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The Cranial Nerve Assessment for Nurses

The Cranial Nerve Assessment for Nurses

The cranial nerve assessment is an important part of the neurologic exam, as cranial nerves can often correlate with serious neurologic pathology. This is important for nurses, nurse practitioners, and other medical professionals to know how to test cranial nerves and what cranial nerve assessment abnormalities may indicate. This becomes especially important when evaluating potential new strokes.

In school, cranial nerves tend to be something you memorize and then forget the day after the test. But they are important in testing a patient’s neurologic status, as an abnormality in a cranial nerve can indicate a central lesion (stroke, tumor, bleed, etc).

Every nurse should at the least know how to do a basic cranial nerve assessment, specifically the visual acuity and pupillary light reflex. When evaluating a stroke, The NIH scale is a method to evaluate the severity of a stroke. This scale walks you through evaluating many of the cranial nerves, but not all of them. If you want to feel confident when you chart “Cranial nerves II-XII grossly intact”, then keep reading!

1. The Olfactory Nerve (CNI)

The olfactory nerve is responsible for the sense of smell. Although rarely tested in practice, alterations in smell can be caused by serious intracranial pathology (brain tumors, strokes, TBI), neurodegenerative diseases like Alzheimer’s, Parkinson’s, or MS, or benign and transient causes such as the common cold.

If both branches of the olfactory nerve are damaged, this can lead to permanent anosmia (loss of smell) and can lead to food tasting bland and decreased appetite. In most individuals, the sense of smell decreases over time, with up to 75% of individuals older than 80 have some degree of anosmia.

 How to test the Olfactory Nerve

The olfactory nerve is almost never tested within an acute care setting such as in the hospital. However, this is sometimes tested in outpatient neurology offices. To test the olfactory nerve, blindfold the patient and have them smell and identify common scents such as vanilla, cinnamon, coffee, or peppermint while covering up one nostril at a time. Do not use ammonia or alcohol as these can trigger intranasal trigeminal nerve receptors and bypass the olfactory nerve.

2. The Optic Nerve (CNII)

The optic nerve is the second of the cranial nerves and is responsible for vision. This nerve transmits signals perceived in the retina and cones of the retina to the occipital lobe. This is commonly tested within the clinical setting and for a variety of presentations.

Partial or complete loss of vision can be caused by conditions such as:

  • Diabetes
  • Intracranial pathology (ischemia, stroke, tumors)
  • Inflammation or infection of the eye
  • Toxicity

How to test the Optic Nerve

When testing the optic nerve, you need to examine the visual fields, the visual acuity, and the pupillary light reflex. All three are an important part of the cranial nerve assessment, although the pupillary light reflex involves cranial nerve 3 as well.

Testing the Visual Fields (II)

If the patient loses part of their vision on one side, it is termed partial hemianopia, and if they lose complete vision on one side it is complete hemianopia. There are a few different ways to test visual fields, but here is an easy way. Stand one arm length away from the patient and ask them to cover up one eye or do it for them if they are unable. Close your own eye on the same side. Now hold up numbers with your fingers at each of the four corners of their vision. Once satisfied, test the other eye.

Testing the Visual Acuity (II)

Nurses often assess visual acuity, and most emergency departments will have a Snellen eye chart to use. The distance the patient stands depends on the visual acuity chart (it should say). If you do not have easy access to this, there is an app you can get on your phone which is super helpful!

Have the patient stand the appropriate distance away and have them cover up one eye. Do not have them forcibly close the eye as this can somewhat inhibit their ability to see out of their open eye. Ask the patient to read the 20/20 line on the chart. On a standard Snellen eye chart, this would be 20 feet away. If the patient gets more than half wrong, move onto the line above. Stop once the patient gets over 50% right. Mark this down and test the other eye. If they wear glasses – have them wear their glasses for this as well!

Pupillary Light Reflex (II, III)

The pupillary light reflex tests both cranial nerves II and III. First, inspect both pupils and make sure they are equal in size and shape. Then dim the lights if possible and shine a penlight directly into the right eye. Both pupils should constrict and maintain symmetry. Note if they are brisk or sluggish and if they are symmetric. Remove the light source and watch both eyes dilate equally as well. Do the same for the left eye.

