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Management of Increased Intra-Cranial Pressure

Cerebral Blood Flow and Perfusion
1. Blood supplied from where? 2
2. Drains via? 3
3. Recieves how much CO?
4. CPP=?
5. Normal CPP?
6. CPP over what indicates brain ischemia?

1. Supplied from
-internal carotid and
-vertebral arteries

2. Drains via
-cerebral veins and
-dural venous sinuses into the -internal jugular veins

3. Receives 10-15% of CO
4. CPP = MAP – ICP
5. Normal CPP = 70-90 in adults
6. CPP > 50 indicated brain ischemia


Monroe-Kellie Concept
1. What is ICP?/
2. Volume of brain and constituents inside the cranium is fixed and cannot be compressed. Which parts make this up and what percent do they account for? 3

1. ICP is a function of the volume and compliance of each compartment

-Brain volume = 85%
-Cerebrospinal fluid = 10%
-Blood = 5%


Intracranial Compliance
1. What kind of compliance?
2. What are the initial compensatory mechanisms? 2
3. Once compensatory mechanisms are exhausted what happens to volume and pressure?

1. Nonlinear compliance
1. Initial compensatory mechanisms
-Displacement of CSF into thecal sac
-Decrease in cerebral venous blood

3. Once compensatory mechanisms are exhausted, small increases in volume produce large increases in pressure


Causes of Increased ICP

1. Intracranial mass
2. Cerebral edema
3. Increased CSF production (choroid plexus lesion)
4. Decreased CSF absorption (adhesions)
5. Obstructive hydrocephalus
6. Obstruction in venous outflow (venous sinus thrombosis)
7. Idiopathic (pseudotumor cerebri)


Signs and Symptoms: increased ICP

1. Headache
2. Vomiting
3. Altered consciousness
4. Seizures
5. Papilledema
6. Unequal and/or unreactive pupils
7. Cushing’s triad: bradycardia, hypertension and abnormal respirations
8. Impending herniation


ICP Monitoring Indications

1. Abnormal CT showing mass effect and/or midline shift
2. GCS less than 8
3. High risk for increased ICP (closed head injury)


Non-invasive techniques
for ICP measurement?

1. Ocular sonography – measures optic nerve sheath diameter
2. Transcranial doppler – measures velocity of blood flow in proximal cerebral vasculature
3. Intra occular pressure measurement
4. Tympanic membrane displacement


Management of ICP
1. Optimize Cerebral Venous OUtflow by

1. Promote displacement of CSF from intracranial compartment to spinal compartment
2. Elevate head of bed to 30°
3. Line placement (subclavian vs IJ)


1. How can a fever cause increased ICP?
2. Tx for this?
3. If conventional efforts fail?
-core temp of?

1. Elevated metabolic demand results in increased cerebral blood flow and elevated ICP
2. Acetaminophen and cooling blankets
3. Therapeutic hypothermia can be effective in lowering ICP with conventional efforts failed
-Goal core temperature between 32 and 34°


1. PaCO2 of?
2. Considered what kind of measure?
3. Minimize in pts with what? 2

1. PaCO2 of 35-38
2. Hyperventilation to lower PaCo2 levels: Considered an urgent measure, but should not be chronic
3. Minimize in pts with
-TBI or
-acute stroke
(Vasoconstriction causes decrease in cerebral perfusion and can worsen outcome)


1. hypoxia and hypercapnea increase ICP how?
2. Why should you use PEEP with caution? 3
3. Pre-medicate with what to prevent ICP surge?

1. Hypoxia and hypercapnea can increase ICP

2. Use PEEP with caution
-Impedes venous return,
-decreases blood pressure
-leading to reflex increase in cerebral blood flow
3. Pre-medicate w/ Lidocaine to prevent increased ICP surge


What is the most commonly used osmotic diurectic?



1. Mannitol MOA?
2. Dose?
3. Can be given through what?
4. Good option if also interested in doing what?
5. Monitoring parameters?

1. Draws free water out of brain and into circulation
2. Dose: 20% solution given as 1g/kg bolus, repeat dosing q6-8 hrs as needed
3. Can be given through peripheral line
4. Good option if also interested in lowering BP
5. Monitoring parameters:
-serum Na+,
-serum osmolality and
-renal function


Varying volume and tonicity either as bolus or infusion
1. Which fluid?
2. Which fluid for an ICU or actively herniating pt?
3. What kind of line preferred?
4. Goal serum?

1. 3%
2. 23% (ICU or actively herniating patients only)
3. Administration via central line preferred, but 3% okay peripherally
4. Goal serum Na+ less than 155


1. Decreases ICP by what?
2. What has good effect since it is easily titratable and has a short half life?

1. Decreases ICP by reducing metabolic demand
2. Propofol


Heavy Sedation and Paralysis
1. Used when?
2. Common regimen includes? 4
3. What is the issue with this?

