AACN clinical issues
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Heat stroke (HS) is a serious and potentially life-threatening condition defined as a core body temperature >40.6 degrees C. Two forms of HS are recognized, classic heat stroke, usually occurring in very young or elderly persons, and exertional heat stroke, more common in physically active individuals. An elevated body temperature and neurologic dysfunction are necessary but not sufficient to diagnose HS. ⋯ Long-term neurologic sequelae (varying degrees of irreversible brain injury) occur in approximately 20% of patients. The prognosis is optimal when HS is diagnosed early and management with cooling measures and fluid resuscitation and electrolyte replacement begins promptly. The prognosis is poorest when treatment is delayed >2 hours.
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The hazards of thermoregulatory shivering in the critically ill are often overlooked by caregivers. Shivering may accompany heat loss from bathing, dressing, transport, and many therapeutic activities. Febrile shivering is common during chills of fever, blood product transfusions, administration of antigenic drugs, and chemotherapy. ⋯ Knowledge of the anatomical progression of shivering equips the nurse to recognize or prevent this energy-consuming response. This article discusses measures to prevent shivering as well as evidence-based interventions to manage shivering during fever, aggressive cooling, and postoperative recovery. Detailed information is presented on assessment and documentation of the extent and severity of shivering.
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AACN clinical issues · Apr 2004
ReviewMalignant hyperthermia: pathophysiology, clinical presentation, and treatment.
Malignant hyperthermia (MH) was first described as an inherited highly lethal disorder in 1960. There has since been significant progress in the clinical management, identification of MH susceptible (MHS) persons, and understanding of the underlying pathophysiology. When patients are known to be MHS prior to surgery, an MH episode can easily be avoided by the use of safe nontriggering anesthetic agents. ⋯ MH is triggered in humans by an MH triggering anesthetic agent, which causes the release of calcium from the sarcoplastic reticulum of the skeletal muscle cell at an uncontrolled rate resulting in a hypermetabolic state. Recent molecular genetic studies have shown that MH is related to an abnormal ryanodine receptor that controls the release of calcium from the sarcoplastic reticulum. This article reviews the current understanding of the pathophysiology, diagnosis, clinical presentation, and treatment of MH.