Autonomic Dysreflexia - Coursework Example

Autonomic Dysreflexia Student Name Tutor Course Date Table of Contents level Table of Contents level 2 Autonomic dysfunction (Hyperrreflexia) 3 History of dysreflexia 3 Pathophysiology 5 Difference between above and below the level of injury 6 Non clear mechanisms at the cellular level of autonomic dysreflexia 6 The intensity of injury in spinal cord that leads to autonomic dysreflexia T6-7 7 Central causes of Autonomic Dysreflexia 10 Peripheral nerve injury cause 11 Consequences or complications of autonomic dysreflexia 12 The Role of hypersensitivity of alpha (1 & 2)adrenoceptors in the development of autonomic dysreflexia 12 The role of L-type (nifedipine sensitive) calcium channels in the regulation (increase and Decrease) of Autonomic dysreflexia 13 Nitrates (Nitroglycerine, Depo-Nit, Nitrostat, Nitrol, Nitro-Bid) 13 Works Cited 14 Autonomic dysfunction (Hyperrreflexia) Autonomic Dysreflexia, sometimes referred to as Hyperreflexia, is a condition that is potentially life-threatening which should be considered an emergency medical situation that calls for absolutely attention immediately. It occurs in a situation where the pressure of the blood of a person affected by Spinal Cord Injury (SCI) over T5-6 becomes exceedingly high owing to the vigorous activity portrayed by the Autonomic Nervous System. The major symptoms of autonomic dysreflexia which are common pounding headache, sweating, tingling sensation on the neck and face, blotchy skin around the goose bumps and neck. All these symptoms may not appear simultaneously and the level at which they are severe may vary from one situation to another. In extreme or untreated incidents of autonomic desreflexia, it may result into death or a stroke (Elliott and Krassioukov 389-40). History of dysreflexia Autonomic dysreflexia is a syndrome of huge imbalanced reflex sympathetic discharge happening in patients having spinal cord injury occurring above splanchnic sympathetic outlow (T5-T6). The first establishment was done in the year 1890 when it was demonstrated that excess sweating and erythematous rash of the heads and neck triggered by with bladder catherization in a patient who was eighteen year old with spinal cord injury. A entire portrayal of the syndrome was done in the year 1947. Recognizing and treating the first symptoms and signs as early as they appear can avoid to a great extent blood pressure from escalating. Eltorai argues that autonomic Dysreflexia situation is usually arrived at when a painful stimulus happens beneath the spinal cord injury level. The stimulus is consequently transmitted through the Peripheral Nervous System (PNS) and the Central Nervous System (CNS). The central nervous system is made up of the brain together with the spinal cord, which are in control of end organs and voluntary acts through their respective nerves. The peripheral nervous system is comprises of cranial nerves which are twelve pairs in number, peripheral nerves and spinal nerves. The peripheral nervous system is further dived into the autonomic nervous system and the somatic nervous system. The autonomic nervous system has the responsibility or is in charge of symptoms and signs of autonomic dysreflexia. The autonomic nervous system in normal circumstances is responsible for the maintenance of the body homeostasis through its two branches, that is; the sympathetic autonomic nervous system (SANS) and the parasympathetic autonomic nervous system (PANS) (358-9). These branches owe each other complimentary roles via a negative –feedback system; for instance, when one branch is suppressed, the other branch is stimulated. The spinal cord is throughout surrounded by rings of bone referred to as vertebra. These bones make up what is referred to as spinal column. Generally, the higher in the spinal cord column the injury happens, more dysfunction a person becomes. The vertebra is given names based on their location. Cervical Vertebra refers to the eight vertebra in the neck. The top vertebra is C-1; the next is C-2 and so on. Cervical spinal cord injury usually will result in the dysfunction in the legs and an arm, occasioning what is known as quadriplegia. The chest vertebra which are twelve in number are referred to as Thoracic Vertebra. The thoracic vertebra lying first is labeled T-1, it is where the top rib attaches. Injuries occurring in the thoracic area usually affect the legs and the legs resulting into paraplegia (Cross 609). The Lumbar Vertebra lies in the lower back that exists between the thoracic vertebra, where the ribs attach with the pelvis bone (hip bone). They are labeled as L-1 to L-5. The sacral vertebra begins from the pelvis towards the end of the spinal column. They are labeled as S-1 to S-5. Injuries to the sacral vertebra and lumbar vertebra will cause dysfunction in the legs and the hip. Pathophysiology This feature happens after the period of spinal shock where by reflexes return. Patients having injury above the main splanchnic outflow may in turn develop autonomic dysreflexia. In the case of patients with below the injury intact peripheral sensory nerves transmit impulses that go up in the posterior and spinothalamic columns to bring about sympathetic neurons that are found in the intermediolateral gray matter in the spinal cord. The inhibitory outflow that is above the spinal cord injury emerging from cerebral vasomotor centers is more activated, but cannot pass under the block of the spinal cord