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Trauma of the Brain and Spinal Cord
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Fernando D. Goldenberg, Ali Mansour
Hypotension following trauma is most commonly caused by blood loss, hypothermia, and cardiac dysfunction. However, neurogenic shock should be considered in patients with suspected SCI, especially when the injury is above T6. The loss of sympathetic outflow causes vasodilation, which leads to distributive shock. Unlike hypovolemic shock, distributive shock secondary to neurogenic shock often presents with bradycardia and widened pulse pressure. SCIs at this level can disrupt pathways reaching the midthoracic spinal cord where the sympathetic splanchnic nerves (which have an important role in maintaining vascular tone) arise. The sympathetic outflow to the cardiac native pacemaker can also be affected. Up to 20% of patients with spinal injuries at the cervical level may experience neurogenic shock with an even higher incidence of bradycardia in the acute phase of the disease.24
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Distributive shock is caused by a lack of ability of the vessels to maintain sympathetic tone; thus, systemic vascular resistance falls dramatically, and perfusion pressure is not maintained. Clinically, a patient with distributive shock may feel warm, but the perfusion pressure is not adequate to deliver oxygen to the tissues, so anaerobic metabolism and acidosis swiftly follows. Categories of distributive shock are anaphylactic, septic, (discussed in Chapter 12) and neurogenic (discussed in Chapter 9).
Integrated Cardiovascular Responses
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Distributive shock is characterized by profound systemic vasodilatation resulting in an inadequate perfusion pressure and inappropriate distribution of blood despite an adequate cardiac output. This is observed in septic and anaphylactic shock.
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
General classifications of shock include hypovolemic, cardiogenic, obstructive, and distributive shock. One of the most common types of circulatory shock is distributive or vasodilatory shock (VS). Classically, distributive, or VS is characterized by normal or increased cardiac output (CO) and a low systemic vascular resistance (SVR), leading to hypotension, organ hypoperfusion, inadequate delivery and utilization of oxygen, metabolic acidosis, and eventually organ failure. Causes of VS include vasoplegic syndrome after anesthesia or cardiopulmonary bypass (CPB), infection-related septic shock, severe adrenal insufficiency leading to shock, neurogenic shock, and allergin-induced or anaphylactic shock. Multiple mechanisms of shock may be coincidental. An example would be in severe sepsis, where VS can be coupled with cardiogenic shock either from a preexisting cardiomyopathy or from an infection-related cardiac effect.
A deadly capillary leak attack. Clarkson’s disease: a narrative review
Published in Acta Clinica Belgica, 2022
E De Tandt, D Van Sassenbroeck, L Heireman, J Dierick, A Luyckx, S Verelst
In conclusion, we presented a case that most likely corresponded to Clarkson’s disease, although septic shock as an alternative diagnosis could not be excluded. Clarkson’s disease is a clinical diagnosis by exclusion, with a high mortality, certainly if not recognised and hereby improperly managed. The difficulty of diagnosing this disease has already been shown by Eo et al., where 36.6% of cases were not properly diagnosed during the first attack and have been mistaken by a hypovolemic shock or a septic shock [34]. Because of its presentation, especially emergency and intensive care physicians should be aware of the existence of this condition in the event of an unexplained refractory distributive shock. In the event, a patient presents with signs of a distributive shock, in combination with haemoconcentration and hypoalbuminemia, Clarkson’s disease should be included in the differential diagnosis. In that case, further investigations with protein electrophoresis are recommended, and a highly elevated serum VEGF-concentration could confirm the presumptive diagnoses. If, despite maximum conservative therapy, the clinical condition deteriorates, treatment with IVIg should be initiated. Unfortunately, in some patients presenting with a grade IV flare of Clarkson’s disease, all treatment options seem futile.
Pathophysiological profile of awake and anesthetized pigs following systemic exposure to the highly lethal ricin toxin
Published in Clinical Toxicology, 2022
Reut Falach, Michael Goldvaser, Pinchas Halpern, Amir Rosner, Anita Sapoznikov, Yoav Gal, Orr Goren, Tamar Sabo, Chanoch Kronman, Shahaf Katalan
Lethal intramuscular (systemic) exposure to ricin differs clinically and pathophysiologically from intra-tracheal (inhalational) exposure. As described in our previous study [8], intra-tracheal exposure to ricin leads mainly to a respiratory syndrome culminating in end stage acute respiratory distress syndrome (ARDS). Herein we describe a totally different clinical syndrome ensuing exposure to the same toxin by the intramuscular route: terminal distributive shock with no apparent respiratory involvement. The diagnosis of distributive shock reported in this study is determined from the global homodynamic variables described here and corroborated by preliminary microcirculation imaging. Systemic exposure to a lethal dose of ricin results after a 24-hour deterioration to an irreversible shock. At this stage, the result of the intoxication is irreversible, as evidenced by the fact that equine-derived anti-ricin F(ab′)2 antibodies treatment led to partial rescue when given 24 h post exposure and to no rescue at all when given 30 h after intramuscular ricin exposure.