3. The Oculomotor Nerve (CNIII)

The oculomotor nerve controls the majority of the extraocular muscles. It is primarily responsible for eye movement, eyelid movement, and pupillary constriction. If there is any oculomotor nerve impairment, there will be a pupillary dilation, ptosis (drooping eyelid), and outward deviation of the eye – termed abduction. When a patient has diplopia (double vision), it is often due to a unilateral lesion on this cranial nerve. In most cases, third nerve palsy resolves over weeks to months.

Causes of oculomotor nerve palsy include:

  • Intracranial aneurysm
  • Microvascular ischemia (in diabetics especially)
  • Trauma: Severe blows to head with skull fracture

Testing Extraocular Muscles (III, IV, VI)

To test the oculomotor nerve, you need to assess the EOMs. Testing the EOMs also tests cranial nerves IV and VI, as all three nerves are responsible for eye movement.

Hold your finger or a pen 2 feet in front of the patient’s eyes midline and have the patient focus on it with both eyes. Ask the patient to follow your finger or pen with only their eyes, moving the pen to the right, back to the midline, and then to the left and back again. Do this again for up and down. Lastly, do this again to the down-left diagonal angle, and then the down-right diagonal angle. You should have tested a total of 6 different directions – termed the “6 cardinal directions”.

Eye movement should be symmetric, smooth, and moving in all directions. At each extremity of vision, you should be observing excessive nystagmus. Nystagmus is repetitive uncontrolled eye movement.

Conjugate nerve palsy is when both eyes are unable to look in a specific direction during your testing. This most commonly occurs in the horizontal directions. This is usually due to a stroke within or near the brain stem.

The pupillary light reflex listed above is also used to assess the oculomotor nerve.

4. CN IV: The Trochlear Nerve

The fourth cranial nerve, the trochlear nerve, innervates the superior oblique muscle of the eyes. This means it controls the downward movement of the eyeball and prevents it from rolling upward. When there is a fourth nerve palsy, patients will often complain of vertical diplopia and/or tilting of objects. This may be most noticeable when in a downward gaze such as when going down the stairs. They may also have a head tilt, as the visual changes improve with tilting of the head. On exam, the eye will with deviated upward and rotated outward.

Testing the trochlear nerve involves evaluating the patient’s extra-ocular movements as described above.

5. CN V: The Trigeminal Nerve

The Trigeminal nerve is the 5th cranial nerve and responsible for facial sensation, as well as moving the muscles involved with biting and chewing. This has three branches including the ophthalmic V1, maxillary V2, and Mandibular V3. Compression of this nerve root can cause trigeminal neuralgia – a rare but painful condition.

How to test the Trigeminal Nerve

To test the trigeminal nerve, you are testing their facial sensation. Lightly touch both sides of the forehead and ask if they felt the same. Do this on the cheek, and then the chin. If the patient is uncooperative, you can test their corneal reflex. Do this by having the patient look right, then touch their left cornea with a whisp of cotton. They should blink. Do this on both sides.

6. CN VI: The Abducens Nerve

The sixth cranial nerve, the abducents nerve innervates the lateral rectus muscle of the eye. This means its responsible for outward movement of the eyes. Patients with dysfunction of this nerve will be unable to outwardly move their eyes. This causes horizontal diplopia, where the double images are side-by-side, which is worse at far distances.

This nerve is often the first nerve compressed when there is any increased intracranial pressure (ICP). However, more common causes include vascular disease (diabetes, hypertension, atherosclerosis) or trauma.

To test the abducents nerve, test the EOMs as described above.

7. CN VII: The Facial Nerve

Cranial nerve VII is the facial nerve, which controls the muscles of facial expression, as well as the sensation of taste of the front of the tongue. Facial nerve palsy can occur for various reasons, the most common being Bell’s palsy. Some other common causes include stroke, Lymes disease, trauma, or even diabetes.

How to test the Facial Nerve

To test the facial nerve, you must assess the patient’s facial expressions. Have the patient close their eyes tightly, then have them open their eyes. Ask them to frown, looking for symmetry in the forehead muscles. Have them smile and look for any drooping or asymmetry.

