Hematorheology during deep hypothermia

Sands, Murray P.; Mohri, Hitoshi; Sato, So; Mannik, Mart; Hessel, Eugene A.; Dillard, David H.

doi:10.1016/0011-2240(79)90036-1

Cited by 16 publications

(8 citation statements)

References 18 publications

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“… 6 Although we observed an increased PT and an increased partial thromboplastin time in this patient presenting with hypothermia, blood viscosity increases when cooling occurs and it increases once the patient is rewarmed. 7 In an experimental study, Sands et al have found a better correlation between blood viscosity and hypothermia as against that with hematocrit. An increased hematocrit would be related to a systemic capillary leak, mostly reversible with dextran perfusion.…”

Section: Discussionmentioning

confidence: 97%

Severe Aortic Thrombosis and Profound Hypothermia: A Case Report

Schmitt¹,

Esnault²,

Sartre³

et al. 2021

Indian Journal of Critical Care Medicine

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A bstract Background Blood clot formation is a multifactorial process and has been related many times in intensive care units. Here is presented a multiple thrombosis formation in a rewarming patient. Case description A 68-year-old patient was admitted to our intensive care unit after lying on the floor for an unknown time. She presented a severe hypothermia at 26° and a severe cardiogenic shock. Because she was confused and was hypoxemic, she had been intubated at her admission. After intravascular warming, we could stop sedative medications. She presented a right hemiparesis and acute left leg ischemia. Computed tomography (CT) scan revealed a constituted left Sylvian stroke and a massive clot along the aorta. She required a surgical embolectomy and fasciotomy. She died after she presented a severe bowel ischemia on the third day after her admission. C onclusion Relevant hypothesis for blood clot formation in this patient may include prolonged lying position or blood temperature variation. Hypothermia and rewarming responsibilities may explain multiple thrombosis development. How to cite this article Schmitt J, Esnault P, Sartre M, Cungi PJ, Meaudre E. Severe Aortic Thrombosis and Profound Hypothermia: A Case Report. Indian J Crit Care Med 2021;25(5):588–589.

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Section: Discussionmentioning

confidence: 97%

Severe Aortic Thrombosis and Profound Hypothermia: A Case Report

Schmitt¹,

Esnault²,

Sartre³

et al. 2021

Indian Journal of Critical Care Medicine

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“…Cerebral vascular resistance at 20°C increased to 140% of the precooling level. Since resistance is proportional to blood viscosity and vascular resistance itself (Gordon 1972), and blood viscosity at 20°C is 170% of the precooling level (Sands et al 1979), this increase in cerebral vascular resistance at 20°C is due to a rising viscosity rather than vascular constriction. In the groups undergoing 60 min arrest, cerebral vascular resistance was reduced and cerebral blood flow increased immediately after initiation of rewarming.…”

Section: Discussionmentioning

confidence: 99%

Determination of safe interval of circulatory arrest from the cerebral metabolic aspect.

Iguchi

Haneda

Sato

et al. 1986

Tohoku J. Exp. Med.

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To determine the safe interval of hypothermic total circulatory arrest, the cerebral metabolic state was evaluated in 30 dogs. Surface cooling was achieved by deep ether anesthesia and the animals were assigned to three equal groups. Group I : 30 min circulatory arrest and surface rewarming. Group II: 60 min circulatory arrest and surface rewarming. Group III: 60 min circulatory arrest and perfusion rewarming. Brain tissue gas tension was monitored and cerebral 02 consumption was calculated. Cerebral 02 consumption reduced with cooling, parallel to the decrease in cerebral blood flow. Rapid increase in Pot, elevation of Pco2, and decrease of pH in the brain tissue were observed during circulatory arrest. Brain tissue Pot increased significantly after circulatory arrest in Group I, but it remained low during rewarming in Groups II and III. Cerebral 02 consumption was at reduced levels in all groups during rewarming and it remained at 29% of the precooling control level in Group II at the end of rewarming, whereas it recovered to 71% and 57% of the precooling levels in Groups I and III, respectively. It was estimated that cerebral metabolism may be recovered after 30 min circulatory arrest, despite a transient reduction in cerebral 02 consumption. On the other hand, after 60 min circulatory arrest, the recovery of cerebral metabolism was delayed in Group II and organic failure might have occurred in this group. However, even after circulatory arrest for 60 min, cerebral metabolism was recovered in Group III. The safe period of circulatory arrest is considered to be prolonged by use of extra-corporeal circulation.induced hypothermia, surface ; circulatory arrest ; central nervous system ; ether anesthesia Hypothermic total circulatory arrest has been used as an adjunct in cardiac surgery, particulary in small children since Lewis and Taufic (1953) applied it clinically. Although the hypothermia technique has been refined, there still remain several problems in clinical application.Neurological disturbance is the most serious complication following hypothermic circulatory arrest. Clinical and experimental studies regarding the relationship between neurological disturbance and circulatory arrest period have been reported by many investigators (Stevenson

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confidence: 99%

“…In dogs' blood, viscosity is increased by 50% at 25°C but at 30°C it is increased by only 25% (Sands et al, 1979). Platelet counts decrease during cardiopulmonary bypass and not with surface cooling (Sands et al, 1979). Changes in vascular perfusion at low tem-peratures are due to increased hematocrit (Chen and Chien, 1978).…”

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confidence: 99%

Systemic Hypothermia in Treatment of Severe Brain Injury: A Review and Update

Clifton¹

1995

Journal of Neurotrauma

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Laboratory studies of moderate hypothermia (30-33 degrees C) after injury show diminished neuronal loss after ischemia, diminished excessive neurotransmitter release after ischemia, prevention of blood-brain barrier disruption after ischemia and brain injury, and behavioral improvement after brain injury. Clinical literature suggests that brief periods of moderate hypothermia (> or = 30 degrees C) in humans are not associated with cardiovascular, hematologic, metabolic, or neurological toxicity. Clinical studies were, therefore, organized to investigate the potential application of moderate systemic hypothermia in patients after severe brain injury. A study of 21 elective craniotomy patients and 11 patients with severe brain injury led to the conclusion that 32 to 33 degrees C was the lowest safe temperature in patients with severe brain injury. A randomized study of moderate hypothermia in 46 patients with Glasgow Coma Score (GCS) 4-7 gave an indication of improved neurologic outcome in the hypothermia group. A multicenter, randomized protocol to test the effect of moderate systemic hypothermia in patients with severe brain injury is in progress. Funded by the National Institutes of Health, The National Acute Brain Injury Study: Hypothermia tests the hypothesis that systemic hypothermia to 32-33 degrees C if rendered within 6 h of injury improves Glasgow Outcome Scores (GOS) at 6 months after injury in patients with severe brain injury (GCS 3-8).

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Hematorheology during deep hypothermia

Cited by 16 publications

References 18 publications

Severe Aortic Thrombosis and Profound Hypothermia: A Case Report

Severe Aortic Thrombosis and Profound Hypothermia: A Case Report

Determination of safe interval of circulatory arrest from the cerebral metabolic aspect.

Systemic Hypothermia in Treatment of Severe Brain Injury: A Review and Update

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