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  2. INTRODUCTION • Delayed awakening from anaesthesia remains one of the biggest challenges involving an anaesthesiologist. • The principal factors responsible are anaesthetic agents and medications used in the perioperative period.
  3. DEFINITIONS • Recovery from anaesthesia may be defined as “a state of consciousness of an individual when he is awake or easily arousable and aware of his surroundings and identity” • Coma is derived from the Greek ‘koma’ meaning a state of sleep; & is defined medically as “a state of unresponsiveness from which the patient cannot be aroused”.
  4. PHASES OF RECOVERY FROM ANAESTHESIA • Divided into 3 phases : • Immediate recovery This consists of return of consciousness, recovery of protective airway reflexes and resumption of motor activity. This stage Usually lasts for a short time. • Intermediate recovery During this stage, the patient regains his power of coordination and the feeling of dizziness disappears. This stage usually lasts for 1 hr.
  5. • Long-term recovery There is a full recovery of coordination an higher intellectual function. May last for hours or even days
  6. MONITORING RECOVERY FROM ANAESTHESIA GLASGOW COMA SCALE By convention we use the GCS to provide a rapid,reproducible quantification of depth ofunconsciousness. Although the GCS was developed for assessment and prediction of outcome in traumatic brain injury, it remains a useful tool to assess conscious state regardless of the causative factor.
  7. Interpretation • Best possible score - 15 • Worst possible score - 3 • Score of < 8 - coma *When trachea is intubated then , verbal score is designated as “T” • Best possible score while intubated - 10T • Worst possible score while intubated - 2T
  8. DISCHARGE CRITERIA A.PACU Post Anaesthesia Aldrete Recovery Score
  9. B.OUTPATIENTS Post Anaesthesia Discharge Scoring System
  10. • Score of ≥ 9 is required for discharge. • Recovery of proprioception , sympathetic tone, bladder function & motor strength are additional criteria following regional anaesthesia.
  13. 1. EXTREMES OF AGE • Geriatric patient • Elderly patients have increased sensitivity towards general anaesthetics, opioids and benzodiazepines, and slow return of consciousness due to progressive decline in CNS function • The decrease in volume of distribution, clearance rate, and plasma protein binding results in high free plasma concentration of drugs
  14. • Furthermore, muscle relaxants if given on weight basis delay onset of action and prolong drug effect. • Paediatric patients • Because of larger body surface area, heat loss is greater in children resulting in hypothermia, slow drug metabolism, and delayed return of consciousness
  15. 2. GENDER • Men are 1.4 times more likely to have delayed recovery than women. • Lower sensitivity to the hypnotic effect of anaesthetics in women may account for their faster recovery. • The female sex hormone was postulated to play a role in the gender differences in recovery time.
  16. 3. GENETIC FACTORS • Unexpected responses and prolonged somnolence after specific anaesthetic are commonly associated with a genetic defect of the metabolic pathway of the agent or its receptor. • Polymorphic changes in gamma-aminobutyric acid 2 receptor can adversely affect the rapid reversal of propofol anaesthesia. • Also, variable prolongation of suxamethonium apnea Is due to abnormal or absent plasma cholinesterase enzyme
  17. 4. CO-MORBIDITIES • Pre-existing cardiac and pulmonary disease require adjustments in anaesthetic doses to avoid delayed emergence. • Significant lung disease decreases the ability to wash out inhalational agents. • Congestive heart failure and decreased cardiac output prolong somnolence.
  18. • The renal or hepatic disease can prolong action of anaesthetic agents dependent on hepatic metabolism or renal excretion. • Subclinical hypothyroidism may be diagnosed for the first time as hypothermia and delayed emergence. Response to l-thyroxin and thyroid profile will confirm the diagnosis. • Adrenal insufficiency can also present as delayed recovery.
  19. 5. BODY HABITUS • Obesity with increased fat mass requires higher drug doses to attain the same peak plasma concentration than a standard sized person. • Underweight patients are having a higher risk of slow recovery after vascular surgery and cardiopulmonary bypass graft surgery.
  20. 6. COGNITIVE DYSFUNCTIONS • Patients with Parkinson's disease are more prone to postoperative confusion and hallucinations. Inhaled anaesthetic agents have complex effects on brain dopamine concentrations. • Patients with Down's syndrome or mental retardation are particularly susceptible to delayed awakening. • IV sedation in cerebral palsy increases the risk of hypoxia, and delayed recovery of >60 min is expected.
