Neuro ICP & Pharmacology

Question 1

What is ICP a measure of?

Answer 1

Intracranial pressure refers to the supratentorial CSF pressure.
-Measured in the lateral ventricles or in subarachnoid space over cerebral cortex.
-ICP is measuring the compliance within the cranium

Question 2

What is contained in the Cranial Vault?

Answer 2

-Brain-80-90%, Blood-12%, CSF-8%, Intracellular H2O
-Small increases in volume are tolerated well.

Question 3

What is the Monro-Kelly Doctrine?

Answer 3

-The brain is enclosed and non-compressible.
-Any increases in total intracranial volume = increased ICP.
-Because the skull is rigid, any expansion of one of these compartments must be compensated by a reduction in size of the others if ICP is to remain constant.

Nagelhout:
The brain is enclosed within the cranium, and because the brain is not compressible any increase in total intracranial volume produces an accompanying increase in ICP.

Question 4

What are Compensatory Mechanisms for increased ICP?

Answer 4

Initially, displacement of CSF from cranial to spinal compartment.
-Increase in CSF absorption
-Decrease in CSF production
-Decrease in total blood volume (mainly venous drainage)

Question 5

What is normal ICP in adults?

Answer 5

5-15 mmHg

Question 6

What ICP is Intracranial HTN?

Answer 6

> 15 mmHg
-Treatment is needed if >20 mmHg

Question 7

What does increased ICP due to CPP & CBF?

Answer 7

Marked increases in ICP can decrease CPP & CBF and cause regional or general ischemia. (!!)

Question 8

What is Cushing’s Triad?

Answer 8

A sign of severely increased ICP indicating impending brain herniation.
-Widening Pulse pressure (↑systolic ↓diastolic)
-↓HR
-irregular RR

Question 9

What are the S/Sx of increased ICP?

Answer 9

-Headache
-n/v
-Papilledema
-focal neurologic deficits
-altered ventilatory function
-decreased consciousness (LOC)
-seizures
-coma

Question 10

What are causes of increased ICP?

Answer 10

-Trauma
-Hemorrhage
-Infection (encephalitis)
-Edema (3 different kinds)
-Increased CBF or decreased venous outflow (thrombosis)
-Systemic hypertension
-Inadequate CSF absorption
-Post traumatic seizure
-Mass effect from tumors, abscesses, bleeds

Question 11

What are the kinds of edema associated with increased ICP?

Answer 11

1) Cytotoxic
2) Vasogenic
3) Interstitial

Question 12

What is Cytotoxic Edema?

Answer 12

Increased intracellular water.
-Cells lose their ability to regulate what comes in and out.
-Traumatic brain injury and stroke.

Question 13

What is Vasogenic Edema?

Answer 13

A loss of BBB integrity; proteins flow out and causes an osmotic gradient with more fluid following.
-Tumors
-Steroids are good here to get rid of edema around the tumor

Question 14

What is Interstitial Edema?

Answer 14

hydrocephalus, extracellular water

Question 15

What is the gold standard for ICP Monitoring?

Answer 15

Intraventricular catheter
-Requires skill to place
-Low cost, accurate, reliable

Nagelhout:
-Very precise
-Highly invasive
-Can drain CSF to lower ICP
-Infection risk

Question 16

What are other methods of ICP monitoring?

Answer 16

-Intraparenchymal: small hole, can’t recalibrate.
-Subarachnoid, subdural, and epidural aren’t used much.

Question 17

What increases the risk of infection with a Ventricular Drain?

Answer 17

-Drain in place > 5 days
-Other infection in body
-Previous Craniotomy
-Hemorrhage
-CSF leaks

Question 18

What is important to know regarding Intraparenchymal Probes?

Answer 18

-Popular method of measuring ICP
-Low risk of infection
-Inserted through burr hole and tunneled subcutaneously
-ICP may be localized and not equal ventricular CSF pressure
-Only measures local pressure. Not equal to ventricular pressure. Trend it.

Question 19

What is a Transcranial Doppler?

Answer 19

-Non-invasive blood flow velocity measurement
-Most often measures Middle Cerebral Artery (MCA) flow velocity, also used for PCA, ACA and the basilar artery
-Flow velocity that is greater than expected = stenosis, emboli, or vasospasm
-Cannot determine actual CBF

Question 20

What are strategies to maintain brain protection?

Answer 20

-Perfusion: optimization of MAP (80-90 mmHg) & CPP (60-70 mmHg)
-Avoid hypo/hyperglycemia
-PaCO2 levels should be normal or slightly decreased to 30-35
-Hyperventilation can work for short-term brain relaxation and decreases CBF (6 hours)
-Temperature: Normal or hypothermic
-Prevent seizures (increases CMRO2)

Goal is to maintain physiologic homeostasis!

