IntensiveCare Medicine

Intensive Care Med (1990) 16:69-72

9 Springer-Verlag 1990

Case report Accidental hypothermia with cardiac arrest: complete recovery after prolonged resuscitation and rewarming by extmcorporeal circulation R Husby 1, K.S. Andersen 2, A. Owen-Falkenberg 1, E. Steien 1 and J. Solheim 2 Departments of 1Anesthesiology and 2Thoracic and Cardiovascular Surgery, University of Bergen, Haukeland Sykehus, Bergen, Norway Received: 4 December 1988; accepted: 5 May 1989

Abstract. A 51-year-old male remained immersed in sea water (6 ~ for 40 min. Brought ashore, the ECG showed asystole. Advanced life support was immediately commenced. On arrival in hospital his rectal temperature was 27 ~ but continued to fall to 24 ~ The ECG remained isoelectric. Cardiopulmonary resuscitation was continued until extracorporeal circulation was established 190 rain after rescue. Upon rewarming ventricular fibrillation occurred which was converted to sinus rhythm with a bolus of lignocaine followed by D.C. conversion at 31.5 ~ When rewarming was complete after 60 rnin, signs of severe heart failure became evident. Sternotomy and pericardiotomy were performed to exclude cardiac tamponade. After 60 min of re-perfusion the patient was be weaned from bypass supported by a high-dose vasopressor infusion and nitroglycerine. He was discharged after 13 days with no evidence of any permanent organ damage. Given the advantage of providing circulatory support, extracorporeal circulation may be useful when rewarming hypothermic victims with cardiac arrest. Key words: Hypothermia - Asystole - Resuscitation - Extracorporeal circulation

The presence of circulatoy arrest as a consequence of accidental hypothermia poses a multiplicity of therapeutic challenges. The improved prognosis during the last two decades may be due to better intensive care management both in hospital as well as in the pre-hospital period [1]. Several recent reports suggest the improved prognosis is also related to the rewarming method [2, 3]. The following case history illustrates the successful resuscitation of a severely hypothermic patient who had asystole for a period of four hours. The use of ex-

tracorporeal circulation allowed a rapid increase in temperature and was of value in giving circulatory support during a period of severe heart failure which occurred during the process of rewarming.

Case report A 51-year-old fisherman fell into seawater (6 ~ and remained immersed for about 40 min before being pulled from the water. On being brought to land he was attended by paramedics who found him lifeless with no signs of respiration or circulation. His ECG was isoelectric. He was rapidly intubated and ventilated, external cardiac massage was instituted and he was transferred to hospital. On arrival his ECG was still isoelectric. His rectal temperature was 27 ~ but fell to 24 ~ before rewarming could be started. Central venous and arterial lines were established. An acidosis was corrected with sodium bicarbonate. Rewarming was not started before facilities for extracorporeal circulation were available; meanwhile ventilation and cardiac massage (blood pressure 60/40 mm Hg) was continued. Extracorporeal circulation was established 190 minutes after commencement of resuscitation via the femoral artery and vein using standard equipment for open heart surgery consisting of a Bentley AF 1025 filter, two OTC cells (Bentley) and a Bentley 10-plus bubble-oxygenator with integrated heat exchanger. The prime consisted of 2250ml Ringer Acetate, 150ml Mannitol 15% and 100 ml sodium bicarbonate. The mixture was kept at a temperature of 25 ~ before the start of bypass. Heparin 3 mg/kg body weight was given as a bolus injection. The estimated haemodilution was to haemoglobin 77 g/1. A flow of 4.3 1/min was calculated as equivalent to a cardiac index of 2.41/min/m2 BSA (37 ~ A process of rapid rewarming was initiated. 13 rain later (at an oesophageal temperature of 30.5 ~ ventricular fibrillation occurred. Two unsuccessful attempts were made at D.C. conversion. On reaching 31.5~ a bolus of lignocaine (50mg) was given and ventricular fibrillation converted to sinus rhythm. During the early stages of rewarming the patient required a large amount of volume to meet the calculated flow (6000ml Ringer acetate and 6 units of erythrocyte concentrate). On reaching normal temperature after 60 rain, the patient exhibited signs of severe heart failure with low perfusion pressure. CVP rose from being initially high, (25-30 mm Hg) to a severely elevated level (35 mm Hg). Sternotomy was performed to exclude cardiac tamponade secondary to prolonged cardiac massage. No such lesion was found and the heart was seen to be dilated. Pericar-

