Naloxone for shock

Boeuf, Benoît; Poirier, Véronique; Guerguerian, Anne‐Marie; Roy, Christian; Farrell, Catherine; Lacroix, Jacques

doi:10.1002/14651858.cd004443

Cited by 121 publications

(19 citation statements)

References 52 publications

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“…9 Although the reported cardiac depression and antidiuretic effect of opioids have not consistently been duplicated clinically, the SNS depression has been supported by several clinical studies showing improvement in mean arterial pressure with administration of opioid antagonists. 10 Given the deleterious effect on homeostasis restoration and the association of opioids with greater resuscitation volumes in the current study and in that of Sullivan et al's, 17 judicious administration of opioids is needed. Opioids, in particular morphine, are central to pain control in burn patients.…”

Section: Outcome Variablesmentioning

confidence: 79%

“…42 Administration of lowdose opioid antagonists such as naloxaone may be another maneuver to help prevent the SNS depression without effecting analgesia. 10 This may be particularly effective during the resuscitation phase. Finally, nonpharmacologic means of dealing with pain such as massage, imagery, and distraction need to be explored more fully to assess their role in analgesia management of the burn patient.…”

Section: Outcome Variablesmentioning

confidence: 99%

“…In critically ill septic patient studies, opioid administration has also been associated with increased fluid needs and mortality. 10 We sought first to determine if our resuscitation volumes had increased. Second, we sought to determine factors related to that trend and, in particular, the effect of opioid administration.…”

mentioning

confidence: 99%

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The Impact of Opioid Administration on Resuscitation Volumes in Thermally Injured Patients

Wibbenmeyer

Sevier

Liao

et al. 2010

Journal of Burn Care & Research

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Administration of resuscitation volumes far beyond the estimates established by burn-body weight resuscitation formulas has been well documented. The reasons behind this increase are not clear. We sought to determine if our resuscitation volumes had increased and, if so, what factors were related to their increase. A retrospective chart review identified 154 patients admitted with burns greater than 20% of their BSA during the years of 1975-1976 (period 1), 1990-1991 (period 2), and 2006-2007 (period 3). Charts were reviewed for total fluids (crystalloid, colloid, and blood products) and opioids given before admission, during the first 8 hours of treatment, the next 16 hours of treatment, and the following 24 hours of treatment. Opioids were converted to opioid equivalents (OE). Multiple regression analysis was performed to determine the effects of variables of interest and control for confounders. Significance was assumed at the P < .05 level. Resuscitation fluid volumes increased significantly among adults from 3.97 ml/kg/%BSA during the first period to 6.40 ml/kg/%BSA during the third period (P < .01). The same trend in children <30 kg was not seen (P = .72). Fluid administered during the first 24 hours was significantly associated with age, BSA, intubation, latter two study periods, and opioid administration. Fluid administration was consistently associated with opioid administration at all measured time points. At 24 hours postburn, patients who received 2 to 4 OE/kg required an average of additional 3,650 +/- 1,704 ml of fluid, those receiving 4 to 6 OE/kg had required an average of 25,154 +/- 4,386 ml, and those who received >6 OE kg had required an average of 32,969 +/- 3,982 ml. In this single center retrospective study, we have shown a statistically significant increase in resuscitation fluids (from 1975 to 2007) and an association of resuscitation volumes with opioids. Opioids have been shown to increase resuscitation volumes in critically ill patients through both central and peripheral effects on the cardiovascular system. Because increased fluid resuscitation has been associated with adverse consequences in other studies, further research on alternative pain control strategies in thermally injured patients is warranted.

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Section: Outcome Variablesmentioning

confidence: 79%

Section: Outcome Variablesmentioning

confidence: 99%

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The Impact of Opioid Administration on Resuscitation Volumes in Thermally Injured Patients

Wibbenmeyer

Sevier

Liao

et al. 2010

Journal of Burn Care & Research

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“…Coimbra et al (158) have studied the phosphodiesterase inhibitor, pentoxifylline, already widely used for vascular disease because of its rheologic properties, as a treatment for hemorrhage because it reduces neutrophil activation and adhesion. A Cochrane review recently analyzed data on the opiate antagonist, naloxone, which has been studied based on the finding that central mu, epsilon, kappa, and delta receptors are activated during hemorrhagic shock and inhibit calcium channels; the data suggested that further clinical trials are needed to determine if the beneficial effects on blood pressure by the administration of naloxone result in any durable improvements in survival (159). A common thread across all of these potential agents is that they are already in wide clinical use for other disorders.…”

