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The Journal of ExtraCorporeal Technology logoLink to The Journal of ExtraCorporeal Technology
. 2011 Dec;43(4):252–257.

Hypothermic Cardiac Arrest in the Homeless: What Can We Do?

Fabrizio Sansone 1, Roberto Flocco 1, Edoardo Zingarelli 1, Guglielmo Mario Actis Dato 1, Giuseppe Punta 1, Francesco Parisi 1, Pier Giuseppe Forsennati 1, Gian Luca Bardi 1, Iulia Imbastaro 1, Claudia Chiolero 1, Adalberto Balossino 1, Paolo Borin 1, Viviana Peretto 1, Stefano del Ponte 1, Riccardo Casabona 1
PMCID: PMC4557429  PMID: 22416606

Abstract:

Accidental deep hypothermia with body temperature <28°C induces high mortality rates for neurological and cardiac complications. Although several reports described successful treatment of hypothermic arrest by extracorporeal membrane oxygenation (ECMO), the field of warming in the homeless is almost completely unquestioned although the malnutrition and the co-morbidities are usually believed as relevant risk factors for poor outcome. This article describes the experience of successful warming by ECMO in two homeless victims of unwitnessed cardiac arrest, who survived without neurological or cardiac complications. In conclusion, this is an initial experience and further research is required, although our results are appreciable in this high risk subset of population.

Keywords: alcoholism, cardiac arrest, extracorporeal membrane oxygenation, homeless, hypothermia, hypothermic cardiac arrest, resuscitation, warming

OVERVIEW

A 40-year-old homeless woman and a 50-year-old homeless man were found in unwitnessed cardiac arrest in a railroad car. Core temperatures were measured at 23° and 25° Celsius, respectively. Both patients were placed on ECMO to rewarm. Bypass was discontinued after 8 and 6 hours and both patients survived with no neurological or cardiac sequelae and an uneventful postoperative course.

Treatment Protocol

The ECMO system is a centrifugal, paracorporeal device that provides flow up to 7 L. The advantages of ECMO are the ease of implantation and management, although the lifespan is usually limited to few days or weeks. Among the different applications of the ECMO, the use for the cardiac support was preferred and achieved thanks to the insertion of an arterial and venous cannula through the surgical exposure of the femoral vessels. The pump was set to provide a flow greater than 2 L/m2 to ensure an adequate organ perfusion. Both the circuits and the oxygenator (Quadrox PLS Bioline) were Bioline coated (MAQUET Cardiopulmonary AG, Hirrlingen, Germany). Bioline Coating combines heparin and polypeptide, which is adsorbed on the extrinsic surface and is linked to the heparin molecules. Stable attachment of the heparin molecules is achieved by the formation of covalent bonds and ionic interactions between the heparin molecule and the immobilized polypeptide (1) and it allows to maintain lower ACT values, among 180 and 200 seconds. Anticoagulation was achieved by intravenous administration of heparin (25,000 UI in 500 mL of saline solution) at infusion rate adjusted on ACT values (starting from 1000 UI per hour) (2).

Protocol for Re-warming—The protocol for re-warming was to initially, begin at 10 minutes at patient temperature (rectal and esophageal). Then, the temperature was increased by 1–2 degrees over 10 minutes.

The drugs used were:

  • high doses of steroids (methylprednisolone sodium succinate) and barbiturates (thiopental) to reduce the cerebral edema and the brain injury;

  • antibiotics (cefazolin and vancocin) to prevent infections;

  • fentanyl citrate and cisatracurium for anesthesia and paralysis; and

  • pressors after the ECMO weaning (when required).

From November 2009 until May 2010, two homeless people were found in unwitnessed hypothermic arrest in a railroad car and were successfully resuscitated by ECMO re-warming. In our city, homeless are found frequently under shelter in the rail coaches and they may be victims of hypothermia, mainly in cases of acute ethanol intoxication, which is quite common among these communities (3). High blood levels of ethanol (over 3 g/dL) may impair the neurological function, delaying the reflexes with considerable risks of loss of consciousness (4) and severe hypothermia by peripheral vasodilatation (5).