70

P. Husby et al.: Recovery from cardiac arrest due to severe hypothermia

diotomy was performed to relieve the mechanical obstruction. A Swan-Ganz catheter was introduced and revealed a PCWP of 3 0 - 3 5 mm Hg and an infusion of nitroglycerine was started in addition to an infusion of dobutamine. Circulatory support by the use of prolonged extracorporeal circulation, was continued for 60 min after which time the circulation improved sufficiently for extracorporeal bypass to be discontinued with the support of adrenaline and nitroglycerine infusions. Postoperatively the patient was moderately hyperventilated ( p C O 2 : 4 - 4 . 5 kPa) and given mannitol. He was extubated 24 hours later without neurological sequelae. During the next 12 days the patient recovered from a bronchopneumonia. More extensive neuropsychological testing six months later revealed no deleterious effects of this treatment.

7 -

9

CK

0 O A

LD ALAT ASAT ALP ~GT

41,

6 -

5 -

10

C) x

Laboratory results A series of blood tests were taken from the arterial line to evaluate his biochemical status. The results of the serum acidbase determinations as well as the serum electrolytes are given in Table 1. Serum enzyme concentrations of LD, CK, ALAT, ASAT and the myocardial isoenzyme CK-MB were severely elevated on occasion during the first days of treatment as shown in Fig. 1. ALP, Gamma-GT and serum-amylase were normal. Serum osmolality (365 mOsm/1) and serum lactate concentration (22.5 mmol/1) were elevated during the first 24 h of treatment. Serum-ethylalcohol concentration was measured to 1.55 g/kg blood. Serum glucose was initially slightly elevated. Serum creatinine was normal on admission but increased slightly during the first 48 h, whereafter normal values were obtained. Blood thrombocyte count was subnormal during the first 5 postoperative days. Other parameters were within nor-

ul

E

>, N

2

-

Time (Doys after admission)

~

0 -I

, 0

~ 2

11

Time

'I /,

(Days

t

i 6

i

I 8

i 10

after admission)

Fig. 1. Serum enzymes during the first 10 days after admission. CK = creatine kinase; LD, lactate dehydrogenase; ALAT, alanineaminotransferase; ASAT, aspar tate-aminotrans ferase; ALP, alkaline phosphatase; Gamma-GT, gamma-glutamyl-transferase; CK-MB, the MB-fraction of the total creatine kinase activity. Values are given in Units/l

Table 1. Acid base and serum-electrolyte changes during the first day pCO 2 and pO 2 are given in kPa. Other parameters are presented in m m o t / L . Temperature (temp): ~ Date/ Time

pH

pCO 2

BE

pO 2

Na +

K+

Ca + +

Mg + +

C1-

Temp.

5.12. 0930 1000 1130 1200 1245 1315 1420 1800 2000 2200 6.12. 0400 0800 7.12. 0800 8.12. 0800 9.12. 0800

6.97 7.20 7.33 7.41 7.54 7.43 7.29 7.48

9.4 8.9 7.1 4.9 2.9 3.8 7.3 5.4

- 15.7 - 3.0 + 1.0 -0.9 - 1.0 - 3.6 - 2.2 + 6.4

1.8 3.1 4.5 51.3 50.8 42.2 58.8 26.2

148

2.4

2.25

1.22

104

27 24 24 27 a 35

149 143 150

2.4 3.3 3.5

2.81

1.21

37

2.17

0.90

96 99 103

7.60 7.55 7.46 7.41 7.40 7.39

4.1 4.3 5.3 6.2 5.5 5.1

+ 10.5 +6.7 + 4.4 +3.7 +0.2 - 1.8

18.3 15.2 16.5 18.8 10.9 13.0

148 146 146 139

4.3 4.2 4.2 4.3

2.03 2.10 2.13 2.05

0.98 1.00 0.80

109 109 112 107

a Indicates first acid-base determination after initiation of extracorporeal circulation. Acid base values are not temperature-corrected

P. Husby et al.: Recovery from cardiac arrest due to severe hypothermia

mal range. Sequential ECGs and echocardiograms revealed no abnormalities.