1. Used in refractory increased ICP
2. Common regimen includes
-morphine and
-Lorazepam and
-analgesia/sedation and
-Cisatracurium or Vecuronium for paralysis
3. Cannot closely monitor neuro exam


1. Bypasses what?
2. this alone will lover ICP by what?
3. Craniectomy including removal of dura will lower ICP up to?
4. Complications include? 4

1. Bypasses Monroe-Kellie doctrine
2. Craniectomy alone will lower ICP by 15%
3. Craniectomy including removal of dura will lower ICP up to 70%
4. Complications include
-herniation through bony defect,
-spinal fluid leak,
-infection, and
-epidural and subdural hematoma


What defines Cushings Triad?

Bradycardia, Hypertension, Abnormal Respirations


A patient presents with right sided hemianopsia and memory loss. This is indicative of an ischemic stroke of what vessel?



Which of the following is the not an effective measure of decreasing elevated intracranial pressure?
A. Heavy sedation/paralysis
B. Hypertonic saline infusion
C. Surgical Craniectomy
D. Induced Hypoventilation

Sorry Lauren, ill change this when i find out :)


DX of Vertigo
1. N/V more severe with what etiology?
2. Gait disturbances more pronouced with?
3. Describe the differences in peripheral vs central length of symptoms?

4. Important
-Get good hx
Thorough PE looking for what? 2
-Look at risk factors for more serious central disease

1. N & V more severe w/ peripheral causes
2. Gait disturbances more pronounced w/ central etiologies
3. Generally central etiologies last for hours to days, while peripheral are recurrent and last for a few minutes to 2-3 hours

-nystagmus and
-focal neurologic signs


Transient Ischemic Attack (TIA)‏
1. Most last how long?
2. If neuro defects last 4 hours pts often have?
3. Sx of TIAs? 5

1. TIAs: most sx last 5-20 min, rarely longer than an hour, without evidence of acute infarction
2. If neurological defects last 4 hours or longer pts often have infarcts on MRI
3. Sx of TIAs include:
-Hemiparesis, hemiparesthesia
-Dysarthria, dysphasia, dysploplia
-Circumoral numbness
-Monocular blindness


TIA Work Up
Depends on suspected area affected:
1. Low flow areas? 3

-Int carotid


Depends on suspected area affected:
Low flow: Imaging for these?
1. Int carotid?
2. MCA?
3. Vertebrobasilar?
4. Embolic? 2
5. Lacunar?

1. duplex US or transcranial doppler
2. MRA or CT angiography
3. CT angiography

-Cardiac monitoring looking for atrial fibrillation

5. r/o others—diagnosis of exclusion


1. What is myasthenia gravis

2. What is myethenic crisis?
3. Symptoms? 2

1. Myasthenia gravis: a disorder of neuromuscular transmission affecting the ocular, bulbar, limb and respiratory muscles

2. Myasthenic crisis occurs when there is severe enough weakness to necessitate intubation

-Severe bulbar weakness produces dysphagia and aspiration that often complicates respiratory failure
-Often the pt experiences generalized weakness as a warning


MG crisis management:
1. If the pt presents with weakness and not acute respiratory failure how can we proceed with management?

2. Elective intubation should be considered if what?

3. At times because of the weakness of oropharyngeal muscles secretions cannot be handled and the pt is at risk for aspiration so we should do what?

4. If the pt is in obvious respiratory failure what is done?
-but what is preferable?

5. What are done for treatment? 2

1. the forced vital capacity (FVC) can be monitored every 1-2 hours

2. serial measurements of the FVC consistently decline approaching 15 mL/kg body weight

3. elective intubation is done in this setting

4. emergent intubation is done,
-elective intubation is preferred

5. Plasmapharesis or IVIG


Multiple Sclerosis
1. Describe the accute exacerbations of this?
2. Treated with?

1. Acute exacerbations that result in functionally disabling symptoms with objective neurologic impairment (e.g. loss of vision, motor and/or cerebellar symptoms)‏

2. Treated w/ high dose IV glucocorticoids
such as methylprednisolone 1000 mg IV a day for 5 days


Neuropathic Pain Syndromes
1. What is this?
2. If its a chronic pain exacerbation discuss w/ patient level of pain and options for treatment. Such as? 4

1. Generally patients with chronic pain, may be on prophylactic medications to control pain, but are having breakthrough pain

2. If its a chronic pain exacerbation discuss w/ patient level of pain and options for treatment
-1 time IM dose of Demerol
-1time dose of PO opioid
-Start or increase prophylactic med
-Importance of regular follow up with primary medical provider and/or pain specialist


Neuropathic Pain Syndromes
1. Do not do what?
2. Assess them for associated what?

1. DO NOT give prescriptions for narcotics

2. Assess for associated depression and/or anxiety that may be making pain worse and make appropriate referral


Guillian-Barre’ Syndrome
1. Weakness patterned how?
2. Starts where?
3. Progressses to what?
4. timeline?
5. Sensory issues?
6. Often severe pain where?
7. Voice problems?
8. Other symtpoms? 6

1. Symmetric ascending muscle weakness
2. Weakness usually starts proximal legs
-Begins in arm and facial muscles 10% patients

3. Progresses to severe respiratory muscle weakness
-30% of patients will need ventilatory support

4. Can happen quickly
80% will have paresthesias in hands/feet
5. Sensory abnormalities on exam often mild
6. Often severe back pain
7. Dysautonia-70%

-urinary retention,
-loss of ability to sweat