When a warming strategy becomes a silent injury — mechanisms, evidence, risk factors, and prevention.
There is a quiet irony in modern anaesthesia. We fight hypothermia with the discipline of a watchmaker — warmed fluids, forced-air blankets, core probes, and protocolized targets. The monitor finally shows 36.7 °C. Everyone exhales.
And yet, rarely — but undeniably — the drapes come off and a blister appears. No flames. No smoke. No alarms. Just heat, sustained and unopposed.
Heat can be a blanket… or a slow scalpel.
A low-temperature burn (also called a low-heat or contact thermal injury) is not caused by dramatic heat. It occurs when moderate temperature is applied for a long enough duration to injure tissue. In the operating room, this typically involves warming devices where the surface or delivered air is warm, but exposure is sustained and sometimes concentrated.
Time + Temperature + Context determines injury.
The number on the device matters — but duration, distribution, pressure, and perfusion often matter more.
Thermal injury behaves less like an on-off switch and more like an exponential curve. Around 43 °C, injury can occur with prolonged exposure; as temperature rises, the time to injury drops steeply. This is why “low-temperature burns” are fundamentally time-dependent.
Conceptual Time–Temperature Pattern (Not a clinical dosing chart)
43 °C → hours (risk increases with vulnerability + pressure)
45 °C → minutes
50 °C → seconds
In anaesthesia, “hours” is not abstract. It is the duration of a spine case, a prolonged abdominal surgery, or an unexpectedly complex airway + resuscitation scenario. When time stretches, the risk window opens quietly.
Awake patients complain, shift, withdraw. Under general anaesthesia, the body’s behavioural defenses are gone. Thermoregulatory thresholds are altered, and the patient cannot respond to heat discomfort or pain.
It is not just that the patient is asleep — it’s that the warning system is offline.
Skin tolerance to heat depends heavily on perfusion. Intraoperative hypotension, vasopressors, diabetes mellitus, peripheral vascular disease, advanced age, and malnutrition can all shrink the margin.
When perfusion is compromised, even moderate heat can tip tissue into microvascular failure.
Pressure alone can cause ischaemia; heat alone can cause protein denaturation. Together, they amplify risk. Classic supine pressure points — occiput, scapulae, sacrum, heels — become the “quiet corners” where injury develops.
If you had to remember one metaphor: pressure closes the escape routes, heat builds the fire. 🔥🧱
Forced-air warming remains widely used and recommended for prevention of inadvertent perioperative hypothermia. In the published literature on injuries, a recurring theme is not routine correct use — but misuse or stacked risk factors.
“Hosing” refers to directing warmed air from the hose toward the patient without the manufacturer’s diffuser blanket attached. This concentrates heat in a small area instead of distributing it. Multiple published reports and safety advisories highlight this mechanism as a major contributor to severe burns.
Never direct the warming hose at the patient.
Hose → must connect to the correct blanket/diffuser system.
Many systems include a high setting around 43 °C. Clinical protocols may use such settings safely under defined conditions, but prolonged exposure, impaired perfusion, moisture, pressure points, or combined warming can shrink the safety margin. Published case reports describe injuries in prolonged cases where multiple risk factors converge.
In the OR, time is elastic — and tissue pays the interest.
Underbody warming surfaces place heat and pressure on the same tissue bed. In prolonged surgery, especially in elderly or vasculopathic patients, this can increase the risk of both pressure injury and thermal injury — sometimes simultaneously.
Forced-air warming + warmed fluids + radiant heat can be clinically appropriate, but additive thermal load can be underestimated. The patient cannot report discomfort; therefore, monitoring and reassessment become the compensatory defense.
These injuries often appear after the case — in recovery, in the ward, or even the next day. Because onset can be delayed, the association may be missed unless a team actively looks for it.
“If the device is under 45 °C, burns cannot happen.”
Reality: injury is time-dependent and context-dependent.
“Forced-air warming is unsafe.”
Reality: it is standard of care; injuries are rare and often linked to misuse or stacked risks.
Start
│
├─► Assess patient risk (diabetes/PVD/vasopressors/age/frailty)
│ │
│ ├─► High risk? ─► YES ─► Moderate setting + pressure-point plan
│ │ + early step-down target
│ │
│ └─► NO ─► Standard setting with continuous temperature monitoring
│
├─► Normothermia achieved (≥ 36 °C)?
│ │
│ ├─► YES ─► Step down setting + reassess every 30–60 min
│ │
│ └─► NO ─► Continue warming + check placement, perfusion, stacking
│
├─► Prolonged case (> 3–4 h)?
│ │
│ ├─► YES ─► Re-check pressure points (occiput/scapulae/sacrum/heels)
│ │
│ └─► NO
│
└─► Post-op skin check in PACU/ward (especially high risk) → Document
Clinicians often hesitate above 40 °C not because the number is “evil,” but because the safety margin narrows: the time-to-injury shortens, and vulnerability factors (pressure + perfusion impairment) become more relevant.
Heat alone doesn’t decide harm.
Harm emerges when temperature + time + concentrated delivery + low perfusion + pressure align.
Low-temperature burns can lead to institutional review and medicolegal scrutiny. Good documentation is not defensive — it’s patient-centered clarity.
Warm the patient — and warm the system with vigilance. 🛡️