Horner Syndrome Secondary to Bullet Fragments

Horner syndrome occurs when ipsilateral oculosympathetic innervation is compromised and results in 1 mm to 2 mm of eyelid ptosis, pupil miosis, and facial anhidrosis.¹ Numerous causes exist, but the most common are idiopathic, carotid artery dissections, and surgical/iatrogenic.^2-4 In the following case, we diagnosed Horner syndrome in a patient with a longstanding chest injury from retained gunshot shrapnel.

CASE REPORT

A 72-year-old Black male presented to our clinic for a second opinion on the presence of anisocoria. The patient had no visual complaints, but reported a medical history of diabetes mellitus, hypertension, chronic obstructive pulmonary disease, and myocardial infarction. He had a remote history of a gunshot wound to his left thoracic cavity 26 years earlier, which resulted in nine bullet fragments becoming lodged in his left upper lung. He had also been a cigarette smoker for 60 years.

The patient’s VA was 20/25 OS. Confrontation visual fields and extraocular motilities were normal OU. A 2-mm ptosis of the upper left eyelid was noted. Pupils were equally reactive to light, but showed anisocoria with left pupillary miosis that was worse in the dark than in bright light conditions (Figure 1). Apraclonidine 0.5% was instilled OU to check for denervation hypersensitivity; after 45 minutes, reversal of anisocoria was noted, confirming the diagnosis of Horner syndrome OS (Figure 1).

The remainder of the patient’s eye examination was normal, except for mild cataracts OU. Brain, neck, and chest CT scans were performed due to the known presence of metal foreign bodies. Brain and neck CT were within normal limits, but the chest CT clearly showed the longstanding bullet fragments from the patient’s previous trauma (Figure 2).

DISCUSSION

The oculosympathetic pathway involves three neurons and travels ipsilaterally from the hypothalamus to approximately the T1-T2 vertebrae, where the second-order neuron eventually travels over the apex of the lung to synapse at the superior cervical ganglion. The third-order neuron ascends back to the eye via the internal carotid arteries.^1,5 Given the proximity of the bullet fragments to the upper parts of the patient’s left lung, it is apparent that his Horner syndrome can be attributed to the trauma to his second-order neuron.

Historically, hydroxyamphetamine or cocaine eye drops have been used to help localize lesions to central/preganglionic and postganglionic pathways.⁶ However, these particular substances can be difficult for the average eye care provider to obtain. Apraclonidine has shown excellent efficacy in helping to diagnose Horner syndrome in patients with denervation hypersensitivity of the affected eye due to its weak alpha-1 receptor agonism, resulting in reversal of anisocoria and improved ptosis.⁶ One recent article recommends that apraclonidine now be considered the gold standard in place of cocaine testing for Horner syndrome, as it is more reliable and more widely available.⁷ Infrared photography and digital pupillometry have shown to be helpful tools in documenting anisocoria, as in this case.^8,9

It is important to be mindful of specific case history details in patients presenting with Horner syndrome. In this case, the patient’s 60-year cigarette smoking habit was certainly concerning for the development of lung cancer at the apex of the lung (ie, Pancoast tumor), which can be a cause of Horner syndrome.^2,4,5 However, the absence of a tumor on the chest CT scan ruled out lung cancer at this time. Regardless, we feel that such patients should still be counseled on smoking cessation.

pay attention to detail

A thorough case history can help identify an underlying cause of Horner syndrome when encountered clinically. This case highlights the importance of proper pharmacologic testing and neuroimaging in previously undocumented cases of Horner syndrome.