injury. This huge sympathetic outflow instigates the letting loose of various neurotransmitters (dopamine, dopa-b-hydroxylase, norepinephrine), resulting into piloerection severe vasoconstriction in the arterial vasculature and skin pallor. The outcome is unexpected increase vasodilation and blood pressure way beyond the level of injury. Patients will frequently exhibit a headache triggered by vasodilation of intracranial vessels that are pain sensitive. Reflexes in vasomotor brainstem try to bring down the blood pressure by escalating parasympathetic stimulation to the heart via the vagus nerve to occasion compensatory bradycardia. The reflex action cannot make up for severe vasoconstriction, outline by the Poiseuille formula, where by pressure in a tube is influenced to the fourth power by alteration in the radius (vasoconstriction) and specifically linearly by alteration in the rate of flow (bradycardia). Parasympathetic nerves become more common above the level of injury, which may be accompanied by vasodilation together with skin flushing and profuse sweating. It has been established that genetic handling that are site-directed of the fiber emerging in the spinal dorsal horns ina compression rate of the model would change the level of hyperreflexia after bowel distention, portraying that endogenous spinal cord neural emerging has importance in the pathophysiology of autonomic dysysreflexia. Difference between above and below the level of injury The above level of injury happens above T-6. The below types of injury happens below T-6. The end results of spinal cord injury mainly depend upon the kind of injury sustained and the level of that particular injury. Spinal cord injury may possibly be divided into incomplete and complete types of injury. A complete injury translates to no function below the level of the injury, no voluntary movement and no sensation. The both sides of the body are affected equally. An incomplete injury there is presence of some level of performance below the primary level of the injury. An individual having an incomplete may be in a position to move one limb more than the other, is able to feel the body parts that cannot be moved, or may possess more functioning on one side of the body above the other (Mathias and Frankel 447-8). Non clear mechanisms at the cellular level of autonomic dysreflexia Spinal cord injury (SCI) refers to the is the injury that is caused to the spinal cord resulting into loss of functions such like feeling and mobility. More common causes of damage are trauma such as that resulting from falls, car accident, and gunshot or disease including spina bifida, Friedreich’s Ataxia, and polio. It is not a must for the spinal cord to be completely severed for it not to function. The spinal cord may be intact while damage caused to it cause loss of functioning. Spinal cord injury is very much different from back injuries for example spinal stenosis, pinched nerves and ruptured disks. One can ‘break his neck or back’ without sustaining spinal cord injury if at only the bones around the vertebrae are damaged while the spinal cord is not affected. In such circumstances the person may not be affected by paralysis so long as stabilization of the bones is done (Anton and Townson 170). The intensity of injury in spinal cord that leads to autonomic dysreflexia T6-7 With advancement in acute treatment of spinal cord injury, consequently incomplete injuries are more prevalent. The injury level is very essential in predicting what parts of the body may be affected by paralysis and dysfunction. According to Hughes, there will be variations in prognoses in case of incomplete injuries. Hawkins notes that cervical injuries in many circumstances will result in quadriplegia. Injuries that occur above the C-4 level may bring in the issue of a ventilator to aid the person to breath. C-5 injuries will occasion biceps and shoulder control while there will be no control in the hand or at the wrist. C-6 injuries on the general result in wrist control but on the other hand there is no hand function. Individuals with T-1 and C-7 injuries will straighten their arms but still may possess dexterity problems with the fingers and hand. Injuries below and at thoracic level will result into paraplegia, with the hand not affected. At T-8 to T-1 there would be usually control of the hands, but resulting in poor trunk control as occasioned by lack of abdominal muscle control (laydon and Krassioukov 1717). According to Barton, lower T-injuries, that is, between T-9 and T-12 allow good abdominal muscle control and also good trunk control. In the situation sitting balance is generally good. Sacral and Lumbar injuries result into decreasing control of the legs and hip flexors. Apart from loss of motor functioning and loss of sensation, persons with Spinal Cord Injury also will experience other changes. For instance, they may go through dysfunction of the bladder and the bowel. Sexual functioning in most cases accompanies spinal cord injury; on the other hand generally women’s fertility is not affected. Critical injuries involving C-2 and C-1 might occasion loss of various involuntary functions even ability to breathe, necessitating breathing aids like diaphragmatic pacemakers or ventilators. Other effects of spinal cord injury include inability to sweat below the injury level, chronic pain and decreased control of body temperature (84). Diagram B The sympathetic nervous system is concerned with flight-or-fight