Special Articles

SPECIAL ARTICLE – Perioperative hypothermia in pediatric patients: diagnosis, prevention and management

Sukhminder Jit Singh Bajwa, MD, MBA*, Swati MD**

*Associate Professor, Department of Anesthesiology and Intensive Care, Gian Sagar Medical College & Hospital, Ram Nagar, Banur, Punjab (India).

**Assistant Professor, Govt Medical College and Hospital, Sector-32, Chandigarh, India

Correspondence: Dr.Sukhminder Jit Singh Bajwa, House No-27-A, Ratan Nagar, Tripuri, Patiala, Punjab-147001 (India); Phone: 09915025828, +911752352182; E-mail: sukhminder_bajwa2001@yahoo.com


Hpothermia is the most common perioperative disturbance in pediatric patients. Pediatric patients are highly vulnerable to hypothermia and its associated complications, e.g. respiratory embarrassment, metabolic acidosis, hypoglycemia, hypoxemia, cardiac disturbances, coagulopathy, and a higher incidence of wound infection etc. This higher vulnerability is mainly due to increased heat loss from larger head size, thin skin, lack of subcutaneous pad of fat and limited ability of compensatory thermogenesis from brown fat. As such it is mandatory to design appropriate diagnostic, preventive and therapeutic strategies which can effectively protect pediatric population from the potential catastrophic complications associated with hypothermia during perioperative period. The current review aims to refresh the basic mechanism of hypothermia and discussion of evidence based management strategies to minimize the incidence of hypothermia in pediatric patients.

Key words: Perioperative, Hypothermia, Thermoregulation, Thermogenesis

Citation: Bajwa SJS and Swati. Peri-operative Hypothermia in pediatric patients: diagnosis, prevention and management. Anaesth Pain & Intensive Care 2014;18(1):97-100


Inadvertent hypothermia, defined as a core temperature below 36˚C, is the most common form of perioperative disturbance in pediatric population. The incidence of hypothermia can be up to 20% among patients undergoing major surgical procedures. Perioperative hypothermia is associated with several complications, which can adversely affect the patient outcome, especially in high risk patients.1 A combination of proportionately higher heat loss, a diminished ability to produce endogenous heat and a diminished thermoregulatory response makes infants highly vulnerable to developing hypothermia.2 Although, not as well described in literature as in adults, perioperative hypothermia has been associated with a number of serious complications in infants.3 The current review aims to discuss the importance of maintaining normothermia in pediatric patients, predisposing risk factors for inadvertent perioperative hypothermia and methods to detect and prevent perioperative hypothermia in children.

Thermoregulatory Mechanism during Anesthesia

Normal thermoregulation in infants in response to hypothermia is primarily augmented by vasoconstrictor response and nonshivering thermogenesis. Vasoconstrictor response is characterized by shunt vasoconstriction as an initial response to cold exposure. The thermoregulatory threshold is decreased by general anesthetic agents. While volatile anesthetics cause inhibition nonlinearly, higher concentrations being more effective; propofol and opioids cause a linear inhibition.4-7

The most effective thermoregulatory response in infants is nonshivering or brown fat thermogenesis. Brown fat is located at nape of the neck, interscapular region, axillae, and groin and around the kidneys and adrenals. Oxidation of triglycerides releases fatty acids to be consumed in generation of heat which is distributed through the blood stream to various parts of the body. Clinically significant nonshivering thermogenesis is thought to be present up to 2 years of age. It might, however, be inhibited by anesthetics agents and this fact may play a critical role in development of intraoperative hypothermia.8-10

Minimal development of musculoskeletal mass makes shivering an insignificant mechanism of thermogenesis in infants. The shivering response probably does not become important until early childhood, although age dependence has never been firmly established.11 Protective mechanisms from hypothermia and shivering mechanism even in the higher age group to some extent are influenced by pharmacogenomics and pharmacogenetic factors.12

Perioperative period is the time when child is exposed to a cold environment of operating room (OR) due to administration of non-warmed intravenous fluids, and potential evaporation from the operated areas. However, these factors alone usually do not cause hypothermia as such. Caution has to be exercised even during the recovery phase and in postoperative wards which mandates the need for postoperative rounds by the anesthesiologists.13 Although thermoregulatory vasoconstrictive mechanism is efficient in infants and children, they are functionally similar to adults in being unable to increase the metabolic rate in response to even mild hypothermia under anesthesia. In fact, it is the failure of effective thermoregulatory defenses which induces hypothermia in a child.

