PARA210 Group Assignment PDF

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Group assignment on autonomic dysreflexia, includes lots of info....

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AUTONOMIC DYSREFLEXIA (AD) Title Autonomic dysreflexia (AD) is a potentially life-threatening condition defined as uncontrolled episodic hypertension (Systolic increase over 20-40mmHg) and concurrent baroreceptor mediated bradycardia (1-5,7,9). Autonomic dysreflexia usually develops following spinal cord injury at T6 or above (1-4,6,9). Injury at this level disrupts supraspinal modulation to sympathetic preganglionic neurons (4,6-8). Without this control noxious stimuli below the level of injury cause hyperresponsiveness of the sympathetic nervous system resulting in vascular constriction and hypertensive episodes (2,4-9). If left untreated the acute uncontrolled hypertension can result in cerebral haemorrhage and even death (1,2,6,8). Autonomic dysreflexia is characterised by sudden extreme hypertensive episodes along Clinical Features with concurrent baroreflex mediated bradycardia (2,4-5,9). Clinically Autonomic dysreflexia is indicated when systolic BP rises above baseline by at least 20-40mmHg but individuals with SCI are typically hypotensive so even a rise towards normal BP range could suggest AD (1-2,4,7). Autonomic dysreflexia is often hard to diagnose as signs and symptoms vary between patients and occasionally is asymptomatic (1,5,7). Key clinical features indicating autonomic dysreflexia include a pounding headache as the result of vasodilation and hypertension, flushing blotchy skin above the injury, chills without a fever, shortness of breath and feelings of anxiety (2,4-6-9). Other common signs and symptoms include sweating above the site of injury, nasal congestion, blurred vision, skin pallor and piloerection below the site of injury as well as irritability or combative behaviour (2,4-6-9). These symptoms are not often all simultaneously present however headache and sweating above the site of injury occurs 88% of the time (4,8). If left untreated autonomic dysreflexia can be life threatening putting the patient at high risk of seizures, intracranial haemorrhage, hypertensive encephalopathy and myocardial infarction (1,2,6-8). AD comes as a condition associated with spinal cord injury at the neurological level of Aetiology injury T6 or above (10,11). AD can develop in 20% - 70% of T6 or above spinal cord injury (SCI) patients (10-12). The higher level of the spinal cord injury, the greater the risk with up to 90% of patients with cervical spine or high thoracic SCI being susceptible (11). AD is more common in people with complete injuries compared to incomplete SCIs (10,13) The severity and frequency of these episodes are also associated with the completeness of the SCI (12). Rarely lesions as low as T8 can cause AD (10,11). AD in the first month after SCI is rare (10), and is more commonly seen in chronic SCI any time from months to years after the spinal shock phase (1,4,5,7,10,11,14,15). Risk factors for the development of AD are caused by a variety of noxious stimuli that can trigger a sympathetic response in a spinal cord injury patient, these stimuli occur below the neurological level of injury (10,11). The most common noxious stimuli occur in the genitourinary system; such as bladder distention, UTI or calculi which account for more than 75% of AD episodes (10,11), followed then by bowel distention or faecal impaction. Weaver (10,16) further notes that all noxious stimuli below the level of injury have the capacity to cause AD including pressure injuries, fractured bones, ingrown nails and menstruation (5). Labor is also a risk factor for developing AD, Ko (10) states that it can occur during labor in up to two-thirds of women. Autonomic dysreflexia describes the stimulation of noxious visceral or somatic stimuli Pathophysiology below the neurological level of spinal cord injury. With the loss of supraspinal control over sympathetic preganglionic neurons, the condition characteristically impacts patients with lesions superior to T6, as the innervation of splanchnic nerves occurs through T5 to T12 (17). The stimulus of afferent neurons by noxious stimuli in the intermediolateral grey matter of the spinal cord, elicits reactionary sympathetic nervous system responses (18). The release of noradrenaline via the SNS, stimulates vasoconstriction in the inferior twothirds of the body, prompting an increase in arterial blood pressure (19,22-24). Definition