Section: Alternatives To Conventional Fluid Resuscitationmentioning

confidence: 99%

Fluid Resuscitation

Santry

Alam

2010

Shock

215

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Hemorrhage remains a major cause of preventable death following both civilian and military trauma. The goals of resuscitation in the face of hemorrhagic shock are restoring end-organ perfusion and maintaining tissue oxygenation while attempting definitive control of bleeding. However, if not performed properly, resuscitation can actually exacerbate cellular injury caused by hemorrhagic shock, and the type of fluid used for resuscitation plays an important role in this injury pattern. This article reviews the historical development and scientific underpinnings of modern resuscitation techniques. We summarized data from a number of studies to illustrate the differential effects of commonly used resuscitation fluids, including isotonic crystalloids, natural and artificial colloids, hypertonic and hyperoncotic solutions, and artificial oxygen carriers, on cellular injury and how these relate to clinical practice. The data reveal that a uniformly safe, effective, and practical resuscitation fluid when blood products are unavailable and direct hemorrhage control is delayed has been elusive. Yet, it is logical to prevent this cellular injury through wiser resuscitation strategies than attempting immunomodulation after the damage has already occurred. Thus, we describe how some novel resuscitation strategies aimed at preventing or ameliorating cellular injury may become clinically available in the future.

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“…58, 59 Other treatments currently under investigation in children include plasmapheresis, IV immunoglobulins, naloxone, and recombinant bactericidal/permeability-increasing protein. [60][61][62][63] Trauma Patients with hemorrhagic shock require aggressive fl uid resuscitation to treat hypovolemia and require blood products for hypotension that does not rapidly respond to fl uids. Supplemental oxygen is an important adjunct in the setting of anemia.…”

Section: Beyond the Golden Hourmentioning

confidence: 99%

Circulatory Emergencies: Shock

Cho¹,

Rothrock²

2008

Pediatric Emergency Medicine

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Shock is an abnormal physiologic state of inadequate tissue perfusion that is a common end point for various diseases.Physiologic subtypes of shock include hypovolemic, cardiogenic, distributive, and obstructive shock. Multiple subtypes of shock can be present with a single disease.With the exception of cardiogenic shock, the most common mistake in management is not administering enough fl uids in a timely fashion.Use of goal-directed therapy for fl uid-refractory septic shock improves outcome.with only minimal changes in vital signs. 4,5 The term compensated shock is used for patients with shock physiology, but preservation of normal blood pressure. Decompensated shock is used when the patient has hypotension, and is usually a late sign of shock. If untreated, decompensated shock will become irreversible, leading to eventual death.Physiologic subtypes of shock include hypovolemic, cardiogenic, distributive, and obstructive shock. Hypovolemic shock is due to a defi ciency in intravascular volume either through insuffi cient intake or excessive loss of fl uid. Cardiogenic shock is due to failure of the heart to provide suffi cient cardiac output. Distributive shock is defi ned as a change in vascular capacitance resulting in peripheral vasodilation and abnormal redistribution of blood fl ow. Obstructive shock is due to an obstruction of outfl ow from the heart. The differential diagnosis for each type of shock is extensive (Table 8-1).While it is useful to distinguish between the physiologic subtypes of shock, recognition and treatment of the specifi c disorders that lead to shock is equally important. In addition, some diseases have multisystem involvement with several different subtypes of shock. For example, children with septic shock may be hypovolemic from fl uid loss and inadequate intake, and may have sepsis-induced myocardial depression that directly limits contractility and cardiac output. Recognition and ApproachKnowledge of physiologic compensatory responses can help clinicians identify shock subtypes and initiate appropriate management. Cardiac output is regulated by both the heart rate and the stroke volume of each contraction. Preload, cardiac contractility, and afterload determine stroke volume. Preload refl ects both the absolute intravascular volume and changes in venous capacitance. Afterload is related to systemic vascular resistance. The primary physiologic response to compensate for shock is via the sympathetic nervous system. Baroreceptors in the carotid sinus and chemoreceptors in the aorta and carotid bodies sense hypovolemia and hypoxemia, respectively, and activate the sympathetic adrenergic response. The release of catecholamines activates α 1 receptors in peripheral vascular smooth muscle, causing peripheral vasoconstriction. 6 Presynaptic α 2 receptors in the heart and vasculature are activated by norepinephrine released from sympathetic nerves and mediate negative feedback inhibition of further norepinephrine release.

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Naloxone for shock

Abstract: Naloxone improves blood pressure, especially mean arterial blood pressure. However, the clinical usefulness of naloxone to treat shock remains to be determined, and additional randomized controlled trials are needed to assess its usefulness.

Cited by 121 publications

References 52 publications

The Impact of Opioid Administration on Resuscitation Volumes in Thermally Injured Patients

The Impact of Opioid Administration on Resuscitation Volumes in Thermally Injured Patients

Fluid Resuscitation

Circulatory Emergencies: Shock

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