Glasgow Coma Score: Total score after resuscitation <9.
Motor score <3. Eye opening <2. Verbal response <2.
Pupils Dilated or abnormal response to light.
Oculocephalic or oculovestibular: Absent reflexes.
Injury severity scale: >40. (Ann Emerg Med 2001;37:318–332)
Adult risk factors for blunt cerebrovascular injury (BCVI) were identified in 91% of children diagnosed with this injury (J Trauma 2011;71:559)…. clinicians should use existing adult guidelines when evaluating children for BCVI….Adult risk factors for BCVI were present in the 52 patients who underwent diagnostic tests as follows:
Basilar skull fracture: 41 patients, 7 (17%) with BCVI
Glasgow Coma Scale score 8: 16 patients, 5 (31%) with BCVI
Cervical spine fracture: 13 patients, 3 (23%) with BCVI
Soft-tissue neck injury: 3 patients, 1 (33%) with BCVI
Neurological findings of concern for BCVI: 2 patients, 2 (100%) with BCVI
Le Fort II/III facial fracture: no patients
Major thoracic injury was present in six of the nine children with carotid artery injury, and cervical spine fracture was present in the two patients with vertebral artery injury.
Tx: ETT intubation, fluid resuscitation, ventilation, oxygenation, sedation, consider pharmacologic paralysis. If herniation or decortication –> decr ICP by hyperventilating to PaCO2 of 25-28 mmHg, controversial as may aggravate cerebral ischemia long term.
• Mannitol 0.5-1g/kg IV lasts 4hr, works in 30 min by osmotic gradient/ free radical scavenging/ incr RBC deformability = decr viscosity/ decr intracranial elastance/ decr CSF production/ incr CO. Can also control IC pressure with Phenobarbital @ 15mg/kg IV load, then titrate to effect.
Diuretics 1mg/kg (~40-80mg) Furosemide (Lasix) PRN. Consider sz prophylaxis with Phenytoin (Dilantin) @ 15mg/kg load, then 5mg/kg/d.
• To stop sz use Diazepam @ 1-5mg IV. Chlorpromazine 10-25mg IV. Injury above clavicle assumed to have spinal injury until proven otherwise so immobilize until lateral C-spine. EEG may be one of the best parameters for predicting a pt’s outcome following a severe head injury.
Therapeutic hypothermia: target temp of 32-33C x 24hr and rewarming within 24hrs, may reduce the mortality and poor neurologic outcomes in adults with traumatic brain injuries (JAMA 2003;289:2992-99). IV MgSO4 added to an antishivering pharmacological regimen hastens temperature reduction when used with a surface cooling technique, MgSO4 also appears to increase subjects’ comfort level (Stroke 2004;35:2331-233). Inducing hypothermia (cooling to about 32.5° C esophageal temperature for 24 hours — initiated within eight hours of the injury) does not appear to improve neurologic outcomes for children suffering traumatic brain injury, and it might actually increase mortality, a multicenter trial showed (NEJM 2008; 358: 2447-2456).
Fluids: Acute restoration of fluid volume for pt’s with severe traumatic brain injury should be done with saline rather than albumin (SAFE study. NEJM 2007;357:874-84)….mortality rate at two years was 63% lower among pt’s resuscitated with saline rather than albumin (P=0.003)….researchers suggest that a mechanism might be that albumin exacerbates vasogenic or cytotoxic cerebral edema.
• Pt’s with traumatic brain injury and hypotension had similar outcomes whether they received prehospital hypertonic saline (7.5%) or Ringer’s lactate solution in addition to standard IV resuscitation fluids (JAMA 2004;291:1350-1357).
• The trial found that care focused on maintaining monitored ICP at or below 20 mm Hg (as guidelines recommend) in order to avoid poor outcome was not superior to care based on serial CT and neurologic clinical examination in pt’s with severe traumatic brain injury (TBI) (N Engl J Med. Published online December 12, 2012)…..Mortality at 6 months was also similar: 39% in the ICP group and 41% in the ICE group….The median length of ICU stay was also similar in the 2 groups, although the number of days of brain-specific treatments administered in the ICU (hyperosmolar fluids and hyperventilation) was lower in the ICP group than in the ICE group (3.4 vs 4.8; P = .002). The distribution of serious adverse events was similar in both groups.
Other: Neuroendocrine abnormalities occur early and with high frequency in survivors of traumatic brain injury (TBI) and may have significant implications with respect to rehabilitation and recovery (Endocrine Society 2004 Abstract OR40-2. Presented June 19, 2004) (80% had gonadotropin deficiency and low sex steroid concentrations, hyperprolactinemia in 52%, DI in 26%, 14% had SIADH, may have GH and cortisol abnormalities). Corticosteroid therapy does not reduce 2-week mortality rates in pt’s with head trauma, but may increase it (Lancet 2004;364:1321-8, 1291-2).
Progesterone: In adult pt’s with acute traumatic brain injury, progesterone tx may improve outcomes — especially in cases of moderate injury (Ann Emerg Med 2007;49:391-402)….a loading dose of 0.71 mg progesterone/kg for over first hour, followed by an infusion of 0.5 mg/kg/hr for the next 11 hours, then 5 additional 12-hour infusions were given, for a total of 3 days of tx. Progesterone pt’s remained in coma longer than control pt’s, the report indicates, but fewer pt’s in the progesterone group (13%) died within 30 days of injury compared with the control group (30.4%). Those with moderate traumatic brain injury who had received progesterone were significantly less disabled than those who had received placebo. Head injury patients treated with injections of progesterone in an investigational protocol had improved survival (18% vs 32% in patients receiving placebo at 6 mo’s) and better function after six months in a small randomized trial with 159 adults (Critical Care 2008;17:1-5)….Patients were randomized to placebo or 1 mg/kg of progesterone by intramuscular injection beginning no more than eight hours after the injury…..Injections were repeated twice daily for five days.
Info: Fashion hair accessories are often difficult to identify following cranial trauma, neurosurgeons warn, but they must be considered in the differential diagnosis and removed (J Neurosurg Pediatrics. 2008;2:424-426)…..plastic hair beads are radiolucent and thus are difficult to differentiate on radiologic scans from the adjacent soft tissue — the air-filled hollow core may be mistaken for benign air that became entrapped at the time of injury. Elevated intraocular pressure (IOP) identifies children with intracranial pressures (ICP) above 20 cm H2O (Pediatr Crit Care Med 2010;Jan 14;e-pub ahead of print)…..Investigators conclude that IOP is a useful screening tool for children with suspected increased ICP but that it lacks the accuracy needed for precise ICP management…..could help in the assessment of critical multitrauma patients who are too unstable to undergo CT or in rural settings with limited availability of CT and neurosurgical specialty consultation, to help direct the need for emergent intervention and appropriate transfer destinations.
Skull fx is strongly associated with other more serious intracranial abnormalities. Studies have shown that 40-100% of all intracranial abnormalities are associated with skull fx. The skull fx itself, however, is typically of little clinical consequence to the pt.
S/s: Palpate for depressions, step-off or crepitus. Look for raccoon eyes, Battle’s sign, hemotympanum, scalp lacerations. Check for CSF rhinorrhea or otorrhea (double ring sign). Check Head CT w/o contrast to r/o associated injury. Observe all pt’s for signs of incr ICP.
