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What’s Causing a Man’s Weight Loss, Cough, Axillary Pain, Ptosis, and Miosis?

AUTHORS:
Colton Bitely, MD1 • Emily K. Dodge, MD1,2 • David Effron, MD1,2

AFFILIATIONS:
1MetroHealth Medical Center, Cleveland, Ohio
2Case Western Reserve University School of Medicine, Cleveland, Ohio

CITATION:
Bitely C, Dodge EK, Effron D. What’s causing a man’s weight loss, cough, axillary pain, ptosis, and miosis? Consultant. 2020;60(10):17-19. doi:10.25270/con.2020.05.00007
Received December 23, 2019. Accepted April 7, 2020.

DISCLOSURES:
The authors report no relevant financial relationships.

CORRESPONDENCE:
David Effron, MD, MetroHealth Medical Center, 2500 MetroHealth Dr, Cleveland, OH 44109 (deffron@metrohealth.org)


A 68-year-old man with limited previous medical care was sent to the emergency department (ED) after having been seen at a primary care office to establish care for the first time in more than 15 years. The patient’s concerns included an interment nonproductive cough, left-sided neck and axillary pain, fatigue, and a significant weight loss of 36.3 kg over the past 3 to 4 months.

The man smokes about 1 pack of cigarettes per day and drinks 5 to 6 beers per day. He told the ED staff that he was concerned about a possible infection because of an elevated white blood cell count and possible pneumonia on a screening computed tomography (CT) scan of his chest performed during the office visit earlier in the day (Figure 1). The CT appeared to show a left upper lobe mass invading the mediastinum and left upper chest wall.

Figure 1
Figure 1. Chest CT showed a left upper lobe mass invading the mediastinum and left upper chest wall.

The patient’s initial vital signs included a heart rate of 103 beats/min, a blood pressure of 110/54 mm Hg, a respiratory rate of 18 breaths/min, an oxygen saturation of 96% on room air, and a temperature of 36.8 °C. Physical examination findings were significant for decreased breath sounds in the left upper lung fields and left-sided ptosis and miosis (Figure 2). Neurologic examination findings were otherwise normal, including visual acuity. The neck was supple without masses or lymphadenopathy, and no bruits could be heard.

Figure 2
Figure 2. Physical examination findings included left-sided ptosis and miosis.

Answer: Cancer

A demyelinating disorder such as multiple sclerosis would likely be associated with additional neurologic findings that would help localize the lesion, if present. Such findings could include motor deficits, sensory deficits, or neurogenic bladder.1

The patient denied any history of trauma or injury to the neck or head, making trauma an unlikely etiology.

Vascular malformation or injuries such as dissection and aneurysms typically present with ipsilateral neck pain and may be precipitated by numerous events, but they can occur spontaneously, as well.2,3 The patient’s symptom of neck pain should bring this high on the differential; however, his additional symptoms of weight loss, axillary pain, and cough make a malignancy more likely.

The patient had had no establishment of care in the past 15 years and no previous surgical procedures, so an iatrogenic injury is not the cause. The iatrogenic etiology generally involves vascular procedures and even anesthetic complications.4,5

DISCUSSION

This patient had Horner syndrome due to a left-sided Pancoast tumor. Horner syndrome is a neurologic syndrome with 3 classic components: ptosis, miosis, and anhidrosis. It can be caused by a variety of conditions in adults and children. The condition arises from lesions that involve any of 3 neurons along a complex oculosympathetic pathway, making the differential broad, while many cases remain undifferentiated.6 Certain clinical features can help distinguish the diagnosis, which highlights the importance of a careful history and physical examination so as to avoid unnecessary testing. Some patients present with isolated painless Horner syndrome and require further testing and imaging to localize a source, especially considering that one of the most commonly found causes is carotid dissection. The most appropriate imaging modality remains unclear in such cases.7,8

First-order lesions causing Horner syndrome are the least frequent of the 3 etiologies. These lesions can occur from the hypothalamus, brainstem, and the intermediolateral spinal cord from C8 through T2. These lesions may be due to stroke, trauma, and tumors. Second-order lesions can occur anywhere from the ventral nerve roots of C8 through T2, to the apex of the lung, up the mediastinum, and into the cervical sympathetic chain. The differential here remains broad, as well, but again, there are associated symptoms that can help localize lesions. Third-order or postganglionic lesions may arise from the superior cervical ganglion, extending along the carotid artery, cavernous sinus, and to the eye itself.

The treatment of Horner syndrome generally involves targeting the underlying source. Vascular interventions may be required in instances of dissections, and reducing tumor burden may help in cases where mass effect is the culprit. Medically treating and preventing strokes and trying to reduce the effects of a demyelinating disorder would be beneficial in those cases. Additionally, thrombosis may be associated with some lesions, requiring anticoagulation.

This patient’s presentation of weight loss, cough, and axillary pain helps distinguish the diagnosis of tumor affecting the lung apex, causing a second-order lesion. A chest radiograph was obtained in the ED prior to admission (Figure 3) and demonstrated a large left apical mass, with additional masses in the right and left hilar regions, consistent with metastatic disease.

Figure 3
Figure 3. A chest radiograph obtained in the ED prior to admission showed a large left apical mass with additional masses in the right and left hilar regions consistent with metastatic disease.

There was also concern for possible venous occlusion leading to thrombosis. He underwent a contrast study, the results of which revealed right-sided internal jugular venous thrombosis. He was started on therapeutic enoxaparin and subsequently was admitted to inpatient medicine for further workup and anticoagulation. Rivaroxaban was initiated, and the patient was discharged for outpatient workup of the mass.

An outpatient oncology workup revealed stage IV small-cell lung cancer with metastasis to the contralateral lung and some bony lesions, as well. He declined chemotherapy and radiation and elected for palliative care options; he died from the cancer at home 5 months after his initial presentation.

REFERENCES:

  1. Guluma K, Lee JE. Ophthalmology. In: Walls RM, Hockenberger RS, Gausche-Hill M, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Vol 1. 9th ed. Elsevier: 2018:790-819.
  2. Furlan JC, Sundaram ANE. Sudden-onset anisocoria in a patient with upper respiratory tract infection. CMAJ. 2014;186(1):57‐61. doi:10.1503/cmaj.130581
  3. Morgan RD, Kreckler S, Lintott P. Painless Horner’s syndrome through occupational exposure. Am J Med. 2011;124(6):e5-e6. doi:10.1016/j.amjmed.2010.12.024
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  5. Chambers DJ, Bhatia K. Horner’s syndrome following obstetric neuraxial blockade—a systematic review of the literature. Int J Obstet Anesth. 2018;35:75-87. doi:10.1016/j.ijoa.2018.03.005
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  7. Beebe JD, Kardon RH, Thurtell MJ. The yield of diagnostic imaging in patients with isolated Horner syndrome. Neurol Clin. 2017;35(1):145-151. doi:10.1016/j.ncl.2016.08.005
  8. Mollan S, Lee S, Senthil L, Burdon M. Comment on ‘Adult Horner’s syndrome: a combined clinical, pharmacological, and imaging algorithm.’ Eye (Lond). 2013;27(12):1423-1424. doi:10.1038/eye.2013.198