  21. 7. SEIZURES • A postictal state may well mimic unconsciousness. • Antiepileptic drugs are known to reduce the responsiveness of neuromuscular blocking . agent when given chronically
  22. 8. STROKE • Surgical procedures with increased risk of embolization are coronary artery bypass graft, orthopedic particularly joint replacement surgery, peripheral vascular surgery, and valvular and aortic surgery. • Fat embolism from closed chest massage, corticosteroid therapy, or tissue trauma may present as delayed return to cognitive function.
  24. 1. RESIDUAL DRUG EFFECTS • A heavy premedication or the relative overdose of general anaesthetic agents may be the cause of delayed awakening.
  25. 2. POTENTIATION BY OTHER. DRUGS • Drugs such as tranquilizers, antihypertensives, anticholinergics, clonidine, antihistamines, penicillin-derived antibiotics, amphotericin B, immunosuppressants, lidocaine, and alcohol will potentiate the CNS depressant effects of anaesthetic drugs and delay emergence from anaesthesia.
  26. 3. DRUG INTERACTIONS • Patient taking MAOIs or SSRIs may experience severe drug interactions with IV agents that can result in hyper/hypotension and postoperative coma or a full-blown serotonergic syndrome. • lithium, ondansetron, metoclopramide, codeine, fentanyl, and oxycodone are among many others.
  27. • Patients taking bromocriptine or pergolide are prone to excessive vasodilatation exacerbating hypotension • Pharmacological interactions with neuromuscular blocking agents such as aminoglycosides, diuretics,calcium channel antagonists, lithium, polymyxinB, echothiophate, OCPs, LA etc., will prolong neuromuscular block • Neurotoxic effect of chemotherapeutic drugs such as l-asparaginase and vincristine can also produce CNS depression.
  28. 4. DURATION AND TYPE OF ANAESTHETIC USED • The selection of anaesthetic technique and anaesthetic drugs determines the duration of unconsciousness • Recovery may be delayed if soluble volatile agents are continued until the end of surgery or long-acting drugs are given toward the end of the procedure
  29. OPIOIDS • Opioids produce analgesia, sedation and respiratory depression. • Dose–response is affected by co-administered sedatives and analgesia and by patient factors. • There are two major mechanisms resulting in coma: respiratory depression and direct sedation via opioid receptors. • The sensitivity of the brainstem chemoreceptors to CO2 is reduced by opioids with consequent dose- dependant respiratory depression and resultant hypercapnia.
  30. • This may affect clearance of volatile agents and CO2; both can cause unconsciousness. • Active metabolites of morphine and meperidine(pethidine) prolong the duration of action, especially in the presence of renal failure. • T/t – I.V. Naloxone @ 0.5-1 mcg/kg every 3-5 mins , until adequate ventilation or alertness is achieved. Max 0.2 mg.
  31. BENZODIAZEPINES • Benzodiazepines are used for anxiolysis & premedication; co-induction facilitates the hypnotic and sedative properties of other agents. • Used alone, benzodiazepines are unlikely to cause prolonged unconsciousness except in susceptible, elderly patients or when given in overdose. • However, CNS depression can prolong the effects of other anaesthetic agents.
  32. • Benzodiazepines combined with high-dose opioids can have a pronounced effect on respiratory depression, producing hypercapnia and coma. • T/t – I.V. Flumazenil @ 0.2 mg/min untildesired degree of reversal is achieved . Usually total dose is 0.6 – 1 mg.
  33. INTRAVENOUS ANAESTHETIC AGENTS • Propofol has a large volume of distribution at steadystate and a relatively long elimination half-life. The effect of propofol after TIVA is prolonged. • Delayed emergence from thiopentone is observed in Huntington's chorea • Norketamine contribute in prolonging the effect of ketamine • Duration of unconsciousness is affected by context sensitive half-life, amount of drug, co-administration with other drugs, and patient factors.
  34. VOLATILE ANAESTHETIC AGENTS • Emergence from volatile agent anaesthesia depends upon pulmonary elimination of the drug and MACawake • The speed of emergence is directly related to alveolar ventilation and inversely related to blood gas solubility. • Hypoventilation lengthens the time taken to exhale the anaesthetic agent and delays recovery.
  35. • Prolonged duration of anaesthesia causes increased emergence time due to tissue uptake depending upon the concentration used and drug solubility. • If vaporizers are not calibrated correctly, higher than expected dose may be delivered, especially if end tidal drug concentrations are not measured. • Release of bromide ions after halothane anaesthesia may produce postoperative drowsiness.