Discussion

Several hypothermic victims can survive for long periods with few or no signs of cardiopulmonary function [2, 3]. The body responds to severe hypothermia by redistributing the circulation to the core resulting in preferential perfusion of vital organs. Metabolic activity and oxygen demand fall in parallel with temperature and the reduced perfusion may well be adequate for organ survival [4]. During asystole, which can be a presenting feature in some patients, safety margins for organ viability will be less. Under field conditions it is difficult to make an adequate assessment of circulation and respiration in severe hypothermic victims. The patient may appear dead. Any doubt should be to the patient's benefit. Resuscitation with external cardiac massage should begin and continue until the patient can be transported to a hospital where rewarming can be initiated. If possible the patient should be intubated. This procedure seems no more likely to provoke ventricular fibrillation than other forms of manipulation [5]. As for external compression of a cold heart, circulation is probably achieved via changes in intrathoracic pressure rather than compression of the heart muscle [6]. Almost all cases of severe hypothermia are complicated during rewarming by some degree of heart failure. Compared with other rewarming procedures, extracorporeal circulation provides the advantage of circulatory support should heart failure occur. It is the most rapid method for core rewarming and it improves tissue perfusion by using hemodilution. Our decision not to rewarm the patient until effective, controlled, rewarming could be instituted is in line with previous recommendations [7]. Rewarming should only begin once effective cardiopulmonary resuscitation is underway. Increasing body temperature before this wilt only increase metabolic demand without increasing supply leading to an increased risk of ischemia. Many chemical parameters are of limited diagnostic value in hypothermic patients [8]. Increased levels of ASAT, ALAT, CK, CK-MB and LDH were found in our patient. We interpret this to be a result of hypoperfusion and relative hypoxia causing diffuse tissue damage. Despite severe hypoxia, acidosis, prolonged external cardiac massage, and an increase in isoenzyme CK-MB to 13% of the total CK activity, we found no signs of myocardial injury in serial ECG's and echocardiography.

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No coagulopathy was observed though a thrombocytopenia occurred early after rewarming. This has previously been described as a consequence of severe hypothermia [9], but in our patient factors such as extracorporeal circulatory devices and massive transfusion may have contributed to the thrombocytopenia. The low values for PaO2 despite continuous ventilation with 100%0 02 are hard to explain. Our case seems to demonstrate that tissue survival is possible in hypothermic subjects despite severe hypoxia [10]. Ethanol has been shown to reduce the threshold for lethal arrythmias by about 2 - 5 ~ [11, 12]. Thus, an adequate circulation can be maintained at a lower temperature. That our patient was ethanol intoxicated would be a factor in his favour. In conclusion, any patient with cardiorespiratory arrest due to severe hypothermia has the potential for complete recovery. Therefore extensive resuscitative efforts should be maintained for considerably longer periods than under normothermic conditions. Death cannot be appropriately diagnosed before the patient becomes normothermic. We support the idea of rewarruing by extracorporeal circulation even if the patient has to be transported to a hospital with such facilities. Such a strategy has recently been demonstrated as successful [2] and has previously been advocated by others [13]. Acknowledgement. Gratitude is expressed to Professor Per Lilleaasen, previous head of Department of Anesthesiology, Haukeland Hospital, University of Bergen, for support during the handling of this case.

References 1. Zell SC, Kurtz KJ (1985) Severe exposure hypothermia: a resuscitation protocol. Ann Emerg Med 14:339-345 2. Althaus U, Aberhard P, Sch~ipbach P, Nachbur BH, Mihhlemann W (1982) Management of profound accidental hypothermia with cardiorespiratory arrest. Ann Surg 195:492 - 495 3. Feiss P, Mora C, Devalois B, Gebeaux R, Christides C (1987) Hypothermie profonde accidentelle et arr~t circulatoire. Traitement par circulation extracorporelle. Ann Fr Anesth Reanim 6:217-218 4. Maningas P, Guzman L, Hollenbach S (1986) Regional blood flow during hypothermic arrest. Ann Emerg Med 15:390-396 5. Gillon J, Vogel M, Holterman R (1986) Ventricular fibrillat ion during orotracheal intubation of hypothermic dogs. Ann Emerg Med 15:412-415 6. Criley J, Niemann J, Rossborough J (1981) The heart is a conduit in CPR. Crit Care Med 9:373-374 7. Moss J (1986) Accidental severe hypothermia (Review). Surg Gynecol Obstet 162:501-513 8. Lonning PE, Skulberg A, A,byholm F (1986) Accidental hypothermia - review of the literature. Acta Anaesthesiol Scand 30:601-613

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P. Husby et al.: Recovery from cardiac arrest due to severe hypothermia

9. Villalobos TJ (1985) A cause of the thrombocytopenia and leukopenia that occurs in dogs during deep hypothermia. J Clin Invest 37:1 10. Hauty MG, Esrig BC, Hill JG, Long WB (1987) Prognostic factors in severe accidental hypothermia: experience from the Mt Hood tragedy. J Trauma 27:1107-1112 11. White DC, Nowell NW (1965) The effect of alcohol on the cardiac arrest temperature in hypothermic rats. Clin Sci 28:395-399 12. Webb WR, Harrison N, Dodds R et al (1968) Protective effect of ethyl alcohol in profound hypothermia. Cryobiology 4:290- 294

