Resuscitation
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Spinal cord injury (SCI) is recognised to cause hypotension and bradycardia (neurogenic shock). Previous studies have shown that the incidence of this in the emergency department (ED) may be low. However these studies are relatively small and have included a mix of blunt and penetrating injuries with measurements taken over different time frames. The aim was to use a large database to determine the incidence of neurogenic shock in patients with isolated spinal cord injuries. ⋯ Fewer than 20% of patients with a cervical cord injury have the classical appearance of neurogenic shock when they arrive in the emergency department. It is uncommon in patients with lower cord injuries. The heart rate and blood pressure changes in patients with a SCI may develop over time and we hypothesise that patients arrive in the ED before neurogenic shock has become manifest.
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Special clinical situations where general hypothermia cannot be recommended but can be a useful treatment demand a new approach, selective brain cooling. The purpose of this study was to selectively cool the brain with cold saline circulating in balloon catheters introduced into the nasal cavity in pigs. ⋯ Inducing selective brain hypothermia with cold saline via nasal balloon catheters can effectively be accomplished in pigs, with no major disturbances in systemic circulation or physiological variables. The temperature gradients between brain and body can be maintained for at least 6 h.
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Most survivors of out-of-hospital cardiac arrest (OHCA) will die subsequently from post-anoxic encephalopathy. In animals, the severity of brain damage is mainly influenced by the duration of cardiac arrest and also by the cerebral blood flow (CBF) and oxygen extraction (CEO2) abnormalities observed during the post-resuscitation period. The aim of our study was to describe CBF and CEO2 modifications during the first 72 h in OHCA patients treated by induced mild hypothermia. ⋯ Cerebral haemodynamic and oxygenation values are altered considerably but evolve during the first 72 h following resuscitation after cardiac arrest. In particular, these changes may lead to a mismatch between CBF and CEO2 leading to a "luxurous perfusion" in non-survivors.
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A 77-year-old woman was admitted to the intensive care unit after successful cardiopulmonary resuscitation for out-of-hospital cardiac arrest due to pulseless electrical activity. She was treated with mild therapeutic hypothermia to minimise secondary anoxic brain damage. After a 24 h period of therapeutic hypothermia with a temperature of 32.5 degrees C, the patient was rewarmed and sedation discontinued. ⋯ Autopsy showed massive brain swelling and tentorial herniation. Hyperthermia possibly played a pivotal role in the development of this fatal insult to this vulnerable brain after cardiac arrest and therapeutic hypothermia treatment. The acute histopathological alterations in the brain, possibly caused by the deleterious effects of fever after cardiac arrest in human brain, may be considered a new observation.
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Colloid solutions have been suggested to improve microvascular perfusion due to their anti-inflammatory properties. Whether this also applies for the gut, an important immunological organ vulnerable to hypoperfusion is unknown. This study investigated intestinal microcirculation of endotoxaemic rats after volume therapy with colloid solutions such as hydroxyethyl starch (HES) and gelatin or isotonic saline (NaCl). ⋯ Also mesenteric leukocyte-endothelium interaction was not significantly influenced by either treatment. In conclusion, early volume therapy with HES or gelatin, but not with NaCl, preserved gut microvascular perfusion during endotoxaemia but did not have a significant effect on tissue oxygenation nor morphological appearance in this experimental model. An anti-inflammatory effect of colloid solutions was not seen and fails to explain the changes in intestinal microcirculation.