response, resulting into pupils’ dilation, increase heartbeat rate, decreased tone of the gut and peristalsis, vasoconstriction, release of norepinephrine and epinephrine, accompanied by other effects. The impact of parasympathetic autonomic nervous system are exactly opposite of the sympathetic autonomic nervous system; largely, there is decreased heartbeat rate, pupil’s constriction, together with increased tone of the gut and peristalsis. Sympathetic autonomic nervous system ad parasympathetic autonomic nervous system departs at varied points in the central nervous system. The parasympathetic autonomic nervous system exits through pons, the middle brain, sacral level of the spinal cord and the medulla (cranial nerves [CN] X, IX, VII and III) (Furusawa 225). There exist main sympathetic output referred to us the splanchnic outflow between L2 and T5. In a person with high level of Spinal Cord Injury, intact lower motor neurons sense the painful stimuli under the injury level and mediate the message up the spinal cord as shown in diagram B above. At spinal cord injury level, the pain signal is prevented and interrupted from being conveyed to the cerebral cortex. The spinal cord injury site also intercepts the two of the autonomic nervous system and result in disconnection of the feedback loop, actualizing the two branches to function independently. The information ascending arrives at the major splanchnic sympathetic outflow (T6-T5) and in turn stimulates a sympathetic response (Braddom and Rocco 238). Arnold notes that the sympathetic response occasion vasoconstriction which causes hypertension, visual change, pounding headache, pallor, anxiety, and of course goose bumps below the level of injury. This hypertension results in the stimulation of the baroreceptors in the aortic arch and carotid sinuses. The parasympathetic autonomic system is unable to deal with these effects via the injured spinal cord; nevertheless, it attempts to maintain homeostasis through slowing down the rate of the heart. The heart is stimulated by the brainstem via the vagus nerve resulting into vasodilation and bradycardia above the level of injury. The parasympathetic autonomic nervous system is not able to go down past the lesion, and as a result of this no changes happen below the level of injury (268). Central causes of Autonomic Dysreflexia Pine argues that there exist various stimuli that result into dysreflexia. Anything that could have been uncomfortable, physically irritating or painful before the injury might result into autonomic dysreflexia following injury. The most prevalent cause is apparently the overfilling of the bladder. This may be as a result of a blockage in the device of urinary drainage, inadequate bladder emptying, bladder infection (cystitis), possibly stones in the bladder and bladder spasms. The second much known cause is a bowel that it is full of gas or stool. Every stimulus directed to the rectum, for example digital stimulation, may instigate a reaction, resulting to autonomic dysreflexia. Other causes include wounds, skin irritations, burns, pregnancy, pressure sores, appendicitis, and ingrown toeneils (Curt et al. 474). According to Braddom and Rocco the usual purpose of the urinary bladder is to store and remove urine in a coordinated fashion. The coordinated activity is regulated by the peripheral nervous system and central nervous system. Neurogenic bladder refers to a term applied to refer to a urinary bladder that is not functioning wellowing to neurologic dysfunction coming from external or internal trauma, injury, or disease. Signs of neorogenic bladder range from detrusor over-activity to destrusor under-activity depending very much on the location of neurologic insult. Urinary sphincter may also be affected occasioning its over-activity or under-activity and subsequent loss of coordination with the functioning. Successful outcome and appropriate therapy are speculated following correct diagnosis by means of carefully medical and with variety of clinical examinations together with voiding history. This also includes selective radiographic studies and urodynamics (239). Peripheral nerve injury cause Frost notes that HIV/AIDS and diabetes mellitus are two of the main conditions causing peripheral neuropathy that result in the retention urinary. These diseases damage the nerves leading to the bladder and might result into silent, painless distention of the bladder. Patients with persistent and recurring diabetes consequently lose the sensation of the bladder filling first, prior to the bladder decompensate. Replica to injury occurring on the sacral cord, the affected patient will experience difficulty in urinating. They may also experience hypo-contractile bladder. Other disease that shows this condition are Guillain-Barre syndrome, extreme herpes occurring in the genitor-anal region, Poliomyelitis, neurosyphilis (tabes dorsalis), and pernicious (1325). According to Dykstra Peripheral nerves are a formation of intricate network of pathways for receiving and sending information through the entire body. The nerves commence from the main trunk of the spinal cord and diverge in different directions to enclose the whole body. Nerves convert the external and internal environmental stimuli to electrical signals in order for the human body to understand stimuli as on of the ordinary senses such as sight, hearing, touch, smell and taste. The urethral sphincters and the bladder are under control of their