Correspondence A case of the peanut syndrome in an adult Dear Sir, The diversity of the pulmonary effects relating to the inhalation of peanuts is well described and the problems they present are particularly apparent in young children. We report an unusual case in which an adult developed severe arterial hypoxaemia which was probably inflammatory in origin and required prolonged mechanical ventilation and corticosteroid therapy. Our patient, whilst under severe emotional stress, inhaled some peanuts which he was eating. This incident resulted in a violent fit of coughing but over the next few days he became progressively breathless and cyanosed, and this led to him being transferred to The Intensive Care Unit 7 days after the incident. On admission to the Intensive Care Unit marked arterial hypoxaemia was observed (blood gas measurements - P a t 2 4.6 kPa, P a C t 2 4.6 kPa, Sa of 0.66 and inspired oxygen fraction 0.21). Fibreoptic bronchoscopy demonstrated very inflamed bronchi and a purulent plug of sputum partially obstructing the left main bronchus was removed. No foreign matter was observed. The patient required tracheal intubation, controlled ventilation with an inspired oxygen concentration of 66% and PEEP ranging from 5-15 cm water for a period of 3 weeks. On the 9th day the calculated pulmonary shunt was 36% and the static pulmonary compliance (syringe technique) was 80 ml/cm water. A thoracic CT scan on 14th day revealed bilateral alveolar consolidation affecting the upper lobar ventral segments, the medial segment of the middle lobe and the anterial and lateral segments of the lower lobe. His antibiotic therapy included Cefotaxime from the 7th to the l l t h day followed by Erythromycin. Viral serology and Legionella serology on several occasions were negative. In view of the severity of the acute respiratory failure and the possibility of a severe acute inflammatory reaction to peanut oil, a 10 days course of steroids (Prednisolone 1.5 mg/kg) was instituted on the 12th day, following an initial bolus of 1 g of Methylprednisolone intravenously. The patient's course was complicated by a nosocontial pneumonia (Klebsiella pneumoniae) and the an-

13. Kugelberg J, Schaller H, Berg B, Kallum B (1967) Treatment of accidental hypothermia. Scand J Thorac Cardiovasc Surg 1:142-146

Dr. P. Husby Department of Anaesthesiology University of Bergen Haukeland Sykehus N-5021 Bergen Norway

timicrobial therapy was modified on the 13th day to Pefloxacin and Amikacin. There was a gradual improvement from the 14th day, (blood gas measurements - P a t 2 9.3 kPa, inspired oxygen fraction 0.6 and PEEP 15 cm water) which was confirmed on a CT scan examination on 22nd day. The patient was discharged from the Intensive Care Unit after 3 weeks of assisted ventilation. Two months after the incident respiratory function tests revealed the following results: FEV 1 2.72L (predicted normal 3.40L), FEV 1/FVC) ratio 77%, and TLC 5.22 L (predicted normal 6.98 L). Whilst many cases of inhalation have been observed particularly in the paediatric population, it appears that inhaled vegetable substances are more noxious than other foreign matter such as metal or plastic. Apart from the problem of mechanical obstruction, there are the allergic and chemical reactions associated with antigenic protein (organic acids and oils) which may cause a pneumonitis. However, it is unusual to find such severe respiratory failure requiring prolonged mechanical ventilation as in this case, since the usual clinical picture consists of a chronic pneumonia with dilatation of the obstructed bronchi [1]. Peanut butter apparently produces a very severe inflammatory reaction increasing the obstructive element and leading to bronchiectasis, pneumonia and atelectasis as confirmed by autopsies [2]. In the case of our patient, it is possible that the pulmonary effects were due to an inflammatory reaction observed during the first bronchoscopy. In addition, it is possible that the 10 day course of steroids may have had a beneficial effect on the clinical, radiological and physiological evolution of the disease. Yours sincerely, P. Leroy, R. Dorne, B. Palmier, J.P. Baechle and J. Escarment

References

1. Aytac A, Yurdakul y, Ikizler C, Olga R, Saylam A (1977) Inhalation of foreign bodies in children: report of 500 cases. J Thorac Cardiovasc Surg 74:145-150 2. Atlas DH (1977) "Cafe coronary" from peanut butter. N Engl J Med 296:399 Dr. B. Palmier, Intensive Care Unit, Desgenettes Hospital, 108, Bd Pinel, F-69275 Lyon Cedex 03, France