Accidental Hypothermia

Core Rewarming with Partial Bypass

Per Wickstroti, MD,’ Minneapolis, Minnesota

Ernest Ruiz, MD, Minneapolis, Minnesota

0. Patrick Lilja, MD, Minneapolis, Minnesota

J. Peter Hinterkopf, MD,t Minneapolis, Minnesota

.iohn J. Haglin, MD, PhD, Minneapolis, Minnesota

Accidental hypothermia due to exposure is not un-

common and can result in a high mortality [l-6].

Although successful resuscitation without active

rewarming has been reported [2,5], profoundly hy- pothermic patients will often reach a state of poiki- lothermia in which the normal physiologic mecha-

nisms of conserving heat are lost [S]. These patients

then must be actively rewarmed. There are essentially two methods of active re-

warming: the external and the internal. External rewarming of profoundly hypothermic patients has

been accomplished with warming blankets [ 741 and with submersion in a warm bath [8,9]. Internal re-

warming has been conducted successfully in a variety

of ways. Linton and Ledingham [ID] and Coughlin

[II] performed thotacotomy on their hypothermic patients, both of whom had lapsed into ventricular

fibrillation. They rewarmed the hearts by bathing them in warm fluid while administering internal cardiac massage. After the hearts were rewarmed,

they were defibrillated. Lash, Burdette, and Turan [12] employed peritoneal dialysis to rewarm a hy- pothermic young woman. Several physicans have

now reported single cases of profoundly hypothermic patients, some of whom were in ventricular fibrilla-

tion, successfully resuscitated by utilizing partial bypass with the heart-lung machine and the heat exchanger [13-171.

There are problems with external rewarming that make internal rewarming the method of choice in

severe cases when it is available. With external re- warming an initial vasodilatation takes place that can result in hypotension or “rewarming shock.” With internal rewarming the cardiac output is increased as the vasodilatation occurs, thus making “rewarming shock” less likely [3]. Furthermore, external re-

From the Departments of Surgery and Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota.

Reprint requests should be addressed to Ernest Ruiz, MD, Hennepin County Medical Center, Fifth and Portland South, Minneapolis, Minnesota 55415.

* Present address: Ellsworth AFB Hospital, Ellsworth AFB, South Dakota 57706 (until July 1976).

+ Present address: Treasurer, Sudan Interior Mission, Cedar Grove, New Jersey 07009

warming increases the metabolic needs of the pe-

ripheral tissues before increasing tissue perfusion,

whereas just the opposite is true with internal methods. Therefore, subsequent tissue loss should

be less with internal rewarming [6].

There also appears to be several theoretic advan- tages to partial bypass over other methods of internal

rewarming. Partial bypass can be instituted rapidly,

using local anesthesia and a groin incision, with little morbidity and mortality. It is the fastest method of

rewarming reported so far and it provides the obvious advantage of circulatory support in a situation in which potentially fatal arrhythmias are likely to

occur. Our experience with central rewarming of pro-

foundly hypothermic patients utilizing partial bypass

consists of three patients.

Case Reports

Case I. The patient (MP), a sixty-five year old white woman, was brought to our emergency room on the after- noon of April 7, 1972 after being found lying on the floor of an abandoned building. On arrival she was unresponsive and flaccid with fixed and dilated pupils. The cardiac monitor revealed ventricular fibrillation. Rectal temper-‘ ature was 25OC (VP). Initial blood gas data was pH 7.31, pCOs 59 mm Hg, ~0s 28 mm Hg, potassium 6.5 mEq/L, and hemoglobin 16.9 gm/lOO ml. The blood gases were not corrected for temperature and were thought to be from venous blood.

Initial resuscitative measures included intubation, ventilation, external cardiac massage, and intravenous sodium bicarbonate. After several unsuccessful attempts at electroversion, the patient was prepared for partial by- pass with cannulation of the right femoral artery and right iliac vein.

