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The Case Files is an anecdotal collection of emergency medicine cases to enable physicians and researchers to find clinically important information on unusual conditions.

Case reports should focus on:

    • Unusual side effects or adverse interactions.
    • Unusual presentations of a disease.
    • Presentations of new and emerging diseases, including new street drugs.
    • Findings that shed new light on a disease or an adverse effect.

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Tuesday, September 18, 2018


A 66-year-old woman with a history of type 1 diabetes, hypertension, and end-stage renal disease (ESRD) on hemodialysis presented via EMS to the emergency department with altered mental status. She lived with her family, and they noted that she refused to go to dialysis for her past four sessions and had increasing lethargy for two days.

She was afebrile, and her other vital signs were blood pressure 136/92 mmHg, heart rate 77 bpm, respiratory rate 20 bpm, and oxygen saturation 96% on room air. She was agitated and reaching for objects in the sky. Her cardiopulmonary exam was notable for a regular rate and rhythm with coarse breath sounds bilaterally, and she was alert and oriented x 1 (baseline of AOx3). Her speech was slurred, and her exam was limited due to little patient cooperation and altered mental status.

She was also experiencing asterixis to her arms, and she had 2+ pitting edema bilaterally to her legs, extending to distal knees. An ECG revealed a normal sinus rhythm of 82 and peaked T-waves, with a prolonged PR interval and QT interval concerning for hyperkalemia.

Chest radiography revealed bilateral pulmonary vascular congestion and bilateral pleural effusions. (Images A and B.) A CT of the head without IV contrast was negative for any acute process. Pertinent laboratory evaluation was notable for a white blood cell count of 11.2, hemoglobin of 6.8 g/dL, hematocrit of 21.3, and a platelet level of 370. Basic metabolic panel revealed a hyponatremia of 129, hyperkalemia of 7.8 (non-hemolyzed), blood/urea/nitrogen (BUN) of 81, creatinine of 8.3, glomerular filtration rate (GFR) of 4.5, and blood glucose of 99. Arterial blood gas was notable for a pH of 7.51, pCO2 28, p02 54, HCO3 22, and a lactic acid of 1.6. Other relevant laboratory abnormalities included an ammonia level of 45, brain natriuretic peptide (BNP) of 2572, and troponin of 0.05.

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Image A.

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​Image B.

Nephrology was consulted immediately for emergent dialysis for her hyperkalemia and altered mental status secondary to uremic encephalopathy and medical noncompliance with hemodialysis. The patient received 10 mg albuterol breathing treatment, 10 units of regular insulin intravenous with an amp of d50, and 3 gm of calcium gluconate while preparing for dialysis. Lasix was held because the patient was not making urine. Her acute hypoxic respiratory failure and hypervolemic hyponatremia was likely secondary to volume overload and missed hemodialysis. Her anemia was secondary to renal failure, and she was transfused 1 unit of pRBCs in dialysis. She continued to improve clinically over her hospital course, and was dialyzed three times. Repeat chest radiography showing significant improvement in pulmonary vascular congestion and bilateral pleural effusions.

Uremia is a clinical condition associated with declining renal function and end-stage renal disease. It is associated with electrolyte imbalances, fluid imbalances, and metabolic abnormalities, and is most often seen in patients with ESRD and also may occur in acute kidney injury. (StatPearls, June 15, 2017;

Dysfunction occurs at multiple levels when the kidneys are not functioning effectively, which affects acid-base homeostasis, hormone production/secretion, fluid regulation, electrolyte regulation, and waste elimination. The result can be severe metabolic disturbances and conditions like hypertension, acidosis, hyperkalemia, anemia, and hypothyroidism, and the increased anion-gap metabolic acidosis can lead to lethargy, muscle weakness, hyperventilation, and congestive heart failure. A buildup of uremic toxins contributes to the development of coagulopathy secondary to diminished platelet adhesion, increased platelet turnover, and reduction in the number of platelets, ultimately resulting in a bleeding diathesis. These toxins also contribute to the development of uremic pericarditis, pericardial effusions, and may further worsen valvular function with resulting suppression of myocardial contractility.

