A 56-year-old male presented to the Emergency Department with a chief complaint of painful eyelid swelling and itching upon waking up. He reported no history of trauma or fever. He had one similar episode in the past which was self-limiting. The patient denied vision loss, diplopia, pain with extraocular movement, and ophthalmoplegia.
Acute dacryocystitis. Dacryocystitis is defined by inflammation or infection of the nasolacrimal sac. Whether acute or chronic, acquired or congenital, inflammation is caused by obstruction of the nasolacrimal duct usually from infection, trauma, or a space-occupying lesion. The most common infectious organisms are Staphylococcus and beta-hemolytic streptococcus species. The classic clinical presentation is a sudden onset of swelling, erythema, and tenderness in the medial part of the orbit. Conjunctival injection and swelling around the entire orbit can suggest the development of preseptal cellulitis. Complications of dacryocystitis include orbital abscess, orbital cellulitis, vision loss, ophthalmoplegia, and eyelid necrosis. The differential diagnosis includes dacryoadenitis, lacrimal sac or sinonasal tumor, ethmoid sinusitis, and infected sebaceous or dermoid cyst.
Treatment for dacryocystitis depends on the severity and clinical manifestations of the disease. In mild cases, symptoms will resolve with the application of warm compresses, lacrimal sac massage (Crigler technique), and topical antibiotics if indicated. Severe cases may require oral or parenteral antibiotics and surgical decompression.
Dacryocystitis is inflammation of the medial nasolacrimal sac preceded by obstruction and may be acute or chronic, congenital or acquired.
Dacryocystitis exhibits a bimodal age distribution. The common congenital form is found in infancy, and in adulthood at age of 40 years older.
Dacryocystitis is occasionally mistaken for dacryoadenitis (inflammation of the nasolacrimal gland with superolateral eyelid edema). Far less common, dacryoadenitis is associated with systemic inflammatory conditions such as malignancy, Sjogren syndrome, sarcoidosis, Crohn’s disease, and other autoimmune diseases.
Proper recognition and prompt treatment may prevent serious complications including orbital cellulitis, vision loss, and sepsis.
Alsalamah AK, Alkatan HM, Al-Faky YH. Acute dacryocystitis complicated by orbital cellulitis and loss of vision: A case report and review of the literature. Int J Surg Case Rep. 2018;50:130-134. doi: 10.1016/j.ijscr.2018.07.045. Epub 2018 Aug 9. PMID: 30118963; PMCID: PMC6098209.
Carlisle RT, Digiovanni J. Differential Diagnosis of the Swollen Red Eyelid. Am Fam Physician. 2015 Jul 15;92(2):106-12. PMID: 26176369.
A 69-year-old Caucasian female with a past medical history of seizures, cerebral vascular accident, and Parkinson’s disease presents by EMS for evaluation of a 30-minute episode of left upper and lower extremity weakness and left facial drooping. The patient complains of a right-sided “migraine-type” headache similar to that experienced with her prior stroke.
Port-wine stain birthmark. This birthmark typically occurs on the forehead, scalp, or around the eye, and is unilateral. It is a manifestation of an overabundance of capillaries near the surface of the skin and exhibits a classic light pink to dark red discoloration.
When located around the eye, port wine stains have been associated with an increased incidence of glaucoma. Large port wine stains on the arm or leg have been associated with extra growth in that limb known as Klippel-Trenaunay syndrome. Port wine staining of the face, forehead, and scalp, when associated with cerebral leptomeningeal angiomas that elicit migraine headaches, seizures, strokes, and intellectual impairment as in this patient, are the classic findings of Sturge-Weber syndrome.
Sturge-Weber syndrome is the third most prevalent neurocutaneous disorder impacting 1 in 20,000 live births. It is a sporadic congenital neurocutaneous disorder that is caused by somatic activating mutations in the GNAQ gene.
Sturge-Weber syndrome is characterized by a facial port-wine stain, leptomeningeal angiomatosis, and glaucoma. Brain involvement can begin early in infancy, and manifests as seizures, strokes, stroke-like episodes, and a variety of neurological impairments.