Question 21

How can we improve ICP via the blood compartment?

Answer 21

Flow related:
↓Venous congestion
↑HOB
Head neutral
↓Airway pressure or peep
↓Inhalation
↓CO2
↓CMRO2 (↑sedation, avoid histamine releasing NMB, Succ, vasodilators, prevent seizures)

Question 22

How can we improve ICP via the CSF?

Answer 22

-Administer meds that decrease production
-Drain (no more than 20mL/hour)

Question 23

How can we improve ICP via the Interstitial Compartment?

Answer 23

-Diuretics (Mannitol can decrease the size of brain during surgery)
-Steroids

Question 24

How can we improve ICP via the cellular compartment?

Answer 24

-Remove tumors via surgery

Question 25

What is the treatment for increased ICP?

Answer 25

-HOB elevated 30 degrees -Make sure neck is straight (promotes drainage) -Hyperventilate to PaCO2 of 30-25 mmHg -No PEEP, remove airway obstructions -Reduce brain water with diuretics, Hypertonic Saline (Lasix, Mannitol) -Metabolic suppression (barbs, propofol = uncoupling) -Corticosteroids: Decadron (NO steroids if TBI, check BS) -Ventricular Drain (no more than 15-20 mL/hr) -Emergency craniectomy to prevent herniation -Control seizures -Hypothermia

Question 26

PaCO2 is ___ mmHg higher than EtCO2.

Answer 26

The PaCO2 is approximately 2 to 5 mm Hg higher than end tidal carbon dioxide (ETCO2) (!!!)

Question 27

Why should you avoid rapid administration of Mannitol?

Answer 27

May produce vasodilation, increases in CBF, a transient rise in ICP, and a transient increase in circulating blood volume. -Push slowly over 20-30 minutes, especially in patients with underlying cardiac dysfunction (risk of pulmonary edema)

Question 27

What is Mannitol?

Answer 27

An Osmotic Diuretic. -Decreases ICP within 15 minutes by increasing plasma osmotic pressure and drawing fluid into the circulation. -It also causes vascular smooth muscle relaxation. -0.25 - 1 gm/kg. -Lasts about 2 hours -1-2 L of urine/hour -May cause hypovolemia, plasma hyperosmolarity, hypokalemia hypochloremic alkalosis

Question 28

What is the dose of 3% Normal Saline?

Answer 28

-Therapeutic dose: 1.4 ml – 2.5 ml/kg of 3% NaCl -Check Serum Na before starting gtt or giving bolus Nagelhout: -Like mannitol, hypertonic saline produces an osmolar gradient causing shrinkage of brain tissue and reduction in ICP.

Question 29

Why do you want to avoid rapid increases in Serum Na Concentration when administering 3% NS?

Answer 29

A rise in serum sodium concentration >9 mEq/L in 24 hours can lead to an osmotic demyelination syndrome, also known as central pontine myelinolysis. -Side effects: secondary bleeding due to platelet aggregation and delayed coagulation time, hypokalemia, hyperchloremic acidosis

Question 30

What are the effects of Volatile agents on ICP?

Answer 30

-Dose dependent increase in CBF -Decrease in CMRO2 and decrease in Luxury Perfusion or Cerebral steal Nagelhout: -Inhalation agents decrease mean arterial pressure (MAP) and increase ICP, reducing cerebral perfusion pressure (CPP). Isoflurane produces the greatest increases in CBF and ICP, followed by sevoflurane and desflurane. -All inhalational agents are known to increase CBF, CBV, and ICP.

Question 31

What is the effect of Isoflurane on CBF?

Answer 31

Isoflurane at 0.6 to 1.1 MAC no increase in CBF. However, at 1.6 MAC, CBF doubles.

Question 32

What are the effects of Nitrous Oxide on CBF?

Answer 32

N20 increases CBF and CMRO2 Nagelhout: -N2O can produce increases in CBF, CMRO2, and ICP. -N2O is more soluble than nitrogen and expands closed-gas spaces. Its use should be avoided in patients with an intracranial or intravascular air compartment such as pneumocephalus.

Question 33

What are the effects of Propofol on CBF?

Answer 33

-↓ CBF, CMRO2 -CPP may drop if BP drops Nagelhout: -The cerebral effects are a dose-dependent reduction in CBF and CMRO2. -PP may decrease because of reductions in blood pressure after bolus induction doses; however, the reduction in CBF appears to be independent of systemic hemodynamic changes. They are most likely due to the metabolic depressant effect and cerebral vasoconstriction. Reductions in systemic blood pressure produce corresponding reductions in CPP.