Baroreceptors stimulated in the carotid sinus by an increase in blood pressure, thus mediate parasympathetic responses (20). Peripheral vascular resistance is regulated through the limitation of the vasoconstrictor sympathetic preganglionic neurons of the thoracolumbar spinal cord, resulting in vasodilation (17-19, 21). This compensatory parasympathetic activity is unable to transmit below the level of paralysis, due to the loss of supraspinal control over sympathetic preganglionic neurons (17, 22). With unopposed sympathetic outflow, comprehensive vasoconstriction below the site of injury continues, producing systemic hypertension (23, 24). Above the level of injury, activated efferent impulses oppose sympathetic stimulation, causing vasodilation and associated baroreflexmediated bradycardia (24). Autonomic Dysreflexia is characterised by paroxysmal periods of SNS stimulation Evaluation and accompanied by hypertensive crises (25). It is known to occur in patients who have Risk assessment suffered SCI at the level of T6 or above (25) and hence, paramedics should always suspect AD in patients with SCI and signs of sympathetic innervation. Furthermore, AD and its presenting sympathetic overdrive are typically triggered by stimuli below the area of SCI and so paramedics should seek to perform a thorough head-to-toe assessment to determine if there are any notable noxious or non-noxious stimuli present (UTI, impacted bowel etc.) (25). The major diagnostic sign for AD is paroxysmal hypertension (32). The degree of this hypertension varies across studies with some sources reporting a 40mmHg increase in systolic BP whereas others report a 20mmHg rise being sufficient for AD diagnosis (30, 32). Individuals suffering high SCI typically have a BP 15-20mmHg lower than able-bodied persons, and so, even seemingly normal BP may be diagnostic for AD (27). It can be useful to ask the patient if they are aware of their usual blood pressure in order to determine the actual increase in blood pressure. Paramedics should continuously monitor blood pressure, every 2-5 mins to detect any improvement or deterioration in patient condition (31). Other diagnostic signs and symptoms which paramedics should be looking for in AD include profound headache (particularly in frontal and occipital areas), profuse sweating above the level of injury, piloerection, blurred vision, anxiety or stuffy nose (25, 29, 30). Although these symptoms are not consistently present, headache and sweating above the area of spinal cord injury occur in 88% of cases and consequently are often key clinical indicators of the condition (32). Headache, sweating, and cutaneous vasodilatation are considered a triad of diagnostic signs of AD (25).Through patient questioning, history taking and a detailed secondary assessment, paramedics should be able to find sufficient evidence in clinical signs, symptoms and past medical history to make an accurate provisional diagnosis of AD in the prehospital field. Rapid recognition of AD is essential in improving patient outcomes and preventing the onset of life-threatening complications (25, 28). These life-threatening consequences include intracranial haemorrhage, myocardial infarction, retinal detachments, seizures, cardiac arrhythmias and death (25, 27). AD can vary largely in intensity, sometimes being completely asymptomatic and other times presenting as a life-threatening emergency (29, 30). Therefore, it is vital that paramedics assess their patient to determine the time criticality of the illness. The major clinical sign that provides insight into the acuity or time criticality of the patient is blood pressure. Acute hypertension is characteristic of AD and a continuing increase in BP reflects a worsening and more time critical condition. In severe cases, systolic BP has been reported to climb higher than 300mmHg. Conditions that may clinically manifest in a similar way to AD include stroke, toxaemia of pregnancy, pheochromocytoma, posterior fossa neoplasms, migraine, cluster headaches Differential Diagnosis and hypertensive encephalopathy (25). Essentially, any cause or condition associated with hypertension can mimic the symptoms of AD (26). Due to the time criticality and likely poor outcomes of a stroke, paramedics should rule this condition out immediately by determining their patient as FAST negative. Due to the large number of possible differential diagnoses, it is vital that paramedics look

