Porth's Essentials of Pathophysiology, 4e

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Nervous System

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sympathetic effector responses below the level of injury is disrupted; the ability to control blood vessel responses that conserve or dissipate heat is lost, as are the abili- ties to sweat and shiver. Higher levels of injury tend to produce greater disturbances in thermoregulation. In tetraplegia and high paraplegia, there are few defenses against changes in the environmental temperature, and body temperature tends to assume the temperature of the external environment, a condition known as poiki- lothermy. Persons with lower-level injuries have various degrees of thermoregulation. Disturbances in thermo- regulation are chronic and may cause continual loss of body heat. Treatment consists of education in the adjust- ment of clothing and awareness of how environmental temperatures affect the person’s ability to accommodate to these changes. DeepVeinThrombosis and Edema. Persons with SCI are at high risk for development of deep vein thrombo- sis (DVT) and pulmonary embolism, particularly dur- ing the first 2 to 3 weeks after injury. 60,66 The high risk for DVT in patients with acute SCI is due to immobil- ity, decreased vasomotor tone below the level of injury, and hypercoagulability and stasis of blood flow. Current preventative interventions include mechanical and phar- macological methods. 18,60 Mechanical methods of pre- vention include intermittent pneumatic compression, thigh-high graduated elastic compression stockings, and neuromuscular electrical stimulation. Pharmacologic methods include oral anticoagulants and low–molecu- lar-weight heparin. Local pain, a common symptom of DVT, is often absent because of sensory deficits. Thus, a regular schedule of visual inspection for local signs of DVT (e.g., swelling) is important. Testing of persons at high risk for DVT includes plethysmography and duplex ultrasonography. Edema is also a common problem in persons with SCI. The development of edema is related to decreased peripheral vascular resistance, decreased muscle tone in the paralyzed limbs, and immobility that causes increased venous pressure and abnormal pooling of blood in the abdomen, lower limbs, and upper extremities. Edema in the dependent body parts usually is relieved by position- ing to minimize gravitational forces or by using com- pression devices (e.g., support stockings, binders) that encourage venous return. Skin Integrity. The entire surface of the skin is inner- vated by cranial or spinal nerves organized into derma- tomes that show cutaneous distribution. The CNS and autonomic nervous system also play a vital role in skin function. The sympathetic nervous system, through con- trol of vasomotor and sweat gland activity, influences the health of the skin by providing adequate circulation, excretion of body fluids, and temperature regulation. The lack of sensory warning mechanisms and voluntary motor ability below the level of injury, coupled with cir- culatory changes, place the spinal cord–injured person at major risk for disruption of skin integrity (see Chapter 46). Significant factors associated with disruption of

centers that coordinate sphincter control (i.e., a UMN lesion). Persons with UMN lesions or spastic bladders lack awareness of bladder filling (i.e., storage) and vol- untary control of urination. In LMN lesions or flaccid bladder dysfunction, lack of awareness of bladder fill- ing and lack of bladder tone render the person unable to urinate voluntarily or involuntarily (see Chapter 27). Bowel elimination is a coordinated function involv- ing the enteric nervous system, the autonomic nervous system, and the CNS. Persons with SCI above S2 to S4 develop spastic functioning of the defecation reflex and loss of voluntary control of the external anal sphincter. Damage to the cord at the S2 to S4 level causes flac- cid functioning of the defecation reflex and loss of anal sphincter tone. Even though the enteric nervous system innervation of the bowel remains intact, without the defecation reflex, peristaltic movements are ineffective in evacuating stool. Sexual function, like bladder and bowel control, is mediated by the S2 to S4 segments of the spinal cord. 18,65 The genital sexual response in SCI, which is mani- fested by an erection in men and vaginal lubrication in women, may be initiated by mental or touch stimuli, depending on the level of injury. The T11 to L2 cord segments have been identified as the mental-stimulus, or psychogenic, sexual response area, where autonomic nerve pathways in communication with the forebrain leave the cord and innervate the genitalia. The S2 to S4 cord segments have been identified as the sexual-touch reflex center. In T10 or higher injuries, reflex sexual response to genital touch may occur freely. However, a sexual response to mental stimuli (T11 to L2) does not occur because of the spinal lesion blocking the com- munication pathway. In an injury at T12 or below, the sexual reflex center may be damaged, and there may be no response to touch. In men, the lack of erectile ability or inability to experience penile sensations or orgasm is not a reliable indicator of fertility, which should be evaluated by an expert. In women, fertility is normally reestablished with the return of menses, which usually occurs at about 3 to 5 months after injury. There are hazards to preg- nancy, labor, and use of birth control devices relative to SCI that require the services of knowledgeable health care providers. Disruption of Other Functions Temperature Regulation. The central mechanisms for thermoregulation are located in the hypothalamus. In response to cold, the hypothalamus stimulates vaso- constrictor responses in peripheral blood vessels, par- ticularly those of the skin. This results in decreased loss of body heat. Heat production results from increased metabolism, voluntary activity, or shivering. To reduce heat, hypothalamus-stimulated mechanisms produce vasodilation of skin blood vessels to dissipate heat, and sweating to increase evaporative heat losses. After SCI, the communication between the ther- moregulatory centers in the hypothalamus and the