Tx: Elevate head of bed if CSF leak is present, if CSF leak persists >10days, surgical repair is needed, but monitor closely for signs of meningitis. Consider prophylactic Abx’s. Any depressed skull fx requires OR elevation if depression is > the thickness of the skull. If open skull fx, cover with occlusive sterile dressing and get STAT neurosurgery evaluation.
Closed Skull Fx’s: Use CT scan for dx because CT shows fx’s and other associated injuries. Admit for observation. Detected primarily on noncontrast CT scan. Because these fx’s are often associated with more serious injury, it is prudent to evaluate the injury with CT scan rather than plain skull x-rays. There is no specific tx for linear skull fx’s.
Tx: Close observation is recommended to detect the development of an epidural hematoma after an initially negative CT scan. Pt’s with isolated closed skull fx’s with no evidence of brain injury require admission to the hospital for a minimum of 24 hours of observation.
Open Skull Fx’s: Use CT scan for dx because CT shows fx’s and other associated injuries. Underlie scalp lacerations. High risk of infection. Open fx’s underlie scalp lacerations and are often palpated during evaluation of the scalp laceration. These fx’s have a serious risk of infection. Definitive dx is made with noncontrast CT scan, and more serious intracranial abnormality should be ruled out. Open skull fx is likely if pneumocephalus is noted on CT scan.
Tx: Initiate IV Abx’s such as cefazolin, and refer the pt to the appropriate surgical subspecialty for possible operative debridement. 3.
Depressed Skull Fx’s: Often found with inspection or palpation. Use CT scan for dx because CT shows fx’s and other associated injuries. Depressed skull fx’s are often palpable or visible during examination. However, swelling around the area of the injury can mask a depressed skull fx and make it appear to be a simple hematoma. Like all skull fx’s, depressed skull fx’s are often associated with more serious intracranial injury, and pt’s need to be evaluated accordingly. Noncontrast CT scan is the test of choice to determine whether the pt has intracranial injury or depressed skull fx.
Tx: Depressed skull fx’s without intracranial injury represent a cosmetic situation. Open depressed skull fx’s are at high risk of infection, similar to open nondepressed skull fx’s. Pt’s should be admitted to the hospital for observation and referred to the appropriate surgical subspecialist for possible elevation of the depression and debridement if the fx is open.
Basilar Skull Fx’s: Use CT scan for dx because CT shows fx’s and other associated injuries; may be missed on CT. Associated with hemotympanum, Battle sign, raccoon’s eyes, cerebrospinal fluid leaking from ear or nose, or hearing loss. Basilar skull fx’s are skull fx’s at the base of the skull, typically at the petrous portion of the temporal bone. Clinical signs include hemotympanum, Battle sign (ecchymosis along the mastoid area of the skull), raccoon’s eyes (periorbital ecchymosis), cerebrospinal fluid leak from the nose or ear, or hearing loss. Pt’s with any of these signs should undergo noncontrast CT evaluation for possible basilar skull fx and to rule out more serious intracranial abnormality.
Tx: Initiate IV Abx’s such as cefazolin. Pt’s with documented basilar skull fx or significant signs of a basilar skull fx should be admitted for observation. If a more serious intracranial abnormality is present, obtain neurosurgical consultation.
Acute Spinal Cord Injury (SCI):
Links: Incomplete Cord Injury and Spinal Cord Dysfunction | Head Trauma |
Assume that every pt with multiple trauma or head injury has a spina cord injury. Control the airway, give O2. Nasotracheal intubation is preferred. Treat neurogenic shock with fluids & Dopamine. Immobilize the unstable C-spine.
Neuro assessment:
Sacral sparing –> preservation of sensation in perianal region (2nd-4th sacral vertebrae).
The clinical evaluation of a pt with suspected SCI begins with a careful history focusing on the presence or absence of sx’s related to the vertebral column (most commonly pain) or any motor or sensory deficits. A report of complete bilateral loss of sensation or motor function below a certain level is indicative of a spinal cord injury. Ascertaining the mechanism of injury is also important in identifying the potential for spinal injury. The American Spinal Injury Association (ASIA) has established some pertinent definitions. The neurologic level of injury is the lowest (most caudal) level with normal sensory and motor function. A C5 quadriplegic has, by definition, abnormal motor and sensory function from C6 down.
Neurological assessment in SCI motor strength:
0: No contraction or movement
1: Minimal movement
2: Active movement but cannot overcome gravity
3: Active movement against gravity
4: Active movement against resistance
5: Active movement against full resistance
Assessment of sensory function recognizes the different pathways for light touch, proprioception, vibration and pain. Pin prick should be used for the evaluation of pain sensation. Differentiating a nerve root injury from SCI can be difficult. The presence of neurological deficits that indicate multilevel involvement is suggestive of SCI rather than a nerve root injury. In the absence of spinal shock, motor weakness with intact reflexes indicates SCI, while motor weakness with absent reflexes indicates a nerve root lesion. The clinical assessment of pulmonary function in acute spinal cord injury begins with a careful history of respiratory complaints and review of underlying cardiopulmonary comorbidity such as COPD or heart failure. The physical examination should focus on careful evaluation of respiratory rate, chest wall expansion, abd wall movement, cough, chest wall and/or pulmonary injuries. ABGs and pulse oximetry are especially useful as the bedside dx of hypoxia or CO2 retention may be difficult. The degree of respiratory dysfunction is ultimately dependent on pre-existing pulmonary comorbidity, level of spinal cord injury and the presence or absence of chest wall or lung injury. Any or all of the following determinants of pulmonary function may be impaired in the setting of spinal cord injury:
Loss of ventilatory muscle function from denervation and/or associated chest wall injury. Lung injury, such as pneumothorax, hemothorax or pulmonary contusion. Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs. There is a direct relationship between the level of cord injury and the degree of respiratory dysfunction. With very high lesions (i.e., C1-C2), vital capacity (VC) is only 5-10% of normal and cough is absent. At C3-C6, VC is 20% of normal and cough is very weak and ineffective. High thoracic cord injuries (i.e., T2-T4) have VCs at 30-50% of normal and cough is weak. With descent to lower cord injuries, respiratory function improves. At T11 respiratory dysfunction is minimal; VC is essentially 100% of normal and cough is strong.
Agitation, anxiety or restlessness. Poor chest wall expansion. Decreased air entry, rales, rhonchi. Pallor, cyanosis. Increased heart rate. Paradoxical movement of chest wall. Increased accessory muscle use. Moist cough. In all pt’s assessment of deep tendon reflexes and perineal evaluation is critical. The presence or absence of sacral sparing is a key prognostic indicator.
The sacral roots may be evaluated by documenting the following: Perineal sensation to light touch and pin prick. Bulbocavernous reflex (S3-S4). Anal wink (S5). Rectal tone. Presence of urine retention or incontinence. Presence or absence of priapism.
X-rays: The standard three views of the cervical spine; AP, lateral and odontoid views, are recommended for the cervical spine. AP and lateral view are recommended for the thoracic and lumbar spine. The x-rays must adequately visualize all vertebrae.
