The tear film is made up of three layers. The outer lipid layer, the middle aqueous layer, and the inner mucin layer. The lipid layer is produced by meibomian glands. The meibomian glands retard evaporation and provide a smooth, lubricated surface for the eyelid to move across. The aqueous layer makes up the majority of the tears. It is composed of anti-bacterial substances, water, and proteins that are secreted by the lacrimal gland and accessory lacrimal glands to get rid of toxins and debris in the tear film. The mucous layer is composed of goblet cells, which secrete mucin. Mucin can bind and trap bacteria and viruses to keep them from penetrating the surface. A common symptom of dry eye is excess tearing. The patient is experiencing excess tearing because the ocular surface is dry and irritated from exposure of the globe and lack of lubrication. Reflex tears are protective and produced to fight the irritation and dryness with an increase in tear flow rate. Another possible cause of excessive tearing could be due to ectropion. An ectropion is the eyelid turning outward.When this occurs, the lacrimal punctum is also turned away from the globe, preventing the tears from properly draining out of the eye into the nasolacrimal system. Tear break-up time (TBUT) is a common test performed to help diagnose dry eye and assess the tear film stability. Fluorescein sodium is instilled into the patient’s tear film by either drops or wetting a fluorescein strip with saline, shaking off the excess, and touching the strip to the inferior bulbar conjunctiva. The tear film is observed with the slit lamp and a cobalt blue filter. The patient is instructed to blink – times so the dye spreads across the tear film and ocular surface, and then tell the patient to hold their eye open as long as possible, without blinking. After a blink, the lipid layer of the tear film begins to break down, resulting in the appearance of dry spots. Count how many seconds it takes for a dry spot to appear in the tear film. Repeat the test two more times and take the average of the measurements. The TBUT is recorded as the time between the completion of the blink and the first appearance of a dry spot (hypofluorescent regions). A TBUT of less than seconds is indicative of an abnormal tear film. The patient had a TBUT of seconds. A TBUT of greater than seconds is considered normal, but there is variability with this test. Fluorescein staining of the cornea indicates where the tight junctions of the epithelial cells are disrupted. Fluorescein is considered a vital dye, however it is dying or damaged cells that uptake the dye, resulting in a stain. Fluorescein dye is most commonly used, but lissamine green and rose bengal can also be used to show staining of the cornea. Lissamine green and rose bengal are more sensitive for conjunctiva staining and fluorescein is more sensitive for corneal staining. Lissamine green and rose Bengal both stain dead or devitalized cells, but lissamine green is tolerated more by patients because it does not sting like rose bengal.
Rose bengal is toxic to epithelial cells. The patient is experiencing changes in her facial expression and feeling on the right side of her face. During the history, asymmetry of the right side of her face is observed, along with prolonged periods between blinks. Possible causes of facial asymmetry include: Bell’s palsy, a stroke, tumor, Ramsay Hunt syndrome, sarcoidosis, and Lyme disease. Some possible causes of incomplete closure of the eyelids are: Bell’s Palsy, tumor, Myasthenia Gravis, and Ramsay Hunt Syndrome. If the patient had a stroke she would also experience numbness or weakness of her extremities on the affected side of the body. A tumor would have more of a gradual onset, unlike this patient who described her signs and symptoms as a sudden onset. Ramsay Hunt syndrome causes facial paralysis, but also presents with a pronounced prodrome of pain, and often a vesicular rash in or around the ear. A patient with Lyme disease can have facial paralysis, often has a rash, and a history of tick exposure. And sarcoidosis is usually bilateral, affecting both of the facial nerves. It’s recommended that the patients sees her primary care physician so that these other conditions, like a stroke or tumor, can be completely ruled out. Also to make sure that no other cranial nerves are involved. Bell’s Palsy is a diagnosis of exclusion; therefore, all other possibilities need to be eliminated first, in order to diagnose the patient with Bell’s Palsy. The patient is diagnosed with Bell’s Palsy.
Bell’s Palsy is an acute weakness or paralysis of one side of the face, resulting from peripheral facial nerve palsy. Bell’s Palsy is defined as idiopathic, but some possible etiologies include: viral infection, specifically reactivation of herpes simplex virus type (HSV-), or inflammation of the facial nerve.
Clinical features of Bell’s palsy are excessive tearing and dry eye due to the inability to completely close their eye, sagging of the lower eyelid, drooping of the corner of the mouth on the same side, pain in or behind the ear, ipsilateral impaired or loss of taste sensation, feeling of numbness on the same side of their face, and absence of wrinkling on ipsilateral side of the forehead. It’s significant that the patient in this case has smoothing of the right side of her forehead because this is a common finding in Bell’s Palsy, and it helps differentiate it from a stroke. A patient that has had a stroke can typically still control the upper part of their face, and therefore will have wrinkling of their forehead. The patient’s paralysis is localized to only her face in this case; if she had a stroke she would be experiencing numbness or paralysis in her arms and legs as well. Another way we can differentiate the diagnosis of Bell’s palsy from a stroke is the patient’s speech and motor function. The patient is able to communicate and answer questions normally, so a stroke is unlikely. Bell’s palsy and a stroke can cause acute facial paralysis, but a stroke is much more acute in onset (within seconds to minutes). The onset of Bell’s palsy is within hours to days. The age of the patient is another considerable factor, she is only years old, and an acute stroke usually occurs in people older than.
