The homeostasis values are unremarkable; central neurological causes must be considered. Even though there is no suspicion of a cerebral perfusion disorder, hypotensive or hypoxic phases during the anesthesia – especially caused by the abrupt alleviation of long-standing hypertension – could explain the confusion.

Clinical experience shows, however, that there isn’t always a clear, direct correlation between postoperative confusion and hypotension and hypoxemia during general or regional anesthesia techniques. A possible explanation is that pulse oximetry and blood pressure are very unreliable measurements of brain perfusion. In order to detect perioperative cerebral ischemia, the markers for neuronal damage, e.g., the neuron-specific enolase of the calcium binding Protein S100B, must be measured [5]. Both markers, however, have the disadvantage that false-positive elevations lead to incorrect diagnosis. They are therefore only recommended in organic brain disorders which result from traumatic brain injury, stroke, or subarachnoid hemorrhage.

Apart from the organic changes, residual anesthetic agents or known paradoxical medication effects (such as that of benzodiazepine in elderly patients) must be taken into consideration.

Lastly, a central anticholinergic syndrome (CAS) could explain the signs and symptoms.

>> Mrs. Baker was now beet red in the face, felt hot, and was flailing about wildly in bed. The nurses made every attempt to calm her and explain where she was, but it was useless. Mrs. Baker believed that she was on a farm and she was shooing away all the nurses who had nothing to do with her farm.

Dr. Benjamin was impressed with the nurses’ determination to calm the patient, but the nurses gave him accusing looks. He must find help.

The findings can’t be explained by any other cause, so CAS is the most likely diagnosis.

The pathophysiological cause of CAS is a functional block of central and peripheral muscarinic choline receptors or deficiency of acetylcholine in synaptic space [4]. The functional block can occur directly (e.g., by belladonna alkaloids, antipsychotics, antidepressants, antihistamines, Parkinson’s medications) or indirectly (through opioids, IV and volatile anesthetics, local anesthetics, benzodiazepines, H₂ receptor blockers).

Trigger substances are lipophilic and penetrate the blood–brain barrier. The diagnosis is difficult, because the clinical picture is complicated and the clinical presentation can vary. The fearful, agitated type symptoms with hallucinations – sometimes accompanied by myoclonus and seizures – is differentiated from the type predominated by a decrease in the level of consciousness – and possible coma and apnea. Following anesthesia, the prolonged somnolence is more common than the agitated form [7]. The symptoms of CAS are divided into central and peripheral (Table 19.2). When CAS is suspected, at least one central and two peripheral symptoms must be present for diagnosis. If the CAS suspicion arises after an anesthesia during which muscle relaxants were antagonized with peripheral cholinesterase inhibitors, the peripheral symptoms may be absent.