In our experience, despite the unwitnessed cardiac arrest and the incomplete neurological evaluation for the emergency conditions, the decision to treat to this patient group depended on the young age of the patients and on the potassium level (<4.0 meq/L), which is a strong predictor of survival in case of hypothermia (6).

PATIENT ONE

A 40-year-old homeless woman, who was a smoker, affected by arterial hypertension, and was 170 cm and 70 kg, with acute ethanol intoxication (3.15 g/L), was found in a railroad car on December 21, 2009 in unwitnessed cardiac arrest at the body temperature of 23°C. Basic Life Support (rescue breathing and chest compressions) was started immediately after discovery until the hospital admission (about 39 minutes later) and admission to the following ECMO institution (about 2 hours later) (Table 1).

Table 1.

Schematic sequence of resuscitation events.

Patient 1: Found December 21, 2009 Patient 2: Found May 4, 2010


Hour Events Hour Events
13:40 Found in unwitnessed cardiac arrest 6:40 Found in unwitnessed cardiac arrest
13:40 Started with Basic Life Support 6:40 Started with Basic Life Support
14:19 Arrived at the hospital 7:19 Arrived at the hospital
14:19 Started with Advanced Life Support 7:19 Started with Advanced Life Support
14:19 Infusion of warm solution 7:19 Infusion of warm solution
15:20 Arrived at the operating room 8:00 Arrived at the operating room
15:40 Started the ECMO support 8:15 Started the ECMO support
23:00 Stopped the ECMO support 12:08 Stopped the ECMO support

Surgical exposure of the femoral vessels was carried out under cardiopulmonary resuscitation and the ECMO institution took about 15 minutes for the insertion in the groin both of the arterial cannula (OPTISITE™ arterial perfusion cannula, Edwards Lifesciences LLC, Irvine, CA) of 20 French (Fr) and of the venous cannula (femoral venous cannula, Edwards Lifesciences LLC) of 20 Fr. Patient was not re-warmed during the initial 10 minutes at the ECMO institution, to avoid the progression of the brain injury. After 10 minutes of ECMO support, the temperature was slowly increased by 1–2°C each 10 minutes up to 25°C when the ventricular fibrillation was converted to sinus rhythm by external shock (360J). The infusion of pressors (noradrenaline up to 0.1 γ/Kg/min) was required to improve the systemic blood pressure. When the body temperature reached 30°C, the patient was transferred to the intensive care unit (ICU) where he was awakened 6 hours later despite the agitation. Noradrenaline was replaced by dobutamine on postoperative day (POD) one up to 5 γ/Kg/min (weaned on POD 2) and the ECMO was removed about 8 hours later for an untreatable bleeding of the groin. However, there was a complete recovery of the cardiac function with progressive normalization of the chemistry (Table 2) and patient was extubated in 10 hours. Unfortunately, patient was restless and AVBG values were poor. Patient was re-intubated and was on the ventilator until POD 2. The patient was discharged early on POD 6 without any complication or harmful events.

Table 2.

Patient 1: Changes in blood gas analysis from the admission until few hours later, ECMO weaning.

