SAEM Clinical Images Series: A Rash You Don’t Want to Miss

rash

A 54-year-old female with a past medical history of diabetes presented to the Emergency Department (ED) for evaluation of unresponsiveness. The patient was found unresponsive by her spouse, who notes she had missed several doses of insulin over the past few days. EMS notes the glucometer read ‘HIGH’ on fingerstick. The patient remains unresponsive on presentation and is unable to contribute further history.

Vital Signs: BP 148/105; HR 120; RR 24; Pulse Oximetry 98% on room air; Temperature 97.7°F

Constitutional: Patient is morbidly obese, unresponsive, and toxic-appearing.

Cardiovascular: Regular rhythm with tachycardia. No murmur.

Pulmonary: Pulmonary effort is normal. Lungs clear to auscultation bilaterally.

Abdomen: Abdomen is soft and non-distended. Unable to assess for tenderness given unresponsiveness.

Skin: Cool, pale, mottled. Large gangrenous, draining, foul-smelling wound on proximal left thigh. There is necrotic, malodorous, black skin noted over the left lower abdomen and left upper thigh.

Neurological: Unresponsive. GCS 3.

White blood cell (WBC) count: 20.5

Comprehensive metabolic panel (CMP): K 5.8; Cr 2.06; BUN 86; Glucose >600

Venous blood gas (VBG): pH<7; lactate 3.4; bicarbonate 7

These photographs show advanced Fournier’s Gangrene, a form of necrotizing fasciitis located in the genitals, perineum, or perianal region. Rapid involvement of our surgical colleagues is crucial, as these patients will not recover without the debridement of affected tissues. Aggressive fluid resuscitation and broad-spectrum antibiotics can be initiated after a surgical consult is made.

This patient presented with impressive visual evidence of advanced disease including severe ecchymosis, but our clinical suspicion must be high as Fournier’s is rapidly progressing and carries a high mortality rate (may be upwards of 30%). Earlier symptoms are genital or perineal pain which may be associated with itching, lethargy, or fever. The biggest exam finding to keep in mind is ‘pain out of proportion to the exam’ as up to 40% of these patients may present without localized symptoms. Advanced disease, as seen in this patient, can present with crepitus and severe ecchymosis of tissue involved. This patient was also found to be in DKA, as evidenced by her laboratory findings. This case should serve as a reminder that it is vital to perform a proper skin examination in patients presenting with hyperglycemia. Ultimately in this case, the patient was intubated for airway protection and started on vasopressors for cardiovascular support in the setting of septic shock. She went into VTach arrest and was successfully defibrillated before further decompensating and becoming asystolic.

Take-Home Points

  • The first task after suspected diagnosis of Fournier’s Gangrene is a page to your surgery service for evaluation and emergent debridement in the OR (depending on your institution this may be general surgery, urology, or both). After your patient is on the path to definitive management, you can begin aggressive fluid administration and broad-spectrum antibiotics (gram-positive, gram-negative, and anaerobic coverage needed).
  • Fournier’s Gangrene is a clinical diagnosis. Imaging may assist in atypical or borderline cases, but should never result in delay of surgical evaluation and treatment. Crepitus and ecchymotic tissue are very late findings; have high clinical suspicion inpatients with signs of swelling, erythema, and pain.

  • Shyam DC, Rapsang AG. Fournier’s gangrene. Surgeon. 2013 Aug;11(4):222-32. doi: 10.1016/j.surge.2013.02.001. Epub 2013 Apr 8. PMID: 23578806.
  • Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit Care Med. 2011 Sep;39(9):2156-62. doi: 10.1097/CCM.0b013e31821cb246. Erratum in: Crit Care Med. 2011 Nov;39(11):2592. Dosage error in article text. PMID: 21532474.
  • Harbrecht BG, Nash NA. Necrotizing Soft Tissue Infections: A Review. Surg Infect (Larchmt). 2016 Oct;17(5):503-9. doi: 10.1089/sur.2016.049. Epub 2016 Aug 2. PMID: 27483003.
  • Singh A, Ahmed K, Aydin A, Khan MS, Dasgupta P. Fournier’s gangrene. A clinical review. Arch Ital Urol Androl. 2016 Oct 5;88(3):157-164. doi: 10.4081/aiua.2016.3.157. PMID: 27711086.
  • Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009 Feb;208(2):279-88. doi: 10.1016/j.jamcollsurg.2008.10.032. Epub 2008 Dec 12. PMID: 19228540.
  • Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. p.592- 593.