Tx: If obvious neurologic spinal cord deficit give Methylprednisolone IV bolus @ 30mg/kg, then 5.4 mg/kg infusion X 23 hours if able to initiate within 3hr or X48hr if initiate within 3-8hrs of injury. This enhances blood flow to the cord and suppresses lipid peroxidation/ hydrolysis and vasoactive by products from damaging membranes. Transfer to spinal cord injury unit ASAP. DVT prophylaxis with pneumatics or heparin. Prevent pressure sores, +Foley, Baclofen for spasticity. Ileus is common. A nasogastric (NG) tube is essential. Aspiration pneumonitis is a serious complication in the SCI pt with compromised respiratory function. Antiemetics should also be used aggressively.
The indications for intubation: Decreased level of consciousness (LOC) (GCS < 9). Increased respiratory rate with hypoxia. PC02 > 50. Vital Capacity < 10 ml/kg. It can be difficult to diagnose hemorrhagic shock in SCI because of the limitations of the history and physical examination in the presence of autonomic dysfunction. Disruption of autonomic pathways prevents the tachycardia and peripheral vasoconstriction that normally characterizes the shock state. This vital sign confusion may falsely reassure the physician. Occult internal injuries with associated hemorrhage may be missed. In all SCI with hypotension, a diligent search for sources of hemorrhage must be made before the hypotension can be attributed to neurogenic shock. In acute SCI, shock may be neurogenic, hemorrhagic or both. The following clinical pearls are useful in distinguishing hemorrhagic from neurogenic shock:
Neurogenic shock only occurs in the presence of acute SCI above T6. Hypotension and/or shock in association with acute SCI at or below T6 are invariably caused by hemorrhage. Hypotension in the presence of a spinal fx alone, without neurological deficit is probably due to hemorrhage. Pt’s with SCI above T6 may not show the classical physical findings associated with hemorrhage (e.g., tachycardia and peripheral vasoconstriction). This autonomic system dysfunction is common in SCI and may confuse the physician. Due to the vital sign confusion in acute SCI and a high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made.
BA-210 (Cethrin): FDA approved 12/05 orphan drug for the tx of acute thoracic and cervical spinal cord injuries. A recombinant protein Rho GTPase antagonist and a fibrin sealant to optimize its delivery during spinal restabilization surgery. After acute injury, axon regeneration inhibition is exacerbated by enhanced activity of the Rho/Rho kinase pathway that induces apoptosis in neurons, astrocytes, and oligodendrocytes. It promoted neurite regrowth, reduced injury-related apoptosis, and improved locomotor functional recovery.
Thoraco-lumbar Injury: most stable fx’s are managed conservatively with bed rest and a brace for 8-12 wks. Operative fusion if unstable injury with incomplete cord lesion.
Complete Cord Transection: all sensory modalities and reflexes impaired below the level of severance (pinprick loss most valuable). Flaccid (paraplegia, tetraplegia), fasciculations, urinary/ rectal sphincter dysfunction. Sweating, piloerection diminished below the lesion. Genital reflexes lost, priapism common. The highest complete spinal cord injury level that can live independently without the aid of an attendant is a C6 complete tetraplegia. This pt would have to be extremely motivated. Feeding is accomplished with a universal cuff for utensils. Transfers require stabilization of elbow extension with forces transmitted from shoulder musculature through a closed kinetic chain. Bowel care is performed using a suppository insertion wand or other apparatus for digital stimulation. C7 level is the usual level for achieving independence.
Common Incomplete Cord Injuries: May have combination of all types. Look for sacral sparing (normal light touch and cold sensation at anus) as a sign of incomplete damage. All have a better prognosis than complete cord transection.
Brown-Sequard Syndrome: Constitutes 2%-4% of all traumatic spinal cord injury. Results from a lesion that causes spinal hemisection, often from a penetrating (knife or gunshot) wound. Leads to ipsilateral loss of motor (weakness)/vibr/ position sense 2 segments below the lesions and contralateral loss of light touch/ pain/ temp (uninjured side). Rare recovery. Because tracts cross at different locations, deficits affect different sides. This syndrome is commonly due to an extra- medullary lesion (spinal cord hemisection syndrome): Ipsilateral (to the lesion) spastic paresis due to involvement of the lateral corticospinal tract. Ipsilateral lower motor neuron weakness due to involvement of anterior horn cells or roots. Ipsilateral loss of vibration and joint position sense due to involvement of the posterior column. Contralateral loss of pain and temperature sense due to involvement of spinothalamic tract.
Central cord syndrome: the most common syndrome. Results from an injury involving the center of the spinal cord. It is predominantly a white matter peripheral injury. Intramedullary hemorrhage is not common. It may occur at any age, but is more common in older pt’s. Produces sacral sensory sparing, greater motor weakness in the upper limbs than the lower limbs. Anatomy of the corticospinal tracts is such that the cervical distribution is medial and sacral distribution is more lateral. Since the center of the SC is injured, upper extremities are more affected than lower extremities.
Pt’s may also have bladder dysfunction, most commonly urinary retention. Variations in sensory loss below the level of the lesion. Lower extremities recover first and to a greater extent. This is followed by improvement in bladder function, then proximal upper extremity, and finally intrinsic hand function.
Central Cervical Spinal Cord Syndrome: hyperextension injury –> weakness and flaccid paralysis of UE (face and arms), often with sparing the LE secondary to concentric-lamellar pathways. Prognosis is good (recovery in hours). Vest-like loss of pain & temp. Sacral sparing (implies an intramedullary central cord lesion).
Functional Transection: most often caused by trauma from motor vehicle or diving accidents, must be at or below the level of the C4 cervical nerve segment if the pt is to survive. If transection occurs above this level, the diaphragm ceases to function and breathing stops. For the quadriplegic pt, breathing is maintained solely or predominantly by the diaphragm. Quadriplegic pt’s who have a preserved phrenic nerve and diaphragmatic function (C7 spinal cord transection) almost never progress to hypercapnic respiratory failure unless a major pulmonary complication supervenes or CNS-depressant drugs are administered. The diaphragm is less effective with the pt in the upright position, and platypnea may result. Abdominal binders serve to replace lost abd muscle tone and should be used whenever tidal volume falls with the pt upright. An inflatable anterior air bladder in the binder may be used to assist ventilation in pt’s with marginal respiratory function. External abd compression may be used to help these pt’s cough. Quadriplegic pt’s have a mild degree of bronchial hyperresponsiveness caused by parasympathetic tone from the uninjured vagus nerve that is unopposed by sympathetic tone from the spinal cord…they may need a albuterol and/or Atrovent NEBS.
Anterior Cord / Spinal Artery Syndrome: Neck flexion injury/ vertebral burst fx –> paralysis, but retain position/vibr/pain/temp/touch.
May recover. A lesion involving the anterior two thirds of the spinal cord preserving the posterior columns, such as: Anterior spinal artery lesions, direct injury to the anterior spinal cord, bone fragments or a retropulsed disc. Polyarteritis nodosa, angioplasty, aortic and cardiac surgery, and embolism, can result in injury to the anterior two-thirds of the spinal cord.
Anterior Horn: pain & temp loss below the lesion, proprioception spared. Flaccid areflexia, fasciculations, urinary/ rectal sphincter dysfunction. No dysautonomias. Anterior horn cell disease is most commonly seen in pt’s with amyotrophic lateral sclerosis (ALS). The disease causes weakness of the muscles of breathing and an associated restrictive abnormality in most pt’s, but only a minority of pt’s have respiratory sx’s at presentation. Sporadic cases of poliomyelitis still occur in the United States and other countries.
