Acta Neurochir (2006) [Suppl] 96: 44–47
6 Springer-Verlag 2006
Printed in Austria
Rewarming following accidental hypothermia in patients with acute subdural
hematoma: case report
K. Kinoshita, A. Utagawa, T. Ebihara, M. Furukawa, A. Sakurai, A. Noda, T. Moriya, and K. Tanjoh
Department of Emergency and Critical Care Medicine, Nihon University School of Medicine, Tokyo, Japan
Summary
A 57-year-old man was admitted to the Emergency and Critical
Care Department with accidental hypothermia (31.5 C) after resuscitation from cardiopulmonary arrest (CPA). Brain CT revealed an
acute subdural hematoma. Active core rewarming to 33 C was
performed using an intravenous infusion of warm crystalloid. The
patient underwent craniotomy soon after admission, with bladder
temperature maintained at 33 to 34 C throughout the surgery. Therapeutic hypothermia (34 C) was continued for 2 days, followed by
gradual rewarming. After rehabilitation, the patient was able to continue daily life with assistance.
Traumatic brain injury (TBI) following CPA is associated with extremely unfavorable outcomes. Very few patients with acute subdural hematomas presenting with accidental hypothermia and CPA
have been reported to recover. No suitable strategies have been
clearly established for the rewarming performed following accidental
hypothermia in patients with TBI. Our experience with this patient
suggests that therapeutic hypothermia might improve the outcome
in some patients with severe brain injury. It also appears that the
method used for rewarming might play an important role in the therapy for TBI with accidental hypothermia.
Keywords: Traumatic brain injury; hypothermia; cardiac arrest.
Introduction
The neurological outcomes of traumatic brain injury (TBI) are extremely poor in patients resuscitated
from cardiopulmonary arrest (CPA). In fact, TBI
with hypoxia/hypotension is reported to be one of
the most common causes of secondary brain damage.
Several studies have shown at least a doubling of mortality in brain-injured patients with hypoxia and hypotension [9, 11, 14]. In this study we describe a patient
who received intensive treatment and ultimately survived after presenting with CPA involving accidental
hypothermia in the aftermath of a traumatic brain injury.
The optimal strategy for rewarming from accidental
hypothermia in TBI patients remains unclear. Our patient with accidental hypothermia (31.5 C) underwent
active core rewarming from to 33 to 34 C, followed
by therapeutic hypothermia with slow rewarming.
This experience may prove useful when considering
the need for warming and the method by which it is
applied. Specifically, the present case suggests that rewarming is important in patients with TBI involving
accidental hypothermia and that therapeutic hypothermia has the potential to improve outcome in selected patients with severe TBI.
Case history
A 57-year-old man was discovered in front of a restaurant in coma with a gasping respiration pattern. By
the time emergency medical services reached the scene,
the patient’s body temperature had fallen to 31.5 C.
On arrival at our emergency room, bladder temperature was 31.8 C and no spontaneous respirations
were present. Carotid pulse was absent. Electrocardiogram indicated pulseless electrical activity. Active core
rewarming to 33 C was performed using a warming
blanket and intravenous infusion of warm crystalloid.
Cardiopulmonary resuscitation (CPR) had been administered with an intravenous injection of epinephrine (adrenaline, 1 mg) and atropine (1 mg). Return
of spontaneous circulation was finally observed 25
minutes after the onset of CPA.
A brain computed tomography (CT) revealed an
acute subdural hematoma with e¤acement of the basal
cisterns (Fig. 1A). The cause of the brain injury was
unclear, as no witnesses had been present at the scene
and the patient had been comatose at hospital admission. An emergency craniotomy was performed after
Rewarming following accidental hypothermia in patients with acute subdural hematoma: case report
45
Fig. 1. Sequential changes in brain CT after admission. (A) Brain CT revealed an acute subdural hematoma on admission. (B) No brain swelling was observed on CT 4 days after admission. (C) Ventricular dilatations were observed at 6 weeks after admission
rapid rewarming to 33 C, with bladder temperature
maintained at 33 to 34 C during the surgery. No brain
swelling or episodes of intraoperative hypotension
were observed. The pupils measured 3.5 mm after
surgery, but both were unreactive to light. Therapeutic
hypothermia was induced using a water-circulating
blanket to confer brain protection. The patient re-
ceived sedation by intravenous administration of
midazolam (0.1 mg/kg body weight/h initially) and
buprenorphine (0.05 mg/h), with dose adjustments as
needed for the management of mechanical ventilation.
Paralysis was induced by a continuous infusion of
pancuronium (0.05 mg/kg body weight) to prevent
shivering.