Anticonvulsants, low-dose aspirin, and glaucoma medications are often employed in the management of Sturge-Weber syndrome as well as skin pulse dye laser therapy as desired for cosmesis. The prognosis of this condition depends on the extent of leptomeningeal involvement and the severity of glaucoma.
Higueros E, Roe E, Granell E, Baselga E. Sturge-Weber Syndrome: A Review. ActasDermosifiliogr. 2017 Jun;108(5):407-417. English, Spanish. doi: 10.1016/j.ad.2016.09.022. Epub2017 Jan 23. PMID: 28126187.
A 67-year-old caucasian male experiencing homelessness was “found down” in a parking lot. EMS reported that he had a GCS of 6 with a systolic blood pressure in the 80’s, finger stick glucose of 100, and no response to intranasal naloxone. He was intubated in the field and arrived to the emergency department unresponsive with a BP of 95/60, HR 125, T 38°C, and O2 Sat 100%. Hemodynamic stabilization was achieved with central venous access, and laboratory and imaging studies for the evaluation of altered mental status ensued.
In the appropriate clinical scenario, especially those involving respiratory, cardiac, and neurologic findings where invasive procedures were utilized, the diagnosis of venous air embolism should be entertained.
Immediate management of an air embolism involves administration of 100% oxygen by nonrebreather mask (NRM) or ventilator and placement of the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg positions. Hyperbaric oxygen therapy has also been used if there is no clinical improvement.
The purpose of the Durant maneuver and Trendelenburg position is to trap air along the lateral right ventricular wall, preventing right ventricular outflow obstruction and embolization into the pulmonary circulation.
Gordy S, Rowell S. Vascular air embolism. International Journal of Critical Illness and Injury Science. 2013;3(1):73. doi:10.4103/2229-5151.109428 Malik N, Claus PL, Illman JE, Kligerman SJ, Moynagh MR, Levin DL, Woodrum DA, Arani A, Arunachalam SP, Araoz PA. Air embolism: diagnosis and management. Future Cardiol. 2017 Jul;13(4):365-378. doi: 10.2217/fca-2017-0015. Epub 2017 Jun 23. PMID: 28644058.
A 52-year-old male with a past medical history of prostate cancer status post radiation therapy 10 years prior presents to the emergency department (ED) with the chief complaint of low back pain worsening over the past year. He characterizes the pain as a “dull, aching stiffness” associated with decreased motility.
The classic clinical presentation is an older male with increasing back pain and stiffness that is worse in the morning, as seen in 80% of affected individuals. Common labs are unremarkable in patients with DISH. Peripheral joint involvement is possible, especially in joints that are not normally affected by primary osteoarthritides, such as the foot and ankle. Heel spurs, Achilles tendinitis, and plantar fasciitis may be seen as well. Differentiating features of DISH compared to ankylosing spondylitis include older age of presentation, preservation of facet joints and disk spaces, and no association with HLA-B27.
This patient has an increased risk of spinal fractures. Thus, if an older patient with known DISH presents with acute back pain following minor trauma, the workup will require a comprehensive neurovascular exam and imaging of the entire spine due to the patient’s disposition to spinal fractures.
Diffuse idiopathic skeletal hyperostosis (DISH) is an occult noninflammatory disorder of unknown etiology characterized by calcification and ossification of spinal ligaments and entheses on imaging.
Diagnostic criteria include linear calcification and ossification along the anterolateral aspect of multiple consecutive vertebral bodies, most often seen in the thoracic spine and less commonly seen in the cervical and lumbar spines.
Therapy for patients with DISH is similar to that of chronic lower back pain: physical therapy, exercise, and symptomatic pain management with acetaminophen or NSAIDs.
Patients should be educated to monitor acute changes in localized spine pain or neurologic disturbances, as DISH predisposes patients to fractures, even from minor injuries.
A 53-year-old caucasian male with a history of alcohol and amphetamine abuse presents to the Emergency Department via ambulance immediately after sustaining a fist-blow injury to the right eye. The patient denies loss of consciousness and complains of eye pain with the inability to see.
This procedure is easily performed at the bedside in the ED and the transected lateral canthal tendon and inferior/superior crus can be repaired during the repair of the presenting injury. Patients report improvements in pain and sometimes vision in as little as 10 minutes after the procedure.
