D elayed recovery

1. Delayed recovery Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics PhD (physio) Mahatma Gandhi Medical college and research institute , puducherry , India

2. Definition • Recovery by definition • is “to regain possession of”. Whatever it is !!

3. In anaesthesia • It is the same • It is usually and conventionally ascribed to General anesthesia

4. What is the dynamics ?? • It is a spectrum of clinical condition varying • from a patient who has undergone a coronary surgery shifted on a ventilator • to a patient who underwent a curettage going home in two to three hours

5. When to say delayed recovery ?? • If a patient does not generate a meaningful, directed response to ordinary levels of verbal or tactile stimuli within 30 minutes of PACU admission, he or she is exhibiting prolonged unconsciousness that requires a differential diagnosis.

6. Definition of delayed recovery • Intriguing • . It can be simply stated that when the patient does not recover when he is supposed to. • The mode of recovery may vary with the technique of anesthesia used like intravenous, inhalational or using neuromuscular blockers.

7. Response to External Stimulus • Sharp loud voice telling the first name • Tactile stimuli • Pinch and pain but no physical injury • Trapezius squeeze test

8. Why we need to do better ?? • shorter-acting intravenous agents • lower solubility inhalational anesthetics, • and the use of depth of anesthesia indicators, such as end-expired volatile agents ,processed EEG monitoring.

9. Induction and recovery- differences • First, on induction the effect of solubility to hinder the rise in alveolar anesthetic concentration could be overcome by increasing the inspired anesthetic concentration– • the inspired concentration cannot be reduced below zero • Second, on induction all the tissues initially have the same anesthetic partial pressure-zero. On recovery the tissue partial pressures are variable.

10. Why should there be a delay ?? Exhaustive list

11. Causes of Prolonged Unconsciousness After Anesthesia • Residual sedation from opioids • Residual sedation from inhalational agents • Residual sedation from premedications antiemetics • Hypercarbia or hypocarbia • Hypoxemia • Hypothermia • Cerebral hypoperfusion • Hypoglycemia or hyperglycemia • Hyperosmolar or hypoosmolar states • Coexisting medical illness • Central neurologic events

12. Pneumonic • AROSE • SCOTCH

13. BASIC CARE • Airway – maintain a clear airway , give O2 reintubate if indicated • Breathing:- Ensure adequate respiration. If indicated ventilate the patient effectively via an endotracheal tube. Monitor SpO2. • Circulation:- Assess blood pressure, heart rate, ECG, Peripheral perfusion, conscious level and urine output. Resuscitate as indicated

14. Continue basics before steps for evaluation • Continue basics before steps for evaluation • Continue basics before steps for evaluation

15. Approach - Step 1 • STOP ALL THE ANAESTHETICS • Vaporisers switched off • Back flown drugs in the IV set removed • Change the breathing circuit • Check the machine and gas sources

16. Can we wash off this ?? Rectal drugs

17. Step 2 • LOOK FOR POSSIBLE CAUSE • The history, investigations and peri operative management including anaesth. chart and the timings of drug administration are analysed to spot a possible cause.

18. Take special note of preexisting medical conditions • cerebral vascular disease, transient ischemic attacks, stroke, intracranial tumor, cerebral aneurysm, or previous head trauma. • The presence of supraventriculardysrhythmias such as atrial fibrillation or flutter should lead one to consider the possibility of cerebral thromboembolism

19. Take special note of preexisting medical conditions --- contd • . A history of congenital heart disease, septal defect, endocarditis, or heart murmur may point toward paradoxical cerebral embolization with thrombus, vegetations, air, or fat. • Cirrhosis, chronic hepatitis, or other disorders of liver function may indicate an element of hepatic encephalopathy. • medications on a chronic basis

20. Intra op events • intraoperative events such as transient airway obstruction, • periods of low arterial oxygen saturation • prolonged decreases in systemic blood pressure, dysrhythmias, • or blood loss

21. Intra op events • Level of responsiveness before induction • Extreme or unusual intraoperative positioning • Interventions near the cerebral circulation

22. Intra op events • Intracerebral structures can be damaged during sphenoid sinus procedures or middle ear procedures • In patients with facial fractures or those who have undergone transsphenoidal surgery, the inadvertent passage of nasogastric or nasotracheal tubes through the cribiform plate into the intracranial cavity can obviously produce severe brain injury intraoperatively.

23. Midazolam is metabolized by the same P450 iso-enzyme as alfentanil, such that co administration prolongs the actions of both drugs.

24. STEP – 3 • ELIMINATION OF REMNANTS OF ANAESTHETICS IN THE PATIENT • 100% O2 for 10 – 15 minutes • IPPV • Hyperventilation • Forced diuresis

25. Sometimes these may not be eliminated herbal medications

26. STEP – 4 • WARMING THE PATIENT • Forced air warming with warm air blankets (Bair hugger) or similar device is the most effective method. • However wrapping in blankets and/or in foil sheets, ensuring the room is kept warm, and giving warm IV fluids, will all help.

27. STEP – 5 • CORRECTION OF METABOLIC ABNORMALITIES • Hypoglycemia: • Can occur in small children and those who have been given insulin or oral hypoglycaemic drugs. It may also occur in liver failure, in the presence of alcohol excess and in septicaemia and malaria.

