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The Cryonics Institute’s 89th Patient: By Ben Best

by System Administrator / Friday, 30 May 2008 /

The 89th patient of the Cryonics Institute is a German woman who deanimated in Switzerland on the day following her 80th birthday. The woman's only son had moved to Switzerland 20 years ago. When her husband died 14 years ago she moved to Switzerland to live with her son.

Cause of cardiac arrest was not determined. Three years previously she had experienced a Transient Ischemic Attack (TIA) from which she recovered. She also had signs of arrhythmias. But immediately prior to deanimation she was simply "sick", finding it hurtful to eat and drink.

Arrangements were made for CI Scientific Advisor Klaus Sames and a German Alcor Member to do standby for the patient in Switzerland. But these men were still on their way to Switzerland when deanimation occurred early in the morning of Friday, May 30, 2008. Klaus Sames submitted the following report of his connection to this case:


On Thursday 29.5.08, 6.30 p.m. German time, Barry Fowden informs Klaus Sames about a patient in Switzerland. The son of the patient has already been in preliminary contact with the DGAB and with CI. Klaus calls the son, who explains that his mother has been chronically ill and is now in terminal condition. She was visiting her son in Switzerland and is now checked into a small hospital. The doctors are unsure of the prognosis, stating that she might die in next hours or might make it another week or two. Klaus tells the son to speak with the doctors about cooling and medicine and asks him to find ice before arrival of the mortician and try to produce some circulation of ice water around the patients head. The son asks if Klaus can come to Switzerland to help him out.

Klaus proposes to send the doctors an email with instructions as a first step and then to consult the other German cryonicists for help. Torsten Nahm is ready to accompany for a standby. Torsten organizes the travel, while Klaus corresponds with the doctors.

Klaus and Torsten plan some type of limited standby with the option to leave after about 3 days. If the patient has not deanimated by then, they will leave detailed instructions with the son and the doctors. Klaus informs the son about the time of arrival. Following this, the German team is informed by email about the arrangements.

Klaus leaves Hamburg at 3.17 a.m. on Friday by train, with Torsten to join him when the train stops at Frankfurt at 7.45 a.m. At around 5.30 a.m. the son calls Klaus on his cell phone and informs him of the deanimation of the patient. The night doctor is with the son. Klaus speaks to her and discovers that unfortunately the email with instructions had not reached her. Klaus repeats the instructions by phone and asks if there is any ice in the hospital, but the doctor seems somewhat helpless. He urges her to apply 100000 U heparin and do a heart massage. She says that she cannot make this decision, but promises to pass it on to the physician in charge. She also does not know if a venous catheter has been left in place. The patient is already in the cooling room. Torsten and Klaus abort the standby.

At around 6 a.m. Torsten calls the son and urges him to get the doctors to apply ice and heparin, but he seems rather passive. Torsten then calls the mortician, and reaches him at 6.30 a.m. The mortician informs him that the heparin has been applied, but that no ice had been applied before his arrival.

At around 4 p.m. Mr Fowden informs Klaus that the patient had deanimated at 4.50 a.m. and that the local mortician had arrived at 6 a.m. Unfortunately, he was not able to obtain the necessary papers for patient transport to Detroit before the weekend.


The British-born and enthusiastically-friendly Frankfurt funeral director Barry Fowden arranged for a direct flight to Detroit from Frankfurt for Saturday, May 31, but this plan was thwarted by new (Spring 2008, since the time of CI's Australian patient in March 2008) shipping regulations imposed by American authorities on human remains entering the United States. As if the problems of out-of-country shipment of cryonics patients were not bad enough, the new regulations require approval by the US Health Department and State Department. There is only a narrow window daily in which the overlap of business hours in the United States and Europe allow officials to speak with each other. The American Consulate now insists on an original death certificate and will no longer authorize shipment on the basis of a FAXed copy. Cause of death on the death certificate must comply with American standards, not European standards. These regulations are not specific to cryonics, but apply to all shipment of human remains into the United States.

