Frozen rigor, also known as accidental hypothermia, refers to a systemic condition characterized by a core body temperature (CBT) below 35°C alongside neurological and cardiovascular system impairment. This condition occurs in individuals with normal hypothalamic function who are exposed to cold environments (below -5°C). Onset typically takes place within six hours of cold exposure. The prognosis worsens as CBT decreases, and successful resuscitation becomes difficult when CBT falls to 25–27°C. Tissue damage caused by frostbite or necrosis resulting from cold exposure is not within the scope of this discussion.
Etiology
A significant number of cases exhibit regional and seasonal patterns. Frozen rigor occurs most commonly under the following circumstances:
- Prolonged exposure to cold environments without adequate insulation or insufficient heat supply, such as in mountaineers, skiers, or military personnel stationed in cold, high-altitude areas.
- Elderly individuals, those with physical frailty, chronic health conditions (e.g., dementia, mental disorders, hypothyroidism), or severe malnutrition may develop hypothermia even in settings with low indoor temperatures.
- Accidental submersion in cold or icy water.
Pathogenesis
The severity of frozen rigor is influenced by various factors, including the temperature, humidity, wind speed, duration, and exposed body parts in the cold environment as well as the nutritional status and cold tolerance of the individual. Cold stimulation results in sympathetic nervous system excitation and peripheral vasoconstriction. Prolonged exposure leads to morphological changes in tissues and cells, endothelial damage to blood vessels, increased vascular permeability, extravasation of blood plasma components, aggregation of cellular elements, thrombosis, and consequent circulatory disturbances and tissue necrosis. Cellular dehydration and degeneration contribute to metabolic dysfunction. Metabolic changes during frozen rigor vary depending on the patient’s core body temperature (CBT):
Mild Hypothermia (CBT 35–32°C)
Cold stimulation heightens sympathetic nervous system excitability, leading to increased skin vasoconstriction, elevated heart rate and respiratory rate, increased cardiac output, higher blood pressure, increased cerebral blood flow, and cold diuresis. The body responds defensively by reducing heat loss and increasing basal metabolic rate. During cold exposure, elevated muscle tone and shivering consume more energy, accelerating cold-related damage.
Moderate Hypothermia (CBT 32–28°C)
Body temperature regulation mechanisms fail at this stage, resulting in the cessation of shivering and a significant slowdown in metabolism, which can lead to multi-organ dysfunction syndrome (MODS) or multi-organ failure (MOF). Each 1°C decrease in CBT corresponds to a 7% reduction in cerebral blood flow and a roughly 6% decline in metabolic rate. When CBT drops below 30°C, slowed sinoatrial node activity leads to bradycardia, reduced insulin secretion, elevated blood glucose levels, and insulin resistance in peripheral tissues.
Severe Hypothermia (CBT <28°C)
The heat conservation mechanisms controlled by endocrine and autonomic systems collapse, and basal metabolic rate decreases by 50%. The threshold for ventricular fibrillation lowers significantly, and breathing slows dramatically. Below 24°C, systemic vascular resistance decreases to the point where blood pressure becomes undetectable, consciousness is lost, pupils become dilated, and death results from circulatory and respiratory failure.
Clinical Presentation
Mild Hypothermia
Symptoms include fatigue, memory loss, polyuria, muscle tremors, elevated blood pressure, increased heart rate, and accelerated respiratory rate. Incomplete intestinal obstruction may also develop progressively.
Moderate Hypothermia
Symptoms include apathy, mental confusion, speech impairment, abnormal behavior, motor incoordination, or lethargy. Electrocardiograms may reveal atrial flutter or fibrillation, premature ventricular contractions, and a signature J wave (also referred to as an Osborn wave) located at the junction of the QRS complex and the ST segment. Shivering ceases, consciousness is lost, pupils dilate, and bradycardia sets in when the CBT drops to 30°C. Electrocardiograms show prolonged PR intervals, QRS complexes, and QT intervals.
Severe Hypothermia
Symptoms include oliguria, loss of pupillary light reflex, slowed respiration, and ventricular fibrillation. As CBT decreases to 24°C, rigid facial features reminiscent of rigor mortis appear. Below 20°C, the skin becomes pale or cyanotic, heartbeat and respiration cease, pupils remain fixed and dilated, limb muscles stiffen, and joints lose flexibility. Electrocardiograms or electroencephalograms show isoelectric lines.
Diagnosis
Diagnosis is generally straightforward based on the patient’s history of prolonged exposure to a cold environment and their clinical manifestations. Measurement of CBT provides definitive confirmation. CBT is assessed from two anatomical sites:
Rectal Temperature Measurement
The thermometer probe is inserted 15 cm into the rectum for temperature assessment.