The facial nerve (CN VII) supplies all of the muscles of facial expression, and taste sensation from the anterior two-thirds of the tongue. Bell’s palsy is associated with a lower motor neuron, while an upper motor neuron is associated with a cerebrovascular accident. A lesion of the lower motor neuron causes weakness or paralysis of all muscles of facial expression, the frontalis muscle (forehead), and closure of the eye. An upper motor neuron lesion does not affect blinking or eye closure and the frontalis is preserved. A stroke causes central facial weakness, which involves the lower facial muscles contralateral to the lesion in the brainstem and Bell’s palsy causes peripheral facial weakness, which involves all of the facial muscles ipsilateral to the side of facial nerve that is damaged. Bell’s Palsy is defined as idiopathic because there is no specific cause that has been determined. No lab or imaging tests are usually required to diagnose Bell’s palsy because it is diagnosed by exclusion of other possibilities of facial paralysis. A CBC, blood glucose, and hemoglobin Ac were performed by the physician on this patient because diabetes is a risk factor for Bell’s palsy. More than percent of patient’s with Bell’s palsy also have diabetes mellitus. The severity of the nerve damage is determined by the House-Brackmann grading system. The grading system is also useful as a baseline to watch progression and recovery of the facial palsy before starting treatment. Grade I is characterized as normal facial function in all areas. Grade II is described as slight dysfunction. There is slight weakness on close inspection, very slight synkinesis (abnormal involuntary facial movement), complete eye closure with little effort, and only slight mouth asymmetry. Grade III is described as moderate dysfunction, and presents with obvious, but not disfiguring difference between the sides, noticeable but not severe synkinesis, complete eye closure with maximum effort, and hemi-facial spasm. Grade IV is moderate-severe dysfunction with obvious weakness and/or disfiguring asymmetry, asymmetric mouth with maximum effort, and incomplete eye closure. The patient is graded as IV on the House-Brackmann scale. Grade V is severe dysfunction and presents with just barely perceptible motion, incomplete eye closure, and slight mouth movement. Grade VI is described as total paralysis, so there is no movement.
The patient was prescribed prednisone. Prednisone is a corticosteroid; it is an anti-inflammatory and immunosuppressant drug. It is best to administer the steroid within hours of the onset of symptoms, in order to get the full effect of the steroid. The patient was prescribed prednisone to reduce inflammation and swelling of the facial nerve. The facial nerve pathway travels from the pons, through the facial canal, and exits the skull at the stylomastoid foramen. The swelling and inflammation of the nerve can result in the nerve being compressed due to the pressure of the bony canal of the stylomastoid foramen pressing on it. This leads to a lack of innervation to the facial nerve, resulting in ipsilateral facial muscle paralysis. In a randomized control trial, the recovery rate of patients with Bell’s palsy taking prednisone was % at months, and.% in patients that were not taking prednisone. So there proved to be some benefit to the steroid. The patient was also prescribed an anti-viral medication, oral acyclovir. This drug is usually taken to treat HSV. The reason oral acyclovir was prescribed is because the inflammation of the facial nerve could be related to HSV-. It was prescribed in combination with prednisone because with prednisone being an immunosuppressant, there’s an increased potential for HSV to erupt. If the virus became active the patient’s would be prone to an ocular infection and signs and symptoms would be exacerbated. Currently there is no evidence to prove there’s benefit to using an antiviral drug alone, and it’s uncertain if it’s beneficial to take with corticosteroids.
Erythromycin is a macrolide antibiotic ointment to treat bacterial infections of the eye. The antibiotic stops the growth of bacteria by inhibiting protein synthesis. This could be of benefit for the patient because she is at an increased risk of infection due to her eye not closing completely. The patient already has progression of inferior keratitis which could be the result of her cornea being exposed or from a bacterial infection. Erythromycin could also benefit the patient because her dry eye symptoms could likely be caused by MGD. MGD is the cause of dry eye symptoms in over % of patients with dry eye. MGD occurs when the glands are clogged, decreasing the amount of oil or lipid reaching the ocular surface. It can develop from bacterial infections, usually due to poor lid hygiene. The patient’s keratitis can lead to a corneal ulcer, so you want to try and prevent this by using erythromycin ointment. Keratitis is inflammation of the cornea, and a corneal ulcer is an open sore on the cornea. A corneal ulcer often occurs due to a bacterial infection or viral infection, such as herpes simplex virus. It can also occur from dry eye disease and any disorders that prevent your eye from completely closing, such as Bell’s palsy. A patient may be instructed to tape their eyelid shut to help heal an epithelial defect or to avoid exposure keratitis when they cannot close their eyelid normally. Lightweight and waterproof tape is recommended for the patient to avoid a skin reaction on the eyelid. Before applying the tape, make sure the eyelid is clean and dry, and apply the top half of the piece of tape to the lower half of the upper eyelid and the bottom half of the tape below the bottom eyelid. The patient should not be able to open the taped eye.
Another useful method is creating a moisture chamber by adhering plastic wrap to the eyelid for an airtight seal. Other methods used to treat or manage Bell’s palsy and exposure keratitis are eye patches, scleral lenses for protection and dryness, tarsorrhapy surgery if the exposure keratitis is severe, and eyelid weights are a non-surgical treatment that can help with eyelid closure in patients with facial palsy. Physical therapy with facial exercises, and electrical stimulation are non-drug therapy options for Bell’s palsy, and have been used to speed up recovery; but there is no current evidence to prove any significant benefit of these. Surgical decompression has been recommended in the past for patients experiencing persistent loss of function at two weeks of the onset.
The incidence of Bell’s Palsy is about per, people per year, or about in to people in a lifetime. The symptoms of Bell’s palsy vary from mild to severe paralysis, but prognosis is typically good. Approximately % of patients with Bell’s palsy that do not receive treatment will have a full recovery. The reoccurrence rate of Bell’s palsy is low, only about % of patients will have a reoccurrence, and there’s equal incidence of ipsilateral and contralateral recurrence.