The patient arrived in Michigan on the afternoon of Tuesday, June 3rd after having spent several days sitting in Barry Fowden's cooler while packed in ice. The patient had suffered more than five days of cold ischemic time before perfusion was begun.

The patient's son requested perfusion of the body as well as the head. In the past, efforts to perfuse the bodies of patients who have experienced long ischemic. times have been forced to stop due to edema. Using glycerol rather than ethylene glycol in the body seems to increase the ability of the bodies of ischemic patients to tolerate body perfusion.

Clamped vessels
[ Clamped vessels ]

The plan was to use the same perfusion method as had been used for the previous patient (CI's 88th patient), namely open the chest and perfuse into the ascending aorta. The expectation was that when the body became edematous, vessels leading to the body (descending aorta and subclavial arteries) would be clamped. Then perfusion to the head would continue until the refractive index of the effluent from the superior vena cava indicated that the brain was vitrified.

Jim Walsh, CI's funeral director, opened the chest by cutting the rib cage on both sides using a scalpel rather than the sternal saw. He refused to cut the sternum until I got him a "chest spreader". He said that cutting ribs with a scalpel would result in less damage than using the sternal saw. Nonetheless, vessels were severed and for the entire perfusion he was suctioning blood from the chest cavity. There was evidence of clotting.

Cryonicist Mike Darwin had advocated that CI begin perfusion with 5% glycerol rather than 10% so as to reduce damage to endothelial cells and thus reduce edema. CI had stopped beginning perfusions with pure washout solution (carrier solution) because beginning with 10% solution seemed to result in less edema. I thought that beginning with 10% glycerol might be better than beginning with 10% ethylene glycol because glycerol is more dehydrating.

The patient was perfused with 7 liters of 10% glycerol followed by 1.5 liters of 10% ethylene glycol and then 4 liters of 30% ethylene glycol. THe patient received a full 24.3 liters of 70% CI−VM−1.

The 10% solutions were perfused at over 2 liters per minute, with pressures of under about 90 mmHg. Although line pressure is still being measured, the values should be much closer to patient perfusion pressure than was the case with the metal cannulae because the single cannula has a wide (8 millimeter diameter, "24 French") mouth. With the 30% ethylene glycol flow rate was dropped to 1.68 liters per minute at a pressure of about 100 mmHg. Perfusion with 70% CI−VM−1 began with a flow rate of 1.13 liters per minute and a pressure of 105 mmHg. As the perfusion with CI−VM−1 proceeded flow rate continued to be reduced to compensate for rising pressure. At the end of the perfusion flow rate was down to 0.43 liters per minute with a pressure of 117 mmHg.

The previous patient, who had experienced only 7 hours of cold ischemia was perfused in the same manner as this patient and showed no sign of edema whatsoever, despite receiving some of the 70% CI−VM−1 in her body. But this patient, who had experienced over 5 days of cold ischemia, showed considerable edema -- as expected, but not where expected. There was no evidence that the legs were perfused at all, as their appearance remained unchanged throughout the perfusion. The arms seemed to perfuse perfectly, first dehydrating and then rehydrating with cryoprotectant. There was swelling of the abdomen, but this was not as serious as had been seen with previous cases where abdominal swelling caused body perfusion to stop.

There was bad edema to the head, however, which was very swollen. It seems likely that there was edema to the brain also. Burr holes have traditionally been used to monitor brain edema in cryonics, but the burr holes used in CI perfusions have been too small in diameter to allow visualization of the brain. No burr holes were made in this case. It would be good to know about brain edema, but that knowledge would not have changed the procedure. The operating assumption that a swollen head means a swollen brain is reasonable, but confirmation would help.