  36. NEUROMUSCULAR BLOCKERS • Occurs secondary to absolute or relative overdose or incomplete reversal of nondepolarizing muscle relaxants or in a patient with suxamethonium apnea • The patient may become distressed or agitated, typically twitchy movements of partial reversal may also be seen. • Electrolyte disturbances cause cell-wall hyperpolarization and prolong block.
  37. • Hypothermia decreases metabolism and acidosis donates protons to tertiary amines, increasing receptor affinity. • Prolonged apnea following suxamethonium is due to abnormal or absent plasma cholinesterase enzyme • Acquired cholinesterase deficiency is seen in pregnancy, liver disease, renal failure, starvation, and thyrotoxicosis.
  38. • Patients with myasthenia gravis are very sensitive to nondepolarizing muscle relaxants. • Increased sensitivity to muscle relaxants is also seen in patients with muscle dystrophies • T/t – Cholinesterase inhibitors for antagonism of non-depolarising neuromuscular blockers.
  39. LOCAL ANESTHETIC SYSTEMIC TOXICITY • Repeated doses of local anaesthetics in highly vascular area, intracranial spread of local anaesthetics after spinal anaesthesia, or accidental subarachnoid injection during epidural or interscalene brachial plexus block may cause prolonged somnolence, seizures, coma, and cardiorespiratory arrest
  41. 1. HYPOGLYCAEMIA • Hypoglycemia can occur in children with prolonged fasting. • It may also occur in starvation, liver failure, end-stage renal disease, alcohol intoxication, septicemia, and malaria. • As the brain is totally dependent on glucose for energy, hypoglycemia may manifests as restlessness, sweating, confusion, blurring of vision or diplopia, seizures, and coma.
  42. • Diabetic patients on insulin and/or oral hypoglycemic may sometimes present with hypoglycemia and delayed emergence. • Salicylates and ethanol given preoperatively may exacerbate hypoglycemia in starved patients. • Hypoglycemia can occur during manipulation of insulin-producing tumor of pancreas or retroperitoneal carcinoma.
  43. Causes of hyperglycemia and hypoglycemia
  44. 2. HYPERGLYCAEMIA • Hyperglycemia occurs in known diabetics as a result of inadequate provision of insulin or injudicious glucose supplementation. • Hyperglycemia in hyperosmolar hyperglycemic nonketotic acidosis causes an osmotic diuresis and intracellular dehydration.
  45. • The effects of dehydration range from drowsiness to acidosis. • Intraoperative cerebrovascular accident may occur as a result of cerebral vascular occlusion, especially in patients with micro..or macrovascular disease. • Diabetic ketoacidosis, stress response of prolonged surgery, and. dexamethasone therapy can also lead to severe hyperglycemia.
  46. 3. HYPONATRAEMIA • Mild hyponatraemia is usually asymptomatic, but serum sodium concentration <120 mmol/litre may cause confusion and irritability. Serum sodium concentration <110 mmol/litre causes seizures, coma and increased mortality. • Cerebral salt-wasting syndrome may also occur in the brain injured patient, and infusion of mannitol can futher cause dehydration. Here, sodium loss from the kidneys is thought to be mediated by ANP secretion. Cerebral oedema results in cerebral irritation and coma.
  47. • Fluid overload and hyponatraemia may occur when large volumes of glycine solution,is a hypotonic solution (220 mmol /litre) is absorbed by open venous sinuses during TURP, i.e. TURP syndrome which results in pulmonary oedema and cerebral oedema causing variable cerebral signs, including coma. • SIADH can result from brain trauma, subarachnoid haemorrhage and administration of drugs (e.g. opioids, haloperidol, vasopressin).
  48. • T/t –Sodium deficit = total body water (TBW) × (desired serum Na − measured serum Na), where TBW = body weight (kg) × Y. , Y= Children 0.6 Adult male 0.6 Adult women 0.5 Elderly male 0.5 Elderly women 0.45
  49. • Correction rates – • Mild symptoms - @ 0.5mEq/L/hr or less • Moderate symptoms - @1 mEq/L/hr or less • Severe symptoms – @1.5 mEq/L/hr or less • Pharmacotherapy • Demeclocycline • Vaptans (conivaptan & tolvaptan)
  50. 4. HYPERNATRAEMIA • Hypernatremia (plasma Na+ >145 mmol/L) during hepatic hydatid cyst removal may also hinder the process of recovery from anesthesia due to cerebral dehydration, vascular rupture, and intracerebral hemorrhage. • Symptoms include thirst, drowsiness, confusion, and coma.