PreECMO During ECMO Post ECMO



Value Hour 14:53 Hour 16:00 Hour 17,18 Hour 18:51 Hour 5:20
pH 7.256 7.437 7.369 7.365 7.538
pO2 40.0 mmHg 375.0 mmHg 168.0 mmHg 260.0 mmHg 193.0 mmHg
pCO2 57.4 mmHg 23.9 mmHg 29.9 mmHg 35.0 mmHg 33.6 mmHg
HCO3 24.7 mmol/L 19.2 mmol/L 16.8 mmol/L 19.5 mmol/L 29.9 mmol/L
Base excess −3.0 mmol/L −7.5 mmol/L −7.1 mmol/L −4.8 mmol/L 6.0 mmol/L
Glucose 92 mg/dL 140 mg/dL 53 mg/dL 86 mg/dL 202 mg/dL
K+ 3.5 meq/L 3.0 meq/L 3.0 meq/L 3.0 meq/L 3.7 meq/L
Na+ 146.0 meq/L 145.0 meq/L 143.0 meq/L 145.0 meq/L 147.0 meq/L
Ca+ .90 mmol/L 3.48 mmol/L 3.46 mmol/L 3.46 mmol/L 3.74 mmol/L
Cl 115.0 meq/L 116.0 meq/L 115.0 meq/L 118.0 meq/L 132.0 meq/L
Lactate 3.6 mmol/L 6.7 mmol/L 7.1 mmol/L 6.9 mmol/L 2.9 mmol/L
mOsm 298.0 mmol/Kg 298.4 mmol/Kg 288.9 mmol/Kg 295.7 mmol/Kg 305.0 mmol/Kg
Hb 13.9 g/dL 12.0 g/dL 9.1 g/dL 7.9 g/dL 10.1 g/dL

NA, not available; HCO3, bicarbonate; K+, potassium; Na+, sodium; Ca+, calcium; Cl, chloride; mOsm, osmolarity; Hb, hemoglobin.

Patient’s pH before ECMO was 7256 with serious impairment of blood gas analysis (pO2: 40.0 mmHg; pCO2 57.4 mmHg) and a normal value of potassium (3.5 meq/L), while after the ECMO institution there was a significant improvement of blood gases and urine output (Tables 2 and 3).

Table 3.

Patient 1: Evolution of the chemistry from the admission until first postoperative day.

Value December 21, 2009 Hours 15:01 December 21, 2009 Hours 18:01 December 23, 2009 Hours 8:00 December 25, 2009 Hours 8:00
Blood alcohol level 3.15 g/L NA NA NA
Creatinine .3 mg/dL .4 mg/dL .5 mg/dL .4 mg/dL
GFR >90 mL/min/1.73 mq >90 mL/min/1.73 mq >90 mL/min/1.73 mq >90 mL/min/1.73 mq
Total bilirubin 2.0 mg/dL 1.3 mg/dL 7.0 mg/dL 4.4 mg/dL
Direct bilirubin 1.1 mg/dL .7 mg/dL .2 mg/dL 1.3 mg/dL
LDH 796 U/L 602 U/L 2711 U/L 1328 U/L
CK NA 551 U/L 2590 U/L NA
Total protein NA 4 g/dL 5.8 g/dL 6 g/dL
Troponin I <.06 ng/mL NA NA NA
INR 1.85 4.3 1.54 1.74
AST 141 U/L 103 U/L 1090 U/L 437 U/L
ALT 37 U/L 32 U/L 173 U/L 135 U/L
WBC 5.6 × 10E3 c/uL 5.8 × 10E3 c/uL 9.41 × 10E3 c/uL 8.44 × 10E3 c/uL
RBC 5.27 × 10E6/uL 2.89 × 10E6/uL 3.39 × 10E6/uL 3.37 × 10E6/uL
PLTs 81 × 10E3 c/uL 93 × 10E3 c/uL 79 × 10E3 c/uL 49 × 10E3 c/uL

NA, not available; GFR, glomerular filtration rate; INR, international normalized ratio; AST, aspartate amino transferase; ALT, alanine transferase; WBC, white blood cells; RBC, red blood cells; PLTs: platelets.

Lactates increased about 2 hours after cardiac arrest (up to 7.1 mmol/L) while a serious hepatic dysfunction was noted later (aspartate amino transferase up to 1090 U/L and alanine transferase up to 173 U/L on POD 2; bilirubin 7.0 mg/dL on POD 2; international normalized ratio 4.3 few hours after cardiac arrest). Renal function was normal over the length of the in-hospital stay despite the amount of necrosis enzymes as lactate dehydrogenase (LDH) or creatine kinase (CK) increased up to 2711 U/L and 2590 U/L, respectively.