At some point in the perfusion (there was a deficiency in record keeping which prevents me from knowing exactly when) the descending aorta and the subclavian arteries were clamped. Unlike the case with the previous patient where effluent from the superior vena cava became clear, at not time did effluent from the superior vena cava ever show an absence of blood. The refractive index of the effluent rose to about 1.41, which would indicate adequate brain vitrification IF the brain had been saturated at that level. More likely, however, edema prevented much of the brain from being saturated with CI−VM−1. The best we can say is that the patient did receive cryoprotectant to her brain and that freezing damage was reduced below what it would have been if no perfusion had been performed.

For the next patient we receive which has experienced considerable ischemic damage, I will direct that more concentrated cryoprotectant be introduced much sooner in the hope that the risk of osmotic shock will be more than offset by the possibility of greater dehydration and less edema. If this works, in the future we will tailor the perfusion protocol to the patient rather than continue to search for a perfusion protocol which is to be applied uniformly to all patients, irrespective of their history of ischemic damage.

For this patient three suture rings were used on the cannula in the ascending aorta rather than one, and at no time did the cannula slip from the aorta. Unfortunately, when Mr. Walsh removed the cannula at the end of perfusion he lost two of the suture rings in the patient.

Temperature control was a bit better with this patient than with the previous one. The patient had been packed in finely crushed ice which was excellent for cooling the head. Nasopharyngeal temperature was maintained below 6.7ºC, and reached as low as 3.8ºC. Lower temperatures have been achieved with other patients when perfusing with cold CI−VM−1 from the freezer. This is another indication that head and brain perfusion was poor because of the edema. As per usual, when perfusion was finished the patient's head was surrounded with dry ice pellets in a slurry of isopropyl alcohol during transport from the funeral home to the CI facility.

Cooling curves for CI Patient 89
RED=under skull skin (controller), GREEN=naso-pharyngeal (brain core), BLUE=body
Full 4 days First 19 hours
[ Full  4 days ] [ First 19 hours ]











The patient received the usual cooling protocol for a vitrification patient. Cooling took place over four days, with initial cooling as rapid as possible down to about −115ºC for the brain surface temperature (skull, controlling temperature), with another half-out of cooling for brain surface to reach −120ºC. Brain surface temperature was held at −120ºC for 15 hours. It took about six hours for brain surface temperature to drop to between −115ºC and −120ºC, after which time brain cor (green) temperature more slowly approached brain surface (red) temperature.


Cooling curves for CI Patient 89
RED=under skull skin (controller), GREEN=naso-pharyngeal (brain core), BLUE=body
3 hours of annealing Last 56 hours
[ 3 hours of annealing ] [ Last 56 hours ]











Between about the 16th and 17th hour an attempt was made to warm the brain surface temperature about 4ºC from −120ºC to −116ºC. Although the brain surface temperature briefly rose above brain core temperature, the lasting effect was not very great -- meaning there was not much increase in brain uniformity or closeness of brain surface and core temperatures.

By about 45 hours the body temperature came within 10ºC of brain temperature. Whereas the temperature fluctuations of the controlling thermocouple (red) in under the skin of the skull (brain surface) were in a range of about 2ºC at 50 hours (−150ºC), the range had increased to about 5ºC at 80 hours (−180ºC). This was probably due to an increasing relative warming effect of the residual nitrogen gas in the pipes on the ambient temperature in the cooling box as the temperature of the box (and the patient) got lower.

Cooling curve for CI Patient 89
RED=under skull skin (controller), GREEN=naso-pharyngeal (brain core), BLUE=body
Last 20 hours
[ Last 20 hours ]












In the last hour of cooling, brain core and body temperature plummeted to liquid nitrogen temperature not long after the brain surface temperature reached liquid nitrogen temperature. This is due to a "dousing" effect of the liquid nitrogen from the cooling bar in the cooling box as brain surface temperature reaches liquid nitrogen temperature. The liquid nitrogen from the cooling bar increasingly becomes a spray rather than a vaporizing liquid, thereby dousing the patient with liquid nitrogen.

The patient was wrapped in her sleeping bag, tied to her backboard, and placed in an HSSV cylindrical cryostat.