We have herein described a patient who developed TLOC immediately after TP. The most striking feature of this case was the mixed acid–base disorder with hyperglycemic state after pancreatectomy. Although it tends to be hyperglycemic state after TP, TLOC after TP has been reported as a result of hypoglycemic state [8,9,10]. Only one case was reported to be TLOC and die from diabetic ketoacidosis, but it occurred 5 months after surgery [8]. As far as we know, there has been no report regarding the case of TLOC immediately after TP accompanied by hyperglycemic state. Because the ∆PaCO2 was less than expected from the ∆HCO3 during the second episode of TLOC, the acidosis was considered to have been influenced by both metabolic and respiratory disorders [12,13,14]. Although consciousness disorder with hyperglycemic state is the same clinical condition as diabetic ketoacidosis, the serum ketone (β-hydroxybutyrate) concentration and anion gap are usually higher than in the present case [15]. Hyperventilation is a well-known compensatory mechanism in diabetic ketoacidosis, but it was interrupted by lingering effect of fentanyl in this case (pCO2 was 55.9 mmHg at the timing of TLOC). Therefore, although serum ketone level was not elevated very much, pH kept decreasing, which resulted in TLOC for this patient. From above the consideration, we considered that the metabolic acidosis and respiratory acidosis both worked on the occurrence of TLOC. The acidemia improved promptly and spontaneous ventilation recovered after the initiation of continuous insulin infusion and termination of fentanyl, supporting this possibility. Of course, fentanyl is well-known anesthesia medication to cause postoperative loss of consciousness independently. However, the fentanyl concentration of central nerve system analyzed by Tivatrainer software was low and decreasing at the timing of TLOC (Fig. 3). Therefore, fentanyl was not considered to be the only cause of TLOC. In this simulation, the possible change of fentanyl metabolism accompanied by surgery was not incorporated. However, the fentanyl metabolism was not considered to be altered through the TP, because the hepatic blood flow, which was thought to play the greatest effect on fentanyl metabolism [16], was not changed by this procedure. Also, the renal function of this patient was slightly deteriorated because of previous nephrectomy. However, the proportion of renal extraction of fentanyl is less than 8.0% [17], thus, the influence of which on fentanyl metabolism seemed low.
Other possible causes of TLOC include syncope and epileptic seizure [18,19,20]; however, both were unlikely in our patient. After the operation, continuous monitoring revealed stable vital signs and electrocardiographic indices. Furthermore, preoperative/postoperative CT and magnetic resonance imaging showed no signs of vascular disease, and the patient had no signs of syncope. TLOC due to epileptic seizure was also unlikely because he did not present with convulsions, and his serum lactate concentration remained stable. Electrocardiographic examination and magnetic resonance imaging on POD 10 and 11 showed no remarkable abnormalities.
TP changes glycometabolism in a dynamic manner because of the lack of glucose-raising and -lowering hormones. Despite the high frequency and severity of pancreatogenic diabetes after TP, no generally accepted guidelines on its management have been established [9, 21]. The American Diabetes Association suggests classification of pancreatogenic diabetes as type 3c and proposes glycemic management according to the guideline for type 1 diabetes; i.e., induction of continuous insulin infusion at 0.1 U/kg/h is recommended [9, 22,23,24]. In the present case, the continuous insulin infusion was not initiated until the second episode of TLOC because the postoperative blood glucose level was maintained at 140 to 190 mg/dL. Previous reports have indicated that intensive glucose control increases mortality among patients in the intensive care unit [25]. By contrast, some authors have proposed a target postoperative glucose level of < 140 mg/dL, which is associated with low rate of postoperative complications [21, 26, 27]. Thus, the optimal range of the glucose level after TP may be narrow, and frequent glucose checks are required. In this case, earlier intravenous insulin infusion with tight glycemic control might have prevented repeated TLOC. In Japan, perioperative safe and strict glycemic control using bedside artificial pancreas system has been developed since 2010 [28]. In this case, earlier insulin administration might prevent TLOC. Thus, more aggressive introduction of an artificial pancreas should be considered.
