A case of profound accidental hypothermia without loss of spontaneous cardiac output
Oxford University
Hospitals
Matthew Maton-Howarth (CT1 Anaesthetics), Amar Bhat (ST6 Acute Medicine), Jon Walker (Emergency Medicine Consultant)
NHS Foundation Trust
We present a case of profound accidental hypothermia in a previously fit and well 56-year-old male. He presented critically unwell, though spontaneously
perfusing, with an admission rectal temperature of 21.7°C. Cardiac output is almost globally absent below 24°C – indeed an extensive search of the literature
has not found any reported case of spontaneous perfusion at any temperature lower than in this case1.
CASE SUMMARY:
A 56-year-old man was admitted to the Emergency Department after being found semi-conscious in a rural location.
Pre-hospital he was spontaneously ventilating and had perfusing cardiac output. Rectal temperature was 21.7°C.
He had been reported missing from his home 14 days previously, and an extensive Search & Rescue operation had
been ongoing since that time. Nocturnal atmospheric temperatures throughout this period were consistently below
0°C. He was found by rescue dogs on day 14 of the operation.
ECG rhythm strip on admission to A&E.
He was previously fit and well and did not drink alcohol.
On arrival at the Emergency Department he was markedly bradycardic (25 bpm), hypotensive (77/60 mmHg) and
bradypnoeic (8 breaths / minute). He had strong central pulses, and was self-ventilating with oxygen saturations of
99%. He had a Glasgow Coma Score of 10/15; (E4,V1,M5), and his pupils were equal and sluggishly reactive to
light. He was globally areflexic.
INVESTIGATIONS:
Initial venous blood results revealed a profound hyperkalaemia (>10mmol/L) in a non-haemolysed venous sample.
There was rhabdomyolysis (CK=1929U/L), associated acute kidney injury, and a hypothermic coagulopathy
(INR=1.4). Other results were unremarkable. Paracetamol, salicylate and alcohol levels were all 0mmol/L.
Arterial blood sampling demonstrated a lactic acidosis (pH=7.19, lac=6.6) and again confirmed the hyperkalaemia
(7.6mmol/L following initial treatment).
Chest radiography and computed tomography (CT) of the brain were unremarkable.
15:05 17:45 18:35 19:35 20:25 22:30 23:35 00:45 02:10 04:45
pH:
-
7.19 7.2
pO2 (kPa):
-
53.2 16.1 8.9
FIO2:
-
0.8
0.35 0.35 1.0
pCO2 (kPa):
-
5.2
HCO3- (mmol/L):
-
sO2 (%):
-
Base excess (mEq/L): -
7.24 7.18 7.18 7.2
7.25 7.3
7.3
8.1
7.7
8.3
10.4
1.0
1.0
0.7
0.7
0.55
6.2
6.45 7.02 7.2
8.1
7.7
5.4
5.35
15
17
18
17
19
18
19
19
19
99
98
89
97
81
87
87
96
92
-12.2 -9.2
-6.5
-8.1
-4.9
-7.1 -6.1 -6.1 -6.3
14.3 7.2
Lactate (mmol/L):
-
6.6
5.1
4.0
5.4
3.1
3.7
4.1
3.1
3.0
Sodium (mmol/L):
138
157
156
155
155
153
153 153
149
149
Potassium (mmol/L): 7.6
3.0
3.0
3.4
3.5
4.0
3.8
4.3
4.5
4.8
119
118
119
135
136 141
138
137
Haemoglobin (g/L):
-
119
Haematocrit (%):
-
36.6 36.5 36.4 36.5 41.5 41.8 43.3 42.5 42.2
Glucose (mmol/L):
-
4.6
3.2
2.4
5.1
5.5
4.2
5.3
8.1
8.9
Serial arterial blood gases during rewarming.
Initial electrocardiogram rhythm strip revealed an irregular bradyarrhthmia at a rate of 26 beats per minute, profound
QRS broadening (275ms), QT prolongation (QTc:556ms), Osborn waves, ST depression and T-wave inversion.
REWARMING:
Non-invasive warming was immediately commenced with forced-air warming blankets. Intravenous fluids were
warmed to approximately 43°C and infused rapidly via two wide-bore intravenous cannulae. A urethral catheter was
inserted and warmed bladder lavage was performed.
Rewarming over time during ini
Hyperkalaemia was treated with 30mL of 10% calcium gluconate and with an insulin-dextrose infusion. Broad
spectrum antibiotics were given empirically and anti-tetanus antitoxin administered.
Fluid-resistant hypotension necessitated cautious use of bolus-dose vasopressors.
The gentleman was transferred to the critical care unit where emergent continuous veno-venous haemodiafiltration
(CVVHDF) was commenced to allow electrolytic clearance and for rewarming at approximately 2°C/hour.