SAEM Clinical Images Series: ‘Tis Not the Season to be Wheezing

wheezing

A 2-year-old male with a history of solitary kidney presented with greater than one month of daily coughing, wheezing, and decreased appetite. The patient was previously seen by his primary care physician after three weeks of symptoms where he was prescribed albuterol as needed for viral bronchospasm. The patient’s wheezing did not improve after two weeks of albuterol treatment so a chest x-ray was ordered. The patient’s mother denied any fevers, vomiting, diarrhea, weight changes, or night sweats.

Vitals: BP 131/60; Pulse 148; Temp 36.7 °C (98.1 °F) (Axillary); Resp 28; Wt 15.7 kg (34 lb 9.8 oz); SpO2 95%

General: Alert; well appearing

HEENT: Pupils equally reactive to light; moist mucous membranes; nares with normal mucosa without discharge

Cardiovascular: Regular rate; regular rhythm; normal S1, S2; no murmur noted; distal pulses 2+

Pulmonary: Good aeration throughout all lung fields; clear breath sounds bilaterally; prolonged expiratory phase; stridor with agitation

Abdomen: Soft; non-tender; non-distended

White blood cell (WBC) count: 56.1/uL (Blasts 58%)

Platelets: 288/uL

Uric acid: 8.3 mg/dL

LDH: 2231 iU/LD

D-Dimer: 3.22 ug/mL

Fibrinogen: 463 mg/dL

Bronchospasm, bronchiolitis, viral infection, pneumonia, foreign body aspiration, space-occupying lesion, vocal cord dysfunction, cardiac dysfunction, and acute chest in patients with sickle cell disease.

The radiograph shown demonstrates a mediastinal mass. This patient was ultimately diagnosed with T-cell acute lymphoblastic leukemia. T-ALL can present with fatigue, fevers, weight loss, easy bleeding/bruising, paleness, or a mediastinal mass. Mediastinal masses found on chest x-ray require further evaluation to determine the diagnosis, location, and treatment. If malignancy is suspected, an oncology referral and bone marrow sample will be necessary.

Take-Home Points

  • In patients with first-time wheezing that does not improve with bronchodilator therapy, consider alternative diagnoses and further evaluation.
  • A mediastinal mass is found at the time of diagnosis in 10% to 15% of children with acute lymphoblastic leukemia.

  • Steuber, P (2021). Overview of common presenting signs and symptoms of childhood cancer.UpToDate. Retrieved January 2, 2021.2.
  • Juanpere, S., Cañete, N., Ortuño, P., Martínez, S., Sanchez, G., & Bernado, L. (2013). A diagnostic approach to the mediastinal masses. Insights into imaging, 4(1), 29–52.https://doi.org/10.1007/s13244-012-0201-0

SAEM Clinical Images Series: An Enlarging Scalp Mass

scalp mass

A 27-day-old female infant born at 34 weeks 4 days with a prenatal history of maternal syphilis treated with penicillin presented with an enlarging scalp mass since birth. Since birth, the patient has had a 1 cm erythematous and flat lesion on her scalp. Since that time, the lesion has continued to grow and develop scales. On the day of presentation, the lesion was noted to be 7-8cm in diameter with multiple surrounding smaller lesions. There is some clear to bloody drainage coming from the main lesion. The patient has otherwise been growing and developing normally. No fevers or other sick symptoms. Feeding well. Mom has no concerns with bowel movements or voiding habits.

General: She is active. She is not in acute distress. She is well-developed.

HEENT: No congestion or rhinorrhea. Mucous membranes are moist. No posterior oropharyngeal erythema.

Cardiovascular: Normal rate and regular rhythm. Normal pulses. No murmur heard.

Pulmonary: Respiratory effort is normal. No retractions. Normal breath sounds. No wheezing.

Skin: Skin is warm. Capillary refill takes less than 2 seconds. On the left side of the scalp, there is a large raised keratinized plaque with a stuck-on appearance. Some red blood is noted when tapped with a white sheet. The plaque is firm and non-tender. On the rest of the scalp, there are several peeling flat lesions with hair attached, and intermittent alopecia.

Neurological: No focal deficit present. She is alert. Suck is normal.

Scalp ultrasound: Posteriorly exophytic left parietal lesion is peripherally echogenic, possibly representing a calcified lesion or cephalohematoma. CT or MRI may be useful for further evaluation, as clinically indicated.

a. Seborrheic Dermatitis: A common, self-limiting eruption consisting of erythematous plaques with greasy, yellow-colored scales that distribute to the areas of the body with sebaceous glands.

b. Atopic Dermatitis: Erythematous, scaly, crusted lesions that are poorly demarcated. It is pruritic and commonly involves the cheeks, scalp, and extensor surfaces.

c. Psoriasis: Uncommon in infants, but can mimic seborrheic dermatitis with sharply demarcated, shiny, erythematous plaques with fine silvery scales in non-intertriginous regions.

d. Tinea Capitis: While rare, tinea can present with a scaly scalp rash in infants. There may be a mild to moderate inflammatory reaction associated as well as hair loss.

e. Langerhans Cell Histiocytosis (LCH): LCH can present as refractory seborrheic dermatitis. There may also be papules or reddish-brown nodules that appear with the rash.