Induction of general anesthesia results in a three-phase decrease in core temperature; core-to-peripheral heat redistribution, linear core temperature decline, and core temperature plateau.14 Initially, vasodilatation caused by anesthetic agents results in redistribution of heat from the core to the periphery. Body heat content remains unchanged. Infants and children experience little heat redistribution because of their small extremities with respect to torso. As a result, redistribution may have a less contribution to intraoperative hypothermia.15

The initial phase of redistribution is followed by a stage of thermal imbalance in which there is net heat loss to environment. The heat is lost mainly by radiation, convection, conduction and evaporation. Radiation is responsible for maximum heat loss up to an extent of 40% and is proportional to environment / core temperature difference. Convection is the other major source of heat loss and denotes the loss of heat to air molecules surrounding the body. Conductive heat loss is due to difference in temperature between body and surfaces in contact. Evaporation refers to heat loss from skin, respiratory, bowel and wound surfaces. The pediatric patients are vulnerable to intraoperative hypothermia because of increased heat loss due to their large surface area to weight ratio, large head with thin scalp and skull, thin skin which increases evaporative losses and lack of subcutaneous fat.16

After three to four hours during intra-operative period, core temperature reaches a plateau reflecting a state in which heat loss is equal to heat production. Usually the core temperature plateau occurs at a lower temperature,17 although the core temperature is maintained during this phase. This may mask a continuing decrease in body heat content as the loss from extremities continues unabated.

There have been few studies identifying specific risk factors for intraoperative hypothermia in pediatric age group. Tander et al, evaluated the factors responsible for predisposing to intraoperative hypothermia in sixty neonates and infants.18 The study concluded that infants had less decrease in temperature than neonates during both major and minor surgery and that the operating room temperature below 23˚C could significantly interfere with the maintenance of the neonate and infant’s core temperature during anesthesia.18 A study in children under 18 years of age by Pearce B et al, revealed that hypothermia was significantly associated with preoperative lower baseline temperature and the type of surgery (major or minor).19


If the ongoing hypothermia is not taken care of, many complications can occur in neonates, infants and children. Respiratory embarrassment3 or apnea2 can be dangerous complications. Both non-shivering and shivering thermogenesis increase oxygen consumption leading to hypoxemia and carbon dioxide retention, metabolic acidosis, hypoglycemia and a shift of oxygen dissociation curve to the left with resultant decreased oxygen delivery to the tissues.20 Adult studies have shown that hypothermia may cause cardiac problems, impaired platelet function and clotting factor enzyme function, thus increasing the requirement of allogenic blood transfusion. It also facilitates wound infections. Moreover, there can be altered metabolism of drugs,21 thermal discomfort,22 an impact on the patient outcome and resultant increased costs.23


Continuous temperature monitoring in children receiving general anesthesia is recommended as per the guidelines laid down by American Society of Anaesthesiologists (ASA). Any site which appropriately measures core body temperature can be chosen for such diagnostic intervention. The choice of method used to measure temperature is based on the level of invasiveness and the degree of accuracy.24 There are a variety of sites, each with its specific merits and demerits which can be summarized as Table 1.

Table 1: Probable sites for temperature monitoring


Clinical Significance

Pulmonary Artery Catheter

measures core temperature most accurately

However it is reserved for patients requiring intensive hemodynamic monitoring due to its invasiveness and cost of the catheters

Distal Esophageal Measures accurately core temperature but may be affected by humidified gases and in surgeries where chest cavity is opened like during open heart or lung surgery
Nasopharyngeal May be affected by inspired gases
Bladder Efficiency may be affected with low urine output, lower abdomen procedures
Tympanic Non invasive measure of core temperature

Patency of external auditory meatus is a must

Rectal Accurately reflects the core temperature but results might be effected by stools and bacteria that generate heat
Axillary  For accurate measurement probe should be positioned over the axillary artery and the arm to be kept at the patient’s side
Skin temperature measured over the carotid artery Using a simple correction factor of +0.52°C,this is an accurate noninvasive measure of nasopharyngeal temperature

Avoid risk of nose bleeding ,infection [25]


Prevention is better than cure. This proverb has probably not been more true in any other situation than in prevention of hypothermia in infants and children.