Spinal muscular atrophy (SMA): represents a heterogeneous collection of heredofamilial d/o’s that primarily involve spinal motor neurons. A study has found a gene on the X chromosome that causes X-linked infantile spinal muscular atrophy (XL-SMA) (Am J Hum Genet. 2008;82:188–193). The X-linked form of SMA, which occurs only in males, is similar to type 1 SMA with additional joint involvement.
SMA affects approximately 25,000 Americans.
S/s: reduced muscle tone, lack of reflexes, and congenital contractures, all caused by the loss of anterior horn cells — the motor neurons that transmit impulses from the spinal cord to muscles. SMA is classified by severity:
Type 1 affects the respiratory muscles before or shortly after birth, leading to death in the first 2 years.
Type 2 appears at age 6 to 18 months, with life expectancies ranging from childhood to adulthood.
Type 3 appears after 18 months of age, with life expectancies near normal. Sodium Phenylbutyrate: FDA approved in 3/07 as and orphan drug for the tx of SMA. A histone deacetylase inhibitor that has been identified in in vitro systems and animal models as an agent that can increase the level of SMN protein. Data collected from in vitro studies and pilot clinical work suggests that phenylbutyrate tx in SMA pt’s may improve motor function.
Posterior Cord Syndrome: loss of proprioception, preservation of power and pain/temp sensation.
Spinal cord injury without radiologic abnormality (SCIWORA): Primary spinal cord injury may occur in the absence of spinal fx or dislocation. Occurs primarily in children. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction with or without flexion/extension of the vertebral column may result in primary SCIWORA.
Spinal Cord Dysfunction:
Leads to nonprogressive loss of sensory and motor function distal to the point of injury. The leading causes of spinal cord injury are motor vehicle accidents, gunshot wounds, falls, sports (especially diving) injuries, and water injuries. Pt’s are generally categorized into three groups. The first consists predominately of younger individuals who sustained their injury from a high-energy traumatic accident. The second consists of older individuals with cervical spinal stenosis caused by congenital narrowing or spondylosis. The third group consists of people with gunshot wounds.
Tetraplegia: (preferred to quadriplegia) refers to loss or impairment of motor or sensory function (or both) in the cervical segments of the spinal cord with resulting impairment of function in the arms, trunk, legs, and pelvic organs. Impairment or loss of motor and/or sensory function in the cervical segments of spinal cord due to damage of neural elements within spinal canal. Does not include brachial plexus lesions or injury to peripheral nerves outside neural canal.
Paraplegia: Impairment or loss of motor and/or sensory function in thoracic, lumbar, or sacral segments of spinal cord. Trunk, legs, pelvic organs may be involved, arm function spared. Refers to cauda equina and conus medullaris injuries, but not to lumbosacral plexus lesions or injury to peripheral nerves outside the neural canal. Arm function is intact but, depending on the level of the cord injured, impairment in the trunk, legs, and pelvic organs may be present.
Complete Injury: This term refers to an injury with no spared motor or sensory function in the lowest sacral segments.
Incomplete Injury: Incomplete injury refers to an injury with partial preservation of sensory or motor function (or both) below the neurologic level and includes the lowest sacral segments.
C4 level function: cervical lesions above C4 may have impairment of respiratory function, depending on the extent of injury, and may require a tracheostomy and mechanical ventilatory assistance. Pt’s with high tetraplegia can use chin or tongue controls to operate an electric wheelchair with attached respiratory equipment. Mouth sticks that are lightweight rods attached to a dental bite plate enable pt’s to perform desktop skills, operate push-button equipment, and pursue vocational and recreational activities.
C5 level function: the key muscles are the deltoid and biceps muscles, which are used for shoulder abduction and elbow flexion. If these muscles are weak, the pt will benefit from mobile arm supports attached to a wheelchair. Mobile arm supports are balanced to exert a vertical force to counteract gravity. This enables the pt with poor muscle strength to feed independently and perform other functional tasks with the hands. A ratchet wrist-hand orthosis (WHO) with a fixed wrist joint and a passively closing mechanism attached to the thumb and fingers enables the pt to grasp objects between the thumb and fingers.
C6 level function: the key muscles are the wrist extensors, which enable the pt to manually propel a wheelchair, transfer from one position to another, and even live independently. If wrist extensor strength is poor, an orthosis is indicated. A WHO with a free wrist joint and a rubber-band extensor-assist mechanism will enable the pt to complete wrist extension. A wrist-driven WHO with a flexor hinge mechanism that causes the metacarpophalangeal joint to flex when the wrist is extended will enable the pt to actively grasp between the fingers and thumb. Some pt’s will develop a natural tenodesis of their thumb and finger flexor muscles owing to myostatic contracture or spasticity, and this tenodesis enables them to grasp without the need of an orthosis. Most pt’s with good wrist extensor strength are able to operate a manual wheelchair but may require an electric wheelchair for long distances. These pt’s may also be able to transfer independently if they have no elbow flexion contractures and they can passively lock their elbows in extension while transferring.
C7 level function: the key muscle is the triceps. All pt’s with intact triceps function should be able to transfer and live independently if no other complications are present. Despite their ability to extend the fingers, these pt’s may also require a WHO with a flexor hinge mechanism.
C8 level function: the key muscles are the finger and thumb flexors, which enable a gross grasp. The functioning flexor pollicis longus enables pt’s to obtain lateral pinch between the thumb and the side of the index finger. Intrinsic muscle function is lacking, and clawing of the fingers is usually present. A capsulodesis of the metacarpophalangeal joints will correct the clawing and improve hand function. Active intrinsic function can be gained by splitting the superficial finger flexor tendon of the ring finger into four slips and transferring these tendons to the lumbrical insertions of each finger.
Shoulder or arm pain: The hemiplegic shoulder is a common source of pain. A variety of different factors contribute to the painful shoulder: reflex sympathetic dystrophy, inferior subluxation, spasticity with internal rotation contracture, adhesive capsulitis, and degenerative changes about the shoulder. If early range-of-motion exercises are performed and the extremity is properly positioned with a sling to reduce subluxation, severe or chronic pain at the shoulder can usually be prevented or minimized.
Shoulder contracture: Contracture of the shoulder can cause pain, hygiene problems in the axilla, and difficulty in dressing and positioning. Shoulder adduction and internal rotation are caused by spasticity and myostatic contracture of four muscles: the pectoralis major, the subscapularis, the latissimus dorsi, and the teres major.
Elbow flexion contracture: persistent spasticity of the elbow flexors causes a myostatic contracture and flexion deformity of the elbow. Frequent accompanying problems include skin maceration, breakdown of the antecubital space, and compression neuropathy of the ulnar nerve.
Clenched fist deformity: A spastic clenched fist deformity in a nonfunctional hand causes palmar skin breakdown and hygiene problems. Recurrent infections of the fingernail beds are also common.
1. Sensory level of injury: Most caudal segment of the SC with normal (2/2) sensory function on both sides of the body for pinprick, and light touch
For the sensory examination there are 28 key sensory dermatomes, each tested separately for light touch (with a cotton tip applicator) and pinprick (with a safety pin). The face is used as the normal control point.