Uremia can result in numerous clinical presentations (WikEM, February 2017;, including but not limited to:

  • Cerebrovascular accident (as a result of hypertension, bleeding dyscrasias, and trauma)
  • Peripheral neuropathy (parasthesias, weakness, dizziness, impaired proprioception in 60-100% of dialysis patients)
  • Subdural hematoma (10 times more likely than the general population to develop this as a result of platelet dysfunction)
  • Uremic pericarditis (seen in about 75% of cases, blood urea and nitrogen >60, and a loud friction rub)
  • Tamponade (patients present with hypotension, dyspnea, and altered mental status and seldom present with the classic Beck's triad)
  • Pulmonary edema and congestive heart failure
  • Hematologic abnormalities (anemia and bleeding diathesis with an increased risk of spontaneous intracranial hemorrhage, hematoma of the liver, and gastrointestinal hemorrhage secondary to an impairment in platelet function)
  • Dermatologic abnormalities (crystallized nitrogenous waste from sweat results in uremic frost, often seen with BUN >200)
  • Renal bone disease (amyloidosis, hyperparathyroidism, and metastatic calcification)
  • Increased anion gap metabolic acidosis
  • Uremic encephalopathy

Our patient presented with uremic encephalopathy, a toxic metabolic encephalopathy, which is considered a rare and life-threatening disease in patients with acute or chronic renal failure. Early symptoms include anorexia, irritability, drowsiness, nausea, and delayed cognitive function. As the encephalopathy progresses, patients become confused and disoriented, and may present with emotional instability and bizarre behavior, with eventual coma and death. (StatPearls, June 15, 2017; Asterixis, clonus, hyperreflexia, and tremor have been shown to parallel the degree of mental status changes. (UpToDate, Sept. 1, 2016;

Clinical research has shown that uremic encephalopathy is uncommon when the BUN level is <35. (Clinical Gate, February 2, 2015; It has also been shown that the severity and onset of uremic encephalopathy is associated with the degree of azotemia. (UpToDate, Sept. 1, 2016; Patients presenting with a true uremic emergency with hyperkalemia refractory to medical treatment, lactic acidosis, uremic encephalopathy, and symptomatic pericardial effusion, require emergent dialysis. (StatPearls, June 15, 2017; Signs and symptoms of uremia don't often develop until the GFR is 10-15 mL/min, and no minimum GFR indicates an absolute indication for dialysis without symptoms. (UpToDate, March 5, 2018; “A-E-I-O-U” is a mnemonic for clinicians commonly used for dialysis indications. (First Aid Team, April 7, 2014;

A: Acidosis: increased anion gap metabolic acidosis with a pH <7.1

E: Electrolyte abnormalities: rapidly-rising potassium levels or refractory hyperkalemia

I: Intoxications: lithium, isopropanol, methanol, salicylates, and ethylene glycol

O: Overload: patients presenting with volume overload refractory to diuresis

U: Uremia: elevated BUN with signs and symptoms of uremia, including uremic encephalopathy.

Improvement in uremic encephalopathy can take several months, with some patients never returning to baseline. By day four, our patient was alert and oriented x 3, had no complaints, and her mental status was back to baseline and her potassium was within normal limits at discharge.

Dr. Taylor is a captain in the United States Air Force and an emergency medicine resident at Beaumont Hospital in Farmington Hills, MI, a teaching hospital of Michigan State University, where Dr. Cooley is also an emergency physician.

Monday, September 10, 2018


A 70-year-old woman with a history of breast cancer and a lumpectomy and lymph node dissection 20 years before presented to the ED because of redness and itching for two weeks covering the entire surface of her skin. Two weeks before that, she went for a Pap smear and was prescribed fluconazole for Candida vulvovaginitis infection. She took one dose of the fluconazole and an hour later became itchy and red and felt as if her entire body were burning.

The itching and redness were diffuse and had persisted for two weeks, neither worsening nor improving. She had no exacerbating factors: The symptoms did not worsen with water, soap, or sunlight. She reported some change in her voice and some loose stools, but reported no shortness of breath, wheezing, constipation, sore throat, dysphagia, fever, history of allergies, chest pain, abdominal pain, nausea, or vomiting. She also had no environmental changes at home. Her past medical history was significant for hypothyroidism, for which she took levothyroxine.

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An example of exfoliative dermatitis caused by a reaction to phenytoin.

The patient's vital signs were a blood pressure of 138/44 mm Hg, a pulse of 99 bpm, a respiratory rate of 18 bpm, a temperature of 99.0°F, and oxygen saturation of 99% on room air. The skin on her entire body was red, with mild exfoliation, but no other physical abnormalities were found.

Her initial labs consisted of a CBC with differential, CMP, and ECG. She had a very low potassium level (2.6 mEq/L), but no abnormalities were seen in the ECG. She also presented with normocytic anemia. Electrolytes were corrected in the ED, and the patient was admitted to the hospital and discharged the next day with a prescription for hydroxyzine pamoate, prednisone, and triamcinolone acetonide 0.5% cream.

Pain and Itchiness

Erythroderma, or exfoliative dermatitis, presents as diffuse erythema with scaling involving more than 90 percent of the skin surface. Erythroderma can have various etiologies, including inflammatory skin diseases, immunodeficiencies, drug hypersensitivity, and psoriasis. Erythroderma occurs in about one of 100,000 adults. (J Am Acad Dermatol2001;45[5]:675; When erythroderma is caused by a hypersensitivity reaction, it usually has an acute onset. An urticarial eruption starts anywhere on the body and then various patches appear and further increase in size and coalesce into a confluent rash. (“Erythroderma in adults.” UpToDate; April 3, 2018;

The most common complaints are severe skin pain and itchiness. The duration of the rash is highly variant. Some patients experience it for a few minutes, but others will have had the symptoms for more than six weeks. Erythroderma can produce nonspecific lab abnormalities such as anemia, elevated ESR, and eosinophilia. Complications from erythroderma generally occur in the very young, the elderly, and those with comorbidities. These complications may be infections and hemodynamic or metabolic disturbances. The diagnosis is made purely by presentation. Treatment depends on the severity of the symptoms, and ranges from antihistamines to a combination of antihistamines and systemic corticosteroids. (“Erythroderma in adults.” UpToDate; April 3, 2018;

Fluconazole is an antifungal agent member of the triazole family. Its mode of action is inhibiting the cytochrome p450 enzyme that converts lanosterol into ergosterol. Common side effects of azoles are testosterone synthesis inhibition and liver dysfunction. Erythroderma, commonly known as red man syndrome, is almost always a hypersensitivity reaction caused by vancomycin (most common), sulfonamides, and others. Scant cases have been reported of fluconazole causing erythroderma, which made this case intriguing.

Ms. Vazquez is a third-year medical student and Mr. Kasra, top right, is a fourth-year medical student at the University of Medicine and Health Science in Chicago. Dr. Raziuddin is a board-certified emergency physician and internist at Weiss Memorial Hospital, Gottlieb Memorial Hospital (Loyola University), and Westlake Hospital in Melrose Park, IL.​

Tuesday, August 28, 2018


A 30-year-old G5P3 presented to the ED with bilateral lower-extremity edema and headache for three days. She presented one week after an uncomplicated full-term vaginal delivery with an unremarkable pregnancy course and no prior requirement for antihypertensive therapy. The headache was described as achy to sharp, with associated photophobia. She also noted occasional vaginal spotting, which was common a few weeks after delivery. She denied any chest pain, shortness of breath, nausea or vomiting, abdominal pain, or any other symptoms. She admitted to occasional mild cramping with minimal lochia.

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The patient was afebrile. Her vitals on arrival included a blood pressure of 168/94 mm Hg, heart rate of 82 bpm, respiratory rate of 18 bpm, and 100% on room air. Laboratory evaluation was notable for a hemoglobin of 11.1 g/dL, an aspartate aminotransferase of 44 U/L (13-39), alanine aminotransferase of 131 U/L (7-52), and a uric acid of 8.4 mg/dL (2.5-7.5). The clinical presentation and laboratory evaluation were concerning for postpartum preeclampsia.

Hypertensive disorders of the antepartum and postpartum period (preeclampsia, eclampsia, HELLP, and cardiomyopathy) complicate up to 10 percent of all pregnancies around the world. (ACOG, 2017; These become common causes of maternal and perinatal morbidity and mortality. (EMRA. Jan. 31, 2018; Postpartum preeclampsia may occur without any previous diagnosis of preeclampsia or eclampsia. It can ultimately result in permanent neurologic complications and death. Seizures have been shown to occur even without the typical prodromal symptoms of hypertension, proteinuria, and edema. (J Emerg Med 2011;40[4]:380; Postpartum preeclampsia includes the presence of hypertension and proteinuria occurring up to four weeks after delivery, with a systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg. (J Emerg Med 2011;40[4]:380;

A retrospective chart review identified 22 cases of postpartum pre-eclampsia and eclampsia over seven years. (J Emerg Med 2011;40[4]:380; Common presenting complaints to the ED included headache (82%), visual changes (31%), elevated blood pressure at home (23%), nausea (18%), abdominal pain (14%), edema (9%), and neck pain (9%). Presenting signs included an SBP ≥140 mm Hg (95%), edema (84%), DBP ≥90 mm Hg (77%), proteinuria (64%), hyperuricemia (54%), hyperreflexia (47%), and elevated LFT (41%). Commonly noted laboratory abnormalities were elevated aspartate aminotransferase >47 U/L, elevated alanine aminotransferase >47 U/L, or elevated alkaline phosphatase >117 U/L, and uric acid >5.7 mg/dL.

Hydralazine and labetalol are the mainstays in blood pressure management in the ED. Magnesium sulfate (bolus of 4-6 gm IV over 15 minutes, followed by 2 gm IV per hour over 24 hours) prevents the development of eclampsia, and decreases the seizure recurrence in those who had a seizure. Benzodiazepines and phenytoin are commonly used for refractory seizures. (EMRA. Jan. 31, 2018;; emDOCs. June 7, 2018;

Differential Diagnosis

HELLP syndrome, a multisystem disease, is defined as hemolytic anemia with associated schistocytes or microspherocytes on blood smear, elevated liver function studies (lactate dehydrogenase is often >600 IU/L, aspartate aminotransferase/alanine aminotransferase >70 IU/L, and bilirubin >1.2 mg/dL, with associated thrombocytopenia of <100,000). (emDOCs. June 7, 2018; It is often associated with the antepartum period, but 30 percent of HELLP cases occur within 48 hours and up to one week following delivery. (Life in the Fast Lane. July 19, 2014;

Presenting symptoms can include headache, nausea or vomiting, edema, proteinuria, abdominal pain, and hypertension. Treatment is multifactorial and includes magnesium sulfate to prevent seizures, possible transfusions, and anti-hypertensives. Definitive treatment requires delivery of the fetus with recommendation after 34 weeks if multisystem disease is present. HELLP syndrome during the postpartum period is considered rare and a significant cause of maternal morbidity, with associated disseminated intravascular coagulation and multisystem organ failure.

Eclampsia results in posterior reversible encephalopathy with headache, dizziness, confusion, vision loss or vision changes, peripheral edema, and new-onset, generalized tonic-clonic seizure in a patient with preeclampsia. This is diagnosed after the 20th week of pregnancy, but the risk of occurrence remains till six weeks postpartum. One theory for developing eclampsia is that the hypertension of pregnancy results in a disrupted autoregulatory system within the cerebral circulation, leading to edema and eventually eclamptic seizure. (EMRA. Jan. 31, 2018;

This is considered a form of hypertensive encephalopathy secondary to an increase in vascular permeability. Research has shown that 38 percent of all eclamptic seizures occur during the antepartum period, 18 percent during labor, and 44 percent postpartum. (J Accid Emerg Med 2000;17[1]:7; The literature indicates that the initiation of antihypertensives to prevent a stroke is imperative if the blood pressure is ≥160/110 mm Hg, a leading cause of death and disability in eclampsia.

Postpartum cardiomyopathy (also referred to as peripartum cardiomyopathy) is the development of systolic congestive heart failure in the last month of pregnancy and up to five months after delivery in a patient with no prior history of congestive heart failure. (Life in the Fast Lane. July 19, 2014; Risk factors include age over 30, cocaine abuse, postpartum hypertension, multiple fetuses, and preeclampsia or eclampsia. Criteria to make the diagnosis: systolic heart failure within the last month of pregnancy or five months after delivery, absence of prior heart disease, absence of an identifiable cause of systolic heart failure, and an ejection fraction <45% on echocardiography. Treatment is similar to the treatment for acute decompensated heart failure, involving diuresis, nitroglycerine, and BiPAP. With some studies reporting a mortality up to 32 percent, postpartum cardiomyopathy is a must-recognize disease and among the top differential causes of hypertension in the postpartum period. (Am J Crit Care 2012;21[2]:89.)

Obstetrics and gynecology was consulted for our patient, and she was given 4 gm magnesium sulfate IV over 15 minutes and placed on a 20 gm magnesium infusion for 24 hours with magnesium checks every two hours. She was also started on labetalol. The magnesium infusion was completed over the next 24 hours, her headache resolved, and her blood pressure decreased to 130/85 mm Hg, with downtrending liver function tests. The rest of her hospital course was unremarkable. She remained asymptomatic, and was discharged in stable condition on day three on oral labetalol with outpatient follow-up.

Dr. Taylor is completing his emergency medicine residency at Beaumont Hospital in Farmington Hills, MI, a teaching hospital of Michigan State University. He also serves as a captain and physician in the United States Air Force. Dr. El-Alayli is on staff at Beaumont Hospital as core faculty and a clinical instructor in emergency medicine for Michigan State University.

Tuesday, August 21, 2018


A 47-year-old woman presented to the emergency department with a chief complaint of pain and swelling on her left index finger two days after she was bitten by her cat. Her vitals were within normal limits. Physical exam was notable for two puncture wounds to the left index finger along the radial aspect of the middle phalanx. Fusiform swelling was noted around the proximal phalanx to the level of the MCP joint, with erythema extending to the distal palmar crease. The index finger was held in slight flexion with pain during passive extension and pain with palpation of the tendon. She was neurovascularly intact.

Plain radiographs did not show any evidence of a fracture or foreign body. Her tetanus was updated, and she was started on 3 gm IV ampicillin/sulbactam. Plastic surgery was consulted for flexor tenosynovitis. She was taken emergently to the operating room, and underwent an exploration of the left index finger and palm, decompression of the flexor tendon sheath, decompressive fasciectomy, tenosynovectomy, and decompressive arthrotomy.

Infectious tenosynovitis, also known as pyogenic flexor tenosynovitis, is a purulent infection of the synovial sheath surrounding a flexor tendon. The incidence is up to 9.4 percent of all hand infections. (Orthobullets; An orthopedic and plastic surgery emergency, infectious tenosynovitis must be recognized rapidly and treated accordingly to prevent severe debility. The mechanism of injury involves bacterial invasion by penetrating trauma to the synovial sheath or direct spread from a septic joint, felon, or deep space infection. (Orthobullets; The most common organisms are Staphylococcus aureus (40-75%), MRSA (29%), skin flora (Staphylococcus epidermidis, beta-hemolytic streptococcus, Pseudomonas aeruginosa), Eikenella corrodens (human bite), Pasteurella multocida (animal bite), and gram-negative organisms in immunocompromised patients. (Eplasty2016;16:ic7;

The clinical presentation usually involves pain and swelling within 24-48 hours localized to the palmar aspect of the digit involved. Several inflammatory and infectious processes on the differential may mimic infectious tenosynovitis, including abscess, herpetic whitlow, cellulitis, septic arthritis, gouty/psoriatic arthritis, felon, and trauma. (Clin Orthop Relat Res2016;474[1]:280;

A high degree of clinical suspicion is necessary for a rapid diagnosis and definitive treatment because it is difficult to distinguish a superficial from a deep space infection. Four physical exam findings, the Kanavel signs, help the clinician in the diagnosis. They include the involved digit held in flexion, tenderness over the tendon sheath, pain with passive extension, and fusiform swelling. (Eplasty 2016;16:ic7; One study involving 75 patients with infectious tenosynovitis showed that 97 percent had fusiform swelling of the affected digit, 72 percent had pain with passive extension, 69 percent held their digit in flexion, and 64 percent had tenderness over the sheath. (J Bone Joint Surg Am 2007;89[8]:1742; Only 54 percent of patients had all four Kanavel signs.

Flexor tenosynovitis is mainly a clinical diagnosis. A complete blood count, ESR, and C-reactive protein can help the clinician, but the specificity and negative predictive value are low, and these tests are often used once the diagnosis is already suspected. (Eplasty 2016;16:ic7; Even with prompt recognition and appropriate treatment, there is still the potential for complications, including the spread of infection, tendon rupture, osteomyelitis, and possible amputation. The majority of these cases, however, are in patients with digital ischemia on presentation to the ED, delayed treatment, age over 43, and comorbidities like diabetes, peripheral vascular disease, and renal failure. (Eplasty2016;16:ic7;

Infectious tenosynovitis is truly an orthopedic and plastic surgery emergency. Nonoperative treatment is rare. Most cases require intravenous antibiotics, hospital admission, and surgery. An often-used antibiotic regimen, as in our case, is ampicillin/sulbactam, given the nature of the cat bite (others include cefoxitin or piperacillin/tazobactam). If there is a history of IV drug abuse, prior MRSA, or the patient is immunocompromised, then vancomycin is recommended as an additional regimen. (J Bone Joint Surg Am 2007;89[8]:1742;

Our patient was admitted on intravenous antibiotics following surgery. Culture results revealed Pasteurella multocida. She progressed well, her erythema resolved, and she was discharged on day three on oral antibiotics with outpatient follow-up.

Dr. Taylor is an emergency medicine resident at Beaumont Hospital in Farmington Hills, MI, a teaching hospital of Michigan State University. He also serves as a captain and physician in the United States Air Force. Dr. McDowell is an emergency medicine core faculty at Beaumont Hospital in Farmington Hills, MI, the chair of the Emergency Center Quality Improvement Committee, and formerly a faculty reviewer of research papers for the American College of Osteopathic Emergency Physicians.

Tuesday, August 21, 2018


A 36-year-old man presented to the emergency department with chest pain that had begun 30 minutes earlier. The patient was a mechanic, and said he was working on his car when he developed sharp, constant, mid-sternal, 5/10 chest pain that radiated to his left arm. He had associated nausea and dyspnea. The patient denied fever, cough, recent travel, recent surgery, malignancy, blood clots, hormone use, calf pain, and calf swelling. He did not take any medication for the pain. He denied smoking cigarettes, and had no family history of cardiac disease.

The patient appeared well-developed, well-nourished, and not in acute distress on exam. He was not diaphoretic. His vital signs were an oral temperature of 97.4°F, a pulse of 45 bpm, respiratory rate of 18 bpm, a blood pressure of 106/73 mm Hg, and 100% oxygen saturation on room air. His body mass index was 25.63 kg/m2. The patient was awake, alert, and oriented. Cardiac exam revealed bradycardia with a regular rhythm and normal heart sounds. The patient was not in acute respiratory distress. He had clear lung sounds bilaterally with normal effort. His abdomen was soft, nondistended, and nontender. His legs were not edematous, and his calf was not tender to palpation.

His initial ECG showed sinus rhythm at approximately 50 bpm with 1 mm ST elevation in lead III, 0.5 mm ST elevation in lead II with reciprocal changes of 1 mm ST depressions in V1-V4 and leads I and avL, consistent with an acute inferior wall myocardial infarct. An interventional cardiologist was consulted, and the patient was taken emergently to the cardiac catheterization lab for percutaneous coronary intervention (PCI). The patient received 324 mg chewable aspirin. Blood work was drawn, and the patient had a chest x-ray that showed a tiny nodule in the right mid-lung without focal infiltrate or pleural effusion.

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Figure 1. Inferior wall STEMI: ST depressions in V1-V4 and leads I and avL and 1 mm ST elevation in lead III.

In the catheterization lab, the patient was found to have subtotal right coronary artery (RCA) disease, with 70% lesion in the proximal RCA that was treated with a drug-eluting stent, 99% lesion in the distal RCA with associated moderate filling defect consistent with thrombus and treated with a drug-eluting stent and thrombectomy. The left ventricular ejection fraction was found to be 40-45 percent with inferior wall hypokinesis. The patient tolerated the procedure well, and had no adverse outcomes. He was subsequently transferred to the ICU for continued cardiac monitoring.​

Heart disease is the leading cause of death in the United States with more than 600,000 deaths annually, according to the Centers for Disease Control and Prevention. ( Risk factors that lead to cardiovascular disease and subsequently a heart attack include high blood pressure, high cholesterol, and smoking. Additionally, unhealthy lifestyle choices such as a poor diet, being overweight or obese, a sedentary lifestyle, and excessive alcohol or cocaine use can all lead to heart disease. (Heart Lung Circ 2016;25[10]:955; J Am Coll Cardiol 2003;41[4]:521.) Medical conditions such as diabetes or a family history of heart disease also dramatically increases one's chance of having a heart attack.

Heart attacks more commonly occur in patients older than 45, but young men and women can still suffer from a myocardial infarction. (Open Cardiovasc Med J 2014;8:61.) Approximately six to 10 percent of heart attacks occur in people under age 45, but the incidence is low. (Am J Med 1999;107[3]:254.) It can, however, have devastating effects on a person in the prime of life.

Many studies and clinical practice guidelines focus on the approach to older patients, and data on younger patients are limited. (Circ Cardiovasc Qual Outcomes 2009;2[5]:500; Eur Heart J 2011;32[23]:2999; Postgrad Med J2005;81[962]:741.)​

Uncommon Cases

The patient had an initial troponin I of 0.047 ng/mL. Subsequent troponins were 6.500 ng/mL, 20.200 ng/mL, and 13.800 ng/mL. Other labs included total cholesterol of 180 mg/dL, triglyceride of 268 mg/dL, HDL of 33 mg/dL, LDL cholesterol of 93 mg/dL, and hemoglobin A1c of 5.8%. An official echocardiogram post-cardiac catheterization revealed an overall left ventricular systolic function between 55%-60% without any significant valvular abnormalities.

The universal definition of a myocardial infarction is an ECG with new ST elevation at the J point in at least two contiguous leads of ≥2 mm in men or ≥1.5 mm in women in leads V2-V3, and/or ≥1 mm in other contiguous chest leads or limb leads, according to the American College of Cardiology Foundation and American Heart Association guidelines. Activation of the cardiac catheterization lab and primary PCI should be accomplished within 90 minutes for patients with STEMI presenting to a PCI-capable hospital. (Circulation 2013;127[4]:529.)

This is a classic case of an acute myocardial infarction that has the increased likelihood of being overlooked because the patient was young and had no identifiable risk factors for acute coronary syndrome. He also had no prior ECG to compare and a single-dynamic ECG that demonstrated only one STE in leads III that did not quite meet the defined STEMI criteria according to the ACCF/AHA guidelines for PCI. Several key markers led to the great outcome of this individual patient: The timely order of the initial ECG within four minutes of the patient's arrival, its completion within nine minutes, and it being immediately brought to the physicians' attention. That led us to get the patient out of the emergency room in under 90 minutes for PCI.

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ECG with resolution of STD in V1-V4, leads I and avL, and minimal STE in lead III status post-cardiac stent placements and thrombectomy.

The patient was placed on aspirin 81 mg, atorvastatin 40 mg, ticagrelor 90 mg, and metoprolol succinate 25 mg. He continued to improve, and was subsequently discharged from the hospital two days later with outpatient cardiology follow-up.

Dr. Huang is an emergency medicine resident at Good Samaritan Hospital Medical Center in West Islip, NY, where Drs. Kelly and Sattler are attending emergency physicians.