1. Parents/caregivers education to keep the child warm during preoperative hospital stay as well as during the transfer to the operating room so as to avoid the risk of hypothermia and its complications. The biopsychosocial perspectives related to various anesthetic techniques and drugs have to be explained to the parents for their complete.26

2. Preoperative assessment should be thorough and should specifically aim at:

– preoperative checking of the temperature

– preoperative warming by covering the child in a cotton blanket or using forced air warming system.27,28 Moreover, the preventive measures have to be devised on the basis of available resources especially in developing nations by innovations and improvisations.29

3. Maintaining normothermia in intraoperative phase by:

– maintaining ambient OR temperature ˃23 ̊ C so as to reduce radiation and convection losses but it may be associated with discomfort to OR team.

– induction of anesthesia should not begin unless and until the patient’s temperature is 36.0°C or above.

– use of warmed intravenous fluids30 alone may not prove to be effective.

– Passive insulation i.e. minimizing heat loss by insulating the child from the environment by using surgical drapes, cotton blankets and metalized plastic covers. The trapped air between the covers and child̓̓́ s surface provides the insulation. Increasing the number of layers does not provide further protection .Reduction in heat loss is by approximately 30% and is directly proportional to the covered surface area.30

– Active skin warming vs. passive protection.

(i) Forced-Air Warming Devices- are the most commonly used and efficient active warming systems.31 These consist of an electrically powered heater blower unit and blanket made of paper to cover the patient. It provides convective heating to keep body warm. To increase the efficiency, prewarming the child is desirable and the largest size of the blanket that covers maximum body surface is preferred.32 These can increase the core temperature by almost 0.75°C/hour.

(ii) Resistive heating (electric blankets) are cheaper and equally efficient as forced-air system.34

(iii) Energy Pads use circulating heated water that comes in contact with patient’s skin.

(iv) Circulating water mattresses are placed over the operating table under the pediatric. This system maintains an acceptable efficiency in pediatric patients as it involves warming the back skin surface which provides larger surface area in children as compared to adults.

(v) Radiant warmers/ overhead heating units generate infrared radiation. The effectiveness depends on the distance between the device and the skin of the patient and its direction. They can be used during induction of anesthesia until the child is covered with surgical drapes.

Disadvantages of warming devices include the risk of burns seen when used incorrectly.35 A combination of them increases treatment costs too.

Internal Warming Systems

Fluid warmers should be used for major surgeries with considerable blood loss and massive fluid shifts. Active and passive inspired gas humidification slightly contributes in maintaining core temperature in anesthetized pediatric patients. Active airway heating and humidification  uses electric humidifiers and passive humidification involves using heat and moisture exchanger. These preserve cilial function and prevent bronchospasm. But recent SCIP24 do not recommend their use.


In conclusion, during pediatric anesthesia infants and small children are prone to perioperative hypothermia due to many inherent factors. This makes it mandatory to monitor their core temperature. Management should involve prevention and/or decreasing the risk by use of a multimodal approach. This includes preoperatively keeping the child warm, increasing ambient OR temperature to 23 ̊-25 ̊ C, use of warm intravenous fluids, passive insulation and use of forced air warming devices.


