Hypothermia, defined as an unintentional decline in the core body temperature to below 35degrees C, is a life-threatening condition. Patients with malnutrition and diabetes mellitus as well as those of advanced age are at high risk for accidental hypothermia. Due to the high mortality rates of accidental hypothermia, proper management is critical for the wellbeing of patients. Accidental hypothermia was reported to be associated with acute kidney injury (AKI) in over 40% of cases. Although the pathogenesis remains to be elucidated, vasoconstriction and ischemia in the kidney were considered to be the main mechanisms involved. Cases of AKI associated with hypothermia have been reported worldwide, but there have been few reports of hypothermia-induced AKI in Korea. Here, we present a case of hypothermia-induced AKI that was treated successfully with rewarming and supportive care.
Acute Kidney Injury/*etiology/therapy ; Aged ; Humans ; Hypothermia/*complications/therapy ; Male ; *Rewarming

OBJECTIVETo investigate the clinical characteristics and significance of thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury (TBI).

METHODSNinety-six inpatients with severe brain injury were randomized into three groups: SBC (selective brain cooling) group (n=24), MSH (mild systemic hypothermia) group (n=30), and control (normothermia) group (n=42). The platelet counts and prognosis were retrospectively analyzed.

RESULTSThrombocytopenia was present in 18 (75%), 23 (77%) and 15 (36%) patients in SBC group, MSH group and control group, respectively (P<0.01). Thrombocytopenia, in which the minimum platelet count was seen 3 days after hypothermia, showed no significant difference between SBC and MSH group (P>0.05). Most platelet counts (37 cases, 90%) in hypothermia group were returned to normal level after 1 to 2 days of natural rewarming. The platelet count in SBC group reduced by 16%, 27% and 29% at day 1, 3 and 5 respectively compared with the baseline value. Good recovery (GOS score 4-5) rate of thrombocytopenia 1 year after injury for hypothermia group (17 cases, 37%) was significantly lower than that of control group (P<0.01).

CONCLUSIONSTherapeutic hypothermia increases the incidence of thrombocytopenia in severe TBI, and patients with thrombocytopenia after therapeutic hypothermia are associated with unfavorable neurological prognosis.

Adult ; Brain Injuries ; therapy ; Female ; Humans ; Hypothermia, Induced ; adverse effects ; Male ; Middle Aged ; Prognosis ; Thrombocytopenia ; etiology

Adult ; Circulatory Arrest, Deep Hypothermia Induced ; adverse effects ; Humans ; Male ; Rhabdomyolysis ; diagnosis ; etiology

Animals ; Humans ; Hypothermia, Induced ; Hypoxia-Ischemia, Brain ; etiology ; therapy ; Infant, Newborn ; Randomized Controlled Trials as Topic

Animals ; Humans ; Hypertension, Pulmonary ; complications ; Hypothermia ; complications ; Hypoxia ; etiology ; therapy ; Respiratory Distress Syndrome, Adult ; complications ; Shock, Septic ; complications

Animals ; Calcium Channel Blockers ; therapeutic use ; Dogs ; Hypothermia ; complications ; Male ; Nimodipine ; therapeutic use ; Ventricular Fibrillation ; etiology ; prevention & control

Aged ; Antitubercular Agents ; adverse effects ; therapeutic use ; Heart Failure ; Humans ; Hypothermia ; diagnosis ; etiology ; Stevens-Johnson Syndrome ; diagnosis ; etiology ; Tuberculosis ; drug therapy

Acute coagulopathy of trauma-shock (ACoTS) occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.
Blood Coagulation Disorders ; etiology ; Complement System Proteins ; physiology ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Hypothermia ; complications ; Inflammation ; complications ; Protein C ; physiology ; Shock, Traumatic ; complications

Central diabetes insipidus (DI), characterized by unexpected fatal hypernatremia, is a rare complication after successful cardiopulmonary resuscitation with therapeutic hypothermia, but may be potentially fatal if recognition is delayed. We describe here a patient who experienced cardiac arrest due to a pulmonary embolism, followed by successful resuscitation after induction of therapeutic hypothermia. The patient, however, suddenly developed unexpected hypernatremia with increased urine output and was diagnosed with central DI as a complication of cerebral edema, and eventually died. Our findings suggest that central DI should be considered as a possible complication following unexpected hypernatremia with increased urine output during therapeutic hypothermia and that desmopressin acetate should be used to treat central DI.
Adult ; Cardiopulmonary Resuscitation/*adverse effects ; Diabetes Insipidus, Neurogenic/diagnosis/etiology ; Fatal Outcome ; Female ; Heart Arrest/complications/therapy ; Humans ; Hypernatremia/*etiology ; Hypothermia, Induced/*adverse effects ; Pulmonary Embolism/complications

OBJECTIVETo study the effects of deep hypothermia on the neuronal ultrastructure and nervous system of monkey after selective cerebral profound hypothermia and blood flow occlusion.

METHODSBrain-local extracorporeal circulation was established by right internal carotid artery deep hypothermic perfusion and homolateral external jugular vein backflow, brain blood flow was recovered from circulatory arrest 60 - 80 minutes late and monkey came back naturally.

RESULTSIn all 7 monkeys, 5 were succeeded in being build up the models except for 2 because of technic problems, and 4 of them lived up for ever. The function of nervous system grade, essential organ and neuronal ultrastructure were normal.

CONCLUSIONSelective cerebral profound hypothermia can increase the ability of brain to endure hypovolemia and hypoxidosis and prolong the time of blood flow occlusion.

Animals ; Brain Ischemia ; etiology ; pathology ; physiopathology ; prevention & control ; Cerebrovascular Circulation ; Disease Models, Animal ; Extracorporeal Circulation ; adverse effects ; Female ; Haplorhini ; Hypothermia, Induced ; Male ; Time Factors