Treatment

CPG Variations

at key distinctive features of autonomic dysreflexia and seek to rule in their diagnosis whilst ruling out other potential causes to ensure that appropriate treatment is initiated. The prehospital treatment and management of AD is aimed at the reduction of elevated blood pressure and the identification and removal of noxious stimuli (10). Both pharmacological and non-pharmacological strategies are described in the evidence based treatment of AD. The paramedic should first assess the patient for an elevated systolic blood pressure (SBP), defined by Eldahan (4) as 20-40mmHg above baseline for adults. If a rise in SBP is observed, then the patient should be placed in a position where their head is lifted and they are sitting upright (1-3). This allows for an orthostatic drop in blood pressure (BP) as net blood flow is towards the extremities of the patient (1-3) causing venous pooling. Eldahan (4) and Breault (3) both stress the importance of monitoring BP every 2-5minutes to check for resolution or exacerbation of increased SBP as blood pressure can fluctuate rapidly in Spinal Cord Injury (SCI) patients. Tight clothing or constrictive devices should then be removed from the patient or loosened in order to enable the blood to flow to the abdomen and extremities (3) as these could also be possible triggering causes of noxious stimuli (1). Eldahan (4) also notes that pressure sores and skin lacerations can also contribute to noxious stimuli, which paramedics should assess the patient for. The identification and removal of noxious stimuli can next lead to AD being reversed, if the general management has not already lowered the patient's SBP. If possible, the paramedics should remove the stimulus before using pharmacological interventions (2) to lower the BP. A common noxious stimulus for SCI patients may be coming from bladder distention or obstruction such as an indwelling catheter that is kinked (3). Paramedics should check for kinks in existing catheters as well as bladder distention if the patient does not have an indwelling catheter. Monitoring of the SBP is paramount during treatment (3) to ensure that sudden decompression does not resolve it (3) and further hypotension is not missed as a consequence. Faecal Impaction is also a common stimulus (1-3) in which paramedic intervention is minimal and further control of blood pressure may result in pharmacological strategies if AD worsens (2,3). Ko (1) notes that if BP cannot be lowered or SBP >150mmHg or diastolic blood pressure (DBP) is >100mmHg, pharmacological management should be considered immediately. Eldahan (2) states that these interventions are mainly aimed at managing hypertension and further fast-acting and short duration antihypertensive agents should be used (1). The most commonly used agents in AD treatment include nifedipine, captopril and nitrates such as glyceryl trinitrate (GTN) and 2% nitroglycerin ointment (1-5). A Meta-analysis conducted by Krassioukov in 2009 (5) on the management of AD stated that there was no clear advantage of any pharmacological agent being used in the treatment of AD. For paramedics, a pharmacological intervention of sublingual (SL) GTN is the most readily available treatment and can be carried out by both ALS and ICP level paramedics. Nitrates are direct acting vasodilators (1). Breault (3) states that 300-600mcg of GTN can be administered SL to the patient for rapid BP control, and it can be repeated every 10 minutes, continuously monitoring the patient's BP for resolution and to avoid subsequent hypotension. It is important to note that GTN administration is contraindicated in patients who have used sildenafil in the last 24hrs due to adverse effects (3). Following pharmacological antihypertensive treatment, the patient should be monitored closely, with BP and pulse taken every 2-5 mins to notice changes (1). Further, if the patient shows signs of hypotension, the paramedics should return them to the supine position (1,3) Transport to hospital for further management and monitoring is recommended (1). Through a comparison of NSW, QLD and VIC State CPGs for the treatment of AD, it is evident that evidence based practice (EBP) has been followed and used to outline the treatments of varying services. All states recognised the importance of patient positioning

in the immediate treatment of AD (6-8), being sat upright with head lifted. Further, the removal of tight clothing or loosening of devices is noted in all three CPGs (6-8), in line with evidence based treatment. All recognised that identifying and eliminating the noxious stimulus, if possible was the preferred treatment before pharmacological antihypertensive interventions (6-8). AV (8) and QAS (9) stated that GTN should be administered if SBP remained >160mmHg, differing from EBP as a SBP of >150mmHg, NSW (6) CPGs differ again as GTN is administered if SBP >170mmHg. The repeated dosage of GTN differs among all states with NSW (6) and QLD (9) repeating every 5 minutes, and AV (8) repeating every 10mins. States follow the EBP of administering 300-600mcg of GTN, with NSW and VIC (6,8) administering 300mcg and QLD (9) 400mcg initial dosages. Repetitive monitoring of BP is noted for all CPGs and transport to hospital (6-8).

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