PATIENT TWO

A50-year-old homeless man, who was a smoker, affected by arterial hypertension, was 165 cm and 60 kg, with acute ethanol intoxication (3.5 g/L), was found in a railroad car on May 4, 2010 in unwitnessed cardiac arrest with a body temperature of 25°C. Basic Life Support (rescue breathing and chest compressions) was started immediately after discovery until the hospital admission (about 39 minutes later) and admission at the ECMO institution (one and a half hour later) (Table 1). Surgical exposure of the femoral vessels was performed under cardiopulmonary resuscitation and the ECMO institution took about 15 minutes for the insertion in the groin both of the arterial (20 Fr) and venous cannula (20 Fr). The protocol for re-warming was the same as the first patient. When the body temperature reached 28°C the onset of ventricular fibrillation was converted to sinus rhythm by external defibrillation (360J) and at the body temperature of 31°C the patient was moved to the ICU where he was awakened about 6 hours later. Patient was weaned from the ventilator and extubated 12 hours later when the neurological function was completely restored and the hemodynamic stabilized by adrenaline 0.1 γ/Kg/min (weaned in POD 2). We were not aware of the previous left pneumonectomy and when the chest X-ray showed a complete clouding of the hemithorax (Figure 1), an unsuccessful percutaneous drainage of the pleural effusion was attempted. Then, computed tomography scanning showed previous left pneumonectomy with compensatory emphysema of the other lung (Figures 2 and 3). The patient was then moved to the general ward on POD 2 without postoperative complications and was discharged on POD 5.

Figure 1.

Figure 1.

The chest X-ray shows the complete clouding of the left hemithorax, indicative of considerable pleural effusion.

Figure 2.

Figure 2.

Computed tomography scanning shows the absence of the left lung for previous pneumonectomy with compensative emphysema of the other lung.

Figure 3.

Figure 3.

Another computed tomography scanning section shows the previous left pneumonectomy.

The following data are listed in Tables 4 and 5. pH before ECMO institution was 6.984 with severe increase of CO2 levels (pCO2 61.8 mmHg) and high O2 values (pO2: 278.0 mmHg) due to mechanical ventilation; blood gas analysis showed low value of potassium, 3.0 meq/L. After the ECMO institution, there was a significant improvement of pH and blood gases and the urine output was quickly restored for the adequate cardiac output and the furosemide administration.

Table 4.

Patient 2: Changes in blood gas analysis from the admission until few hours later, ECMO weaning.

PreECMO During ECMO Post ECMO



Value Hour 08:10 Hour 09:00 Hour 9:55 Hour 11:20 Hour 20:43
pH 6.984 7.420 7.45 7.43 7.45
pO2 278.0 mmHg 206.0 mmHg 322.0 mmHg 202.0 mmHg 247.0 mmHg
pCO2 61.8 mmHg 24.6 mmHg 33.8 mmHg 36.0 mmHg 37.8 mmHg
HCO3 11.4 mmol/L 18.6 mmol/L 24.3 mmol/L 23.0 mmol/L 26.0 mmol/L
Base excess −15.6 mmol/L −8.0 mmol/L −.5 mmol/L −.1 mmol/L 2.4 mmol/L
Glucose NA NA NA NA 94 mg/dL
K+ 3.0 meq/L 4.3 meq/L 4.3 meq/L 3.1 meq/L 4.0 meq/L
Na+ NA NA NA NA 138.0 meq/L
Ca+ NA NA NA NA 4.29 mg/dL
Cl NA NA NA NA 108.0 mmol/L
Lactate 9.5 mmol/L 7.8 mmol/L 5.8 mmol/L 3.9 mmol/L 1.3 mmol/L
mOsm NA NA NA NA 282.0 mmol/Kg
Hb 11.0 g/dL 10.6 g/dL 10.0 g/dL 8.2 g/dL 8.0 g/dL

NA, not available; HCO3, bicarbonate; K+, potassium; Na+, sodium; Ca+, calcium; Cl, chloride; mOsm, osmolarity; Hb, hemoglobin.

