1. How many spinal cord injured clients are living in the US?

What is the initial hospitalization and average lifetime cost? There are 259,000 people living in US with SCI. (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1546) 200,000 currently living with SCI in United States (CDC) Average annual medical cost: $15,000$30,000 per year (CDC) Estimated lifetime cost: $500,000more than $3 million, depending on injury severity (CDC) Average Yearly Expenses Severity of Injury First Year Each Subsequent Year High Tetraplegia (C1-C4) $985,774 $171,183 Low Tetraplegia (C5-C8) $712,308 $105,013 Paraplegia $480,431 $63,643 Incomplete motor function at any level $321,720 $39,077 (Christopher & Dana Reeve Foundation) 2. Why did his heart rate and blood pressure fall during this emergency? Sympathetic nerve fibers dilate pupils, increase HR and rhythm, contract blood vessels and relax smooth muscles of the bronchi (Silvestri, 2011, p. 937) Trauma to the SC causes partial or complete disruption of the nerve tracts and neurons (Silvestri, 2011, p. 945). C-spine injuries may have movement in the shoulders if the injury is C5-C8 and may have decreased respiratory reserve (Silvestri, 2011, p. 947). Why was his breathing rapid and shallow? Respiratory complications correspond to level of injury (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549) Cervical and thoracic injuries cause paralysis of abdominal muscles and often intercostal muscles resulting in diaphragmatic breathing if the phrenic nerve is functioning (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549). If the phrenic nerve is functioning hemorrhage and SC edema can impede its function and cause further respiratory insufficiency (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549) The loss of vital capacity and tidal volume due to loss of abdominal and intercostal muscles that is associated with diaphragmatic breathing always results in hypoventilation (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549). His breathing is rapid due to trying to compensate for the hypercapnea and hypoventilation. His breathing is shallow due to paralysis of abdominal and intercostal muscles and possibly impediment to the phrenic nerve. H Pain may also be a factor in his shallow and rapid breathing. Why was the blood pH below normal? The hypoventilation causes hypercapnic acidosis. 3. What other clinical examination findings were present and why? His sensory perception ends at an imaginary line across his chest about 3 inches above the nipple line and he has some sensation in his arms and can raise his shoulders but not his arms and his lower extremities are flaccid:

He degree of injury is an B = Incomplete C4 SCI on the ASIA scale. He has some sensory function preserved below the level of the neurologic injury but no motor function (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549). His Neurologic injury is C4. The lowest level of normal sensory and motor function (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1547). His Skeletal injury is probably C5. The vertebral level where there is the most damage to vertebral bones and ligaments (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1547).

BP 94/55, HR 64: Neurogenic shock is caused by loss of vasomotor tone and results in hypotension and bradycardia (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1547). Sympathetic nerve fibers dilate pupils, increase HR and rhythm, contract blood vessels and relax smooth muscles of the bronchi (Silvestri, 2011, p. 937) Trauma to the SC causes partial or complete disruption of the nerve tracts and neurons (Silvestri, 2011, p. 945). Any SCI above T6 greatly decreases the influence of the SNS. This results in bradycardia. Cardiac monitoring is necessary. Bradycardia <40 needs to be treated with atropine to increase HR to prevent hypoxia. It also results in peripheral vasodilation which causes hypotension, decreased CO, and hypovolemia due to increased venous capacity. IV fluids and vasopressor drugs may be used to support BP.

O2 sat is 92% on room air: This is explained by the hypoventilation as explained above. Temp is 102 degrees F: The interruption of the SNS in SCI prevents peripheral temperature sensation from reaching the hypothalamus which interferes with temperature regulation (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1551). There is a decreased ability to to sweat and shiver which affects the ability to regulate body temperature (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1551). Cervical injures have a greater loss of ability to temperature regulate (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1551). Cervical and thoracic injuries cause paralysis of abdominal muscles and often intercostal muscles reducing the ability to cough and clear secretions leading to atelectasis and PNA (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1549). This causes infection and fever. The patient has a foley catheter which increases his risk of infection (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1550). The patient is on Corticosteroids which increase susceptibility to infection. Color is dusky, skin warm and dry: His dusky color is explained by his hypercapnea. His skin being warm is explained by the difficulty with temperature regulation. His skin being dry is explained by the inability to sweat below the level of injury. Blood sugar was 562mg/dL: This is most likely do to the Corticosteroid use. He has marked spasms and exaggerated stretch reflexes in his lower extremities: Once spinal shock is resolved the reflexes begin to return. The lack of control from the higher brain cause them to be hyperactive and exaggerated resulting in spasms (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1558). The spasms should be treated with Baclofen, Dantrolene or Tizanidine (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1558). These may be interpreted as a return of function by patient and family and it should be explained that they are reflexes not a return of function (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1558). He has urinary incontinence: Neurogenic bladder is related to abnormal or absent bladder innervation (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1559). Normal voiding requires NS coordination of urethral an pelvic floor relaxation with simultaneous contraction of the detrusor muscle. A neurogenic bladder may have: No detrusor contractions (areflexic, flaccid). Hyperactive reflex detrusor retractions (hyperreflexic, spastic). Lack of coordination between detrusor contraction/urethral relaxation ( dyssynergia). (Lewis, Dirksen, Heitkemper, Bucher & Camera, 2011. p. 1558).