  51. Hypernatremia Water and Na* loss Water loss. Increased Na+ content Replace isotonic loss Replace water deficit Loop diuretic Replace water deficit Replace anv water deficit Algorithm for TT for hypernatremia
  52. • T/t - Water deficit (L)= total body water(TBW) x [(measured Na /140)-1] • This deficit is replaced gradually over 48 hrs. • Most commonly used fluid for correction of hypernatraemia is 5% Dextrose in water
  53. 5. HYPOKALEMIA • Hypokalemia intensifies the effects of nondepolarizing muscle relaxants. • Respiratory alkalosis with PaCO2 <36 mmHg results in reduced intracellular proton concentration and draws K+ into the cells. • There is a reduction of 0.5 mEq/L of K+ per 10 mmHg reduction of PaCO2.
  54. • Hypokalemia can also occur with perioperative use of diuretics, calcium gluconate, sodium bicarbonate, β-adrenergic agonists, glucose, and/or insulin without K+ supplement • Mild preoperative hypokalemia without any clinical features could rapidly deteriorate after iatrogenic hyperventilation or surgical stimulation and delays recovery
  55. • T/t – • Approximately 200 mEq potassium deficit is required to decrease serum potassium by 1 mEq/ L in the chronic hypokalemic state. • In acute situations, the serum potassium concentration falls by approximately 0.27 mEq/L for every 100 mEq reduction in total body potassium stores. • Peripheral iv correction with KCl should not exceed 8 mEq/hr.
  56. • Through central venous catheter , correction @ 10-20 mEq/hr may be administered. Max 240 mEq/day.
  57. 6. OTHER ELECTROLYTE IMBALANCE • Hypocalcemia after thyroid or parathyroid surgery, hypermagnesemia after MgSO4 therapy in preeclampsia, and severe hypercalcemia produce CNS depression.
  58. 7. URAEMIA • Uraemia results in dehydration and cerebral effects attributable to cellular damage and distortion. • The clinical effects of uraemia are varied, but intracerebral changes may produce drowsiness , confusion and coma
  59. 8. HYPOTHERMIA • Neurological and respiratory changes occur with decreasing temperature, e.g. confusion (<35°C), unconsciousness (<30°C), apnoea (<24°C), absent cerebral activity (<18°C). • The direct hypothermic effects on brain tissue are compounded by cardiovascular and respiratory disturbance at less profound degrees of hypothermia.
  60. • Cardiac output decreases with a decrease in temperature and arrhythmias occur. Low cardiac output affects circulation and drug pharmacokinetics, as well as tissue perfusion.
  61. 9. HYPERTHERMIA • Temperature above 40°C leads to loss of consciousness . • Skeletal muscle destruction after malignant hyperthermia can delay recovery from anaesthesia.
  63. • Postoperative respiratory failure causes hypoxaemia, hypercapnia or both. • The causes of respiratory failure may be classified into neurological, pulmonary, and muscular. • Central drive is lost during drug overdose, with intracranial pathology and in patients with COPD or sleep apnoea. • Ventilation is affected by primary muscle problems, metabolic imbalance, obesity and residual neuromuscular block.
  64. • Hypoxaemia with continuing blood supply causes less damage than complete interruption of perfusion, because toxins are removed. • HYPERCAPNIA • Detected by central chemoreceptors, initially stimulates respiration but thereafter depresses the regulatory respiratory centres of the brain causing hypoventilation and apnoea.
  65. • Respiratory acidosis results from hypoventilation rendering the patient acidaemic. • Hypercapnia in a head-injured patient with impaired cerebral autoregulation causes vasodilatation and a consequent increase in intracranial pressure which may result in secondary brain injury
  67. • The common mechanism is ischaemic brain destruction. • Periods of hypoxaemia or ischaemia may occur during surgery; these are often a result of inadequate cerebral perfusion secondary to MAP. • Cerebral autoregulation in the normal brain occurs between 60 and 160 mm Hg MAP. • Carotid surgery and operations in a sitting position present a high risk of hypoperfusion
  68. • Intracranial haemorrhage, thrombosis or infarction can occur in association with intraoperativearrhythmias, hypo- or hypertension, or in patients with abnormal cerebral vasculature. • The outcome from ischaemic events varies between discrete functional deficits, hemiparesis and coma. • In the brain with impaired autoregulation, injury may be caused by hypercapnia, hypoxaemia, low MAP and increased metabolic rate
  69. • Cerebral hypoxaemia may result when epileptic seizures are masked by neuromuscular block, and from intraoperative air embolism. • Finally, the spread of intracranial local anaesthetic can cause unconsciousness. POSTOPERATIVE NEUROEXCITATORY SYMPTOMS • symptoms such as twitching, myoclonic movements, opisthotonus, and seizures can present during induction, maintenance as well as recovery from anaesthesia
  71. CENTRAL ANTICHOLINERGIC SYNDROME • Historically, anticholinergic syndrome was a commonly encountered sequel to anaesthesia • It is thought to be due to a decrease in inhibitory anticholinergic activity in the brain • Symptoms range from cerebral irritation with delirium and agitation to CNS depression with stupor and coma. These accompany peripheral anticholinergic effects i.e. tachycardia, blurred vision, dry mouth and urinary retention.
