In the morning of the following day (the seventh hospital day), his blood pressure further dropped to 75/48 mmHg with sinus tachycardia with a pulse rate of 115 beats/min while he was restlessly moving around with substantial diaphoresis. He insisted that a patient in the unit was his close relative, and he spoke with for a long time, although the person was in fact a stranger to him. His laboratory data (Table
1) showed that he had acute renal failure with a creatinine level of 3.43 mg/dl, which had been 0.59 mg/dl 3 days earlier, and a blood urea nitrogen level of 40.4 mg/dl, which was low at 6.9 mg/dl 3 days earlier. Retrospectively, the patient’s hypotension since the afternoon of the sixth hospital day could not be attributed to overuse of nitroglycerin because the half-life of nitroglycerin oral spray is only ~ 40 min (
https://www.rxlist.com/nitrolingual-pumpspray-drug.htm#description). The fact that his hypotension after the overuse improved in an hour without any intervention supports this view. Also, his hypotension is not considered to be caused by hypotensive drugs, i.e., telmisartan and bisoprolol fumarate, because he had taken them for 7 years without any side effects. A gradual decline in fluid infusion after admission is unable to explain his hypovolemia because it was replaced by his oral food intake and he had consumed almost the full amount of food he was offered when his alcohol withdrawal syndrome was severe (from the fifth to seventh hospital day) and when his hypovolemic shock was observed on the seventh hospital day (Table
1). Although urine output was unable to be measured from the six hospital day due to psychiatric symptoms associated with alcohol withdrawal syndrome, the amount of his total urine output on the fifth hospital day was 1000 ml, suggesting fluid control was well managed at least until the fifth hospital day. Similarly, it is difficult to attribute his hypovolemia only to his fever because his fever on the sixth hospital day only lasted several hours before his hypovolemic shock occurred on the morning of the following day (the seventh hospital day). These data suggested that hypovolemia due to excessive diaphoresis and high fever was the mechanism underlying these medical conditions, i.e., hypotension and acute renal failure. Elevated levels of albumin and hemoglobin on the fourth and seventh hospital days were also indicative of hypovolemia, along with the urine specific gravity of 1.030, which is the upper limit of its normal range. Elevated level of white blood cell count on the seventh hospital day was most likely caused by physical stress with regard to hypovolemic shock as well as fever [
11]. Delirium was considered to be a result of alcohol withdrawal syndrome because other potential factors associated with delirium were ruled out: his serum levels of ammonia and sodium remained normal, and serum glucose was above the lower limit of the normal range (Table
1), suggesting the absence of hepatic encephalopathy, hyponatremia, or hypoglycemia. Likewise, a possibility that hypovolemia and its medical consequences themselves might have caused delirium can be ruled out because his alcohol withdrawal syndrome started with insomnia and tachycardia on the fourth hospital day, when no hypovolemia or renal failure were observed (Table
1). No neurological findings were revealed except for tremor, a hallmark of alcohol withdrawal syndrome, suggesting that no brain damage had occurred, which can also cause delirium. In particular, no signs of Wernicke encephalopathy were found, e.g., ophthalmoplegia, nystagmus, or ataxia, which results from vitamin B-1 deficiency mainly due to alcohol use disorder. It was considered possible that his acute renal failure was caused by rhabdomyolysis, but this was not the case for this patient because his elevation of creatine phosphokinase was 1211 IU/L (Table
1), which is less than 10 times the upper limit of the normal range (248 IU/L × 10, or 2480 IU/L), a standard criterion for rhabdomyolysis [
12]. In addition, the prompt resolution of the acute renal failure contradicts the relatively long duration of renal failure caused by rhabdomyolysis, the resolution of which takes an average of 11 days (7–17) [
13].