الفهرس 
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Abstract
SUMMARY
Wakefulness depends on diffuse cortical activation by the
reticular formation of the brain stem, though afferent sensory
stimuli mediated by reticular activating system (RM). Recent evi-
dence in human and experimental animals has shown that gen-
eral anaesthesia is produced by a variety of neurophysiologic
mechanisms at cortical or subcortical levels according to the site
and mechanism of action of the drug given. Thus mechanism of
prolonged narcosis following anaesthesia are drug dependent and
may involve neural stimulation or depression at cortical and sub-
cortical levels.
Causes of delayed recovery I-Prolonged action of anaesthetic drugs :
This occur in the following conditions :
1-Overdose of anaesthetic agent.
2-Increased central sensitivity due to age, biologic variation
and metabolic effects.
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3-Delayed anaesthetic excretion and decreased protein binding.
4-Anaesthetic redistribution.
5-Decreased hepatic metabolism, drug interaction and bio-transformation. II-Metabolic encephalopathy :
A number of systemic metabolic disturances resulting in CNS de-pression can occur in post anaesthetic period :
1-Liver and renal impairment :
Patients with liver disease and renal impairment can develop EEG slowing and CNS depression after small doses of barbiturates or narcotics. This is probably as a result of enhanced CNS sensitivity to barbiturates as well as decreased protein bind-ing, electrolyte disturbances and acid base inbalance involved this case.
2-Endocrinal disturbances :
Some endocrinal disturbances hypothyroidism, hy-popituitrism and adrenal insufficiency may be accompanied by prolonged postoperative unconsciousness.
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3-Hypoxia and Hypercarbia :
This may be due to postoperative respiratory failure which
can retard excretion of inhalation anaesthetics, CO2 narcosis can
occur in absence of hypoxia.
4-Acidosis :
Decrease in CSF pH due to various causes showing symp-
toms of mental confusion, delirium and coma.
5-Hypoglycemia and hyperglycemia :
Disturbed blood glucose level is a cause of metabolic en-
cephalopathy and prolonged narcosis.
6-Electrolyte disturbances :
Hyponatremia, water intoxication, hypocalcemia and hy-
permagnesaemia are all factors which may be associated with
delayed recovery.
7-Hypothermia and hyperthermia :
Hypothermia prolongs recovery by reduce the rate of bio-
transformation of depressant drugs by increasing the solubility of
inhalation anaesthetics and by direct hypothermic effect on the
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brain. Hyperthermia due to malignant hyperpyrexia one of the
most important cause of delayed recovery. III-Neurologic damage :
Cerebral ischaemia, haemorrhage or embolism can cause
failure to regain consciousness after general anaesthesia. 1-Cerebral ischaemia :
Patients undergone controlled hypotension may suffer
from cerebral hypoxia which leads to brain ischaemia.
2-Cerebral haemorrhage :
This may result secondary to hypotension evoked by
laryngoscopy and tracheal intubation.
3-Cerebral embolism :
Due to entraiment of air, fat or thrombus into the arterial
circulation. The embolus may be air in case of right to left shunt
or thrombus in case of calcified mitral or aortic valve or it may
be fat after bone fracture.
88 IV-Neuromuscular blockade :
Failure to regain respiration may be due to peripheral causes at neuromuscular junction as a result of succinylcholine apnea or prolonged non depolarizing block.