46
K. Kinoshita et al.
Fig. 2. Sequential changes in mean arterial pressure and bladder temperature during hypothermia. Active core rewarming to 34 C was done
using a warming blanket and intravenous infusion of warm crystalloid. Therapeutic hypothermia was continued for 3 days with gradual rewarming of the patient to 37.0 C at a rate of 1 C/day. No hypotensive episodes were observed after craniotomy
The patient was cooled (34.0 C) continuously for 2
days and then gradually rewarmed to 37.0 C at a rate
no faster than 0.1 C/h and 1.0 C/d (Fig. 2). No evidence of intracranial hypertension was observed on
brain CT 4 days after admission (Fig. 1B).
The patient was able to respond to verbal requests
and eat meals by himself after a rehabilitation program, but he remained aphasic for 6 weeks after onset.
He was discharged to a satellite hospital with a rating
of severe disability on the Glasgow Outcome Scale. CT
at the time of discharge showed atrophy of the cerebral
cortex and ventricular dilation (Fig. 1C). The patient
currently lives in a partially-dependent state at the satellite hospital.
Discussion
The CPA su¤ered by this patient might have been
wholly or partially attributable to the following conditions: 1) increased intracranial pressure caused by
brain contusion/hematoma, resulting in brainstem
compression, brain herniation, and subsequent respiratory arrest; 2) secondary brain damage caused by
anoxia-hypoxia and hypotension; 3) hypothermia.
Even when return of spontaneous circulation is ob-
served after successful CPR in patients with TBI, only
a few patients survive over the long term and those
who do have a poor prognosis for daily life. Isolated
brain injuries with hypotension are associated with increased mortality [8].
The recovery of our patient after hypoxia and severe
hypotension was somewhat surprising. In view of this
outcome, this case suggests that therapeutic strategies
after TBI with accidental hypothermia should be considered further. Recent clinical trials of therapeutic hypothermia suggest that this treatment can improve
outcomes after resuscitation from CPA due to cardiogenic origins [1, 2, 13]. Although a clinical study of
TBI failed to identify significant improvements in outcomes with therapeutic hypothermia [3], the present
report suggests that such treatment might be beneficial
in selected patients with TBI.
Two methods are applied for rewarming from accidental hypothermia (30 C to <34 C) [4]: passive rewarming and active external rewarming (truncal areas
only). To avoid the risks of dysrhythmia and coagulopathy [15] that arise when the core temperature drops
below 33 C, the latter method, active external rewarming, is generally preferred [4]. Dysrhythmia and
coagulopathy were not observed in the case reported
Rewarming following accidental hypothermia in patients with acute subdural hematoma: case report
here. A comparison between normothermic (37 to
38 C) and hypothermic (32 to 33 C) groups by Clifton et al. revealed no di¤erence in the incidence of
delayed traumatic intracerebral hemorrhage due to
coagulopathy [3, 12]. Standard rewarming rates from
accidental hypothermia range from 1 to 3 C/h for
cardiac arrest patients [5, 6]. Suitable rewarming rates
from accidental hypothermia with TBI remain controversial, however. Each rewarming method has advantages and disadvantages, and no controlled studies
have been performed to compare them in humans.
Clifton et al. [3] reported that brain-injured patients
with hypothermia on admission should not be rewarmed. They based this advice on a subgroup analysis revealing a significant improvement in the outcome
of brain-injured patients with hypothermia on admission. They did not, however, provide any data or indicate the methods used for rewarming. The present case
suggests that the method of rewarming might play an
important role in improving outcomes in TBI with
accidental hypothermia. Posttraumatic hypothermia
followed by rapid rewarming o¤ered no beneficial effects for neuronal outcome [10]. Our group previously
reported [7] that marked changes in alternation of vascular resistance at rewarming and active core rewarming to normothermia may lead to elevations in cerebral
blood volume and intracranial pressure, which in turn
may adversely a¤ect final outcomes. For these reasons,
we have determined that active core rewarming to normothermia at a rate of 1 to 3 C/h might worsen the
patient outcome. After active core rewarming to 33 to
34 C, therapeutic hypothermia with slow rewarming
could be e¤ective for the treatment of patients with severe brain injuries accompanied by accidental hypothermia < 33 C.
Conclusion
We report the case of a patient with severe brain injury who survived CPA with accidental hypothermia.
Although the neurological outcome was poor, the survival of our patient suggests that therapeutic hypothermia might have the potential to improve survival and
functional outcome in TBI patients with accidental hypothermia who experience hypoxia and hypotension.
This case may provide information useful for planning
rewarming treatment in TBI patients with accidental
hypothermia.
47
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Correspondence: Kosaku Kinoshita, Department of Emergency
and Critical Care Medicine, Nihon University School of Medicine,
30-1 Oyaguchi Kamimachi, Itabashi ku, Tokyo 173-8610, Japan.
e-mail: [email protected]