Background Delayed recovery is multifactorial and includes drug, patient, and procedural factors, acid-base, metabolic or electrolyte abnormalities, hyper/hypothermia, respiratory disorders, and neurological... [ view full abstract ]
Background
Delayed recovery is multifactorial and includes drug, patient, and procedural factors, acid-base, metabolic or electrolyte abnormalities, hyper/hypothermia, respiratory disorders, and neurological complications. Central anticholinergic syndrome (CAS) should be explored as a diagnosis of exclusion. Its clinical spectrum ranges from a depressed to an excitatory state, and if suspected, should be treated with empiric doses of intravenous physostigmine for resolution of symptoms. 1-2
Case Description
A 69-year-old female with morbid obesity, hypertension, atrial fibrillation, obstructive sleep apnea, coronary artery disease, and type 2 diabetes, was scheduled for urgent laparoscopic cholecystectomy. Prior general anesthetics were uncomplicated. The patient was induced with fentanyl, lidocaine, and propofol. After muscle relaxation with rocuronium and intubation, anesthesia was maintained with sevoflurane. After an uneventful intraoperative course, she was given adequate neuromuscular blockade reversal with neostigmine, had sustained tetany for 5 seconds on ulnar nerve stimulation, and met all reasonable criteria for removal of her airway.
Upon PACU arrival, the patient was deeply stuporous and severely hypoxemic. Despite quick resolution of her hypoxemia with bag mask ventilation, she remained unresponsive. Initial ABG showed mild respiratory acidosis with normal electrolytes and glucose. She was hyperventilated but remained unresponsive to aggressive stimulation despite hemodynamic stability and normothermia. Pupil size and reactivity were normal. Another 0.5 mg of neostigmine was given for possible residual blockade. Narcan was dosed without effect. Benzodiazepene antagonism was not indicated.
CAS was considered, and physostigmine 0.5 mg was given with concomitant stroke code activation. Two minutes later, she had a significant response (spontaneous eye opening, tracking, moving all four extremities to pain, and improved respiratory effort). She relapsed and became obtunded after ten minutes. Physostigmine 1 mg, divided over several minutes, was re-dosed with another significant, albeit short-lasting response. A repeat ABG showed worsening respiratory acidosis. She was re-intubated with propofol. At the same time, another dose of physostigmine 0.5 mg was given. After less than one minute on the ventilator, the patient was responsive, tracked, and followed commands in all extremities. Because the stroke code was already activated, she was sedated for a stat CTA brain that was negative and monitored in the ICU. She was extubated several hours later and remained at her pre-op mental status until discharge.
Discussion
CAS is associated with anticholinergics and a long list of other drugs commonly used in the perioperative anesthetic. The diagnosis can be mistaken for prolonged duration of anesthetics, so it is likely underdiagnosed and reported. In our scenario, the diagnosis was delayed. Physostigmine should have been given at a higher initial dose of 0.04 mg/kg i.v. and repeated at 10-30 minute intervals for its short plasma elimination half-life. The centrally-acting anticholinesterase has minimal peripheral side effects in this range and could have avoided costly consultations, diagnostics, intensive care resources, and patient morbidity.2-3
References
- Misal US, et al., Anesth Essays Res 2016;10:164-72
- Martin, B. and Howell P.R., European Journal of Anaesthesiology 1997; 14: 467-470
- Katsanoulas K, et al. Eur J Anaesthesiol 1999; 16: 803-809.
