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Medications used to treat sympathetic storming

Medications used to treat sympathetic storming

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Patients with sympathetic storming must be treated promptly. Intravenous medication can provide immediate control, although the effect is generally temporary, and dosing can be extreme, thus placing the individual at greater risk for respiratory depression. These patients already have significant cerebral compromise and must be treated promptly to...

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... that depress the central nervous system, thus suppressing the sympathetic nervous system, are most commonly used. Opiate receptor agonists, dopamine agonists, β-blockers, α- blockers, γ-aminobutyric acid (GABA) agonists, and sedatives all have been used (Table 4) control these episodes. Although intravenous medications offer rapid control, dosing can be extreme, thus placing the patient at greater risk for respiratory depression. ...

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... 24 These signs and symptoms vary from episode to episode, as well as from individual to individual. 6 The interruption of diaphoresis is used as a mark between the second and third phases, frequently occurring on the 74 th day after the brain injury. 9 When an episode of mixed PSH occurs, the symptoms manifested are miosis, tearing, bradycardia, bradypnea, hypotension, hypothermia, tidal breathing, and yawning. ...
... 16 In the ICU, intravenous drugs such as morphine, fentanyl and midazolam are the first line of treatment. 6 Morphine, an opioid agonist, performs analgesia and alters the extreme changes of the ANS, as well as dystonia by suppressing the sympathetic flow. 9 Sedatives such as dexmedetomidine and propofol are used to manage episodes of PSH in the ICU. ...
... When treated incorrectly, PSH leads to an increased risk of secondary brain injury. 6 The high adrenergic activity of PSH 4 in association with several episodes of the phenomenon can result in secondary morbidities such as elevated intracranial pressure, cardiac injury, metabolic disorders, 19 systemic abnormalities throughout the body, and increased mortality. 21 A hypermetabolic state during sympathetic hyperactivity can reduce body weight by 25% during just one episode. ...
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The present literature review aims to present the physiology of paroxysmal sympathetic hyperactivity (PSH) as well as its clinical course, conceptualizing them, and establishing its diagnosis and treatment. Paroxysmal sympathetic hyperactivity is a rare syndrome, which often presents after an acute traumatic brain injury. Characterized by a hyperactivity of the sympathetic nervous system, when diagnosed in its pure form, its symptomatologic presentation is through tachycardia, tachypnea, hyperthermia, hypertension, dystonia, and sialorrhea. The treatment of PSH is basically pharmacological, using central nervous system suppressors; however, the nonmedication approach is closely associated with a reduction in external stimuli, such as visual and auditory stimuli. Mismanagement can lead to the development of serious cardiovascular and diencephalic complications, and the need for neurosurgeons and neurointensivists to know about PSH is evident in order to provide a fast and accurate treatment of this syndrome.
... Electrophysiological investigations of this phenomenon did not show electroencephalographic activity. Many names were attributed to this syndrome: dysautonomia, sympathetic storming, brainstem attack, autonomic dysregulation, and paroxysmal autonomic instability with dystonia [2][3][4][5]. In 2014, the International Brain Injury Association convened a consensus workgroup to clarify its nomenclature and diagnostic criteria. ...
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Introduction: Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Methods: We searched MEDLINE, ResearchGate, and Google Scholar, for keywords related to PSH and the role of beta-blockers in moderate-to-severe TBI on September 23, 2020. Two authors blindly screened the articles found with Rayyan. Both resolved their conflicts by mutual consent. If no solution was found, a third author was consulted. Simple descriptive data analysis was performed and the results were presented both in a narrative and tabular form. Results: Of the 19 items found, 10 met the criteria for inclusion. 50% were systematic reviews without meta-analysis, 40% were observational studies, and 10% were experimental studies. Propranolol was the main beta-blocker found in 80% of the studies and was the only molecule used in the treatment of paroxysmal sympathetic hyperactivity in 40% of the included studies. Only two studies evaluated and showed a significant association between beta-blockers and mortality rate (5.1% vs. 10.8%; P=0.03), (3% vs. 15%; P=0.002), respectively. Conclusion: Propranolol is the beta-blocker that has been shown to be effective in reducing the length of stay and mortality rate in moderate-severe traumatic brain injury patients with PSH. However, further studies are needed to precisely define the terms and conditions of its use.
