Are urological procedures in tetraplegic patients safely performed without anesthesia? A report of three cases

Vaidyanathan, S; Soni, B M; Selmi, Fahed; Singh, G.; Esanu, Cristian; Hughes, Peter L; Oo, Tun; Pulya, Kamesh

doi:10.1186/1754-9493-6-3

Cited by 10 publications

(17 citation statements)

References 8 publications

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“…Vaidyanathan et al 50 reported a BP increase to 4200/110 mm Hg in tetraplegic individuals without anesthesia. When cystoscopy was conducted again under subarachnoid block, the BP was stable during the procedure, thus demonstrating subarachnoid block as an effective method in preventing the occurrence of AD.…”

Section: Cystoscopy and Transurethral Litholapaxymentioning

confidence: 99%

Iatrogenic urological triggers of autonomic dysreflexia: a systematic review

et al. 2015

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Study design: This is a systematic review. Objective: The objective of this study was to review the literature on iatrogenic urological triggers of autonomic dysreflexia (AD). Setting: This study was conducted in an international setting. Methods: A systematic review was conducted from PubMed search using AD/ autonomic hyperreflexia and spinal cord injury (SCI). Studies selected for review involved iatrogenic urological triggers of AD in individuals with SCI, including original articles, previous practice guidelines, case reports and literature reviews. Studies that did not report AD or blood pressure (BP) assessments during urological procedures were excluded. Results: Forty studies were included for analysis and categorized into four groups: (1) urodynamics and cystometry; (2) cystoscopy and transurethral litholapaxy; (3) extracorporeal shock-wave lithotripsy (ESWL); and (4) other procedures. During urodynamics, the incidence of AD ranged from 36.7% to 77.8%. The symptomatic rate ranged from 50% to 65%, with AD symptoms seen predominantly in cervical SCI patients. The studies imply no consensus regarding the relationship between AD, neurogenic detrusor overactivity and detrusor sphincter dyssynergia. Without anesthesia, the majority of individuals develop AD during cystoscopy, transurethral litholapaxy and ESWL. The effectiveness of different anesthesia methods relies on blocking the nociceptive signals from the lower urinary tract (LUT) below the level of the neurological lesion. Other iatrogenic urological triggers were commonly associated with bladder filling. Conclusion: The LUT triggers of episodes of AD are often associated with iatrogenic urological procedures. AD was more prevalent in cervical SCI than in thoracic SCI. To detect this potential life-threatening complication following cervical and high thoracic SCI, routine BP monitoring during urological procedures is highly recommended.

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Section: Cystoscopy and Transurethral Litholapaxymentioning

confidence: 99%

Iatrogenic urological triggers of autonomic dysreflexia: a systematic review

et al. 2015

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“…This explains why pelvic visceral stimulation is the most commonly implicated [1,7,10,11]. Bladder distension is responsible for 75-82% of AH episodes [3]. Bladder distension may result from blocked or kinked indwelling urinary catheters (one of the commonest causes), urinary tract infection, interventional procedures and catheterization [7].…”

Section: Triggeringmentioning

confidence: 99%

“…Essentially symptoms and signs of AH result from the predominant parasympathetic excitation above the level of injury, and sympathetic excitation below the level of injury [3,5]. Usually, patients with SCI at T6 or above have normal systolic blood pressure of 90-110 mmHg.…”

Section: Symptoms and Signs Of Ahmentioning

confidence: 99%

“…As a consequence of the extensive marked vasoconstriction, a hypertension occurs. A reflex bradycardia usually occurs through the intact vagus nerve and glossopharyngeal nerve (cranial nerves X and IX), because of the spinal cord transection does not interfere with afferent connections of the baroreceptors from the carotid sinus and aortic arch to the cardiac centers in the medulla oblongata [3,5,6]. …”

mentioning

confidence: 99%

“…AH is developed in patients after severe spinal cord injury (SCI) above T6 level as a result of exaggerated spinal sympathetic excitation. It is caused by the spinal reflex mechanisms that re main intact despite the injury of the spinal cord [3,4]. The incidence of AH for spinal cord injuries above T6 is 85% [3][4][5].…”

mentioning

confidence: 99%

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Autonomic Hyperreflexia after Spinal Cord Injury

Richa¹

2015

J Spine

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The most important complication of spinal cord lesions above T6 level is the phenomenon of Autonomic Hyperreflexia (AH). Symptoms and signs of AH result from the predominant parasympathetic excitation above the level of injury, and sympathetic excitation below the level of injury. Various noxious and nonnoxious stimuli below the level of injury can thus trigger off a mass autonomic response. The main triggering factor of AH is related with the urinary tract. The main treatment of AH is removal of the triggering factors. The development of intraoperative AH and hypertension can be prevented either by general anesthesia, which blunts autonomic reflexes, or regional anesthesia (spinal or epidural), which blocks afferent and autonomic efferent neural impulses. Physiopathology of AHAH is initiated by afferent impulses reaching the isolated spinal cord below the level of the spinal cord damage. While the nerve impulses travel up to the spinal cord, they are obstructed at the injury level. The input activates a reflex which increases the response of the sympathetic nervous system and gives a vasoconstriction and an hypertension [3][4][5][6]. The AH develop ment has multifactorial complex mechanisms. Afferent impulses are carried by fibers which synapse within the dorsal grey matter of the spinal cord at various levels and ascend the dorsal and lateral columns until blocked at the level of SCI. As there is a loss of supraspinal control, the terminal boutons of presynaptic fibres divided by the cord transection become disorganized, leading to derangement in neighbouring, intact efferent fibres. Over the weeks following SCI, presynaptic boutons multiply, forming chaotic and inappropriate reflexes. Interneurones excited by the afferent inputs synapse with preganglionic sympathetic neurons in the intermediolateral grey column of the cord [4]. As a result of this process, an exaggerated reaction occurs within the pregangli onic sympathetic neurones as a response to the afferent stimulus. The reason that AH is a feature of lesions at the T6 level or above is related with splanchnic circulation response to this sympathetic overactivity. The latter activity below the injury level results a splanch nic and peripheral vasoconstriction and causes hypertension. As a result of an excessive parasympathetic output above the level of the lesion, a peripheral vaso dilation occurs [5,7,8].The brain is unable to influence the changes below the level of the injury, but above this level, the response of spinal centers is massive, leading to extensive sympathetic stimulation of the cardiovascular system and of the neurologically isolated adrenal medulla [5,6]. The denervated blood vessels are hypersensitive to any sympathetic stimulation and to the catecholamines released by the adrenal medulla [6]. This leads to vasoconstriction in the denervated area and compensatory vasodilation in the innervated area. Therefore, cord damage at T6 level or above is accompanied by increased secretion of adrenal medullary cathecholamines suggesting...

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Autonomic Dysreflexia in Neuro-urological Practice

Krassioukov

Walter

2023

Handbook of Neurourology

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Are urological procedures in tetraplegic patients safely performed without anesthesia? A report of three cases

Cited by 10 publications

References 8 publications

Iatrogenic urological triggers of autonomic dysreflexia: a systematic review

Iatrogenic urological triggers of autonomic dysreflexia: a systematic review

Autonomic Hyperreflexia after Spinal Cord Injury

Autonomic Dysreflexia in Neuro-urological Practice

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