• Hyperthermia is defined as an elevation of core body temperature above the normal diurnal range of 36–37.5°C and is due to a failure of thermoregulation.
• It is not synonymous with fever, which is regulated at the level of the hypothalamus in the setting of inflammation and cytokine release. Febrile patients are commonly encountered in the ICU setting and present perioperatively (for surgery or have postoperative fever). Postoperative fever includes the pneumonic: Wind (pulmonary causes such as aspiration, pulmonary embolism, pneumonia), water (UTI), wound (surgical site infections), walking (deep venous thrombosis), and "what did we do" (medications, blood product transfusions, intravascular, urethral, nasal, and abdominal catheters). Postoperative fever includes the pneumonic:
  • Wind: Pulmonary causes such as aspiration, pulmonary embolism, pneumonia
  • Water: Urinary tract infection
  • Wound: Surgical site infection
  • Walking: Deep venous thrombosis
  • "What did we do:" Medications, blood product transfusions; intravascular urethral, nasal, abdominal catheters
• Hyperthermia has perioperative relevance ranging from passive hyperthermia (excessive heating, most common in infants and children) to drug reactions (malignant hyperthermia [MH] neuroleptic malignant syndrome [NMS]) to increased incidence in laboring patients who receive epidural anesthesia.

• Iatrogenic perioperative causes
  • Conductive warming systems
  • Fluid and blood warmers
  • Warm operating rooms
• Drug reactions
  • Malignant hyperthermia: Succinylcholine, volatile inhalational agents
  • Neuroleptic drugs (NMS)
  • Atropine
  • Salicylates
  • Lithium
  • Sympathomimetics
  • Serotonergic syndrome
• Fever (Wind, water, wound, walking, "what did we do")
  • Urinary tract infections
  • Abscesses
  • Catheter-related infections
  • Sepsis
  • Meningitis
  • Pneumonia
  • Atelectasis
  • Wound infections
• Endocrine
  • Hyperthyroidism
  • Thyroid storm

• Body temperature is maintained within a narrow range and is a balance between heat production and heat dissipation. It is regulated by the thermoregulatory center located in the anterior hypothalamus and varies over the course of the day.
  • Heat production results from metabolic processes as well as heat absorption from the environment.
  • Heat loss is principally via evaporation to the environment (ineffective above a relative humidity of 75%). Other methods of heat dissipation include radiation (emission of infrared electromagnetic energy), conduction (direct transfer of heat to an adjacent cooler object), and convection (direct transfer of heat to convective air currents). However, these processes are inefficient when the environmental temperature exceeds skin temperature.
• Temperature elevation causes increased oxygen consumption and metabolic rate with resultant tachypnea, hypercarbia, and tachycardia; as well as a reduced mixed venous oxygen saturation. Thus, increased oxygen demand can aggravate preexisting cardiac or pulmonary insufficiency. Above 37°C^, each one degree increase corresponds to an ~13% increase in oxygen consumption. Above 42°C (108°F), oxidative phosphorylation is uncoupled, making enzymes nonfunctional and thus putting the patients at risk for multiple organ failure. Hepatocytes, vascular endothelium, and neural tissues are most sensitive to these effects.
• Hyperthermia does not involve resetting the thermoregulatory centers; it remains unchanged and can lead to uncontrolled increases in body temperature that can be rapidly fatal.
• MH is a rare genetic disorder that is triggered by succinylcholine administration or exposure to volatile inhaled anesthetic agents. It manifests as a hypermetabolic crisis with unregulated release of calcium from myocyte sarcoplasmic reticulum. Despite the name "malignant hyperthermia," increased temperature is a late finding and proceeds hypercarbia, tachycardia, acidosis, hyperkalemia, and possibly rhabdomyolysis
• NMS is an idiosyncratic reaction to antipsychotic agents, believed to be the result of central dopamine receptor blockade. It presents as altered mental status, rigidity, fever, and dysautonomia. It is more common with neuroleptic agents (haloperidol, droperidol, fluphenazine); however, all classes of antidopaminergics can result in NMS (clonazpine, olanzapine, metoclopramide, promethazine). Although it is not a dose-dependent phenomenon, higher doses are a risk factor.
• Endocrine disorders. Hyperthyroidism and thyroid storm represent an abnormal increase in basal metabolic rate with resultant heat products.
• Epidural analgesia for labor; patients are more likely to experience hyperthermia and overt clinical fever. Believed to be due to placental and chorioamnio membrane inflammation; however, the mechanism is not completely understood at this time. Because of its potential for neonatal brain injury (cerebral palsy, encephalopathy, learning defects), it can lead to a greater number of Cesarean sections. Additionally, heat transfer to the neonate may result in unnecessary neonatal workup of sepsis.
• Fever is caused by exogenous or endogenous pyrogens. Exogenous pyrogens are mainly microbes or their toxins (lipopolysaccharide endotoxin produced by gram-negative bacteria). Endogenous pyrogens are mainly cytokines (IL-1, IL-6, TNF, ciliary neutrotrophic factor). The interaction of pyrogens with hypothalamic circumventricular vascular endothelium is the first step in raising the thermoregulatory set point to febrile levels.
  • Immediate onset postoperative fever. Occurs in the operating room or a few hours after surgery; they often resolve without therapy and are often unexplained (most often due to trauma, infection, blood transfusion, or due to drugs ).
  • Acute onset postoperative fever. First week after surgery and is commonly due to surgical site infections, ventilator-associated pneumonia, aspiration, intravascular catheter infections, UTI.
  • Subacute onset postoperative fever. 1–4 weeks after surgery and includes fever from antibiotic-associated diarrhea, febrile drug reactions, thrombophlebitis.
  • Delayed onset postoperative fever. Greater than 4 weeks after surgery and includes infections

• Monitoring of temperature intraoperatively can help avoid iatrogenic hyperthermia from excessive warming techniques and assist with early detection of other causes.
• In patients with known history or familial history of MH, avoid triggering agents.
• Surgical site infections are reduced with aseptic technique; prophylactic antibiotics should be considered.
• Central line placement should be performed with maximal barrier sterile technique.
• ICU bundles should be implemented to avoid ventilator-associated pneumonia, deep venous thrombosis, and pulmonary embolism.

• Consider assessment of core temperatures (e.g., rectal).
• End-tidal CO₂ monitor to detect MH
• Invasive monitoring as dictated by the patient's clinical status: Arterial line and ABG, CVP, mixed venous oxygen saturation

• Malignant Hyperthermia
• Blood Transfusions
• Ventilator-Associated Pneumonia
• Hypothermia

995.86 Malignant hyperthermia

• T88.3XXA Malignant hyperthermia due to anesthesia, initial encounter
• T88.3XXD Malignant hyperthermia due to anesthesia, subs encntr
• T88.3XXS Malignant hyperthermia due to anesthesia, sequela

Praveen Kalra , MBBS, MD, FCCP