1through ??) Lumbar (L-1through ??) Complete

 Degree of Injury

Total paralysis and loss of sensory and motor function although arms or rarely completely paralyzed

Incomplete or partial

Degree of Injury

Complete transection
 Total

paralysis and loss of sensory and motor function although arms or rarely completely paralyzed

Incomplete (partial transection)
 Mixed

loss of voluntary motor activity and sensation  Four patterns or syndromes

Incomplete cord patterns

Central cord syndrome More common in older clients
 Frequently

from hyperextension of spine  Weakness in upper and lower ext, but greater in upper.
  

Anterior cord syndrome Posterior cord syndrome Brown-Sequard syndrome

Clinical manifestations of SCI
 Depend on the LEVEL and DEGREE of the injury!  Quadriplegia occurs with C-1 through C-8 injuries.  Paraplegia occurs with T-1 thru L-4.

Clinical Manifestations of SCI
 Respiratory  C1 – C3: Absence of ability to breathe independently.  C4 – poor cough, diaphragmatic breathing, hypoventilation  C5 – T6: decreased respiratory reserve  T6 or T7 – L4: functional respiratory system with adequate reserve.

What is the phrenic nerve?

 The phrenic nerve stimulates the diaphragm to contract.  Two phrenic nerves (right and left) - injury to one or the other paralyzes contraction of only one half of the diaphragm but even hemi- (half) paralysis can significantly interfere with breathing for patients with lung disease.  The nerve arises from branches of the C3,4, and 5 nerve roots.  The phrenic nerve can be damaged by procedures exploring the neck & upper back

 Loss of the phrenic nerve on either side results in paralysis of the diaphragm on that side.  Paralysis of the diaphragm on one side results in less inflation of the lung on that side.  Whether this is physiologically significant (producing respiratory distress, hypoventilation/hypercapnia) depends on other aspects of a patient's pulmonary physiology (namely underlying chronic obstructive pulmonary disease [emphysema, bronchitis], pneumonia, etc.).

Cardiovascular system

C1 – T5 shows decreased or absent SNS influence. BRADYCARDIA AND HYPOTENSION (due to vasodilation)

What is the VAGUS nerve?
 The longest of the cranial nerves- exits out of the medulla and ends in the abdomen  It supplies sensory and motor function to the pharynx  Supplies motor function to the muscles of the abdominal organs  Provides parasympathetic activity to the heart, lungs, and most of the digestive system

Urinary System
 Atonic bladder with RETENTION in spinal shock.  Post acute phase – irritability causing dribbling or frequent urination.  Urinary infection and calculi from retention and distention.  INTERMITTENT CATHETERIZATION!

GI system
    Decreased motility Paralytic ileus Gastric distention – intermittent NG suctioning Increased H2 – administer H2 inhibitors such as Zantac or Pepcid in initial stages  Carafate and antacids later as prophyaxis  Intra-abdominal bleeding! Remember, no pain or tenderness to warn you.  Watch for H/H decrease and impactions

Skin System
Pressure ulcers! Muscle atrophy in flaccid paralysis Contractures in spastic paralysis Poikilothermism – the adjustment of body temp to room temperature  Decreased ability to sweat below lesion    

Peripheral vascular system

 DVT common but not detected easily  Pulmonary embolism a significant cause of death.  Doppler studies, measurement of extremity girth, impedance plethysmography

Post Injury Assessment
 Goals are to
 

Sustain life Prevent further cord damage Against gravity Against resistance Both sides of the body Ask to move legs, hands, fingers, wrists, then shrug shoulders

 Assessment of muscle groups; motor status
   

Post injury assessment
 Thorough motor examination including position sense and vibration.  Sensory examination  Pinprick starting at toes and working upward  ALWAYS HAVE CLIENT CLOSE EYES OR LOOK AWAY! If he can see what you’re doing, he will answer accordingly.  Assess for head injury and ICP  X-ray, CT scan, EMG

Surgical Therapy
 Reduces injury and stabilizes the SC  Done for  Compression  Bony fragments in the cord  Compound fracture  Penetrating trauma

Drug Therapy
 Vasopressors (Dopamine) to keep mean arterial pressure greater than 80mm to 900mm/Hg so that PERFUSION TO CORD is improved.