Pinprick testing: The pt must be able to differentiate the sharp and dull edge of a safety pin. Scores: 0 Not able to differentiate between the sharp and dull edge. 1 The pin is not felt as sharp as on the face, but able to differentiate sharp from dull. 2 Pin is felt as sharp as on the face.
Light touch: a cotton tip applicator is compared to the face sensation. Scores: 2 Normal / same as on face. 1 Impaired / < on the face. 0 Absent.
2. Motor level of injury: Most caudal key muscle group that is graded three-fifths or greater with the segments above graded five-fifths in strength.
A possible score of 100 can be obtained when adding the muscle scores of the key muscle groups (25 points per extremity).
There are 10 key myotomes on the left and right side of the body:
C5 Biceps brachialis Elbow flexors.
C6 Extensor carpi radialis Wrist extensors
C7 Triceps Elbow extensors
C8 Flexor digitorum profundus Finger flexors (FDP of middle finger)
T1 Abductor digiti minimi Small finger abductor
L2 Iliopsoas Hip flexors
L3 Quadriceps Knee extensors
L4 Tibialis anterior Ankle dorsiflexors
L5 Extensor hallucis longus Long toe extensors
S1 Gastrocnemius Ankle plantarflexors
3. Neurologic level of injury: Most caudal segment of the spinal cord with both normal sensory and motor function on both sides of the body, fetermined by the sensory and motor levels. Since the level may be different from side to side, it is recommended to record each side separately.
4. Skeletal level of injury: Level where the greatest vertebral damage is noted by radiographic evaluation.
Complete Vs. Incomplete Lesions:
Incomplete injury: Partial preservation of sensory and/or motor functions below the neurological level, which includes the lowest sacral segment. Sacral sensation and motor function are assessed. Sacral Sparing voluntary anal sphincter contraction or sensory function (light touch, pinprick at the S4S5 dermatome, or anal sensation on rectal examination) in the lowest sacral segments. Due to preservation of the periphery of the SC indicates incomplete injury Sacral sparing indicates the possibility of SC recovery, with possible partial or complete return of motor power. There is also the possibility of return of bowel and bladder function. The concept of sacral sparing in the incomplete SCI is important because it represents at least partial structural continuity of the white matter long tracts (i.e., corticospinal and spinothalamic tracts). Sacral sparing is evidenced by perianal sensations (S4S5 dermatome), and rectal motor function. Sacral sparing represents continued function of the lower sacral motor neurons in the conus medullaris and their connections via the spinal cord to the cerebral cortex.
Asia Impairment Scale: Classifies Complete and Incomplete Injuries: Examine 10 index muscles bilaterally. Examine 28 dermatomes for pinprick and light touch. Complete rectal exam to assess sensation and volitional sphincteric contraction. Determine left and right motor levels. Determine left and right sensory levels. Assign final motor and sensory levels. Determine neurological level, which is the most caudal segment with normal motor and sensory function. Categorize injury as complete or incomplete by ASIA impairment scale (A,B,C,D,E). Calculate motor and sensory score. Determine zone of partial preservation if complete injury (“A” on impairment scale)
A = Complete: No motor or sensory function is preserved in the sacral segments
B = Incomplete: Sensory but not motor function is preserved below the neurological level and includes sacral segments
C = Incomplete: Motor function preserved below the neurological level; more than half the key muscles below the neurological level have a muscle grade < 3.
D = Incomplete: Motor function preserved below the neurological level; at least half the key muscles below the neurological level have a muscle grade of 3 or more
E = Normal: Motor and sensory function
Key Sensory Levels:
C2: Occipital protuberance
C3: Supraclavicular fossa
C4: Superior AC Joint
C5: Lateral side of the antecubital fossa
C6: Thumb (and index finger)
C7: Middle finger
C8: Little finger
T1: Medial ulnar side of antecubital epicondyle
T2: Apex of axilla
T3: Third intercostal space (IS)
T4: Nipple line fourth IS
T5: Fifth intercostal space – fifth IS
T6: Xiphoid sixth IS
T7: Seventh intercostal space seventh IS
T8: Eighth intercostal space eigth IS
T9: Midway between T8 and T10 ninth IS
T10: Umbilicus tenth IS
T11: Eleventh intercostal space eleventh IS
T12: Inguinal ligament at midpoint
L1: Half the distance between T12 and L2
L2: Midanterior thigh
L3: Medial fem condyle
L4: Medial malleolus
L5: Dorsum of foot at third MTP joint
S1: Lateral heel
S2: Popliteal fossa in the midline
S3: Ischial tuberosity
S4 and S5: Perianal area (taken as one level)
ASIA Key Motor Levels
C1C4: Use sensory level and diaphragm to localize lowest neurological level
C5: Elbow flexors
C6: Wrist extensors
C7: Elbow extensors
C8: Finger flexors (FDP of middle finger)
T1: ABD digiti minimi (small finger abductor)
T2L1: Use sensory level
L2: Hip flexors
L3: Knee extensors
L4: DF ankle dorsiflexors
L5: Long toe extensors
S1: Plantar flexors
Reflexes
S1S2: Gastrocnemius (ankle jerk)
L3L4: Quadriceps (knee jerk)
C5C6: Biceps, brachioradialis
C7C8: Triceps, finger flexors
L5: Medial hamstring
Status Epilepticus (SE):
Link: Adult | Child | Complications | See below for Non-convulsive Status Epilepticus (NCSE) | 1st Sz W/u |
= >30 min of sz activity or repeated sz’s w/o clearing of mental status. ~25% of children and 5% of adults with epilepsy will have at least one episode. 13% with SE will have a recurrent bout. Has a 20% overall mortality (higher in elderly and those due to an acute insult (stroke, anoxia, trauma, infection, metabolic), more benign if due to epilepsy, ETOH/ AED withdrawal, tumors, prior strokes. Refractory status (RSE) seen in up to 30% of pt’s.
Causes: withdrawal from anticonvulsant med or benzo, change in med, drugs/ ETOH, bacterial meningitis, encephalitis, stroke, intracranial mass, AVM, hyper/ hypoglycemia, hyponatremia, preeclampsia, electroconvulsive therapy, IV contrast agent.
0-5min: Obtain history. Monitor temp/ BP/ pulse/ RR/ EKG/ EEG. Start IV line with NS.
Check: blood sugar, anticonvulsant levels, lytes, BUN, Ca, CBC, toxic drug screen. Give rectal antipyretics PRN. Perform neuro exam. Consider intubation (intubate if after 20 min) and O2 via nasal canula, check arterial blood gas, injection of 50 mL of 50% glucose IV & 100 mg of thiamine IV or IM. Call EEG lab to start recording as soon as feasible.
If no IV can give IM Fosphenytoin (12-20mg/kg), rectal Diazepam (0.5mg/kg), IM Midazolam (5mg) or intranasal Midazolam (0.1-0.2mg/kg) or an inhalational anesthetic (isoflurane @ 0.5%) then get a saphenous vein cutdown at the ankle.
Adult in Status (in ER, ICU Or monitored bed):
6-9min: Ensure adequate ventilation, oxygenation, blood pressure. Intubate if necessary, based on low oxygen saturation and labored breathing. Insert IV line. Send toxic screen.
• Administer glucose and thiamine in appropriate cirumstances. Bolus 50ml of 50% Glucose. Add Vitamin B complex to IV.
• Assess quickly for cranial and cervical injury if onset of seizures is unwitnessed.