Clinical Tip: To differentiate Bell’s palsy from stroke, assess the patient’s use of their forehead muscles. Peripheral nerve lesions (such as with Bell’s palsy) cause paresis of the entire side of the face. Central lesions tend to only effect the lower portion of the face. This is not always the case though, so you must use clinical judgement. Bell’s palsy should have no other associated neuro deficits. Check out my Infographic for more information!

8. CN VIII: The Vestibulocochlear Nerve

The vestibulocochlear nerve, also called the auditory vestibular nerve, is responsible for hearing and balance. Vestibular neuritis is when the nerve becomes inflamed and can cause vertigo, dizziness, and balancing difficulties – most likely from a viral infection.

How to test the Vestibulocochlear Nerve

While not routinely tested within the hospital, the vestibulocochlear nerve involves testing both hearing and balance. Hearing is tested by holding your fingers a few inches away from their ears and rubbing them together. If they can hear, then that is a pass. Test their balance by assessing their gait while walking. The presence of nystagmus can also indicate vestibular dysfunction.

9. CN IX: The Glossopharyngeal Nerve

The glossopharyngeal nerve is partially responsible for the sensation of taste, pharyngeal sensation, as well as for the gag reflex. A damaged glossopharyngeal nerve can cause a loss of taste in part of the tongue and cause trouble swallowing.

How to test the Glossopharyngeal Nerve

Palatal Movement (IX, X)

Instead of doing the gag reflex which can be very uncomfortable for patients, you can instead assess palatal movement. Do this by having the patient yawn or say “ahh”, and observe their palate movement for symmetry. If this is abnormal, consider testing the gag reflex.

Gag Reflex (IX, X)

When performing the cranial nerve assessment, the easiest way to test the glossopharyngeal nerve is to test their gag reflex, however, this is usually not necessary in the clinical setting. Remember that approximately 20% of people will not have a gag reflex at baseline. Check both sides of the pharyngeal wall by gently poking the pharynx with a cotton swab.

Dysarthria (IX, X, XII)

There is no specific test for this but listen to the patient’s speech. Assess for any slurred speech or abnormality of the voice. Ask the patient or the family if it sounds different than normal.

10. CN X: The Vagus Nerve

The Vagus nerve innervates the hearts, lungs, and digestive tract, along with a few muscles. Most noticeably, it controls the heart rate, GI motility, sweating, and speech. It is also partially responsible for the gag reflex (along with cranial nerve IX).

Overstimulation of the vagal nerve can drop the heart rate and cause syncope, termed vasovagal syncope. Activities that stimulate the vagal nerve include bearing down, holding breath, carotid massage, or extreme fear or stress.

There are even implantable vagus nerve stimulators that can help slow down the firing of neurons within the brain and thus help manage seizures.

How to test the Vagus Nerve

The only real way to test the vagus nerve is via the gag reflex as described above.

11. CN XI: The Accessory Nerve

The accessory nerve innervates the sternocleidomastoid and trapezius muscles. This means it is responsible for tilting/rotating the head as well as shrugging the shoulders. This nerve can be damaged after neck surgery or blunt force trauma.

How to test the Accessory Nerve

To test the trapezius muscle, ask the patient to shrug both of their shoulders at the same time. Then apply some downward pressure with both hands and ask them to shrug both shoulders against the resistance.

To test the sternocleidomastoid, place a hand against their cheek and ask them to rotate their head against resistance in each direction. If you notice weakness, this indicates the opposite side is the weaker muscle.

12. CN XII: The Hypoglossal Nerve

The hypoglossal nerve controls most of the movement of the tongue. This means it is highly responsible for speech and swallowing. Damage to the hypoglossal nerve is rare, but if so are likely to be caused by tumors or gunshot wounds. Other causes include stroke or neurodegenerative disease.

How to test the Hypoglossal Nerve

To test the hypoglossal nerve, ask the patient to stick out their tongue. If the tongue deviates to one side, this indicates hypoglossal nerve dysfunction on the side of deviation. Then ask them to move their tongue from side to side rapidly. Additionally, listen for dysarthria when the patient is speaking as described above.

