case 81 - delayed emergence, coma, brain death Flashcards
What are possible anesthesia caues that can lead to delayed emergence? How would you tx these causes?
Delayed emergence can be due to: anesthesia medications, metabolic derangements, neurologic insult, and pre-existing toxins.
Anesthesia medication effect
1) Prolong BZD
* reverse with flumazenil, IV 0.2 mg up to 1mg
2) prolong opioid
- pinpoint pupils, slow resp rate, high tidal volume
- dx and tx = carefully titrate naloxone IV 40mcg increments up to 400 mcg
- complete opioid redrawl –> tachy, HTN, inc ICP, MI, dysrythmias
3) residual anesthesia (IV or inhaled)
- analyze expired conc of volatile anes
- review anes chart to see meds given prior to emergence
4) residual neuromusclar blockade
-
check TOF (TOF > 0.9 is adequate)
- TOF taken in normal neuromusclar junctions (do not place on hemiplegic areas).
- admin more reversal (neostigmine)
you determine the patient has inadequate reversal of neuromuscular blockade. You attempt to reverse again with neostigmine, but this is inadequate reversal. What could be reasons for prolonged NMBD bockade?
neuromuscular blockade potentiators:
- acidosis
- hypothermia
- magnesium or CCB
- hypocalcemia
- dantrolene
- admin of abx (aminoglycosides)
what are metabolic disorders that can result in delayed emergence?
Delayed emergence can be due to: anesthesia medications, metabolic derangements, neurologic insult, and pre-existing toxins.
Metabolic disorders
1) Hypoglycemia
- glucose check
- if strong suspicion, tx 25g of D50
2) hypoxia or hypercarbia
* obtain ABG and tx accordingly
3) marked hyperglycemia, hyperosmolar coma, DKA, HHS
* glucose check
4) hyponatremia/hypernatremia
* check sodium level
5) hypothyoridsm
* myxedema coma
6) adrenal insuffiency
what are neurosurgical disoders that can cause delayed emergence?
Delayed emergence can be due to: anesthesia medications, metabolic derangements, neurologic insult, and pre-existing toxins.
neurosurgical causes
1) prolong hypotension 2/2 inappropriate cuff position
- ex: cuff placed on calf for sitting post fossa surgery
- CT would NOT show immediete ischemic CVA
2) recent craniotomy c/b intracranial hemorrhage?
- asymmetric pupils? not reactive to light? -> brain herniation
- immediete CT
CT of a patient shows large left thalamic hemorrhage with intraventricular blood and a midline shift. Patient is comoatose. How would you manage this patient in the ICU?
1) Airway
- intubate for airway protection
- normal oxygenation (increase CaO2 to brain)
- mild hyperventilation (dec PaCO2, dec CBF)
2) Hemodynamics
- maintain CPP > 70 mmHg
- CPP = MAP - CVP (or ICP)
- fluids, pressors, inotropes
3) decrease ICP
- increase ICP will compromise CPP
- eleavate bed 30 degree
- ensure no neck ties are compressing jugular
- avoid excessive PEEP (dec venous return from SVC)
- hyperventilate to PaCo2 of 30-35
- mannitol and/or lasix
- ventriculostomy drain –> measure ICP and drain CSF
4) avoid rebleeding
- control BP
- correct coagulopathy, avoid anticoagulants
5) prevent seziures
* administer phenytoin
6) prevent hyperthermia
- hyperthermia increases CMRO2 leading to worsen neurologic insult.
- induced hypothermia is controversial
5) Avoid hypoglycemia and hyperglycemia
- hyperglycemia worsens neurologic insult in spinal cord and cerebral injuries
- hypoglycemia depletes brain of energy = ischemia
- goal < 180. tight vs liberal control debated
6) prevent GI bleeding and DVT
- h2 receptor antagnoist or PPI
- sequental compression stockings; a/c contraindicated in acute bleed
What is the criteria for brain death?
- Irreversible absence of brain function including cortex and brainstem
- absence of hypothermia, toxins (drugs, muscle relaxants, sedatives), metabolic disturbances (hyponatremia, hypothyroid, hypoglycemia)
- determination of brain death
- two clinical assessments of brain function separated by a period of at least 6 hours.
clinical indicators
- 1) coma or unresponsiveness*
- no motor response to verbal command on painful stimuli
- 2) abscence of brainstem reflexes*
- no oculocephalic reflex, no deviation of eyes to irrigation in each ear, no corneal reflex, no gag rfelx to tracheobronchial sunctioning
- 3) apnea*
although clinical criteria alone is sufficent to determine death, is there a confirmatory test available?
- cerebral angiogram showing absence of blood flow to brain
what is apnea test?
- reveals patient’s response to hypercapnia and confirms dx of brain death
- brain dead pts will not respond to hypercapnia
exam
- obtain baseline ABG
- establish reliable pulse ox and disconnect from vent
- deliver O2 into ETT with NC placed deep into ETT lumen
- look closely for resp movements
- measure PaO2, PaCO2, and pH 8 min after.
- reconnect to vent
result
- if resp movement is absent, PaCO2 > 60 or 20 mm Hg increase from baseline = positive test = brain dead