respective nerves. The autonomic nervous system is found out side the central nervous system (1156). Dysreflexia complications Complications of very acute hypertension occasioned by autonomic dysreflexia include pulmonary oedema, seizures, cerebral hemorrhage, and myocardial infarction. The source of autonomic dysreflexia is life threatening and should also specifically investigated and properly treated to avoid unnecessary mortality and morbidity. Consequences or complications of autonomic dysreflexia In normal conditions, the internal urethra sphincter and the bladder are basically are under control sympathetic nervous system. In case the sympathetic nervous system is active, it enables the bladder to enlarge its capacity devoid of escalating resting pressure of detrusor (accommodation) and stimulates the urinary sphincter internally to remain closed tightly. The sympathetic activity also results in inhibition of parasympathetic stimulation. If the sympathetic nervous system is active, micturition reflex is inhibited and urinary accommodation occurs. The parasympathetic nervous system does perform in the opposite to that of the sympathetic nervous system. In perspective of urinary function, the parasympathetic nerves cause the stimulation of the detrusor occasioning it to contract. Instantly following stimulation of parasympathetic, the sympathetic impact on the internal urethra sphincter is suppressed in order for the internal sphincter to relax and open. Besides, the pudendal nerve activity is inhibited to occasion the opening the external sphincter. This facilitate in voluntary urination (Arnold et al. 269) The Role of hypersensitivity of alpha (1 & 2)adrenoceptors in the development of autonomic dysreflexia Stress incontinence may be due to weal urinary sphincter. The sphincter within contains high levels of alpha-adrenergic receptors. Activating the alpha-receptors will result in the contracting of internal urethral sphincter and escalates the resistance of the urethra to urinary flow. Estrogen, tricyclic agents and sympathomimetic drugs increase the level of outlet of the bladder in order to improve signs of stress urinary incontinence. The major categories of drugs utilized in the treatment of urge incontinence include antispasmodics, tricyclic antidepressant agents and anticholinergic drugs. When one drug does not does not give positive result, the used of combination therapy such as imipramine (Tofranil) and oxybutynin (Ditropan) are recommended. Despite differing mechanisms, imipramine and oxybutynin work together towards improving urge incontinence (Frankel and Mathias 297). The role of L-type (nifedipine sensitive) calcium channels in the regulation (increase and Decrease) of Autonomic dysreflexia Nifedipine ( procardia, adat), which is a calcium, ion influx inhibitor, inhibits selectively calcium ion influx within the cell membrane of vascular soft muscle and cardiac muscle while on the other hand maintaining concentrations of calcium serum. In a male patient, Nifedipine result in the creation of a modest fall in diastolic and systolic prerssure while decreasing the resistance of peripheral vascular (Giannantoni 770) . Nitrates (Nitroglycerine, Depo-Nit, Nitrostat, Nitrol, Nitro-Bid) Nitrates may be used in case of acute spasms of autonomic dysreflexia as they do relax vascular smooth muscle resulting in vasodilator impact on peripheral veins and arteries. Postcapillary vessels dilation comprising of encourage peripheral blood pooling and decreases the return of venous to the heart, in the process decreasing left ventricular end-diastolic pressure and blood pressure of arterial. Arterial relaxation results into the reduction of resistance of systematic vascular that ensures the reduction arterial pressure. If sildenafil has been administered within a period of twenty four hours in a patient with spinal cord injury having a possibility of acute autonomic dyresflexia, the utilization short-acting rapid–onset anti-hypersensitive agent is mostly recommended. Nitrates are commonly used after the nifedipine for autonomic dysreflexia management in patients with spinal cord injury. Level 5 evidence the use of nitrates but there is no clinical studies that support the utilization of nitrates in the management of acute of autonomic dysreflexia in spinal cord injury. Works Cited Ackery A. and Tator C. A global perspective on spinal cord injury epidemiology. J Neurotrauma 2004;21:1355-1370. Anton HA and Townson A. Drug therapy for autonomic dysreflexia. CMAJ 2004;170:1210. Arnold JM, Feng QP, Delaney GA, Teasell RW. Autonomic dysreflexia in tetraplegic patients: evidence for alpha-adrenoceptor hyper-responsiveness. Clin Auton Res 1995;5:267-270. 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Autonomic dysreflexia during a bowel program in patients with cervical spinal cord injury. Acta Medica Okayama 2007; 61(4):221-227. Giannantoni A, Di Stasi SM, Scivoletto G, Mollo A, Silecchia A, Fuoco U, Vespasiani G. Autonomic dysreflexia during urodynamics. Spinal Cord 1998;36:756-860. Hawkins RL Jr, Bailey HR, Donnovan WH. Autonomic dysreflexia resulting from prolapsed hemorrhoids. Report of a case. Dis Colon Rectum 1994; 37:492-493. Hughes SJ, Short DJ, Usherwood MM, Tebbutt H. Management of the pregnant woman with spinal cord injuries. Br J Obstet Gynaecol 1991; 98:513-518. Pine ZM, Miller SD, Alonsa JA. Atrial fibrillation associated with autonomic dysreflexia. Am J Phys Med Rehabil 1991;70:271-273. Read More