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The Use of Anesthetics, Steroids, Non-Steroidals, and Central-Acting Analegesics ini the Management of Ocular Pain

Lorne Yudcovitch, OD, MS, FAAO

 



 

INTRODUCTION

It is not uncommon for the optometrist to have patients presenting to the office with complaint of eye pain.  Many ocular conditions can present with varying amounts of pain (Table 1).  Pain is highly subjective, and is dependent on the type and severity of ocular insult, the chronicity of the pain symptom, and the experiential and psychological background of the patient.  As pain is subjective, the amount of pain for the same ocular insult can vary widely from patient to patient.  For example, some patients may not express any pain for a corneal abrasion, while others may relay excruciating pain for a similar injury.  Often a scale of 0 to 10 is asked by the optometrist to help them understand the amount of pain their patient is experiencing (Figure 1).  Elucidating if the pain is “burning”, “stinging”, “sharp”, “dull”, “itching”, “throbbing”, may be of diagnostic use.  Likewise, localizing if the pain is on the surface (i.e. the patient notices it with each blink) versus deeper (i.e. the patient feels a retrobulbar pain on eye movements) is also important diagnostically. 

 

Figure 1. Universal Pain Assessment Tool, incorporating 0 to 10 Scale, Verbal Descriptor Scale, Wong-Baker Facial Grimace Scale, and Activity Tolerance Scale.  From http://www.anes.ucla.edu/pain/FacesScale.jpg

 

The clinician may be hesitant to treat the associated pain, due to misconceptions or fear in using narcotic agents, relying on the primary treatment alone to also reduce the pain, and/or not taking the patient’s symptoms of pain seriously.  Pain can affect the physiological state of cardio-respiratory function (often increasing heart rate and breathing, and causing peripheral vasoconstriction – all potentially leading to systemic hypertension), gastrointestinal function (poor food absorption and gastric ulcer formation), and psychological function (increased anxiety, insomnia, depression, and emotional distress).  Patients may be less willing to adhere to a treatment plan if pain persists.  It is imperative that optometrists judiciously treat for pain along with treatment of the causative eye disease.

This course serves to familiarize the reader to various analgesics used in treating ocular pain, and provide a basic background for the indications and contraindications of each.  It also serves to provide fundamentals of pain pathophysiology and management strategies for various ocular conditions that can have associated pain.

 

Table 1. Various Ocular Conditions that can Present with Accompanying Pain

Acute Angle Closure Glaucoma

Abrasion/Laceration/Foreign Body – Cornea, Conjunctiva, Globe, Adnexa

Adenoviral Keratitis

Blepharitis

Chemical Burn – Cornea, Conjunctiva, Globe, Adnexa

Conjunctivitis

Corneal Edema/Bullous Keratopathy

Corneal Ulcer/Infiltrate

Dry Eye Syndrome

Herpetic Keratitis

Hordeolae

Inflamed Pterygium

Optic Neuritis

Orbital Orbital Fractures/Pseudotumor/Tumor

Pingueculitis

Post-Herpetic Neuralgia

Post-Surgical – LASIK, PRK, Cataract, Keratoplasty

Preseptal/Orbital Cellulitis

Recurrent Corneal Erosion

Referred Orbital/Adnexa Pain – Sinusitis, Dental Disease

Scleritis/Episceritis

Traumatic Ecchymosis

Uveitis

 

Figure 2 shows the physiological pathway of pain.  Specific nerve endings in peripheral tissue (usually in the subepithelial layer), called nociceptors, are activated by mechanical, thermal, or chemical stimulation – these stimuli can be external (outside the body) or internal (within the body).  Figure 3 shows the arachidonic acid pathway, which produces the inflammatory mediators: prostaglandins, leukotrienes, and thromboxanes.  The prostaglandins (primarily PGE2) and leukotrienes sensitize the nociceptors to other inflammatory mediators – bradykinin (cytokine) and histamine, among others – which interact with substance P (preparation – a tachykinin neuropeptide released from the peripheral neurons) to stimulate the nerve endings.  Substance P also stimulates mast cells to release more histamine as well as more prostaglandins and bradykinins, further stimulating the nociceptors.  Substance P also contributes to swelling and redness in the area of pain.