OUTCOME:
Organ System: Features of Hypothermia:
The patient had a turbulent post-resuscitative period.
Cardiovascular:
Five hours following admission, the patient suffered a prolonged generalized tonic-clonic seizure requiring emergent
intubation and ventilation. Furthermore, in the initial 12 hours following admission to the intensive care unit, the
patient developed rewarming shock with hypotension resistant to rapid fluid replacement. Focused intensive care
echocardiography demonstrated a hyperdynamic left ventricular function and evidence of hypovolaemia. Thus,
further intravenous fluids were given and dual inotropic therapy with noradrenaline and vasopressin infusions
commenced.
Bradycardia
ECG changes: QRS broadening, QT prolongation,
elevated J point (Osborn waves), arrhythmias
Myocardial depression
Hypotension
Systemic vasoconstriction
Neurological:
Coma
Peripheral neuropathy
Reduced intracranial pressure
Neuroprotective
Raises seizure threshold
Respiratory:
V:Q mismatch
Bradypnoea
Renal:
Rhabdomyolysis
Acute kidney injury
Hyperkalaemia
Lactic acidosis
Cold diuresis / Hypovolaemia
Gastrointestinal:
Ischaemic colitis
Ileus
Hepatobiliary:
Ischaemic hepatitis
Insulin resistance
Microbiological:
Immunosuppression
Haematological:
Coagulopathy
Haemoconcentration / thrombosis
Hyperviscocity
Thrombocytopaenia
Vascular insufficiency / anasarca
The patient also suffered a range of delayed complications related to the hypothermic episode: On day 2, he
developed an aspiration pneumonitis which improved with intravenous antimicrobial therapy. On day 6, the patient
experienced an episode of large-volume melaena requiring transfusion of 4 units of packed red cells. Urgent
oesophago-gastro-duodenoscopy (OGD) revealed an actively bleeding gastric stress ulcer which was injected with
adrenaline. On day 10, the patient developed a hyperactive delirium requiring reintubation. A full septic screen and
lumbar puncture confirmed a hospital-acquired pneumonia managed with a further course of broad-spectrum
antimicrobials. Additional complications experienced included an ischaemic hepatitis, ischaemic colitis and a
widespread pustulovesicular rash, all of which were managed conservatively.
Following two weeks of intensive care treatment and a four week total hospital admission, he was discharged to a
rehabilitative community hospital, and has since made a complete recovery.
DISCUSSION:
Dermatological:
Frostbite
The human thermoregulatory system provides homeostatic mechanisms by which the body maintains homeostasis
Pustular/bullous skin disease
in response to changes in environmental temperature. Hypothermia can be defined as a state in which these
homeostatic mechanisms are overwhelmed in the presence of a cold stressor2. Hypothermia produces a multi- Physiological effects of hypothermia.
ssystem pathophysiological response affecting myocardial contractility, neuronal excitation and immune function amongst others3.
Despite hypothermia being a condition associated with significant mortality and morbidity, no consensus exists for its management, either with respect to rewarming speed or
method used for rewarming4. Rapid rewarming (>0.5°C per hour) is associated with increased risk of seizures and rewarming shock (both of which our patient experienced)
compared to a slower rewarming protocol5, but exposes the patient to a longer period of cardiac instability and there is cautious consensus that at least an initial phase of
rapid rewarming in profound hypothermia is probably justified.
The consensus gold-standard treatment for cardiovascularly unstable hypothermia is regarded to be veno-arterial extracorporeal membrane oxygenation (VA ECMO) or
cardiopulmonary bypass (CPB)4. These permit the most rapid rewarming rate, and are recognised to reduce mortality4,6,. Veno-venous ECMO and CVVHDF are alternative
options for rewarming, though provide an inferior rewarming speed. However, as with our patient, we would propose that a relative indication for CVVHDF over VA
ECMO/CPB would be patients with cardiovascularly unstable hypothermia in combination with life-threatening electrolytic derangement.
References:
1. Walpoth BH, Walpoth-Aslan BN, Mattle HP et al. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood warming. N Engl J
Med. 1997;337(21):1500-5.
2. Boron WF and Boulpaep EL. Medical Physiology: A Cellular And Molecular Approach. 2009. Philadelphia, PA : Saunders/Elsevier.
3. Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009;Jul;37(7 Suppl):S186-202.
4. Brown DJA, Brugger H, Boyd J et al. Accidental hypothermia. N Engl J Med. 2012;367:1930–1938.
5. Scaravilli V, Bonacina D and Citerio G. Rewarming: facts and myths from the systemic perspec-tive. Critical Care. 2012;16(Suppl 2):A25.
6. Danzl DF, Hedges JR and Pozos RS. Hypothermia outcome score: development and implications. Crit Care Med. 1989;17:227.