0-10min: Lorazepam (Ativan) IV @ 2-4mg or infuse at rate of 2 mg/min to max dose of 15mg (0.1-0.15 mg/kg). Monitor BP closely when higher doses/rates are used. Or
Diazepam IV @ 5-10mg or infuse at rate up to 2mg/min to total of 20mg (0.15mg/kg).
10-20 min: Complete Lorazepam infusion as above.
20+min: Cerebyx (Fosphenytoin) or Phenytoin (Dilantin): 20mg PE/kg IV load (can infuse at 100-150 mg/min rate). Follow this by a repeat dose @ 10mg/kg if no response in 20 min. Can mix in NS or 5% dextrose. IM volume of 10-20ml (12-20mg/kg) in 1-3 injections. Or
Follow with Phenytoin 15–20mg/kg in normal saline at rate no faster than 50mg/min. If still not controlled, repeat Phenytoin at 10mg/kg.
>60min: Phenobarbital: 10-20mg/kg load, then 2mg/kg/hr (0.2-0.4 mg/kg/min) or 100mg/min to loading dose of 20mg/kg, anesthesia and intubate if persists.
Alternative strategies for status include benzodiazepine drip:
Midazolam: 0.2mg/kg load, then infuse at 0.05-2 mg/kg/hr IV) or
Thiopental: 75-125mg load, then infuse at 1-5 mg/kg/hr. Or rapid Depakote (Depakene IV) load.
Caveat: check STAT phenytoin levels immediately after loading pt to ensure adequate serum levels are achieved, and to plan maintenance dosing schedule (target 20 – 30 mcg/ml). R/o CNS bleed/ infection.
Other: Propofol @ 3-5/kg load, then 1-15mg/kg/hr. Versed drip. Adults with acute repetitive seizures, rectal diazepam gel (Diastat) significantly reduces the likelihood of recurrence during the episode, a second dose can be given after 4 hours (Arch Neurol 2002;59:1915-1920). Both isoflurane and desflurane adequately suppress refractory status epilepticus (RSE) (Arch Neurol 2004;61:1254-1259). (New management strategies in the tx of status epilepticus. Mayo Clin Proc 2003;78:508-18)….consider Pseudoseizures. Status epilepticus an independent risk factor for death (Arch Neurol 2008;65:221)…..for patients older than 65 (RR = 5.1) and for subjects who later developed recurrent seizures (epilepsy; RR = 6.3).
Intravenous levetiracetam: appears to be a promising alternative therapy for refractory status epilepticus (J Neurol Neurosurg Psychiatry 2009;80:689-692).
Link: Treatment Steps | Guidelines and Complications |
Status epilepticus (SE), defined as 30 minutes of continuous seizure activity, is about three times more common in infants than in older children (150 vs. 50 per 100,000 per year).
Step #1: ABC’s, then O2, IV. Get glucose, CBC, chem panel, AED levels. If hypoglycemia, bolus with 2cc/kg 50% glucose (10ml/kg D10W if neonate, 4ml/kg D25W in <2yo, 2ml/kg D50W if >2yo). Add 100mg Thiamine if malnourished.
#1 DOC: Lorazepam (Ativan): @ 0.1-0.15mg/kg IV, (max rate at 2mg/min), may repeat q5min X2 to max dose of 5mg. A review recommends IV lorazepam (0.05 to 0.10 mg/kg) and buccal midazolam (0.5 mg/kg) for management of acute generalized seizures in children (Cochrane Database Syst Rev 2008;http://dx.doi.org/10.1002/14651858.CD001905.pub2).
Rectal –> 0.1-0.2mg/kg Or
Diazepam: 0.2-0.3 mg/kg IV, max rate <1mg/min, repeat q5min X2 (max 10mg age >5yo, 5mg @age 30d-5yo).
Rectal –> 0.5mg/kg age 2-5yo, max 20mg. 0.3 mg/kg age 6-11yo, 0.2mg/kg age >12yo Or
Midazolam (Versed): 0.1-0.3 mg/kg bolus then infuse at 0.1-0.4mg/kg/hr,
Nasal @0.1-0.3 mg/kg). Intranasal Midazolam may be a more effective pre-hospital tx of pediatric sz’s than Diazepam (Ped Emerg Care 2004;20:794). Buccal midazolam (2.5 to 10 mg) appears to be a more effective tx for children who require emergency therapy for acute sx than is rectal diazepam (Lancet 2005;366:182-183,205-210) (56% success rate Vs 27%). A meta-analysis reveals that non-IV midazolam (buccal @ 0.5 mg/kg or 10 mg or IM @ 0.2 mg/kg) is as effective as or superior to IV (0.2 or 0.3 mg/kg) or rectal (0.5 mg/kg or 10 mg) diazepam for stopping seizures in children and young adults (Acad Emerg Med 2010;17:575)……midazolam was superior to diazepam for terminating seizures, with a NNT of 7 to demonstrate midazolam benefit…..IM or IN midazolam was as effective as IV diazepam, while buccal midazolam was superior to rectal diazepam in achieving seizure control (NNT, 6).
Intranasal midazolam (0.2 mg/kg; maximum dose, 10 mg) is as effective as rectal diazepam (RD, 0.3–0.5 mg/kg; maximum dose, 20 mg) for home rescue treatment of seizures (Arch Pediatr Adolesc Med 2010;164:747)…RD is awkward to administer, is expensive, and has a short half-life……Parents were instructed to use only one dose of the rescue medicine when a seizure lasted longer than 5 minutes and then to call 911……the median time between medication administration and seizure cessation was 1.3 minutes shorter in the IM group (3.0 vs. 4.3 minutes), the difference was not statistically significant. Frequency of repeat seizures, respiratory complications, and need for emergency services also did not differ significantly between the two groups.
#2: Then IV Phenytoin at 18-20mg/kg at rate no faster than 1mg/kg/min (50mg/min). Or
Fosphenytoin (Cerebyx): 18-20 mg/kg IV, max rate 1mg/kg/min). Monitor ECG & BP, anticipate intubation.
#3: If sz still present at 30-60min give IV Phenobarbital: 20mg/kg load dose at rate no faster than 50mg/min, can repeat with a dose of 5-10mg/kg. Or
If not already given use: Midazolam (above dose), or Lorazepam (above dose) or Diazepam 50mg diluted in NS or D5W and run at 1ml/kg/hr (2mg/kg/hr).
#4: Intubate: give Pentobarbital: 15mg/kg, then 1-5 mg/kg/kg/hr to produce burst suppression pattern on EEG. Or use Propofol (Diprivan) 1-2 mg/kg IV initially, then 1-15 mg/kg/hr. Propofol (max 5 mg/kg/hour, average tx lasting 57 hours) in children with refractory status epilepticus is safe and effective and often resolves the seizure without resorting to thiopental (Neurology. 2005;65:591-592). Or Midazolam 0.15-2mg/kg IV, then 1-18 mcg/kg/min aiming for burst suppression.
Status Epilepticus Guidelines for Evaluation of Children:
(Neurology 2006;67:1542-50)
The guidelines do not support standardized, routine, extensive diagnostic evaluation for every child who develops SE.
Data are insufficient to determine whether blood culture or lumbar puncture should be performed routinely in children in whom there is no clinical suspicion of infection.