  72. • The symptoms are rapidly reversed by physostigmine. • Anti-Parkinsonian, antidepressant and antihistaminic drugs can cause central anticholinergic syndrome
  73. Other rare causes include : – Dissociative coma, – myxedema coma, – thyroid failure, – hunter syndrome (mucopolysaccharide storage disease), – valproate toxicity, – drug abuse, and – lidocaine infusion for arrhythmias
  75. CENTRAL NEURAXIAL BLOCK • Vascular malformations and anticoagulant therapy with increased pressure in the vertebral venous plexus are common causative factors. Diagnosis is established by MRI. • Narrowed epidural spaces, migration of epidural catheter, intrathecal migration of the drug, faulty infusion pump, potentiation by fentanyl and clonidine are possible mechanisms for prolongation of block
  76. PERIPHERAL NERVE BLOCK • Patients with underlying nerve pathology such as diabetic neuropathy, exposure to neurotoxic chemotherapy, or disruption of neural blood supply are more susceptible to peripheral nerve complications. • Neurological deficits may persist for days after high pressure intraneural injection of local anaesthetics.
  77. WOUND INFILTRATION • Brainstem paralysis due to bupivacaine wound infiltration after foramina magnum decompression and field block is also reported
  79. Unresponsive patient Stop all the anaesthetics and stimulate the patient • Vaporizers switched off • Change the iv set • Change the breathing circuit • Check machine and gas source Basic care -Assess vital signs and GCS • Airway - maintain clear airway • Breathing - ensure adequate respiration ,continuous positive airway pressure /intermittent positive pressure ventilation indicated • Circulation - Assessed BP ,HR, ECG, Peripheral perfusion, urine output vasopressors as indicated
  80. looks for possible cause • Review history and investigation - seizures ,diabetes mellitus,Renal or hepatic disease • Review anaesthetic chart - Drug dosage, timing of drug administration • Other perioperative management • Full clinical assessment, neurological examination, Check pupillary response Examination of remnanants of anaesthetics in the patients • 100% O2 for 10-15 min • Hyperventilation • forced diuresis warming the patient - Measure the temperature, warm if <35 cel • Forced air warming ( warm/ Bair Hugger) • wrapping in blanket / foil sheets • the room is kept warm • warm iv fluids
  81. Correction of metabolic abnormalites: Perform ABG - Check oxygenation,co2,blood sugar,electrolytes • Hypogycemia IV dextrose if < 3mmol per liter • hyperglycemia - Insulin • Hyponatremia - 2 mmol/l/hr until the plasma sodium is 120 mmol/ l • Acidosis Reversal of residual NMB • Neostigmine, sugammadex,ulinastetin,milrinone • Amino acide infusion • Substitution therapy - steroids, thyroxine,proteins,antibiotics,fresh blood • Lipid emulsion therapy for local anaesthetic toxicity - 1.5 ml/ kg bolus of 20% intralipid followed by 0.25 ml / kg/min for 10 min Max. 10ml/ kg over 30 min
  82. • Neurological opinion - Stroke therapy ( tissue plasminogen activator) • Monitor the patient in intensive care unite with frequent neurolical examination • Repeat CT scan in 6-8 hours if no improvement
  83. SUMMARY • Delayed recovery from anaesthesia is often multifactorial, and anaesthetic agents may not always be the culprit. • When other causes are excluded, the possibility of acute intracranial event should be strongly considered. • While the specific cause is being sought, primary management is always support of airway, breathing, and circulation.
  84. • Good intraoperative care ensures the patient safety • A calm, comprehensive, and timely management with a systematic approach is highly rewarding. • We, the anaesthesiologists, make the patient sleep, so the recovery from anaesthesia is our responsibility.