Cranial Nerve Assessment Cheat sheetCranial Nerve Assessment Cheat Sheet

How’s that for a refresher?  Although we may have forgotten some of the in’s and out’s of the cranial nerve assessment, this should serve as a reminder for how to examine cranial nerves. Hopefully, after reading this, you can feel more confident in your neurologic assessment!

If you need an easy cranial nerve assessment handout, you can download my handout here! This is the perfect cheat-sheet that you can refer to in practice when assessing cranial nerves!


Gelb, D. (2019). The detailed neurologic examination in adults. In UpToDate. Retrieved from

Lee, A. G. (2019). Third cranial nerve (oculomotor nerve) palsy in adults. In UpToDate. Retrieved from

Lee, A. G. (2019). Fourth cranial nerve (trochlear nerve) palsy. In UpToDate. Retrieved from

Mullen, M. T. (2014). Differentiating Facial Weakness Caused by Bell’s Palsy vs. Acute Stroke. Journal of Emergency Medical Services39(5). Retrieved from

Oculomotor Nerve. (n.d.). Retrieved from

Olfactory Nerve. (n.d.). Retrieved from

Rea, P. (2014). Clinical Anatomy of the Cranial Nerves. Cambridge, MA: Academic Press.

Trigeminal Nerve. (n.d.). Retrieved from

Six Steps for Sepsis Management

Six Steps for Sepsis Management

Sepsis is not a specific disease but rather a clinical syndromewhich represents the body’s response to severe bacterial infection. Sepsis is very common. In fact, within the hospital, you will take care of patients with sepsis in any department. Sepsis is a very serious condition with a poor prognosis. As the medical team suspecting and treating sepsis – there are important management steps that need to be taken in order to maximize patient outcomes and save lives!

Early sepsis– while not clearly defined – is the presence of infection and bacteremia – which can and likely will progress to sepsis without intervention. Sepsis used to be identified using SIRS criteriaSystemic Inflammatory Response syndrome. This syndrome is defined as the presence of at least 2 of the following 4 clinical indicators: Fever >38C or <36C, HR >90bpm, RR > 22/min or PaCO2 <32 mmHg, or WBC >12,000/mm3, <4,000/mm3, OR 10% BANDS. Once SIRS is identified with suspected source of infection – sepsis diagnosis was met. However, the definition of sepsis has changed with 2016. Sepsis is now is defined as life-threatening organ dysfunction in response to infection. Organ dysfunction, usually from hypoperfusion, can be evidenced by hypotension, altered mental status, tachypnea, or increased sofa score by 2 points (see below).  Septic shockis defined as those patients who have received fluid resuscitation and still have a MAP <65 mmHg and a lactic >2.0 mmol/L. These patients require vasopressors and should be monitored in the ICU.

Sepsis can be very serious and even fatal. Because of this – it is important to kn ow the steps to take in sepsis management. Performing these correct steps can literally mean the difference between life and death.

1. Recognition and Early Intervention

The most important aspect of sepsis management is recognizing it’s presence and acting quickly. Common symptoms of sepsis include fever, chills, sweats, and confusion. Common signs include altered mental status, elevated temperature, tachypnea, tachycardia, and hypotension.

Initial management should include investigating the extensiveness of their infection, and applying initial measures to help them. After vital signs are taken an IV should be established and lab work drawn. If the patient’s blood pressure is low – consider starting 2 large-bore IVs. Be sure to draw at least 1 set of blood cultures per IV site (up to 2) as this will need ordered in all sepsis patients. Make sure the blood cultures get drawn before antibiotics are started.

Diagnostics should investigate the source of the infection – sometimes it is not obvious. If unsure – it is a good idea to obtain a urinalysis with culture to r/o UTI and a Chest x-ray to r/o pneumonia should be ordered. A wound culture, sputum culture, or abdominal imaging may be ordered if clinically indicated. Blood work will usually include blood cultures x 2, CBC with differential, CMP, and a lactic acid level. Sometimes in severe cases, an ABG can be ordered to evaluate acid-base status.