  1. Bajwa SJ, Kaur J. Risk and safety concerns in anesthesiology practice: The present perspective. Anesth Essays Res 2012;6:14-20
  2. Jevtovic-Todorovic V, Hartman RE, Izumi Y, Benshoff ND, Dikranian K, Zorumski CF, et al. Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits. J Neurosci 2003;2:876–82.
  3. Ikonomidou C, Bosch F, Miksa M, Vöckler J, Dikranian K, Tenkova TI, et al. Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain. Science 1999;283:70–4.
  4. Bajwa SS, Kalra S. Logical empiricism in anesthesia: A step forward in modern day clinical practice. J Anaesthesiol Clin Pharmacol 2013;29:160-1
  5. Bajwa SS, Takrouri MM. Innovations, improvisations, challenges and constraints: The untold story of anesthesia in developing nations. Anesth Essays Res 2014;8:1-2
  6. Fredriksson A, Pontén E,  Gordh T, Eriksson P. Neonatal exposure to a combination of N-methyl-D-aspartate and gamma-aminobutyric acid type A receptor anesthetic agents potentiates apoptotic neurodegeneration and  persistent  behavioral deficits.  Anesthesiology 2007;107:427-36
  7. Vutskits L, Gascon E, Kiss JZ. Effects of ketamine on the developing central nervous system. Ideggyogy Sz 2007;60:109–12
  8. Slikker W Jr, Zou X, Hotchkiss CE, Divine RL, Sadovova N, Twaddle NC, et al. Ketamine-induced neuronal cell death in the perinatal rhesus monkey. Toxicol Sci 2007;98:145–58
  9. Hayashi H, Dikkes P, Soriano SG. Repeated administration of ketamine may lead to neuronal degeneration in the developing rat brain. Paediatr Anaesth 2002;12:770–4
  10. Loepke AW, Soriano SG. An assessment of the effects of general anesthetics on developing brain structure and neurocognitive function. Anesth Analg 2008;106:1681– 707.
  11. Yon JH, Carter LB, Reiter RJ, Jevtovic-Todorovic V. Melatonin reduces the severity of anesthesia-induced apoptotic neurodegeneration in the developing rat brain. Neurobiol Dis 2006;21:522– 30
  12. Young C, Jevtovic-Todorovic V, Qin YQ, Tenkova T, Wang H, Labruyere J, et al. Potential of ketamine and midazolam, individually or in combination, to induce apoptotic neurodegeneration in the infant mouse brain.Br J Pharmacol 2005;146:189–97.
  13. Bittigau P, Sifringer M, Ikonomidou C. Antiepileptic drugs and apoptosis in the developing brain. Ann N Y Acad Sci 2003;993:103–14
  14. Bajwa S J, Kulshrestha A. Dexmedetomidine:An adjuvant making large inroads into clinical practice. Ann Med Health Sci Res 2013;3:475-83
  15. Stratmann G, Sall JW, May LD, Bell JS, Magnusson KR, Rau V, et al. Isoflurane differentially affects neurogenesis and long-term neurocognitive function in 60-day-old and 7-day-old rats. Anesthesiology 2009;110:834-48
  16. Briner A, De Roo M, Dayer A Muller D, Habre W, Vutskits L. Volatile anesthetics rapidly increase dendritic spine density in the rat medial prefrontal cortex during synaptogenesis. Anesthesiology 2010;112:546– 56
  17. Head BP, Patel HH, Niesman IR, Drummond JC, Roth DM, Patel PM . Inhibition of p75 neurotrophin receptor attenuates isoflurane mediated neuronal apoptosis in the neonatal central nervous system. Anesthesiology 2009;110:813– 25
  18. Bhaskar S B, Bajwa SS. Pharmaco‑genomics and anaesthesia: Mysteries, correlations and facts. Indian J Anaesth 2013;57:336-7
  19. L. Sun. Early childhood general anaesthesia exposure and neurocognitive development. Br J Anaesth 2010;105(S1):i61–i68
  20. Adeniran JO, Abdur-Rahman L. One-stage correction of intermediate imperforate anus in males. Pediatr Surg Int 2005;21:88–90
  21. Korkman M, Kemp SL, Kirk U. Effects of age on neurocognitive measures of children ages 5 to 12: a cross-sectional study on 800 children from the United States. Dev Neuropsychol 2001;20:331–54
  22. Sowell ER, Peterson BS, Thompson PM, Welcome SE, Henkenius AL, Toga AW. Mapping cortical change across the human life span. Nat Neurosci 2003;6:309– 15
  23. Huttenlocher PR, Dabholkar AS. Regional differences in synaptogenesis in human cerebral cortex. J Comp Neurol 1997;387(2):167–78