28. Hypoglycemia • Diabetes, Starvation • Alcohol, Sepsis • Liver failure, Paediatrics • Sulphonylureas, Endocrine tumours • Hypo adrenalism

29. Step 5 - continued • CORRECTION OF METABOLIC ABNORMALITIES Hyperglycemia : May occur in decompensated diabetics i.e., hyperosmotic hyperglycaemic diabetic coma, or diabetic ketoacidosis

30. Hyperglycemia • Ketoacidosis • Hyperosmolar non ketotic acidosis (HONK) • Lactic acidosis • Gestational diabetes • Insulin resistance (acromegally, Cushing’s) • Pancreatitis

31. Step 5 - continued • ELECTROLYTE IMBALANCE: • This may be secondary to the underlying illness or as a consequence of the surgical procedure e.g., hyponatraemia occurring with trans-urethral resection or prostate (where glycine or other hypotonic fluid is used for irrigation).

32. STEP – 6 • SPECIFIC ANTIDOTES • NALOXONE 1 to 4 µg/kg IV, promptly reverses opioid-induced analgesia and depression of ventilation. The short duration of action of naloxone (30 to 45 minutes. • FLUMAZENIL

33. flumazenil • flumazenil is 0.2 mg (8 to 15 µg/kg), which typically reverses the CNS effects of benzodiazepine agonists within about 2 minutes. • duration of action of flumazenil is 30 to 60 minutes, • continuous low-dose infusion of flumazenil, 0.1 to 0.4 mg/hour.

34. Reversal Agents • There are no specific reversal agents available to barbiturates, propofol, phenothiazines, and butyrophenones. • The administration of intravenous physostigmine (1.25 mg) generates a degree of central arousal that can counteract, but not reverse, depression from sedatives, antiemetics, and other depressant medications such as baclofen

35. opioid narcosis - • pin point pupils and slow respiratory rate. In this situation a test dose of naloxone may be given: iv increments of 100 to 200 micrograms are usually sufficient

36. Combination • Sedatives , narcotics, minimal agent with hypercapnia just post op

37. Can happen from back- (centrineuraxial) • The inadvertent subarachnoid injection of local anesthetic in epidural • high concentrations of local anesthetic directly into the intracranial cerebrospinal fluid • Epidural opioid --- subarachnoid === conscious status ??

38. STEP – 7 • Residual neuromuscular blockade results in paralysis, which may be perceived as unresponsiveness though the patient may be fully conscious and aware. • NMJ monitoring

39. Three problems • Scoline apnea • Excess relaxants • Normal dose but more action • myasthenia gravis, muscular dystrophies, renal or hepatic diseases , amino glycosides

40. PRACTICE POINT - Relaxants • Avoid excessive doses of relaxants. • Intermediate acting drugs such as atracurium or vecuronium are easier to use than long acting ones. • Only give repeat doses when necessary (when there is evidence of muscle activity). • When giving repeat doses use 20-25% of the initial dose. • Wherever possible use a NMJ monitor to guide doses and assess reversal.

41. STEP – 8 • SUBSTITUTION THERAPY • Steroids • Thyroxin • Proteins • Antibiotics, • Fresh blood

42. These can also be reasons • Porphyrias • Hunter s syndrome • OSAS • Hypothyroid • Mucopolysacharidoses

43. Central anticholinergic syndrome • follow the use of anticholinergic drugs especially hyoscine, but also antihistamines, antidepressants, phenothiazines and pethidine. • physostigmine 0.04mg/kg slowly iv which acts within 5 minutes, but features may return after 1-2 hours.

44. STEP – 9 • NEUROSURGICAL OPINION AND INTERVENTION AS REQUIRED: • CT brain or anything suggested • In trauma patients or those requiring emergency surgery, the possibility of unrecognized head injury, asphyxia, or exposure to carbon monoxide, environmental toxins, or ingested poisons should be evaluated.

45. What Should Be Done When a Previously Responsive Patient Develops the Acute Onset of Unconsciousness? • Renarcotization,” “bi-phasic responses to opioids,” or “recurarization” are Untrue words and reasons

46. Goes back again ?? • Medication-induced loss of consciousness can occur in a postoperative patient • IV tubing flushing • CNS dysfunction

47. Abnormal position can lead on to -- • surgery is performed in the sitting position, especially with extreme flexion of the neck • Compression of the carotid arteries from external contact or a hematoma in the neck can also impede cerebral perfusion, particularly in patients with severe cerebrovascular disease.

48. Don’t compress neck • Intraoperative interference with cerebral venous return instigated by external compression of the jugular veins, high intrathoracic pressures, jugular venous cannulation, or extreme head and neck positioning can lead to cerebral edema, increased intracranial pressure, and cerebral hypoperfusion.

49. spurious unconscious state • Differentiating between an actual and spurious unconscious state is a clinical challenge. • In a supine patient who is feigning unconsciousness, dropping the patient's hand toward the face will often result in the arm falling to the side rather than toward the nose as gravity would normally direct it. • Bispectral index

50. diabetes insipidus • Delayed recovery from general anaesthesia • Case report • Possible cause = diabetes insipidus • Anaesthesia – 1988 – vol 43 – 1073