Measurement of serum antiepileptic drug levels should be considered when a child with epilepsy who is receiving drug therapy develops SE.
Toxicology testing may be considered when the cause of SE is unknown.
Testing for inborn errors of metabolism may be considered when the initial evaluation for SE reveals no etiology.
An EEG may be considered in children who present with new-onset SE to determine whether there are focal or generalized abnormalities that may influence further diagnostic and therapeutic decisions.
Neuroimaging may be considered for evaluating children with SE if there are clinical indications or if the etiology is unknown.
The data are insufficient to recommend routine neuroimaging in children with SE.
• IM midazolam was superior to IV lorazepam for terminating status epilepticus before arrival at the emergency department (N Engl J Med 2012;366:591)…..The researchers randomized 893 patients to receive either 10 mg IM midazolam by autoinjector followed by IV placebo or IM placebo by autoinjector followed by 4 mg IV lorazepam…..Children estimated to weigh <40 kg received 5 mg of midazolam or 2 mg of lorazepam…..The incidence of termination of seizures without rescue therapy before arrival at the emergency department (the primary endpoint) was 73% in the IM-midazolam group versus 63% in the IV-lorazepam group (P<0.001).
Systemic Complications of Generalized Status Epilepticus:
Metabolic –> Lactic acidosis, Hypercapnia, Hypoglycemia, Hyperkalemia, Hyponatremia, CSF/serum leukocytosis.
Autonomic –> Hyperpyrexia, Failure of cerebral autoregulation, Vomiting, Incontinence.
Renal –> Acute renal failure from rhabdomyolysis, Myoglobinuria.
Cardiac/respiratory –> Hypoxia, Arrhythmia, High output failure, Pneumonia.
Sudden unexpected death in epilepsy (SUDEP): Represents the leading cause of mortality in young adults with drug-resistant epilepsy. Long-term ECG monitoring over several mo’s has detected ictal asystole in 15% pt’s with refractory epilepsy inidcating that this might thus represent the leading cause of SUDEP. No clear recommendations have emerged from the literature regarding the most appropriate therapeutic strategies to prevent the event, apart from the supervision at night of pt’s with refractory epilepsy (Curr Opin Neurol 2006;19:194–199). Sudden unexpected death in epilepsy can also be the result of a seizure-induced respiratory dysfunction. An EEG recording of a sudden death that occurred during an epileptic seizure show abrupt irreversible cerebral electrical shutdown (J Neurol Neurosurg Psychiatry 2007;78:1395-1397)…”the death occurs secondary to primary brain failure.”…The EEG recording, set up at 13:00 the previous day, showed increasing cerebral activity as the day progressed. “Prolonged bursts of high amplitude spikes began to appear towards midnight,” the report indicates, and continued to worsen until paroxysmal activity developed into continuous spike wave discharges, with a seizure onset at 08:27:18. “The seizure activity abruptly terminated at 8:28:14 and the EEG became a ‘flat line’.” Based on movement artefacts that decreased in frequency on the recording, death occurred at 08:31. Preventing the number of tonic-clonic seizures in patients with epilepsy may be one critical strategy in minimizing the incidence of sudden death, which is estimated to be 20-fold greater in this population than in the general population (Lancet. Published online July 6, 2011)……having up to 2 GTCS per year was associated with a nearly 3-fold greater likelihood of SUDEP (relative to no GTCS). Having 3 to 12 GTCS per year raised the risk to greater than 8-fold. With 13 to 50 GTCS per year, the risk was 9-fold higher, and with more than 50 GTCS annually, the risk was 14- to 51-fold higher. A meta-analysis of add-on therapy trials for refractory epilepsy reveals a significantly reduced risk for sudden unexpected death during treatment with effective doses of add-on antiepileptic drugs versus placebo (Lancet Neurol 2011;10:961).
First Aid and Accident Precautions for Seizure Pt’s: Stay calm. Lay the child down with head to the side. Loosen tight clothing. Place something soft under the head. Clear the airway of food, debris, or vomit. Do not place anything in the child’s mouth. If the seizure persists for more than a few minutes, is followed by a prolonged postictal state, or is atypical, the child should be taken to the emergency room.
After the first seizures: Need accident precautions such as no driving, or biking around cars and no climbing higher than one’s height for 6mo’s. Caution around water, even shallow water such as the bathtub. Routine sports are allowed. Older age and etiology (especially life-threatening acute symptomatic etiologies) are associated with worse outcome in SE (J Neurol Neurosurg Psychiatry 2006;77:611-5)…. ~10% of pt’s with first SE episodes experienced recurrent episodes within 7 yrs.
Non-Convulsive Status Epilepticus (NCSE):
Absence status. Prolonged (>30 min) seizure activity in the absence of major motor signs. Can manifest as a change in behavior and/or mental processes from baseline associated with continuous epileptiform discharges in the EEG. Makes up only 1–6% of all clinical forms of status epilepticus in adults. Yet, in pt’s with idiopathic generalized epilepsies, single or recurrent typical absence status epilepticus are common and occur in 3-9% of cases (J Neurol Neurosurg Psychiatry 1996;61:90-92)…Late-onset de novo absence status may occur in pt’s with remitted idiopathic generalized epilepsy or in pt’s without any seizure history.
PP: The neuronal networks that generate absence seizures are completely different from those underlying partial seizures. Thalamocortical neuronal populations are crucial in absence status epilepticus, and neuronal networks within the hippocampal formation and adjacent limbic and neocortical structures (Lancet Neurology 2007;6:4).
S/s: the main clinical feature is an altered state of consciousness but changes in behavior may also be reported. Ranges from disorientation, decreased spontaneity, slow speech, hallucinations; rhythmic blinking. May have slight myoclonic jerking. Pt’s may be able to eat and drink, withdraw from pain, walk about, and respond to simple commands. The duration may range from minutes to days, or weeks (Epilepsia 1993;34:21-S28). The sz can start or end with, or is interrupted by, a generalized convulsive seizure.
On EEG see 2–3 Hz spike-wave discharges, if have stupor may see 0.5–4 Hz spike-wave discharges (Non-convulsive status epilepticus in adults: clinical forms and tx (Lancet Neurology 2007;6:4).
Tx: depends on the type and the cause. Most suggest a less aggressive pharmacological management. Some start with IV diazepam (10mg) or lorazepam (4mg). If seizures continue for >10 min after this tx, these doses can be repeated. Next try IV valproic acid at 25–45 mg/kg (6 mg/kg per min) or phenobarbital at 20 mg/kg (50 mg/kg per min). Recurrent episodes in the institutionalised or home cared can be given buccal, nasal, oral, or rectal benzodiazepines (Lancet Neurol 2005;4:592-593). Some suggest that aggressive pharmacological tx seems to have a greater risk on morbidity and mortality than continuing non-convulsive seizure activity (J Clin Neurophysiol 1999;16:341-352). Topiramate and levetiracetam may be successful. If it cannot be terminated, generalized anesthesia using agents such as midazolam (0.2 mg/kg bolus, 0.1–0.4 mg/kg per h infusion), propofol (2 mg/kg bolus, 5–10 mg/kg per h infusion), thiopental (2–3 mg/kg mg bolus, 3–5 mg/kg per h infusion), or pentobarbital (10–20 mg/kg bolus, 1–3 mg/kg per h infusion) can be given (Eur J Neurol 2006;13:445-450).