  24. Oppenheim RW:Cell death during development of the nervous system. Annu Rev Neurosci 1991;14:453–501.
  25. Bajwa SS, Kalra S. A deeper understanding of anesthesiology practice:the biopsychosocial perspective. Saudi J Anaesth 2014;8:4-5
  26. Kalkman CJ, Peelen L, Moons KG, Veenhuizen M, Bruens M, Sinnema G et al.:Behavior and development in children  and age at the time of first anesthetic exposure. Anesthesiology 2009;110:805–12.
  27. Bartels M, Althoff RR, Boomsma DI. Anesthesia and cognitive performance in children:no evidence for a causal relationship. Twin Res Hum Genet 2009;12(3):246–53
  28. Flick RP, Wilder RT, Sprung J,  Katusic SK, Voigt R, Colligan R, et al. Anesthesia and cognitive performance in children:no evidence for a causal relationship. Are the conclusions justified by the data? Response to Bartels et al., 2009. Twin Res Hum Genet.2009;12(6):611–2; discussion 613–14.
  29. Di Maggio C, Sun LS, Kakavuoli A ,Byrne MW, Li G. A retrospective cohort study of the Association of Anesthesia and Hernia Repair Surgery with Behavioral and Developmental Disorders in Young Children. J Neurosurg Anesthesiol 2009;21:286– 91.
  30. Sprung J, Flick RP, Wilder RT, Katusic SK, Pike TL, Dingli M, et al. Anesthesia for cesarean delivery and learning disabilities in a population-based birth cohort. Anesthesiology 2009;111:302–10.
  31. Wilder RT, Flick RP, Sprung J, Katusic SK, Barbaresi WJ, Mickelson C, et al. Early exposure to anesthesia and learning disabilities in a population-based birth cohort. Anesthesiology 2009;110:796–04.
  32. Flick RP, Katusic SK, Colligan RC, Wilder RT, Voigt RG, Olson MD, et al. Cognitive and behavioral outcomes after early exposure to anesthesia and surgery. Pediatrics 2011;128:1053-61
  33. Hansen TG, Pedersen JK, Henneberg SW, Pedersen DA, Murray JC, Morton NS, et al. Academic performance in adolescence after inguinal hernia repair in infancy: a nationwide cohort study. Anesthesiology 2011;114:1076–85
  34. Ing C, DiMaggio C, Whitehouse A, Hegarty MK, Brady J, von Ungern-Sternberg BS, et al. Long-term differences in language and cognitive function after childhood exposure to anesthesia. Pediatrics 2012;130:476–85
  35. Bajwa SS, Kalra S. Qualitative research in anesthesiology: an essential practice and need of the hour. Saudi J Anaesth 2013;7:477-8
  36. A Multi-site Randomized Controlled Trial Comparing Regional and General Anesthesia for Effects on Neurodevelopmental Outcome and Apnea in Infants (GAS). ClinicalTrials.gov Identifier: NCT00756600.
  37. Sun LS, Li G, DiMaggio CJ,  Byrne MW, Ing C, Miller TL, et al. Feasibility and pilot study of the Pediatric Anesthesia NeuroDevelopment Assessment (PANDA) project. J Neurosurg Anesthesiol 2012;24:382–8.
  38. Bai X, Bosnjak ZJ. Emerging Model in Anesthetic Developmental Neurotoxicity: Human Stem Cells. Int J Clin Anesthesiol 2013;1:1002
  39. Nash R, Krishnamoorty M, Jenkins A, Csete M.  Human embryonic stem cell model of ethanol-mediated early developmental toxicity. Exp Neurol 2012;234:127-35.
  40. Zhao X,  Yang  Z,  Liang  G,  Wu  Z,  Peng  Y,  Joseph  DJ,  et  al.  Dual effects of isoflurane on proliferation, differentiation, and survival in human neuroprogenitor cells. Anesthesiology 2013;118:537-49
  41. Bai X, Yan Y, Canfield S, Muravyeva MY, Kikuchi C, Zaja I, et al. Ketamine enhances human neural stem cell proliferation and induces neuronal apoptosis via reactive oxygen species-mediated mitochondrial pathway. Anesth Analg 2013;116:869-80
  42. Zhao X, Yang, Z,Liang G Wu Z, Peng Y, Joseph DJ, et al. Dual Effects of Isoflurane on Proliferation, Differentiation, and Survival in Human Neuroprogenitor Cells. Anesthesiology 2013;118:537–49
  43. Yaholm B, Athiraman U, Soriano S, Zurakowski D, Carpino EA, Corfas G, et al. Spinal anesthesia in infant rats: development of a model and assessment of neurologic outcomes. Anesthesiology 2011;114(6):1325–35.
  44. McGowan FX Jr, Davis PJ. Anesthetic-related neurotoxicity in the developing infant of mice, rats, monkeys and, possibly, humans. Anesth Analg 2008;106(6):1599–602