Lactic acid levels are very important in sepsis. Lactate is released from cells when they are forced to utilize glycolysis instead of the Kreb’s cycle (throwback to Cell Biology!). This means that there is decreased tissue perfusion due to decreased volume, increased oxygen demand, and decreased oxygen delivery. Lactic levels correlate with severity of sepsis.

Apply oxygen at 2 L/min unless contraindicated – titrate if SPO2 <92%. During sepsis, oxygen demand increases and delivery diminishes. Supplemental oxygen will help put less stress on the body and may help diminish lactic acidosis.

The qSOFA (Quick Sequential Organ Failure Assessment) score is now starting to be used as a clinical tool for sepsis. This is usually used within the hospital to stratify the mortality of patients with sepsis (see infographic for more details).

2. Fluid Resuscitation!

Fluid resuscitation during sepsis is the staple of sepsis management. Evidence shows early fluid intervention decreases mortality. There is such a massive need for fluid because during sepsis there is poor tissue perfusion and often hypovolemia. To correct this – large amounts of fluids are needed.

Typically, 0.9% normal saline is used 9 times out of 10. The recommended standard volume is a 30 ml/kg bolus. So if a patient was 70 Kg, they would receive 2100 ml total. This should be given as quickly as possible – as tolerated. This amount is typically given to anybody recognized as possibly having sepsis, but is especially indicated in those with sever sepsis, fast heart rate, or low blood pressure. Traditionally even larger amounts of fluids were given (5-6 Liters), but several randomized control trials showed no difference in mortality compared with the now-recommended 2-3 Liters.

Exceptions to receiving this bolus includes those with active pulmonary edema. Those with a history of Heart Failure, end-stage renal disease, or severe liver disease should still receive fluids. However – it is recommended to give fluids in 500mL bolus increments and to reassess lung sounds and breathing status after each bolus. If pulmonary edema ensues – the bolus should be stopped and the patient may need diuretics.

3. Timely Antibiotic Administration

Another very important aspect of sepsis management is early antibiotics. The term empiric simply means antibiotics based on the best “clinical guess”.

The choice of empiric antibiotics will be selected based off of the patient’s signs or symptoms and where the likely source – since certain organisms are more likely from one source as opposed to another. This means the antibiotic regimen should be geared towards covering all likely gram-positive and gram-negative organisms. For sepsis – usually a broad spectrum antibiotic like Zosyn or a Carbapenem is combined with another antibiotic of a different lass – such as Vancomycin. Vanco is often added when the patient has risk factors for MRSA.

Correct regimen of antibiotics are important – however timely administration of those antibiotics are just as important. Antibiotics should be initiated within the first hour after suspecting sepsis – especially during severe sepsis or septic shock. This is because several observational studies have shown poorer outcomes with delayed antibiotic initiation. Once again, try to be sure you obtain both sets of blood cultures before you start the antibiotics!

As nurses, it is often up to you to choose which antibiotic to start first as both are often ordered concurrently. If you have both Zosyn and Vancomycin ordered – start with the broad-spectrum antibiotic first. But what exactly is broad-spectrum? This means heavy-hitter antibiotics that cover most pathogens – both gram positive and negative. Contrary to popular belief – vancomycin is NOT broad-spectrum. In fact, it has a very narrow spectrum specific for gram positive organisms such as Staph or Strep. Most cases of sepsis are from gram negative sources. This means starting the Zosyn first should be your priority. Additionally – Zosyn runs much quicker as a loading dose (4.5 grams over 30 minutes) – whereas vancomycin usually runs over 1.5 hours.

4. Hemodynamic Management

Sometimes when sepsis becomes severe – distributive shock can occur. This is termed septic shock. When this occurs – hemodynamic compromise is present.  If blood pressure remains low, the patient’s tissue perfusion continues to suffer and steps need to be taken to improve outcomes.

The patient may require more fluid if they are still hypovolemic after the initial bolus and can tolerate more fluids. However, the mainstay of treatment of septic shock is intravenous Vasopressors. For the most part – Norepinephrine (Levophed) is the go-to pressor for sepsis. However, other choices can be chosen based on clinician discretion (i.e. If very tachycardic consider Vasopressin which has no beta stimulation). Sometimes, multiple vasopressors may need to run concurrently to manage septic shock.