... Autonomic dysregulation arising from a brain injury can manifest itself as distinct changes in heart rate variability parameters. For TBI, it has been suggested that a desynchronisation of the para-sympathetic and sympathetic arms of the ANS caused by cortical and/or hypothalamus dysregulation (Baguley et al., 2008) may be the underlying cause alongside sympathetic storming (Lemke, 2007). These features of autonomic dysregulation originating from childhood brain injury are suggested to mirror those observed in RTT because in both instances the resulting autonomic imbalances cause a cardiovascular dysregulation that is reflected by changes in cardiac physiology. ...
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Rett Syndrome (RTT) is a complex neurodevelopmental disorder with autonomic nervous system dysfunction. The understanding of this autonomic dysregulation remains incomplete and treatment recommendations are lacking. By searching literature regarding childhood brain injury, we wanted to see whether understanding autonomic dysregulation following childhood brain injury as a prototype can help us better understand the autonomic dysregulation in RTT. Thirty-one (31) articles were identified and following thematic analysis the three main themes that emerged were (A) Recognition of Autonomic Dysregulation, (B) Possible Mechanisms & Assessment of Autonomic Dysregulation and (C) Treatment of Autonomic Dysregulation. We conclude that in patients with RTT (I) anatomically, thalamic and hypothalamic function should be explored, (II) sensory issues and medication induced side effects that can worsen autonomic function should be considered, and (III) diaphoresis and dystonia ought to be better managed. Our synthesis of data from autonomic dysregulation in paediatric brain injury has led to increased knowledge and a better understanding of its underpinnings, leading to the development of application protocols in children with RTT.
... Before initial treatment, environmental modification is an important measure. Controlling room temperature to provide a less stimulating environment, and administering daily care for the individual, is of benefit for hyperthermia patients (38,44,88). Recently, a pilot study showed that a lower room temperature was associated with PSH, indicating that environmental interventions could complement pharmacological strategies (e.g., standardization of room temperature and application of a blanket) (89). ...
... Recently, a pilot study showed that a lower room temperature was associated with PSH, indicating that environmental interventions could complement pharmacological strategies (e.g., standardization of room temperature and application of a blanket) (89). A timely and accurately recorded monitoring index may assist the development of an appropriate therapeutic plan (65,88). In this respect, frequency, duration, and severity, and the skills to mitigate the potential triggers of PSH, are thought to play important roles in non-pharmacological treatments (90). ...
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Paroxysmal sympathetic hyperactivity (PSH) has predominantly been described after traumatic brain injury (TBI), which is associated with hyperthermia, hypertension, tachycardia, tachypnea, diaphoresis, dystonia (hypertonia or spasticity), and even motor features such as extensor/flexion posturing. Despite the pathophysiology of PSH not being completely understood, most researchers gradually agree that PSH is driven by the loss of the inhibition of excitation in the sympathetic nervous system without parasympathetic involvement. Recently, advances in the clinical and diagnostic features of PSH in TBI patients have reached a broad clinical consensus in many neurology departments. These advances should provide a more unanimous foundation for the systematic research on this clinical syndrome and its clear management. Clinically, a great deal of attention has been paid to the definition and diagnostic criteria, epidemiology and pathophysiology, symptomatic treatment, and prevention and control of secondary brain injury of PSH in TBI patients. Potential benefits of treatment for PSH may result from the three main goals: eliminating predisposing causes, mitigating excessive sympathetic outflow, and supportive therapy. However, individual pathophysiological differences, therapeutic responses and outcomes, and precision medicine approaches to PSH management are varied and inconsistent between studies. Further, many potential therapeutic drugs might suppress manifestations of PSH in the process of TBI treatment. The purpose of this review is to present current and comprehensive studies of the identification of PSH after TBI in the early stage and provide a framework for symptomatic management of TBI patients with PSH.