Question 34

What are the effects of Etomidate on CBF?

Answer 34

Causes Cerebral Vasoconstriction -Dec CMRO2 -But, causes myoclonus, adrenal suppression, Nausea and vomiting. -Not recommended for ICP issues Nagelhout: -Etomidate, like other CNS depressants, reduces CMRO2 and CBF. Benefits associated with etomidate use include cerebral vasoconstriction, which results in the reduction of ICP without reducing CPP. -Major disadvantages include a high incidence of myoclonia, thrombophlebitis, nausea, vomiting, and suppression of the adrenocortical response to stress. Many clinicians feel that etomidate should be avoided in brain-injured patients.

Question 35

What are the effects of Ketamine on CBF?

Answer 35

↑ CMRO2, CBF by 60-80%, Not used in neurosurgery. Nagelhout: -The primary advantage associated with ketamine is the stable hemodynamic course in the presence of hypovolemia that may occur in patients with traumatic head injury and multisystem trauma. Ketamine is known to produce untoward alterations in cerebral physiology, increasing CBF by 60% to 80% and potentially elevating ICP.

Question 36

What are the effects of Dexmedetomidine on CBF?

Answer 36

-Dose dependent sleep, anxiolysis, no respiratory depression -Easy to do wake up tests -Electrophysiological mapping stays intact and SSEP are maintained when added to desflurane and remifentanil. -Does not change CMRO2 -Cerebral blood flow is decreased because of “uncoupling” (Cerebral vasoconstriction) -Central sympatholytic action decreases catecholamines so neuroendocrine responses to surgery are attenuated -Decreased shivering and emergence delirium

Question 37

What are the effects of opioids on CBF?

Answer 37

No effect on CBF (unless you drop MAP and decrease CPP or over sedate and they become hypercarbic) Nagelhout: -The synthetic opioids produce dose-related reductions in CBF (decrease to 25 mL/100 g/min) and CMRO 2 (40%–50%). Later investigations in patients after acute head injury or in those undergoing supratentorial craniotomy noted increases in ICP and decreases in CPP after administration of induction doses of fentanyl, sufentanil, and alfentanil. These opioid-induced changes in ICP have been suggested to occur secondarily to an autoregulatory response to decreases in MAP.

Question 38

What are the effects of Benzos on CBF?

Answer 38

CBF-minimal change unless you over-sedate and increase CO2 Nagelhout: -Benzodiazepines produce a dose-dependent decrease in CMRO2 and reductions in CBF; however, their effects on ICP are minimal.

Question 39

What are the effects of Succinylcholine on CBF?

Answer 39

-Transient 10-15 mmhg increase in ICP that can last 5-8 min. -Rise in CBF and fasciculations in the neck causing Jugular Vein stasis may be an issue. -Defasiculating dose first! Nagelhout: -Succinylcholine-induced fasciculations can cause transient increases in ICP (transient rise of 10 to 15 mm Hg for 5 to 8 minutes after administration) -The effects on ICP may be inhibited by pretreatment with a small dose of nondepolarizing relaxant. -Furthermore, the administration of an anesthetic induction agent prior to succinylcholine may reduce the potential for ICP increases. -As mentioned previously, succinylcholine is contraindicated in patients with neurologic or denervated muscle because of the potential for life-threatening hyperkalemia. -Succinylcholine should be avoided in patients with cerebrovascular accident, upper and lower motor neuron lesions, coma, encephalitis, closed head injury, and after severe burns and prolonged bed rest.

Question 40

What should be used for intubation in neuro patients?

Answer 40

Roc + Sugammadex for reversal if needed. -Avoid Histamine releasing MRs! Nagelhout: A nondepolarizing alternative, such as rocuronium (at 1.2 mg/kg intubating dose), also facilitates endotracheal intubation within 60 to 90 seconds and avoids the known complications of succinylcholine. Rocuronium is being used with more frequency for rapid sequence induction since the availability of sugammadex, which provides rapid reversal if necessary.

Question 41

What are Beta Blockers used for in neurosurgery?

Answer 41

Beta blockers have great use in control of inotropic & chronotropic effects by sympathetic stimulation (DL, intubation, extubation, pin placements, etc.) -Esmolol – rapid acting, effects on ICP are negligible, forgiving quick on and off -Labetalol – longer lasting

Question 42

Can you use Sodium Nitroprusside or Nitroglycerin in Neuro patients?

Answer 42

No. These increase CBV & ICP, can lead to herniation.

Question 43

Which drugs can help with the prevention of vasospasm?

Answer 43

Calcium Channel Blockers. -Nimodipine (decreases mortality) -Nicardipine