When a patient is in septic shock with hemodynamic compromise – they should have a central venous catheter inserted and/or an arterial line. Vasopressors can be started in a peripheral line, but a central line should be ordered as vasopressors can be caustic and damaging to the peripheral vasculature. Additionally, these catheters can monitor CVP and continuous blood pressures. If a patient is in cardiogenic shock and has inadequate cardiac output – cardiac inotropes can be added such as dobutamine or epinephrine.

Sometimes during severe septic shock, IV glucocorticoids may or may not help. Usually this is ordered if fluid resuscitation and vasopressors have failed.

5. Monitoring

Monitoring is the essential last step to sepsis management. Patient’s with sepsis can respond well to the regimen – or they can decompensate unexpectedly. Sepsis has a high mortality and the patient’s should be monitored very closely.

If the patient has any hemodynamic compromise and are on pressors – they should be monitored in the ICU for a few days until they become stable. Patient’s with mild to moderate sepsis should be closely monitored on a med-surg or telemetry floor. Continuous cardiac monitoring is essential during sepsis. The increased tissue demand for oxygen places the heart at a greater risk for having cardiac events secondary to the sepsis. It is not uncommon for someone with sepsis and cardiac comorbidities to have secondary myocardial ischemia and/or infarctions.

Blood pressure should be monitored closely – especially initially. Normotensive blood pressure should be maintained (SBP >100). However – maybe even more importantly the MAP (mean arterial pressure) should be monitored closely. The goal of MAP should be >65mmHg – this ensures adequate tissue perfusion (i.e. brain). Heart rate is also an important metric to monitor. Tachycardia is usually present – often in the 120s-130s during fever and sepsis – sometimes higher. While giving fluids – heart rate should improve. This can be somewhat helpful in monitoring the response of fluid therapy. Fever should be monitored as well – as sometimes it can become very high and increases insensible water losses and further propitiates hypovolemia. Remember a rectal temperature is preferred in those with suspected sepsis – especially the elderly. Urine output is also often monitored during severe sepsis – as secondary hypoperfusion of the kidneys can cause acute kidney injury and decreased urine output.

Nursing assessments should include skin color and perfusion, mucous membranes (i.e. dry vs moist), mental status, and heart/lung sounds. Nurses should be vigilant in recognizing flash pulmonary edema or cariogenic shock which may develop after rapid administration of fluids with underlying comorbidities (i.e heart failure, ESRD, etc). 

If the initial lactic acid level is elevated > 2 mmol/L, then a repeat level should be drawn in 4 – 6 hours. The lactic acid level should respond quickly to changes in tissue perfusion. CBC should be trended each day to monitor for resolution of the leukocytosis, bandemia, and/or thrombocytopenia. Electrolytes and kidney/liver function should also be monitored closely dpeneding on which abnormalities are present.

6. Patient Disposition and Follow-Up

Last but certainly not least – the patient needs to be sent to the correct unit, needs the correct consults, and needs adequate follow-up. Almost all patients admitted to the hospital with sepsis will warrant an Infectious Disease consultation. Additionally, if they have any pre-existing comorbidities these consults should be made as well (i.e. cardiology for heart failure, nephrology for kidney disease).

Patients should have frequent nursing assessments and daily physician assessments, with close follow-up of labs. Blood cultures can start showing growth at about 24 hours. The pathologist will gram-stain the growth and give a report of “gram positive cocci” a similar description. This tells the clinician if they are on the right track and can guess at the offending organism. At about 48 hours, most clinically significant bacteria will be identified and a sensitivity is done to detect the bacteria’s sensitivity vs resistance to various antibiotics. Urine, wound, and sputum cultures have similar timelines. Antibiotics may be changed depending on the results. Remember, Infectious Disease should likely be involved in this decision.

And those are the six steps to sepsis management. Knowing the general steps to sepsis can help you as the nurse provide high quality care to your septic patients and help improve outcomes. As always, it is a collaborative team effort in offering you patients the best possible care.

Do you have any other sepsis tips? leave them in the comments below!


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