 Increases the recovery of function and is the SOC! IV bolus then continuous IV over a 23 hour period.  Improves blood flow and reduces edema in the SC

Other drug therapy
 Symptom-reducing drugs for  GI problems - zantac, tagamet, pepcid  Bradycardia - atropine  Hypotension - vasopressors  bladder spasticity - anticholinergics  autonomic dysreflexia – blood pressure reduction

Function of Motor Neurons
 Upper motor neurons

Function of Motor Neurons
 Lower motor neurons

Diagnoses and Interventions
 Impaired Gas Exchange r/t muscle fatigue and weakness  Decreased PaO , increased PaCO 2 2
 

Fatigue Diminished breath sounds

Impaired gas exchange
    Maintain patent airway Assess respiratory status q 2 hours Monitor ABGs Provide aggressive pulmonary toilet; chest PT and quad-assist coughing  Assess strength of cough  Suction secretions

Inability to sustain spontaneous ventilation
 Related to diaphragmatic fatigue or paralysis evidenced by
  

Dyspnea Use of accessory muscles Abnormal ABGS

 Provide chest PT  Assist with mechanical ventilation  Provide emotional support

Decreased cardiac output
 Related to venous pooling of blood and immobility as evidenced by
    

Hypotension Tachycardia Restlessness Oliguria Decreased pulmonary artery pressures

Decreased cardiac output
 Monitor blood pressure, pulse and cardiac rhythm  Administer vasopressors to maintain MAP at 80mm/Hg or above  Apply pneumatic compression boots or stockings  Perform ROM at least q8h to aid in muscle contraction and venous return

Impaired skin integrity
 Related to immobility and poor tissue perfusion  Inspect skin and areas around pins or tongs  Turn at least q2h and use kinetic table or other specialty care devices.  Insure adequate nutritional intake  INFORM family and client about risk of pressure ulcers

 Related to location of injury, ↓ fluid intake, diet, immobility AEB
   

Lack of BM in over 2 days ↓ bowel sounds Palpable impaction Hard stool or incontinence

 Auscultate bowel sounds and monitor abdominal distention  Note and report any nausea and vomiting  Begin bowel program when BS return and teach to client and family  Administer suppositories and stool softeners  Ensure appropriate fluid and fiber intake

Bowel program for SCI
 Needs to be consistent  Give suppository after meal and place on toilet approx 30 minutes after.  Do this at same time each day!  Fiber, fluids and activity are important  Constipation leads to AUTONOMIC DYSREFLEXIA!!!

Urinary Retention
 Related to injury and limited fluid intake as evidenced by  Decreased output  Bladder distention  Involuntary emptying of bladder

Urinary Retention
      Palpate bladder every shift During acute phase, insert indwelling catheter Begin intermittent cath program when appropriate Keep I and O and end fluids Monitor BUN and creatinine Crude (pronounced croo-DAY) manuever when voiding/cathing

Risk for autonomic dysreflexia

 Assess for HTN, bradycardia, headache, sweating, blurred vision, flushing, nasal stuffiness/congestion  Reduce or eliminate noxious stimuli such as impaction, urine retention, tactile stimulation and skin lesions or pain!

Autonomic dysreflexia
    Elevate HOB 43 degrees Identify cause and eliminate Take BP and pulse Administer antihypertensives as ordered if hypertensive.  Call physician if interventions not effective  TEACH CLIENT AND CARGIVERS HOW TO PREVENT THIS!

Other diagnoses
       Impaired physical mobility Altered nutrition: < body requirements Sexual dysfunction Risk or injury r/t sensory deficits Altered family processes Risk for ineffective individual coping Body image disturbance

Acute intervention
 Immobilization  Crutchfield tongs  Halo vest  Stryker bed  Roto-rest bed (side to side)

sickness a problem with these.

Respiratory dysfunction
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Intubation if injury is high Decreased tidal volume and shallow breathing lead to pneumonia and atelectasis pain management Prone position may be risky Count to 10 test COUGH technique to assist with ineffective abdominal muscles

Fluids and nutrition
 Paralytic ileus common in 48-72 hours  When bowel sounds return:  High calorie, high protein, high fiber diet  Evaluate SWALLOWING before feeding!  EATING CAN BECOME A POWER STRUGGLE!

Bowel and Bladder mgmt.
    Indwelling catheter initially Intermittent catheterization when able Monitor pH of urine (should be acetic!) Ascorbid acid and Mandelamine (an antiseptic) given to keep down bacteria

Temperature control
 NO vasoconstriction, piloerection or heat loss through sweating below level of injury  Do not over cool or over heat client. They only have the remaining upper portion of their bodies, generally, for temperature adjustment

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