... This finding can be due to the fact that TBI causes loss of consciousness as well as affecting the patients' response to pain based on the severity of brain injury. 37,38 The findings of this study indicate that the varying types of patients` behavioral responses differed according to the extent of TBI. To our knowledge, this finding is the first of its kind. ...
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Introduction: A consistent approach to pain assessment for patients admitted to intensive care unit (ICU) is a major difficulty for health practitioners due to some patients' inability, to express their pain verbally. This study aimed to assess pain behaviors (PBs) in traumatic brain injury (TBI) patients at different levels of consciousness. Methods: This study used a repeated-measure, within-subject design with 35 patients admitted to an ICU. The data were collected through observations of nociceptive and non-nociceptive procedures, which were recorded through a 47-item behavior-rating checklist. The analyses were performed by SPSS ver.13 software. Results: The most frequently observed PBs during nociceptive procedures were facial expression levator contractions (65.7%), sudden eye openings (34.3%), frowning (31.4%), lip changes (31.4%), clear movement of extremities (57.1%), neck stiffness (42.9%), sighing (31.4%), and moaning (31.4%). The number of PBs exhibited by participants during nociceptive procedures was significantly higher than those observed before and 15 minutes after the procedures. Also, the number of exhibited PBs in patients during nociceptive procedures was significantly greater than that of exhibited PBs during the non-nociceptive procedure. The results showed a significant difference between different levels of consciousness and also between the numbers of exhibited PBs in participants with different levels of traumatic brain injury severity. Conclusion: The present study showed that most of the behaviors that have been observed during painful stimulation in patients with traumatic brain injury included facial expressions, sudden eye opening, frowning, lip changes, clear movements of extremities, neck stiffness, and sighing or moaning.
... Penrod, 1993 [28] RCT [37] Clinical Article ...
... This can be caused after the cessation of sedatives and narcotics in the ICUs and should be treated based on their signs and symptoms by initiating planned medications to reduce the activities of the sympathetic nervous system. [37] The patients who receive erythropoietin show lower mortality and better neurological outcome and limit neuronal damage induced by TBI. [38] Naloxone effectively reduce mortality and control ICP in TBI. ...
Article
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Effective nursing management strategies for adults with severe traumatic brain injury (STBI) are still a remarkable issue and a difficult task for neurologists, neurosurgeons, and neuronurses. A list of justified indications and scientific rationale for nursing management of these patients are continuously evolving. The objectives of the study are to analyze the pertinently available research and clinical studies that demonstrate the nursing management strategies for adults with STBI and to synthesize the available evidence based on the review. A comprehensive literature search was made in following databases such as Google Scholar, Cochrane, J‑Gate, ProQuest, and ScienceDirect for retrieving the related studies. In the included studies, data were extracted and evaluated according to the objective. Narrative analysis was adopted to write this review. Patients with STBI have poor prognosis and require quality care for maximizing patients’ survival. With a thorough knowledge and discernment of care of such patients, nurses can improve these patients’ neurological outcomes.
... However, there is no simultaneous increase in myocardial oxygen delivery and subendocardial ischaemia may occur, impaired ventricular function may follow. This can lead to myocardial dysfunction [11][12][13][14][15][16][20][21][22]. Administration of beta-blockers in patients with TBI could attenuate the systemic catecholamine excess, thereby decreasing cardiac complications [10] and support the hypothesis that TBI is a potential risk factor for subsequent myocardial dysfunction. ...
... [19,20] Myocardial dysfunction often occurs as a result of severe brain injury. [21][22][23] The exacerbated stress response, i.e. "sympathetic storm,"results in hypertension, tachycardia, and arrhythmias. Though usually of short duration, it may lead to cardiac dysfunction, cardiac ischemia, myocardial and conduction system necrosis. ...
... Hypernatremia may adversely affect the outcomes for renal and liver transplants (Grade 2A). [22][23][24][25] ...
Article
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Brain stem death is usually followed by an expected pattern of complex multiple organ failure, hence an appropriate support to the donor before and after brain death can increase the number and quality of donor organs. The medical management of organ donor can be broadly divided into cardiovascular management, hormonal or management of metabolic derangement, management of temperature, respiration, hematological parameter, and nutritional support. Early identification of organs for donation helps to optimize the medical strategies. The guidance provided in this statement does not substitute proper clinical decision?making in particular case, but will help intensivists for the management of brain death for organ and tissue donation. Table 10 shows the checklist for the management of potential organ donors.