Esophageal Temperature Measurement
The thermometer probe is placed 24 cm below the throat to measure temperature.
Treatment
Efforts are typically focused on implementing lifesaving resuscitation and supportive measures while minimizing further heat loss. Safe and effective rewarming techniques are applied to prevent complications.
Field Treatment
Patients are moved to a warm environment, with wet clothes removed and their bodies wrapped in blankets or thick quilts. Caution is exercised during handling to prevent fractures.
In-Hospital Treatment
Emergency Treatments
Resuscitation efforts are continued unless definitive evidence of death is obtained. For patients with diminished responsiveness or unconsciousness, airway patency is maintained through intubation or tracheotomy, coupled with inhalation of heated, humidified oxygen. For patients in shock, effective circulation volume is restored prior to rewarming. When CBT is below 30°C, interventions such as atropine, defibrillation, or cardiac pacemakers are often ineffective, although rare success cases with CBT as low as 20.4°C have been reported.
Rewarming Techniques
The selection of rewarming methods and rates depends on the patient’s condition. Special care is taken during rewarming, particularly for elderly or cardiac patients.
Passive Rewarming
Passive rewarming relies on the body's natural heat production. It is suitable for patients with mild hypothermia. Patients are placed in a warm environment and covered or wrapped in thick blankets or quilts. The rewarming rate typically ranges from 0.3–2°C per hour.
Active Rewarming
Active rewarming involves delivering external heat to the patient and is indicated in the following conditions:
- CBT below 32°C.
- Unstable circulatory status.
- Elderly patients.
- Central nervous system dysfunction.
- Endocrine insufficiency.
- Suspected secondary hypothermia.
Active External Rewarming
External heating methods such as heated blankets, hot water bottles, or water baths at 40–42°C are typically used, particularly for previously healthy patients with acute hypothermia. Heat sources are applied to the chest region, while heating the limbs is avoided to prevent added cardiac stress. Rewarming rates are generally 1–2°C per hour.
Active Internal Rewarming
Internal methods include intravenous infusion of warmed fluids (40–42°C), inhalation of humidified oxygen (40–45°C), or gastric, rectal, peritoneal, or pleural lavage using warmed solutions (40–45°C). Internal rewarming rates are approximately 0.5–1°C per hour. Extracorporeal circulation may achieve faster rewarming rates of up to 10°C per hour. For patients experiencing cardiac and respiratory arrest, if no pulse is detected after CBT reaches 28°C, CPR and appropriate medication should be initiated. Efforts are typically discontinued if cardiac and respiratory functions remain unresponsive after CBT reaches 36°C.
Supportive and Monitoring Measures
Supportive Care
Restoration of circulatory volume and heat
Intravenous infusion of saline or 5% glucose-sodium chloride solution (20 ml/kg) is used to restore blood volume. Lactated Ringer’s solution is typically avoided, as the liver's capacity to metabolize lactate is severely impaired in hypothermic patients. Metabolic and electrolyte imbalances are corrected, while energy supplies are replenished.
Maintenance of blood pressure
Early efforts aim to maintain mean arterial pressure (MAP) above 60 mmHg. If blood pressure fails to normalize despite volume restoration and rewarming, intravenous dopamine at 2–5 μg/(kg·min) is administered. For patients with normal blood pressure, small doses of intravenous nitroglycerin may improve blood perfusion in vital organs.
Restoration of consciousness
For patients with impaired consciousness, naloxone and vitamin B1 are often administered.
Monitoring Measures
Placement of a nasogastric tube
Reduced gastrointestinal motility in hypothermic patients often results in gastric dilation or intestinal paralysis. Nasogastric decompression may prevent aspiration triggered by vomiting.
Monitoring of vital signs
CBT is tracked to evaluate rewarming efficacy. Oxygen saturation readings from pulse oximeters are usually unreliable. Continuous cardiac monitoring is used to detect arrhythmias. Swan-Ganz catheter placement is avoided due to the risk of severe cardiac arrhythmias.
Blood glucose monitoring
Elevated blood glucose levels (6.2–10.1 mmol/L) before rewarming do not require insulin therapy to prevent hypoglycemia. After rewarming, insulin secretion typically normalizes, and blood glucose levels gradually return to baseline.
Placement of Foley catheters
Urine output is monitored to evaluate kidney function.
Treatment of Complications
Prolonged hypothermia frequently leads to complications such as non-cardiogenic pulmonary edema, stress ulcers, pancreatic necrosis, myocardial infarction, cerebrovascular accidents, and deep vein thrombosis. Frozen rigor can also trigger bronchorrhea, and protective cough reflex loss often results in pulmonary atelectasis, aspiration pneumonia, or rewarming-induced pulmonary edema. Specific treatments are implemented as complications arise.