Table 5.

Patient 2: Evolution of the chemistry from the admission until first postoperative day.

Value May 4, 2010 Hours 08:45 May 4, 2010 Hours 22:00 May 5, 2010 Hours 8:00 May 7, 2010 Hours 8:00
Blood alcohol level 3.5 g/L NA NA NA
Creatinine .7 mg/dL .5 mg/dL .6 mg/dL .8 mg/dL
GFR >90 mL/min/1.73 mq >90 mL/min/1.73 mq >90 mL/min/1.73 mq >90 mL/min/1.73 mq
Total bilirubin 4.0 mg/dL 1.2 mg/dL 1.2 mg/dL .8 mg/dL
Direct bilirubin 3.5 mg/dL .2 mg/dL .5 mg/dL .42 mg/dL
LDH 686 U/L 790 U/L 969 U/L 921 U/L
CK 913 U/L 2122 U/L 6319 U/L 3209 U/L
Total protein 4.6 g/dL 3.5 g/dL 4.1 g/dL NA
Troponin I .763 ng/mL 16.171 ng/mL 10.01 ng/mL NA
INR 1.64 1.35 1.44 1.11
AST 165 U/L 249 U/L 309 U/L 75 U/L
ALT 8 U/L 50 U/L 66 U/L 77 U/L
WBC 5.38 × 10E3 c/uL 7.98 × 10E3 c/uL 12.37 × 10E3 c/uL 4.4 × 10E3 c/uL
RBC 3.21 × 10E6/uL 3.05 × 10E6/uL 3.38 × 10E6/uL 2.92 × 10E6/uL
PLTs 96 × 10E3 c/uL 81 × 10E3 c/uL 93 × 10E3 c/uL 138 × 10E3 c/uL

NA, not available; GFR, glomerular filtration rate; INR, international normalized ratio; AST, aspartate amino transferase; ALT, alanine transferase; WBC, white blood cells; RBC, red blood cells; PLTs, platelets.

Lactates before ECMO implantation were seriously increased (9.5 mmol/L) and hepatic function slightly impaired (bilirubin 4.0 mg/dL, aspartate amino transferase up to 309U/L and alanine transferase up to 66U/L on POD1; protein value fell up to 3.5 g/dL few hours after ECMO implantation; international normalized ratio value had no significant changes). Renal function was normal over the length of the in-hospital stay while the values of LDH or CK increased up to 969 U/L and 6319 U/L respectively on POD 1. Differing from the other patient, troponin I values raised up to 16 ng/mL in the afternoon after the ECMO implantation.

DISCUSSION

Hypothermia is defined as any body temperature below 35.0°C. It is subdivided into four different degrees: mild 32–35°C; moderate, 28–32°C; severe, 20–28°C; and profound at less than 20°C (7). Successful resuscitation under 13.7°C has never been reported, as this is the lowest value in literature described in a young female resuscitated after hypothermic cardiac arrest (8). However, hypothermia is protective against cell death as happens in cases of aortic arch surgery when a body temperature of 18°C ensures about 30 minutes of safe interval (9). Depending on the degree of hypothermia, brain functions may be impaired leading to loss of consciousness and cardiac cells may be damaged resulting in cardiac rhythm alteration as bradycardia or ventricular fibrillation (10,11). Even with immediate treatment, mortality rates are high (12). Moreover, resuscitation after hypothermic cardiac arrest has poor outcome in cases of pre-existing co-morbidities like poor nutrition (i.e., homeless) or in cases of asphyxia after avalanches (13). However, in this emergency condition it is quite difficult to disqualify patients because quick decision making is mandatory and little information is available. Prognostic factors in case of hypothermic arrest have been discussed and negative indicators of survival after warming with ECMO are: the presence of underlying medical illness, the length of cold exposure, the initial temperature, the mental status, the presence of spontaneous respirations, the presence of cardiac rhythm, and the arterial oxygen tension. Indicators of poor survival are profound hyperkalemia and markedly elevated levels of necrosis enzymes, such as LDH or CK, that indicate cell lysis (6,13).