... Для купирования центрогенной лихорадки при неэффективности НПВС используют методику создания глубокого охранительного торможения центральной нервной системы (ЦНС) с применением барбитуратов, бензодиазепинов, оксибутирата натрия, пропофола [3, 8,9]. В наиболее тяжелых случаях используют опиоиды в условиях контролируемой искусственной вентиляции легких (ИВЛ) [10][11][12]. ...
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Cental fever — fever of infectious origin, complica­ting diseases of the central nervous system. Mechanisms of development are related to the dysfunction of the hypothalamus, which is considered as the center of thermoregulation. Central fever is associated with activation of catabolic reactions, adverse course of underlying pathological process and is hard to control using traditional therapeutic measures, including the use of non-steroidal anti-inflammatory drugs (NSAIDs). The research deals with the comparative study on the efficiency of central fever control in victims with severe traumatic brain injury and cerebral strokes using NSAIDs and a complex of vitamins and antioxidants, which help to improve the processes of association of mitochondrial oxidation and phosphorylation. Increase of this association provides the growth in the synthesis of adenosine triphosphate and inhibits the spread of free energy in the body as a heat. Each of the studied groups included 14 patients with severe injuries of the central nervous system and symptoms of central fever. There was found a significant advantage of treatment regimen that included the combined use of succinic acid, inosine, nicotinamide, riboflavin and thiamine over the commonly used treatment regimen based on the priority use of NSAIDs.
... Several feasible tests can be used in clinical practice for the assessment of parasympathetic and sympathetic functions, particularly in terms of cardiovascular autonomic modulation. Dysfunctions of the sympathetic nervous system (SNS) as well as an increased risk of developing neurodegenerative diseases, such as AD, post-trauma have both been implicated as risk factors in response to traumatic brain injury (TBI) [4][5][6][7][8]. ...
... The SNS, together with the parasympathetic nervous system (PNS), form the ANS which is charged with unconsciously regulating internal organs and bodily functions. The terms paroxysmal sympathetic storm and sympathetic storming have been used to describe the presence of overly active sympathetic signaling after a severe TBI [5]. This sympathetic hyperactivity has been associated with pupil dilation, tachycardia, and hypertension [5]. ...
... The terms paroxysmal sympathetic storm and sympathetic storming have been used to describe the presence of overly active sympathetic signaling after a severe TBI [5]. This sympathetic hyperactivity has been associated with pupil dilation, tachycardia, and hypertension [5]. On top of these symptoms, several other physical symptoms are known to present in an individual who has experienced a TBI [9]. ...
Article
Autonomic dysfunction is very common in patients with dementia, and its presence might also help in differential diagnosis among dementia subtypes. Various central nervous system structures affected in Alzheimer's disease (AD) are also implicated in the central autonomic nervous system (ANS) regulation. For example, deficits in central cholinergic function in AD could likely lead to autonomic dysfunction. We recently developed a simple, readily applicable evaluation for monitoring ANS disturbances in response to traumatic brain injury (TBI). This ability to monitor TBI allows for the possible detection and targeted prevention of long-term, detrimental brain responses caused by TBI that lead to neurodegenerative diseases such as AD. We randomly selected and extracted de-identified medical record information from subjects who have been assessed using the ANS evaluation protocol. Using machine learning strategies in the analysis of information from individual as well as a combination of ANS evaluation protocol components, we identified a novel prediction model that is effective in correctly segregating between cases with or without a documented history of TBI exposure. Results from our study support the hypothesis that trauma-induced ANS dysfunctions may contribute to clinical TBI features. Because autonomic dysfunction is very common in AD patients it is possible that TBI may also contribute to AD and/or other forms of dementia through these novel mechanisms. This study provides a novel prediction model to physiologically assess the likelihood of subjects with prior history of TBI to develop clinical TBI complications, such as AD.