What is the proposed mechanism for the pictured antidote when used as a pressor for refractory vasoplegic shock?
Photo used with permission
The following physical finding would be most consistent with exposure to which of the following?
A 4-year-old male with no significant past medical history presents as a transfer from an outside hospital for suspected inhalation burn secondary to a house fire. The patient was home with his father and sibling when the apartment caught fire from a suspected flame in the kitchen. The patient was evacuated from the building by fire rescue after an unknown period of time. He was intubated at the outside hospital due to concern for inhalation injury. It is unknown if the patient sustained any trauma prior to extraction.
A bottle of nail glue and timolol eye drops (reproduced with permission from BMJ Publishing Group Ltd [1])
Artificial acrylic or “press-on” nails were first invented in the 1950s; however, they did not gain in popularity until the 1980s as nail art became a trend [2]. Shortly thereafter, they fell out of style until a resurgence occurred with the COVID pandemic forcing the closure of nail salons. Compared to pre-pandemic values, Google searches for “press on nails” increased 300% [3]. Application of most nails requires nail glue, which often contains a mixture of alcohol, cyanoacrylate (superglue), or photo-bonded methacrylate [4].
Use of nail glue at home can result in adverse exposures with the most common location being the eye [5]. Because nail glue is often packaged in small containers identical to eye drop bottles, patients can mistake the nail glue for ophthalmic drops — especially those with visual impairment [6]. This exposure was first described in the medical literature in 1982 and has been described many times since despite repeated calls for manufacturers to modify the bottles to be safer [1].
In the presence of water, cyanoacrylate rapidly polymerizes, leading to the bonding effect [5]. If the glue gets into a person’s eye, reflexive blinking pushes the glue to the eyelid margins resulting in the eyelashes or eyelid margins sticking together [5], also known as inadvertent tarsorrhaphy. Methods to open the eyelids include removal of glue with forceps, removal or cutting of the eyelashes, or soaking the eye for hours to days with a moist gauze [1, 6, 7].
Although the most successful solvent to dissolve dried glue is acetone, this can cause corneal and conjunctival injuries [8]. The effectiveness of other solvents has been debated in the literature with mixed reports of efficacy [9].
Our personal experience managing several of these cases suggests that a petroleum-based topical antibiotic ointment, such as Bacitracin, can help loosen the glue bond. It is an inexpensive option with minimal harm to fix inadvertent eyelid adhesion from nail glue (or other superglue). It is worth trying before attempting more aggressive techniques.
Before and after application of topical antibiotic ointment to remove inadvertent nail glue causing eyelid adhesion
A 37-year-old male with a past medical history of type 2 diabetes presents to the Emergency Department (ED) with a rash. Initial symptoms began one week prior with small spots on the right leg with associated itching and burning. He initially presented to an outside facility where he was diagnosed with an allergic reaction versus scabies and was given a short course of oral steroids and topical permethrin that provided some relief. The rash progressed to bilateral lower extremities prompting re-presentation to the ED. He also reports associated dark urine and nausea.
GI: Abdomen soft, non-tender, non-distended.
MSK: No joint swelling, tenderness, erythema or warmth.
Skin: Numerous scattered bright red palpable purpuric papules and plaques, most concentrated on bilateral lower extremities extending to lower abdomen at the level of the umbilicus.
White blood cell (WBC) count: 14.5 k
Creatinine: 1.1 mg/dL on day of presentation, peaked at 2.2 mg/dL approximately 10 days later.
C-reactive protein (CRP): 32.7 mg/L
Erythrocyte sedimentation rate (ESR): 34 mm/hr
Urinalysis: 3+ protein, 2+ blood, 11-20 RBC, 26-50 WBC, rare bacteria
This is a case of IgA vasculitis, formerly called Henoch-Schonlein purpura or HSP. This diagnosis is suspected when a patient has purpuric skin lesions predominantly on the lower limbs as well as at least one of the following: abdominal pain, joint involvement, renal involvement (proteinuria/hematuria), and biopsy demonstrating IgA deposition. This vasculitis is more commonly seen in children and has a male predominance.