About 400,000 people in Europe have sudden cardiac arrest yearly and most of them have serious neurological complication due to brain ischemia (14). Several studies have shown that moderate systemic hypothermia (30°C) or mild hypothermia (34°C) markedly reduces brain injury after cardiac arrest in dogs (15,16) and the outcome of victims of hypothermic arrest is usually better than sudden arrest (13). The mechanism of this protective action is not yet clarified even if a reduction in cerebral oxygen consumption (17,18) and other chemical and physical patterns have been proposed. Among these mechanisms, a retardation of destructive enzymatic reactions, suppression of free-radical reactions, protection of the fluidity of lipoprotein membranes, reduction of the oxygen demand in ischemic regions, reduction of intracellular acidosis, and inhibition of the biosynthesis of excitatory neurotransmitters (16,19) have been proposed. In cases of brain ischemia, the increase of intracellular levels of glutamate, an excitatory neurotransmitter released from presynaptic terminals, activates ion-channel complexes that cause an uptake of the intracellular calcium, leading to the accumulation of oxygen free radicals and the activation of degradative enzymes (19).

Despite the considerations about the protective role of the hypothermia, survival following deep hypothermia (<28°C) with prolonged cardiac arrest is uncommon. The largest series of patients (12) who were victims of deep hypothermia was published more than 10 years ago and the authors retrospectively analyzed 234 patients admitted to the hospital for hypothermia, focusing the attention on 32 patients in hypothermic cardiac arrest treated by warming with ECMO. The patients were almost all young people without cardiac risk factors and the long term outcome was surprising, probably for the following five reasons: deep hypothermia, absence of asphyxia or hypoxic brain damage before hypothermic arrest, young age, experience of rescue organizations (20,21), and the warming technique. In the absence of contraindications such as asphyxia, severe traumatic injury, and extremely elevated serum potassium levels (exceeding 10 mmol per liter), ECMO is the warming method of choice for accidental deep hypothermia with circulatory arrest because it quickly provides an adequate cardiac output. The authors concluded that the long-term outcome of survivors of accidental deep hypothermia with prolonged circulatory arrest and warming with cardiopulmonary bypass is favorable and may be applied when contraindications are absent.

Our limited experience of two homeless people in unwitnessed hypothermic arrest shows appreciable results despite the presence of the following indicators of poor outcome: the shortage of nutrition (homeless), the unknown length of cardiac arrest, and the age of patients. Neurological function was not completely assessed before ECMO implantation because of the emergency condition; differing from other reports, our patients had no neurological sequelae and they had a complete postoperative recovery. Obviously, the awakening was characterized by persistent agitation (as it happens after hypothermic circulatory arrest in case of aortic arch surgery) that was successfully managed by neuroleptic drugs administration. In our experience, the consistent length of the in-hospital stay depended on the social condition of the patients who were homeless without any possibility of health care after hospital discharge. Moreover, the risk of re-admission for hypothermia was significant for the climatic conditions and the surgical incision of the groin needed to be cleaned every day to avoid infection for the lack of hygiene. No specific information was available regarding the presence of specific nutritional deficits although physical examination and their aspect revealed poor nutritional state (chronic alcoholism).

In conclusion, the hypothermic arrest is a life threatening condition that needs close cooperation among different operators and fast decision making to reduce the risks of prolonged hypothermia. Indicators of survival such as potassium levels are helpful for a quick decision about treatment opportunity.

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