Pityriasis Amiantacea secondary to Seborrheic Dermatitis with a significant build-up of crust and scale. Pityriasis amiantacea is an exaggerated inflammatory response to regional dermatitis, most often seborrheic dermatitis. Treatment consists of a keratinolytic and antibacterial ointment. In this patient, 1:4 part vinegar and water soaks were recommended twice daily, followed by mupirocin ointment until the resolution of the lesions.

Take-Home Points

  • Seborrheic dermatitis is a commonly presenting rash in infancy.
  • When rashes are refractory to conservative management, additional diagnoses and sequelae need to be considered.

  • Amorim GM, Fernandes NC. Pityriasis amiantacea: a study of seven cases. An Bras Dermatol. 2016 Sep-Oct;91(5):694-696. doi: 10.1590/abd1806-4841.20164951. PMID: 27828657; PMCID: PMC5087242.
  • Olanrewaju O. Falusi; Seborrhea. Pediatr Rev February 2019; 40 (2): 93–95. https://doi.org/10.1542/pir.2017-0215. PMID: 30709979.

SAEM Clinical Images Series: My Eye is Swollen

eye

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.

Vitals: T 37.4°C; BP 129/73; HR 91; RR 16

General: A/O x 3; well nourished in NAD

HEENT:  Extraocular movements intact in both eyes. Pupils are equal, round, and reactive to light and accommodation bilaterally. Visual Acuity: OD 20/20, OS 20/25.

Left eye: Diffuse swelling and erythema to the left upper and medial lower eyelids with minimal purulent discharge from the lacrimal puncta. Tenderness localized to the medial canthal region.

Right eye: Normal.

Complete blood count (CBC): within normal limits

Comprehensive metabolic panel (CMP): within normal limits

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.

Take-Home Points

  • 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.

By |2022-09-11T10:08:30-07:00Sep 19, 2022|HEENT, SAEM Clinical Images|

SAEM Clinical Images Series: Unilateral Facial Pain

swelling

A 78-year-old male with a past medical history of Lewy body dementia, hypertension on bisoprolol, hypothyroidism, COPD, chronic lower extremity edema on furosemide, and overactive bladder on oxybutynin presented to the emergency department for evaluation of three days of progressively worsening left-sided neck and facial swelling. Associated symptoms included poor oral intake, a nonproductive cough, and one week of sore throat.

The black arrow represents the left parotid gland.

Vitals: Afebrile; normal room air saturation

HEENT: Firm, tender, warm and erythematous swelling over the left mandibular ramus that extended to the cheek, left neck, and spread caudally into the supraclavicular region and anterior chest. There were no identifiable hard masses or areas of fluctuance. Further inspection of the oral cavity revealed dry mucous membranes, poor dental hygiene without identifiable dental abscess, tonsils were normal size and equal bilaterally, and uvula was midline. Direct pressure externally over the area of concern revealed purulent discharge from Stenson’s duct.

White blood cell (WBC) count: 22.15

Comprehensive metabolic panel (CMP): Na 131; BUN 39; Cr 3.3

Lactic acid: 2.9

Acute suppurative parotitis (ASP) is a serious bacterial infection of the parotid gland that occurs in patients with diminished salivary flow, increased susceptibility to infection, and poor oral hygiene. Our patient had multiple risk factors for this disease which can include dehydration, advanced age, sialolithiasis, medications (diuretics, beta-blockers, antihistamines, phenothiazines, tricyclic antidepressants, anticholinergics), and certain disorders including diabetes, HIV, hypothyroidism, Sjogren’s syndrome. The most common organisms responsible for ASP are Staphylococcus aureus and oral flora anaerobes.

The most feared complications include supraglottitis, cervical necrotizing fasciitis, and other deep neck space infections which can be surgical emergencies and rarely cause impending airway obstruction. Further central and vascular complications include brain abscess, central venous thrombosis, and Lemierre’s syndrome

Take-Home Points

  • The role of bedside ultrasound in acute suppurative parotitis can help to rule out a superficial abscess or sialolithiasis. CT scan is beneficial in ruling out deep space infections as a complication from this disease process or other causes of head and neck swelling.
  • ASP-associated complications are rare but can lead to significant morbidity and mortality secondary to the parotid gland’s proximity to vital structures and ability to spread to adjacent deep spaces.
  • Emergency medicine physicians will manage acute suppurative parotitis and must be aware of the potential complications when determining safe disposition and appropriate treatment.