Similar to children with IgA vasculitis, adults presenting with this palpable purpuric rash can have associated joint involvement and GI involvement, though intussusception is less common in the adult population. Renal manifestations are more common in adults with this diagnosis and range from proteinuria and hematuria to renal failure. Our patient initially presented with hematuria/proteinuria and less than two weeks later had a doubled his creatinine. A renal biopsy later confirmed IgA nephropathy.
A 46-year-old female with a history of diabetes and morbid obesity presents to the emergency department (ED) with difficulty walking after she tripped on a curb and fell onto her right knee. You obtain X-rays (Figure 1). What is your suspected diagnosis? What is your initial workup in the ED? What is your management and disposition?
Figure 1. AP/lateral x-ray of the right knee. Author’s own images.
A 32-year-old male with a past medical history of asthma presents with a two-day history of cracked lips and progressively worsening oral pain, associated with white discharge, foul smell, and a metallic taste. The patient presented to urgent care and was sent to the Emergency Department (ED) for a sepsis workup. The worsening sores caused him to eat and drink less, including the gum he normally chews. He endorses oral sex with one female partner one week ago. No recent dental work. He recently completed a prednisone course for the same issue. Denies fevers, tooth pain, tongue pain, dysphagia, odynophagia, chest pain, difficulty breathing, abdominal pain, genitourinary discharge or lesions, sick contacts, trismus, facial swelling, or voice changes.
Vitals: T 102°F; HR 125; BP 114/81; RR 19; SPO2 94%
General: No distress. Alert and oriented.
Skin: Warm and dry, no rash.
Ears: Hearing grossly intact.
Nose: Bilateral nares patent, no bleeding.
Neck: Soft, symmetric, no adenopathy, non-tender.
Extraoral: Ulcerations on upper and lower lips.
Intraoral: 1 small ulcer on tip of the tongue on the right. Inflamed, erythematous and bleeding gingiva and interdental papilla. Uvula midline. Maximal interincisal opening ~ 40 mm. Teeth intact.
Heart: Regular rate and rhythm, no murmur.
Lungs: Clear to auscultation, air entry to bases.
Abdomen: Soft, non-tender, no guarding.
GU: Patient denied symptoms and declined exam.
White blood cell (WBC) count: 11.4
pH: 7.386
Lactic Acid: 1.7
Urinalysis (UA): Negative Blood. Culture sent.
STI workup including HSV titers and HIV testing obtained and pending.
The differential is broad, including ANUG (acute necrotizing ulcerative gingivitis) also known as “trench-mouth” and, more commonly, primary herpes gingivostomatitis and candidal infection. Consideration of periodontitis and dental abscess/pulpitis is necessary. The spectrum of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis is important to include, as well as autoimmune disorders which commonly have mucosal involvement such as systemic lupus erythematosus (SLE), Behcet’s, and Crohn’s disease. Scurvy, although uncommon, can also present with gingival erythema and pain.
Consider the presence of a known autoimmune disorder, chronic systemic disease, or an immunocompromised state. History should include new sexual partners, dietary changes, and changes in dental hygiene. We were concerned given this patient’s vital signs on presentation, and alongside a sepsis workup, called dental to the bedside. They immediately asked the patient about the recent use of chewing gum and its flavor, and the patient described a recent preference for cinnamon gum, which he had been using for about 1-2 weeks. The dental consultant came to the diagnosis immediately. A literature search reveals a phenomenon called “cinnamon-contact stomatitis” which is believed to be caused by a delayed T-cell-mediated hypersensitivity reaction. It is characterized by white patches on the mucosa with erythema and erosions on the buccal mucosa and lateral tongue. Treatment consists of discontinuation of the offending agent, and corticosteroids in patients with severe symptoms. Lesions can take up to two weeks to heal, and appropriate follow-up with dental is needed to monitor for resolution.