One hour after admission, bypass was started. It was continued for an hour and twenty-five minutes during which time the patient was warmed from 25’ to 33V. Blood gas analysis obtained while the patient was on by- pass revealed pH to be 8.21, pCOs 9 mm Hg, and ~0s 600 mm Hg. Because of a lack of improvement in the patient’s neurologic signs and the refractivity of the ventricular fi-

622 The American Journal cl Surgery

Accidental Hypothermia

brillation to electroversion after partial rewarming, the situation was considered futile and the resuscitation was stopped.

Case II. The patient (SW), a forty-five year old Indian woman with a history of a seizure disorder and alcohol abuse, was found the morning of December 7,1973 lying in a snowbank and was brought to our emergency room. On arrival she was comatose with a temperature below 20°C (68OF) which was the lowest reading on our electronic rectal temperature ‘probe. Other vital signs were not recorded except that the pulse was slow and respirations were shallow.

She received ventilation with a mask and bag and several unsuccessful attempts at intubation were made. Thereaf- ter, a cardiac monitor revealed ventricular fibrillation. The patient was successfully intubated, external cardiac mas- sage was begun, and a bicarbonate drip was started. Several attempts at electroversion were of no avail. Blood gases, uncorrected for temperature, with the patient on a respi- rator using 100 per cent oxygen, and after approximately 70 mEq of sodium bicarbonate had been infused, were pH 7.83, pCOz 32 mm Hg, and PO:! 368 mm Hg. The potassium was 3.5 mEq/L and hemoglobin was 14.7 gm/lOO ml.

One hour after admission the patient was placed on partial bypass by cannulation of both iliac veins and the left common femoral artery. A flow of 1,700 cc/min was obtained (37.6 cc/kg/min). External cardiac massage was continudd until electroversion was successful. Two at- tempts were made to defibrillate the heart when the pa- tient’s temperature was between 29’ and 32’C. These re- sulted in short runs of normal sinus rhythm which reverted to ventricular fibrillation. When the patient’s temperature reached 33’C, she was successfully defibrillated.

A bypass of forty minutes was needed to warm the pa- tient to 37’C. After discontinuing bypass the patient’s temperature dropped rapidly to 34°C. Another ten minutes of bypass were needed to rewarm the patient to 37’C. This time the temperature stayed up after cessation of the by- pass. To come off the heart-lung machine with a blood pressure above 90 mm Hg and a central venous pressure of 8 cm of saline, 2 units of blood were added to the crys- talloid prime and 1,000 cc of extra volume was given to the patient.

Postoperatively the patient needed potassium replace- ment and additional volume loading for the ensuing twelve hours. Except for a transient rise in the serum glutamic oxalacetic transaminase, renal and hepatic function tests showed no abnormality. Despite prolonged external cardiac massage she complained of no chest pain except on deep inspiration. Her sensorium cleared after the first postop- erative day. The only complication was pneumonia of the lower lobe of the right lung which responded to pulmonary toilet and antibiotics. She was discharged on the ninth postoperative day with no apparent residual deficits.

Case III. The patient (MB), a sixty-four year old white man, was brought to our hospital early on the morning of

December 31,1973 after being found lying on the sidewalk near his home. He was comatose with a blood pressure of 68 mm Hg systolic and a pulse of 24 beats per minute. Rectal temperature was 23,8OC (75’F). The hands were frozen solid as were the lower extremities below the knees. The cardiac monitor revealed an idioventricular rhythm. X-ray films confirmed the presence of a fracture of the right humerus.

The patient was intubated carefully and respirations were assisted. He was not treated with hyperventilation. Blood gases uncorrected for temperature were pH 6.95, pCOz 50 mm Hg, and ~02 92 mm Hg. The potassium was 5.6 mEq/L and the hemoglobin 16.8 gm/lOO ml. Bicar- bonate was infused slowly as the operating room was readied.