A CT should be ordered after performing a lateral canthotomy and cantholysis to minimize the complications associated with elevated retrobulbar pressure including ischemia and permanent loss of vision. This photograph depicts a patient who presented to the ED suffering from the effects of orbital compartment syndrome (OCS) after being punched in the eye. OCS can develop from as little as 7mL of fluid accumulation in the retro-orbital space and can rapidly lead to permanent blindness if ischemia is present for more than 100 minutes. Symptoms of OCS requiring immediate lateral canthotomy and cantholysis include: proptosis, increased intraocular pressure, Marcus-Gunn pupil, decreased acuity, or restricted ocular movements. Importantly, OCS is a clinical diagnosis, and treatment of this condition should not be delayed for further testing or diagnostic workup. While treatment may not result in the return of vision, there are many case reports of patients regaining full or partial vision up to two hours after the onset of symptoms.
A 30-year-old female with no significant past medical history presents to the Emergency Department with a six-day history of an enlarging, tender, red “bump” on her anterior neck. She reports similar swelling during bouts of pharyngitis. She also reports a recent upper respiratory infection one week ago that was marked by fever, cough, congestion, sore throat, and myalgia. She denies shortness of breath, neck trauma, travel, or animal exposures.
Branchial cleft anomalies are the second most common type of congenital neck mass and present as cartilaginous remnants, sinuses, fistulas, or cysts due to the failure of the branchial apparatus to obliterate. The most common are second branchial cleft anomalies, representing 95% of these cases. Second branchial cleft anomalies are usually located along the anterior border of the sternocleidomastoid muscle on the left side of the neck.
Differential diagnoses include thyroglossal duct cyst, neck abscess, cystic hygroma, cervical lymphadenopathy, metastatic lymph nodes, and cat scratch disease.
The gold standard of treatment necessitates complete surgical excision of the entire branchial cleft anomaly. Branchial cleft anomalies are most commonly diagnosed with computerized tomography (CT) that shows a uniformly hypo-or-anechoic mass with well-defined margins and thin walls. Preoperative fine needle aspiration cytology can be used to view histopathological findings of the mass and help to rule out malignant disease. Ultrasound and MRI can also be helpful for diagnosis, preoperative localization, and preoperative identification of surrounding structures. However, for definitive diagnosis, surgical excision of the entire anomaly and pathology examination is required. If full resection is not achieved, recurrence is possible.
Muller S, Aiken A, Magliocca K, Chen AY. Second Branchial Cleft Cyst. Head Neck Pathol.2015;9(3):379-383. doi:10.1007/s12105-014-0592-y Zaifullah S, YunusMR, See GB. Diagnosis and treatment of branchial cleft anomalies in UKMMC: a 10-year retrospective study. Eur Arch 2013;270(4):1501-1506. doi:10.1007/s00405-012-2200-7
A 44-year-old female presents to the emergency department after noticing swelling of her tongue and face, specifically the cheeks and periorbital area. She states the swelling began two weeks ago and has progressively worsened. She also complains of redness.
Myxedema is a term used to describe the appearance of nonpitting edema in patients with severe hypothyroidism. While the exact mechanism is not completely understood, this edema is thought to be secondary to increased deposition of dermal hyaluronic acid, a glycosaminoglycan that can grow up to 1000x its normal size when hydrated. Carotenemia is another possible manifestation of hypothyroidism and is secondary to impaired conversion of carotenoids to retinol in the setting of low levels of thyroid hormone. Additionally, patients may exhibit patchy alopecia, fatigue, cold intolerance, goiter, coarsening of the skin, and macroglossia.
The presentation of hypothyroidism is widely variable and may be subtle or atypical. Classically, hypothyroidism presents with pretibial myxedema, hyporeflexia, and cold intolerance. In some cases, facial edema may be the predominant feature, as seen in this patient.
Brittle, thinning hair on the scalp and eyebrows is a common feature. Thinning of the hair along the lateral eyebrows is called madarosis, also known as “Queen Anne’s Sign.”
In a patient with Grave’s disease, maintain a high index of suspicion for hypothyroidism, either as part of the natural history of the disease or as a sequela of treatment.