McInerney J J, Breakell A, Madira W, Davies T G, Evans P A
Accident and Emergency Department, The Leicester Royal Infirmary, Leicester, UK.
Emerg Med J. 2002 May;19(3):219-23. doi: 10.1136/emj.19.3.219.
In accidental hypothermia the underlying physiological mechanisms responsible for poor outcome during rewarming through 32 degrees C remain obscure, although possible associations include changes in acid-base balance, divalent cations, and inflammatory markers. This study investigated the metabolic and inflammatory changes that occur during the rewarming of hypothermic patients.
Eight patients, four men and four women, age 45 to 85 years, admitted with core temperatures <35 degrees C were included in the study. Patients were rewarmed with dry warm blankets and fluid replaced by crystalloid at 40 degrees C. Bloods for pH, ionised calcium (Ca(2+)) and magnesium (Mg(2+)), parathyroid hormone (PTH), interleukin 1 (IL1), interleukin 6 (IL6), tissue necrosis factor alpha (TNFalpha), were collected at presentation, during rewarming, and at 24 hours.
Four patients were admitted with mild (32 degrees -35 degrees C) and four with moderate (28 degrees -32 degrees C) hypothermia. Rewarming to 32 degrees C had no significant effect on the presenting acidosis (p=0.1740), although above 32 degrees C pH increased with temperature (p<0.0001). There was a negative correlation between pH and both Ca(2+) (p=0.0005) and Mg(2+) (p=0.0488) below 32 degrees C; above this temperature the relation was significant only for Ca(2+) (p=0.0494). PTH and Ca(2+) correlated positively (p=0.0041) and negatively (p=0.0039) below and above 32 degrees C respectively. There was no relation between IL1 or TNFalpha with Ca(2+) during rewarming, but IL6 and Ca(2+) correlated positively (p=0.0039) and negatively (p=0.0018) when presentation temperature was below and above 32 degrees C respectively.
During rewarming pH remains unchanged until patient temperature approaches 32 degrees C. Ca(2+) and Mg(2+) decline is associated with the pH increase above 32 degrees C. Poor outcome is associated with presentation temperature (<32 degrees C), non-physiological correlation between IL6-PTH-Ca(2+), and age (>or=84 years).
在意外低温症中，体温回升至32摄氏度期间导致不良预后的潜在生理机制仍不清楚，不过可能的关联因素包括酸碱平衡、二价阳离子和炎症标志物的变化。本研究调查了低温患者复温过程中发生的代谢和炎症变化。
纳入8例核心体温低于35摄氏度的患者，4例男性和4例女性，年龄45至85岁。患者用干暖毛毯复温，并通过40摄氏度的晶体液补充液体。在就诊时、复温过程中及24小时时采集血液样本，检测pH值、离子钙（Ca(2+)）、镁（Mg(2+)）、甲状旁腺激素（PTH）、白细胞介素1（IL1）、白细胞介素6（IL6）、肿瘤坏死因子α（TNFα）。
4例患者为轻度低温（32摄氏度至35摄氏度），4例为中度低温（28摄氏度至32摄氏度）。体温回升至32摄氏度时，对就诊时的酸中毒无显著影响（p = 0.1740），不过体温高于32摄氏度时，pH值随温度升高（p < 0.0001）。在32摄氏度以下，pH值与Ca(2+)（p = 0.0005）和Mg(2+)（p = 0.0488）均呈负相关；高于此温度时，该关系仅对Ca(2+)有显著意义（p = 0.0494）。在32摄氏度以下和以上时，PTH与Ca(2+)分别呈正相关（p = 0.0041）和负相关（p = 0.0039）。复温过程中，IL1或TNFα与Ca(2+)无相关性，但就诊时体温低于和高于32摄氏度时，IL6与Ca(2+)分别呈正相关（p = 0.0039）和负相关（p = 0.0018）。
复温过程中，在患者体温接近32摄氏度之前pH值保持不变。Ca(2+)和Mg(2+)的下降与体温高于32摄氏度时pH值的升高有关。不良预后与就诊时体温（<32摄氏度）、IL6 - PTH - Ca(2+)之间的非生理相关性以及年龄（≥84岁）有关。