Link: Neuroimaging |
CBC, BS, lytes, BUN, Ca, Mg, P, Tox, MRI head (CT if urgent, new focal deficit, fever, head trauma, persistent altered MS/ H-A, CA, anticoagulated, immunocompromised), ECG (look for prolonged QT, arrhythmia or ischemia), LP, LFT’s (pseudo sz has no incr CPK, met acidosis or prolactin). ABG can essentially show any pattern.
Consider EEG | Decisions to treat an isolated seizure vary for each individual, and depend upon risks of recurrent seizures, and the implications for such sz’s for that pt, incr risk of 2nd seizure is ~15–60% depending on risk factors, but 80–90% for “epilepsy” after 2nd or 3rd event. Remember to warn pt’s of risks of operating dangerous equipment (incr. cars) and make appropriate reports to Division of Motor Vehicles where statutes apply. One option for isolated seizure: treat with “non-toxic” level of chosen AED for 1–2 years, then consider withdrawal of AED if sz-free.
Neuroimaging: Get a stat CT scan if: suspect a structural lesion or a new focal deficit, persistently altered mental status, fever, recent trauma, h/o cancer, persistent H-A, HIV, on anticoagulants, age >40yo, s/p a partial sz, status epilepticus. Immediate noncontrast CT appears useful for guiding management of a first seizure among pt’s with a predisposing history (AIDS, cancer), focal seizure onset, infants <6 months, or an abnormal neurologic examination in the ED… but not in children with immediate post-traumatic seizures (Neurology 2007;69:1772-1780)…in these pt’s CT findings affected management in 9% to 17% of adults and 3% to 8% of children.
All others as outpatient. Includes child with sz of focal onset, age <1yo & non febrile, no known cause for the sz. (NEJM 2001;344:15) (Ann EM 1996;114). Functional imaging can be done via PET scan, SPECT coregistered MRI (SISCOM) or MR spectroscopy (MRS) (Mayo Clin Proc 2002;77:1251-64).
Elevated serum prolactin assay: measured in the appropriate clinical setting 10 to 20 minutes after a suspected event, is a useful adjunct to differentiate generalized tonic-clonic or complex partial seizures from psychogenic nonepileptic seizure in adults and older children (Neurology 2005;65:668-675) (does not distinguish epileptic seizures from syncope). Its use has not been established in the evaluation of status epilepticus, repetitive seizures, and neonatal seizures. Serum prolactin levels should be representative of the baseline prolactin level when measured more than 6 hours after a suspected episode. Prolactin (PRL) release from the pituitary is controlled by the hypothalamus via a PRL inhibitory factor, now believed to be dopamine. It has been hypothesized that ictal epileptic activity in the mesial temporal structures may propagate to the hypothalamus, altering the hypothalamic regulation of PRL release. In most studies, a serum PLR level of at least twice baseline value was considered to be abnormal. Conditions associated with hyperprolactinemia, including pregnancy, lactation, prolactinomas, primary hypothyroidism, use of phenothiazines or bromocriptine, may reduce the specificity of PRL assays. Epileptic and nonepileptic events may coexist in the same pt.
2007 Guidelines for Evaluating First Unprovoked Seizure in Adults:
(NEUROLOGY 2007;69:1996-2007)
Routine electroencephalography (EEG): should be considered in the neurodiagnostic workup of all pt’s for both its “substantial yield” and “value” in predicting recurrence. EEG revealed epileptiform abnormalities in ~23% of pt’s, and these were predictive of seizure recurrence.
Brain imaging: with either computed tomography or MRI should also be considered routinely. A brain imaging study (CT or MRI) was significantly abnormal in 10% of pt’s, indicating a possible seizure etiology. These significant abnormalities affected pt management and included previously unrecognized brain tumors, vascular lesions, and cerebral cysticercosis. In general, when an imaging study is necessary in a non-emergent situation, MRI is more sensitive and is more likely to show significant abnormalities than is CT.
Labs: There is insufficient evidence to recommend for or against the routine use of blood glucose tests, blood counts, electrolyte panels, LP, and toxicology screening; however, these tests may be useful in certain circumstances (e.g., LP in febrile pt’s). Laboratory tests such as blood counts, blood glucose, and electrolyte panels were abnormal in up to 15% of individuals, but abnormalities were minor and did not cause the seizure. The necessity for such studies should be guided by specific clinical circumstances based on the history, physical, and neurologic examination. Overt clinical signs of infection such as fever typically predicted significant CSF abnormalities on LP.
Outline for seizure assessment: Features of a seizure. Associated factors. Age. Medical history – previous history of similar episodes, prior stroke, brain tumor, systemic illness, mental illness, drug or alcohol abuse. Family history. Developmental status. Behavior. Health at seizure onset – febrile, ill, exposed to illness, complaints of not feeling well, sleep deprived. Precipitating events other than illness – trauma, alcohol, medications, illicit drugs, toxins. The diagnosis of epilepsy and syncope are all too often confused, resulting in unnecessarily high monetary, medical, and emotional costs to misdiagnosed patients (Eur Heart J 2009;DOI:10. 1093/eurheartj/ehp298)……use of an implantable ECG loop recorder that recognizes the distinctive heart rhythms of both conditions while they are occurring can aid in making the right diagnosis.
Symptoms during seizure (ictal): Aura: Subjective sensations.
Behavior: Mood or behavioral changes before the seizure.
Preictal symptoms: Described by pt or witnessed.
Vocal: Cry or gasp, slurring of words, garbled speech.
Motor: Head or eye turning, eye deviation, posturing, jerking (rhythmic), stiffening, automatisms (purposeless repetitive movements such as picking at clothing, lip smacking); generalized or focal movements.
Respiration: Change in breathing pattern, cessation of breathing, cyanosis.
Autonomic: Pupillary dilation, drooling, change in respiratory or heart rate, incontinence, pallor, vomiting.
Loss of consciousness or inability to understand or speak.
Symptoms following a seizure (postictal): Amnesia for events. Confusion. Lethargy. Sleepiness. Headaches and muscle aches. Transient focal weakness (Todd’s paresis). Nausea or vomiting. Biting of tongue.
2006 Guidelines for Pediatric Status Epilepticus (SE): (Neurology. 2006;67:1542-1550).
There is insufficient evidence to support or refute the routine use of blood cultures or LPs in children in whom there is no clinical suspicion of CNS infection. Since ingestion of a toxic substance was responsible for 3.6% of pediatric SE cases, the guideline recommends specific serum toxicology screening be carried out when no apparent etiology is immediately found. There is insufficient evidence to support or refute routine metabolic and genetic testing in children presenting with SE. Metabolic studies may be considered when the initial evaluation reveals no etiology, especially if there is a preceding history that suggests a metabolic disorder. Abnormalities on EEG occur in 62% of children with SE compared with 41% of children with a first unprovoked seizure < 30 minutes long, EEGs should be done in children presenting with new-onset SE. Tthere is insufficient evidence to support or refute the usefulness of EEG testing in nonconvulsive status epilepticus (NCSE). Neuroimaging options, including MRI and CT, should be considered in the evaluation of children with suspected SE if there are clinical indications or if the etiology is unknown. However, such studies should be done only after the child is appropriately stabilized and the seizure activity controlled.
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