  • Markovich A, Ronen O. Factors predicting length of stay in patients hospitalized for acute parotitis. J Investig Med. 2021 Feb;69(2):388-392. doi: 10.1136/jim-2020-001506. Epub 2020 Oct 21. PMID: 33087427.

By |2022-09-11T10:03:16-07:00Sep 12, 2022|HEENT, SAEM Clinical Images|

SAEM Clinical Images Series: Breast Swelling

A female in her 50s with a past medical history of coronary artery disease, pacemaker placement, hypertension, and ESRD presented to the emergency department with the chief complaint of missed dialysis, breast engorgement, and an increase in vascularity in her chest and abdomen. The patient reported an increase in breast swelling and increased vascularity in her belly over the past three months. Additionally, she woke up short of breath on the morning of presentation and reported dyspnea at rest. She denied chest pain, diaphoresis, breast pain, fever, rash, trauma to the breasts, or drainage.

Vitals: T 36.9°C; HR 105; BP 109/74; RR 20; O2 sat 97% on nasal canula @ 3L

Neck: JVD

Lungs: Bilateral crackles

Chest and abdomen: Increased vascularity

Breast: Bilateral breast swelling and redness

Lower extremity: Bilateral pitting edema and varicose veins

Basic metabolic panel (BMP): K 6.9; Cr 9.53

Brain natriuretic peptide (BNP): >35,000

Troponin I: 0.1

DDX: Inflammatory carcinoma, mastitis, superior vena cava syndrome, portal hypertension, pulmonary hypertension, pulmonary embolism.

Superior vena cava (SVC) syndrome results from any condition that leads to obstruction of blood flow through the SVC. Our case was caused by complete occlusion from a thrombus and the patient presented with bilateral breast swelling, skin changes (peau d’orange), and an increase in vascularity in the abdomen and chest (caput medusa). Breast tissue largely drains into the axillary veins, and more proximally into the subclavian veins. Due to occlusion of the SVC, a complete backup of venous flow occurs, resulting in all of the noted collateral hypervascularity.  Often SVC occlusion is caused by malignancy obstructing the superior vena cava or invading the vein.

The CTA demonstrates occlusion of the superior vena cava. There are multiple varices in the chest wall and the imaged upper abdominal wall. There is also diffuse subcutaneous edema with diffuse soft tissue swelling and skin thickening of the bilateral breasts.

Take-Home Points

  • Consider superior vena cava occlusion in patients undergoing hemodialysis who present with the above physical exam findings.
  • Consider occult malignancy as the source or cause of thrombosis.
  • Be sure to fully expose your patient when appropriate and keep your differential broad.

  • Corduff N, Rozen WM, Taylor GI. The superficial venous drainage of the breast: a clinical study and implications for breast reduction surgery. J Plast Reconstr Aesthet Surg. 2010 May;63(5):809-13. doi: 10.1016/j.bjps.2009.02.055. Epub 2009 Apr 3. PMID: 19345164.
  • Friedman T, Quencer KB, Kishore SA, Winokur RS, Madoff DC. Malignant Venous Obstruction: Superior Vena Cava Syndrome and Beyond. Semin Intervent Radiol. 2017 Dec;34(4):398-408. doi: 10.1055/s-0037-1608863. Epub 2017 Dec 14. PMID: 29249864; PMCID: PMC5730434.

SAEM Clinical Images Series: Localized Weakness

sturge-weber

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.

Vitals: Temp 36.5°C; BP 186/74; P 74; RR 18; O2 Sat 95%

General: Alert; no acute distress

Skin: Warm; dry; dark red discoloration localized to the left side of face, neck, chest, and upper extremity

HEENT: Normocephalic; left-sided facial droop; pupils are equal round and reactive to light

Cardiovascular: Regular rate and rhythm; no murmurs or gallops

Neurological: Alert and oriented x 4; CN II-XII grossly intact; slow and sluggish speech with left-sided facial droop; motor strength 4/5 LUE and LLE; tremor consistent with Parkinson’s disease

Comprehensive Metabolic Panel (CMP) and Complete Blood Count (CBC) are within normal limits.

Brain Computed Tomography demonstrates chronic atrophy, subcortical calcification, and microvascular ischemia.

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.

Take-Home Points

  • 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.

  • Comi AM. Sturge-Weber syndrome. Handb Clin Neurol. 2015;132:157-68. doi:10.1016/B978-0-444-62702-5.00011-1. PMID: 26564078.
  • 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.

By |2022-08-18T21:54:43-07:00Aug 22, 2022|Dermatology, Neurology, SAEM Clinical Images|
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