Figure 2.  Physiological pathway of pain.  Injury stimulates peripheral nociceptors, which synapse in the dorsal root ganglion to send signals of pain to the brain.  Inflammatory mediators are released which again stimulate the nociceptors, which in turn release Substance P to create mast cell degranulation and peripheral vasodilation  (From http://instruct1.cit.cornell.edu/courses/psych396/student2006/ the_biology_of_pain_ mac_version/receptor2.jpg).

 

 

 

Figure 3. Arachidonic acid pathway responsible for the inflammatory mediators associated with pain (From: Pharmacotherapy 2003, Pharmacotherapy Publications).

 

Sudden pain stimulus usually produces a fast “reflex arc” response, which may not give a feeling of pain.  The sensory neuron synapses with the motor neuron in the dorsal horn of the spinal cord, resulting in a rapid muscular response.  An example of this would be removing one’s hand from a hot iron.  Soon after this response, a “physiological” response is perceived.  This occurs via the pain signal traveling up the spinal-thalamic tract to the thalamus.  As the thalamus also controls cardiac and pulmonary function, increased heart rate and breathing may occur.  Finally, higher-order synapses in the cerebral cortex create the “pain sensation” perception (Figure 4).  People vary widely in terms of their reaction to and severity of each of these responses.

Figure 4. Thalamic and higher cortical pathway of pain perception.  Afferent fibers, transmitting the pain signal, synapse in the dorsal root ganglion, transferring the signal up the spinothalamic tract to synapse in the thalamus.  A final synapse with primary sensory cortex fibers occurs in the thalamus (From http://www.pharmpedia.com/).

 

 

The transmission of ocular pain is primarily via the trigeminal (V) nerve, which has three main branches – maxillary, mandibular, and ophthalmic (Figure 5).  Of these branches, the ophthalmic branch is the main transmitter of ocular pain.  The corneal nerves are linked to the ophthalmic branch of the trigeminal nerve, and any insult on the corneal nerves is quickly perceived as pain.  Likewise, the nerves innervating the iris are also linked to the ophthalmic branch.  Other nerves which can transmit pain from the ocular area are the facial nerve (VII) - particularly related to eyelid and adnexal disease - and the optic nerve (II) – related primarily to neuritis or compressive insults.

 

Figure 5.  The branches of the trigeminal nerve (cranial nerve V).  The three main branches of the trigeminal nerve are mandibular, maxillary, and ophthalmic.  (from http://www.stjosephsatlanta.org/gamma_knife_center/).

 

Clinical evaluation of these three nerves is fairly straightforward.  The practitioner can perform a cotton wisp test (or use a corneal anesthesiometer) to elicit the blink reflex, indicating sensory transmission of mechanical stimulus via the ophthalmic branch of nerve V (Figure 6).   Nerve VII sensory response can be determined by lightly pressing a dull object (i.e. eraser head) or a sharp object (i.e. needle) randomly on the patient’s skin of the eyelids, adnexa, forehead and cheeks, with the patient’s eyes closed during the testing.  The patient then relays to the doctor if they feel a dull or sharp sensation after each press (Figure 7).  Nerve II sensory response may be determined through the patient relaying a sense of pain behind the eye or eyes upon extraocular motilities.

Figure 6.  Corneal cotton wisp test (corneal anesthesia test) (from http://www.cehjournal.org/extra/ts09_14.htm).

 

Figure 7. Facial nerve (cranial nerve VII) sensitivity testing.

 

 

Healthcare practitioners have an armamentarium of medications (termed analgesic drugs) to control pain.  These medications affect various steps in the pain response, from initial stimulation to final cortical perception.  The three main types of analgesic drugs are:

 

 

Adjuvant agents, although not directly providing analgesic effects themselves, may enhance the pain-killing effect of analgesic agents.  Examples of adjuvant agents are: