A 26-year-old male with no significant past medical history presented to the ED after slipping on wet pavement and hitting his head on the ground three hours prior. He endorsed a constant, achy 7/10 headache accompanied by nausea and photophobia. He denied vomiting, dizziness, diplopia, loss of consciousness, or seizures. Nothing made it better or worse.
This patient has a classic presentation of Mega Cisterna Magna (MCM). MCM is a rare cystic posterior fossa malformation characterized by a 10 mm or larger cisterna magna on midsagittal planes, absent hydrocephalus, and an intact cerebellar vermis. Most cases of MCM are found during prenatal ultrasonography. Adults with isolated MCM are typically asymptomatic and found incidentally on radiographic imaging. No follow-up or treatment is needed.
More than 90% of patients with isolated MCM (such as our patient) have a favorable prognosis and normal development. However, there are multiple conditions that have been found to be associated with MCM. Developmental or cognitive delay occurs in about 8% of patients with MCM, and patients with MCM scored slightly lower than controls when comparing memory, executive functioning, and language fluency. MCM is also associated with other central nervous system (CNS) anomalies; the most common being ventriculomegaly, cerebellar hypoplasia, and arachnoid cysts. Renal defects, such as a horseshoe kidney, are the most common extra-CNS anomalies.
Mega Cisterna Magna is a cystic posterior fossa malformation typically found on perinatal ultrasonography or incidentally on cranial imaging in asymptomatic patients. MCM is a benign condition with no need to follow up or initiate treatment.
Mega Cisterna Magna is associated with developmental and cognitive delay, inferior memory, executive functioning, and verbal fluency, renal defects, and other CNS anomalies.
A 50-year-old Caucasian female with a history of hypertension, coronary artery disease, and insulin-dependent diabetes mellitus presents to the emergency department with a complaint of painful sores on the top of her left foot. She notes that ulcerations have formed over the past two weeks and reports a history of multiple recurrent usually non-tender skin lesions to her lower extremities, forearms, and hands over the past twenty years. She is homeless and medically non-compliant secondary to financial issues.
Skin: Multiple yellow-brown and violaceous plaques on the pretibial lower extremities and feet, some exhibiting ulceration with central necrosis and surrounding erythema. Raised reddish-brown well-demarcated plaques with waxy centers were also noted on the dorsal forearms and hands.
Necrobiosis Lipoidica – This patient had a previous skin biopsy with histopathologic changes demonstrating a granulomatous dermatitis involving the dermis and subcutaneous tissues with necrobiosis of collagen and inflammatory infiltrates of lymphocytes and plasma cells consistent with a diagnosis of necrobiosis lipoidica.
Necrobiosis lipoidica is a rare, chronic, idiopathic, granulomatous disease of collagen degeneration classically associated with type 1 diabetes (with a prevalence of 0.3 to 1.2%). It may present as the first clinical finding of or a precursor to diabetes, although its course is unaffected by glycemic control and it is unrelated to other diabetic complications including renal, ocular, and vascular problems. It has been associated with thyroid disease, inflammatory bowel disease, rheumatoid arthritis, and sarcoidosis. It may be equally common in patients without diabetes, hence was renamed without the term “diabeticorum”.
Necrobiosis lipoidica typically is asymptomatic and presents in females (average onset at age of 30) as small, well-demarcated papules that expand into waxy-centered plaques with indurated borders that may resolve spontaneously (up to 17%) or may be complicated by ulceration, infection, and occasionally transformation to squamous cell carcinoma. The differential diagnosis includes other granulomatous and inflammatory diseases such as granuloma annulare, sarcoidosis, rheumatoid arthritis, and necrobiotic xanthogranuloma. The diagnosis is suggested by clinical presentation and is proven by biopsy.
Complications of necrobiosis lipoidica include long-term scarring, ulceration (more common in males), infection, and when lesions are chronic they may rarely transform into squamous cell carcinoma. There is no cure for necrobiosis lipoidica, and some skin lesions may resolve spontaneously, therefore, treatment is focused on addressing any complications. Multiple medical and surgical interventions have been tried. Topical and intra-lesional corticosteroids have been used to stabilize rapidly enlarging lesions with limited success, however, have the potential to cause further skin atrophy. Surgical interventions including debridement and skin grafting are discouraged as in necrobiosis lipoidica trauma tends to induce the Koebner phenomenon.
A 52-year-old male presents to the Emergency Department with a chief complaint of right lower abdominal pain with urinary frequency and urgency over the past week. The pain radiates from his right groin with 10/10 severity at times. He reports multiple diagnoses of urinary tract infections over the last year requiring oral antibiotics. He claims intermittent constipation, denies any trauma, and is a truck driver by trade.
Vitals: T 97.7 °C; BP 138/75; HR 75; RR 16; O2 sat 96%
General: WDWN obese male, A/O x4, in mild distress
Abdomen: Soft, nondistended, normoactive bowel sounds, no organomegaly. A 5 cm moderately tender soft tissue bulge suggestive of a direct hernia is palpated in the right inguinal area and is reduceable.
This patient’s CT scans demonstrate an inguinal herniation of the urinary bladder, which occurs in less than 4% of all inguinal hernias. The clinical finding of a soft tissue mass in the groin in the setting of recurrent urinary tract infections should include urinary bladder herniation in the differential diagnosis.
Oral or parenteral antibiotics based on clinical presentation and prevalent sensitivities should be given to address urinary tract infections. Emergent or non-emergent (if reduceable) surgical consultation, usually by a urologist, is standard. Surgical reduction and repair techniques that utilize mesh versus non-mesh have been associated with a better prognosis with less recurrence.
Branchu B, Renard Y, Larre S, Leon P. Diagnosis and treatment of inguinal hernia of the bladder: a systematic review of the past 10 years. Turk J Urol. 2018 Sep;44(5):384-388. doi: 10.5152/tud.2018.46417. Epub 2018 Sep 1. PMID: 30487042; PMCID: PMC6134980.
Papatheofani V, Beaumont K, Nuessler NC. Inguinal hernia with complete urinary bladder herniation: a case report and review of the literature. J Surg Case Rep. 2020 Jan 2;2020(1):rjz321. doi: 10.1093/jscr/rjz321. PMID: 31911827; PMCID: PMC6939942.
A 10-year-old male with no past medical history presents to the Emergency Department (ED) by EMS for evaluation of an injury sustained while playing tackle football. The patient was forcibly hit by another child against a tree. He complains of sharp right shoulder and chest pain that worsens with movement of his right upper extremity and he arrives wearing a sling to immobilize the arm.
Cardiovascular: RRR without murmurs, rubs, or gallops, peripheral pulses 2+ throughout
Pulmonary: Bilateral breath sounds, clear to auscultation
Chest: Inability to visualize the right medial clavicular notch or clavicular ridge along with palpable tenderness at the right upper sternoclavicular joint
MSK: The shoulders are asymmetric with the right slightly higher than the left. The right arm is held adducted and internally rotated in a sling. The patient is reluctant to abduct the right arm secondary to pain.
Neuro: No gross motor or sensory deficits were appreciated
SC joint dislocation can occur with anterior or posterior displacement of the medial clavicular head. Anterior dislocations are mostly caused by medial impact to the lateral shoulder. Anterior dislocations are more common and generally regarded as less serious. Conversely, posterior dislocations are more serious but less common. Posterior dislocations usually result from impact directly to the anterior chest wall. High-speed motor vehicle accidents or high-impact sports are common causes of posterior dislocations.
Subclavian vascular injury, pneumothorax, esophageal injury, cardiac arrhythmias, brachial plexus injury, tracheal injury, and thoracic outlet syndrome are all potential complications of an SC joint dislocation. When the medial head of the clavicle is forced posteriorly into the superior mediastinum several structures are at risk of impingement which could cause serious complications. In patients with suspicion of clavicular fracture or dislocation, the presence of dyspnea, stridor, dysphagia, or hoarseness should raise genuine concern for a compressive mediastinal syndrome that may require emergent closed or surgical relocation attempts.
An anterior medial head sternoclavicular dislocation is generally apparent and easily palpable on physical examination, while a posterior dislocation may be difficult to appreciate.
A posterior medial head sternoclavicular dislocation may require computed tomography to diagnose and requires computed tomography angiography to fully assess all mediastinal structures.
Closed reduction is the gold standard for the treatment of non-complicated posterior dislocations. Surgical fixation may be required when compressive complications such as vascular injury are confirmed or when closed reduction is unsuccessful.
Patients with a previous history of sternoclavicular dislocation are at higher risk of developing thoracic outlet syndrome.
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.