Prolonged coma after anesthesia.

Anesthesiologists are pretty much the only doctors who induce controlled and reversible coma medically in their daily practice. The word “coma” derived from a Greek word “Koma” signifies a state of sleep. In medical terms it is defined as a state of unresponsiveness from which the patient cannot be aroused.[1] Therefore any delayed recovery is viewed as anesthetic problem.

Delayed recovery from anesthesia or coma after anesthesia is a major anesthetic complication. The causes for delayed recovery from anesthesia are many. They are patient, surgical, anesthetic, and pharmacological factors. The pharmacological factors include the use of various anesthetic and adjuvant drugs, and their interactions with other drugs, known or unknown. This depends upon the pharmacokinetics, pharmacodynamics, context sensitive half-lives, amount of drug administered, accidental administration, co-administration with other drugs etc. The patient factors such as the extremes of age, obesity, and various co-morbidities like the cardiovascular, renal, liver or other major organ dysfunction can potentiate the effects of the drug used. Some of the rare causes are myxoedema coma, drug toxicity and Addison's disease. However the delayed recovery due to anesthetic causes, excluding hypoxia, usually lasts for a few hours to days.[1]

In the case report published in this issue, the coma lasted for >4 weeks. The authors have eliminated most of the causes of delayed recovery from anesthesia. However the hypoglycemia was detected in the postoperative period when the patient did not recover from anesthesia. The history obtained later revealed that the patient had taken long acting insulin in the preoperative period. The blood sugar level on the morning of surgery was borderline. No blood sugar was estimated during the entire surgical procedure. These factors could have led to profound and prolonged undetected hypoglycemia, which could have led to delayed recovery.

Hypoglycemia of prolonged duration (>30 min) leads to neuroglycopenia and brain damage.[2] The symptoms depend on level of blood glucose and also on time taken to detect and correct hypoglycemia. Even after correcting hypoglycemia, prolonged coma is observed in critical care units. It can produce a variety of symptoms and effects, but the principal problem arising from an inadequate supply of glucose to the brain is impairment of function (neuroglycopenia). Effects can range from mild dysphoria to more serious issues such as seizures, unconsciousness, and (rarely) permanent brain damage and death.[3] Plasma glucose levels are maintained between 4 and 8 mmol/L (72–144 mg/dl) throughout the 24 hours. 3.3-3.9 mmol/L (60-70 mg/dl) is cited as lower limit of blood glucose. However hypoglycemic symptoms do not occur till 2.8-3.0 mmol/L (50-54 mg/dl) of plasma glucose. Under anesthesia hypoglycemic symptoms are not detected. In the case presented the blood glucose level 5 h after preoperative value was 2.2 mmol/L (40 mg/dl). To detect hypoglycemia causing brain damage electroencephalography (EEG) and diffusion-weighted imaging of magnetic resonance imaging (MRI) are useful, both in detection and prognostication. EEG shows theta waves and lambda waves with definite slowing, flat and burst suppression patterns. In this case the EEG changes observed point to hypoglycemia as the factor leading to delayed recovery.

There have been reports of hyper-intense signal intensities in diffusion-weighted (DW) MRI in hypoglycemia.[4] Recently different patterns of DW MRI findings involving the internal capsules, corona radiata and frontoparietal cortex in a patient who recovered from prolonged hypoglycemic coma without neurological deficit have been observed. Therefore, this particular modality might have been useful in diagnosis and prognostication.[5]

Volatile anesthetics have been found to produce neuroprotection in various paradigms. The preconditioning by these agents partially protects perirhinal cortex and striatal dependent functions against moderate to severe neonatal hypoxia-ischemia.[6] Although previous morphological data have suggested that cells die by necrosis, experimental research showed neuronal damage after hypoglycemia has features of apoptosis.[7]

After exclusion of organic and pharmacological causes, coma may be attributed to a dissociative stupor. Reported delays in return to consciousness span time periods from 2 to 30 h, and longer periods of amnesia thereafter. There are four reports in the literature; each excluded other pathology with extensive examination, laboratory tests and radiological imaging. One individual experienced this phenomenon on three separate occasions after tracheal stenosis repairs.[89]

Conclusion

Delayed recovery is usually multifactorial. In the present case report, it looks more like prolonged hypoglycemia leading to delayed recovery. A differential diagnosis of dissociative stupor can be considered when other causes are excluded. The lesson one has to learn as a perioperative physician is to assess the patient thoroughly and investigate according to the need and evidence. An arterial blood gas and blood sugar estimation are needed in prolonged surgeries with multiple co-morbidities particularly in obese individuals.