Two hours after the patient entered the hospital, partial bypass was begun via cannulation of the left femoral artery and left iliac vein. At a flow of 1,300 cc/min (19 cc/kg/min) it took one hour and forty minutes to rewarm the patient from 24’ to 37’C. During this time, blood gases and K potassium were monitored every fifteen minutes. A total of 264 mEq of sodium bicarbonate and 10 mEq of potas- sium chloride were given in slow infusions during the by- pass to,achieve the values of pH 7.36 and potassium 3.6 mEq/L at the end of the bypass. While being rewarmed, the patient’s cardiac rhythm changed from a slow idio- ventricular rhythm to atria1 fibrillation with a ventricular response of 120 beats/min and then to a normal sinus rhythm. The initial central venous pressure was 21 cm of saline. After the bypass it was 4 cm of saline, despite the addition of 1 unit of blood to the crystalloid prime and the termination of bypass with 700 cc transfused from the pump to the patient. During bypass the blood pressure rose from 70 mm Hg systolic to 110 mm Hg as measured by a cuff on the left brachium. There was no urine output during, rewarming. Consequently, 640 mg of furosemide were given in increments.

Postoperatively there was a voluminous response to the furoaemide which necessitated vigorous water and potas- sium replacement for twenty-four hours. The patient had a short attack of what appeared to be delirium tremens. Thereafter, he showed no detectable neurologic abnor- malities. A week after admission the humeral fracture was plated.

During the ensuing months the patient underwent transmetatarsal amputation of one foot but lost no other tissue. A pleural effusion which was present on admission x-ray film persisted despite tube drainage. An open drainage with pleural biopsy was therefore performed. This revealed an adenocarcinoma metastatic to the pleura. Additional workup failed to locate the primary lesion. The patient is now living at home and doing well.

Comments

Recent experience with accidental hypothermia

together with the uiork carried out in the 1950’s and

early 1960’s on therapeutic hypothermia for open

heart surgery provides information that should be of

vohmo 131, May 1979 623

Wickstrom et al

use in the treatment of future hypothermic patients with partial bypass.

The resuscitative effort, once it is begun, should be vigorous and prolonged. It may have been ter- minated too early in our first patient. Popular signs of a fruitless effort such as flaccidity and fixed pupils are not very meaningful in the profoundly hypo- thermic patient [16]. In fact, the patient may be mistaken for dead and yet recover completely with proper treatment [12]. It has been stated that the only criterion for death in the hypothermic patient is the irreversibility of hypothermia [3]. Experi- mentally, hypothermic animals have survived com- plete cardiac arrest for over an hour [18], so the ne- cessity of a prolonged resuscitative effort should not be a source of discouragement. Our second patient, who had ventricular fibrillation, received external massage for an hour before being placed on bypass. Fell et al [15] supported their patient with external massage for three and a half hours, yet she showed no permanent neurologic deficit after rewarming on partial bypass.

Care should be taken not to precipitate ventric- ular fibrillation. In virtually every reported case of successful resuscitation of a hypothermic patient in ventricular fibrillation, including our patient in case II, the fibrillation developed after the patient had entered the hospital. This propensity to fibrillation during resuscitation has been attributed to several factors. The degree of oxygenation and the acid-base status of the patient are important and will be dis- cussed subsequently herein. Ventricular fibrillation in the hypothermic patient has been attributed to the nasopharyngeal stimulation associated with intu- bation [15,19]. Negovskii [18], however, has shown that any physical stimulus can trigger the onset of ventricular fibrillation in hypothermic monkeys. Therefore, gentleness in all handling of hypothermic patients is advised.

Hypothermic patients should be kept well oxy- genated and pH must be monitored closely. At normal temperature the ventricular fibrillation threshold is decreased by acidosis and increased by alkalosis [21]. In hypothermia, however, the oxy- hemoglobin saturation curve is shifted to the left, that is, the affinity of hemoglobin for oxygen is greater at any given ~0s. This shift is accentuated by alkalosis. Therefore, because oxygen is not released, the tissues, including the myocardium, may become hypoxic during profound alkalosis and hypothermia. Edmark [21] and Carson et al [22] have recom- mended induced acidosis by adding hydrochloric acid or carbon dioxide as a means of increasing oxygen availability and thus preventing ventricular fibril-

lation during hypothermia. Others [23] have dis- puted this. Most physicians now working with ther- apeutic hypothermia seem to try for a normal pH. This usually means adding bicarbonate during the rewarming phase [24]. Those who have mentioned the acid-base status of their patients with accidental hypothermia have tended to overtreat [15,16], as have we. Our first two patients received too much bicarbonate, and in our first case this may have ac- counted for our inability to defibrillate the patient after she had been partially rewarmed. In our third case the modification of our bicarbonate infusion by frequent monitoring of blood gases may have allowed us to complete the resuscitation without the devel- opment of ventricular fibrillation.

