Download Delayed recovery mgmc

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
 Recovery by definition
 is “to regain possession of”.
Whatever it is !!
 It is the same
 It is usually and conventionally ascribed to General
anesthesia
 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
 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.
 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.
 Sharp loud voice telling the first name
 Tactile stimuli
 Pinch and pain but no physical injury
 Trapezius squeeze test
 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.
 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.
Exhaustive list
 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
 AROSE
 SCOTCH
 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
 Continue basics before steps for evaluation
 Continue basics before steps for evaluation
 Continue basics before steps for evaluation
 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
Rectal
drugs
 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.
 cerebral
attacks,
vascular disease, transient ischemic
stroke,
intracranial
tumor,
cerebral
aneurysm, or previous head trauma.
 The presence of supraventricular dysrhythmias
such as atrial fibrillation or flutter should lead one
to
consider
the
thromboembolism
possibility
of
cerebral
 . 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
 intraoperative events such as transient airway
obstruction,
 periods of low arterial oxygen saturation
 prolonged decreases in systemic blood pressure,
dysrhythmias,
 or blood loss
 Level of responsiveness before
induction
 Extreme or unusual intraoperative
positioning
 Interventions near the cerebral
circulation
 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.
Midazolam is metabolized by the
same P450 iso-enzyme as alfentanil,
such that co administration
prolongs the actions of both drugs.
 ELIMINATION OF REMNANTS OF
ANAESTHETICS IN THE PATIENT
 100% O2 for 10 – 15 minutes
 IPPV
 Hyperventilation
 Forced diuresis
herbal medications
 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.
 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.
 Diabetes, Starvation
 Alcohol, Sepsis
 Liver failure, Paediatrics
 Sulphonylureas, Endocrine tumours
 Hypo adrenalism
 CORRECTION OF
METABOLIC ABNORMALITIES
Hyperglycemia
:
May occur in decompensated
diabetics i.e.,
hyperosmotic hyperglycaemic diabetic coma, or
diabetic ketoacidosis
 Ketoacidosis
 Hyperosmolar non ketotic acidosis (HONK)
 Lactic acidosis
 Gestational diabetes
 Insulin resistance (acromegally, Cushing’s)
 Pancreatitis
 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).
 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
 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.
 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
 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
 Sedatives , narcotics, minimal agent
with hypercapnia just post op
 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 ??
 Residual
neuromuscular blockade
results in paralysis, which may be
perceived as unresponsiveness though
the patient may be fully conscious and
aware.
 NMJ monitoring
 Scoline apnea
 Excess relaxants
 Normal dose but more action
 myasthenia gravis, muscular dystrophies,
renal or hepatic diseases , amino glycosides
 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.
 SUBSTITUTION THERAPY
 Steroids
 Thyroxin
 Proteins
 Antibiotics,
 Fresh blood
 Porphyrias
 Hunter s syndrome
 OSAS
 Hypothyroid
 Mucopolysacharidoses
 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.
 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.
 Renarcotization,” “bi-phasic responses
to opioids,” or “recurarization” are
Untrue words and reasons
 Medication-induced loss of consciousness
can occur in a postoperative patient
 IV tubing flushing
 CNS dysfunction
 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
particularly
impede
in
cerebral
patients
cerebrovascular disease.
perfusion,
with
severe
 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.
 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
 Delayed recovery from general anaesthesia
 Case report
 Possible cause = diabetes insipidus
 Anaesthesia – 1988 – vol 43 – 1073
 medical risk and expenditure of
resources
 Staff
 Cost
 unresponsiveness may be due to
Deafness
 Tell them to breathe – sometimes
apneic spell are reversed with this
 Language – know to ask in patients
known language
Algorithm
follows
Assess ABC
100% Oxygen, airway adjuncts,
manual ventilation
GCS – stimulate
History, drugs , chart
Glucose, temperature
Arterial blood gas
analysis
Clinical , tests
Where ? Dissociative
test
Naloxone,Flumazenil
Neostigmine,Doxapram
Correct
Correct hypoxia, hypercapnia or
Acidosis , electrolytes
CT head – consider
 “IT IS WE WHO PUT THE PATIENT TO SLEEP
 SO, IT IS WE WHO MUST WAKE THE PATIENT
UP”
 Thank you all