Blood gas measurements in the hypothermic pa- tients .must be corrected for temperature. This is because in most laboratories the gases are measured with the electrode at normal body temperature. In hypothermia, the amount of gas contained in blood for a given partial pressure is greater than that in normothermia. So if blood is drawn anaerobically from a hypothermic patient and warmed for mea- surement, the partial pressure of a gas will rise [25]. The magnitude of the rise in both ~0s and pCOs in the profoundly hypothermic patients presented herein would be roughly 100 per cent. Formulas have been worked out for this [26], but perhaps the best quick reference is the graph constructed by Marshall and Gunning [25]. It should be remembered that although the PO:! and pCOz will rise when a sample is heated for measurement, the gas content of that sample has not changed.

pH measurements are also altered by hypothermia. If blood is drawn from a hypothermic patient and the pH is measured at normothermia, the value obtained will be falsely acidotic. The pH fall is related to the rise in pCO2 [21]. The magnitude of the pH decrease can be simply calculated with the Rosenthal formula [27] which states that for each 10°C (WF) below normothermia, approximately 0.15 should be added to the measured pH to obtain the true pH. Therefore, in our third patient, who was hospitalized with a temperature of 24°C and a measured pH of 6.95, the actual pH would be calculated as follows: he was approximately 13’C below normal, so 13/lO of 0.5 or 0.20 should be added to the measured pH. The actual pH was 6.95 + 0.20 = 7.15.

Potassium concentration also needs special at- tention in the hypothermic patient. Changes in blood pH cause serum potassium shifts in the oppo- site direction. Also, as renal function recovers during rewarming, the potassium concentration in the urine may be higher than normal [28]. In our two survivors,

624 The American Journal of Surgery

Accidental Hypothermia

large quantities of potassium were needed in the early postoperative period.

A certain amount of “rewarming shock” can be expected even with internal rewarming. Both of our survivors needed extra fluid in order to come off partial bypass with a normal blood pressure and normal central venous pressure. Hypothermic pa- tients have vasoconstriction and decreased intra- vascular volumes [29]. In our patients this was evi- denced by elevated hemoglobin levels in each case. On rewarming, the vasoconstriction is released. Then signs of hypovolemia must be searched for and treated quickly.

Pneumonia often develops in patients with pro- found accidental hypothermia after rewarming. Pneumonia developed in most of the patients re- ported on in the literature [13-171 as it did in one of our survivors. This has not been emphasized pre- viously. Consideration should be given to prophy- lactic treatment such as intermittent positive pres- sure breathing and antibiotics for anticipated pul- monary complications.

Summary

Three patients with profound hypothermia were treated by rewarming on partial bypass. Two sur- vived and have normal mental and metabolic func- tions. The resuscitation of the hypothermic patient should be approached with enthusiasm since the outcome is often much better than expected from initial vital signs and neurologic examination. To avoid ventricular fibrillation the patient should be handled gently and an effort should be made to keep the patient well oxygenated and the pH normal. Blood gases should be measured often and corrected for temperature. The potassium concentration and hydration status of the patient should also be moni- tored closely.

The rewarming of profoundly hypothermic pa- tients can readily be accomplished with a pump ox- ygenator and heat exchanger. The indications for this method are not established from our small experience and the few cases reported in the literature. Certainly ventricular fibrillation is a compelling indication. Patients with frozen extremities might also benefit from this method since theoretically tissue salvage would be increased. Finally, those patients who do not respond rapidly to external rewarming may be at less risk of ventricular fibrillation if rewarmed on bypass.

References

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29. Talbott JH, Consolazio WV, Pecora W: Hypothermia: report of case in which patient died during therapeutic reduction of body temperature, with metabolic and pathologic studies. Arch Intern Med68: 1120, 1941.

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