49M with a history of hypertension who presented to his primary physician for routine follow-up and was referred to the ED for an abnormal ECG. He denied chest pain, shortness of breath, or any limitation to baseline exercise tolerance. His vital signs were notable for systolic hypertension and his examination was unremarkable. A chest x-ray showed no acute cardiopulmonary findings. His initial ECG demonstrated a biphasic T-wave in V2 and deep, symmetric T-wave inversions in V3-V6. His initial serum troponin was markedly elevated at 3.499. He was admitted and urgent coronary angiography revealed proximal LAD stenosis (70%), mid-LAD stenosis (85%) and 1st right posterolateral stenosis (85%) which were stented. He was discharged on post-procedure day one and has remained asymptomatic at outpatient follow-up.
Initially described in 1982 where a subset of patients who did poorly with medical management of “impending myocardial infarction” (essentialy unstable angina) were found to have characteristic ECG changes. These patients were noted to be at increased risk for extensive anterior wall myocardial infarctions due to proximal LAD stenosis.
Wellens ECG patterns
- History of chest pain
- Normal or slightly-elevated cardiac enzymes
- No precordial Q-waves
- Isoelectric or <1mm ST-segment elevation
- Pattern present in pain-free state
- Type A (25%): Biphasic T-wave in V2/V3
- Type B (75%): Deep, symmetrically inverted T-waves in V2/V3
Wellens Syndrome (or LAD coronary T-wave syndrome) represents a “pre-infarction” stage of coronary artery disease manifested by critical LAD stenosis. The natural history includes progression to extensive anterior wall myocardial infarction, often associated with severe left ventricular systolic dysfunction, cardiogenic shock and death. These changes may be mistaken for “non-specific” T-wave changes (which in the presence of a non-concerning history and typically non-elevated cardiac markers) may lead providers to inappropriate dispositions such a stress testing which is contraindicated. Recognition of this pattern and its appropriate management (urgent coronary angiography) is critical.
The case presented above is atypical. The patient had no history of chest pain and cardiac enzymes were significantly elevated – two features which are uncommon in Wellens Syndrome. However, the patient’s elevated cardiac biomarkers led to admission and angiography with identification of the characteristic proximal LAD stenosis (and other disease).
- de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103(4 Pt 2):730-736.
- Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. YMEM. 1999;33(3):347-351.
- Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. American Journal of Emergency Medicine. 2002;20(7):638-643. doi:10.1053/ajem.2002.34800.
- Mead N, O Keefe K. Wellen′s Syndrome: An Ominous EKG pattern. J Emerg Trauma Shock. 2009;2(3):206– doi:10.4103/0974-2700.55347.
- Kannan L, Figueredo VM. Images in clinical medicine. Wellens’ syndrome. N Engl J Med. 2015;372(1):66. doi:10.1056/NEJMicm1400946.
34M with a history of HTN, polysubstance abuse, presenting with muscle cramps. He reported onset of diffuse muscle cramping 1-hour prior to presentation while showering. Symptoms involved bilateral upper and lower extremities and resolved spontaneously.
On initial evaluation, the patient was tachycardic and hypertensive. Examination was notable for tremors in bilateral upper extremities with outstretched hands, as well as of extended tongue. Other notable findings included spasm of the upper extremity during blood pressure measurement, hyperreflexia and clonus.
Laboratory evaluation was notable for normal total calcium level, low ionized calcium level, primary respiratory alkalosis, and elevated anion gap metabolic acidosis.
The patient was treated with intravenous fluids, benzodiazepines for alcohol withdrawal, and calcium gluconate 4g IV and was admitted.
- 15% bound to anions (phosphate, lactate, citrate)
- 40% bound to albumin
- 45% free (regulated by PTH, Vit-D)
- Conditions causing changes in total calcium (without affecting ionized calcium)
- Low albumin causes hypocalcemia. Corrected = measured + [0.8 x (4-albumin)]
- Elevated albumin causes hypercalcemia
- Multiple myeloma causes hypercalcemia
- Conditions causing changes in ionized calcium (without affecting total calcium)
- Alkalemia causes increased ionized calcium binding to albumin and decreases ionized calcium levels
- Hyperphosphatemia causes increased ionized calcium binding to phosphate and decreases ionized calcium levels
- Hyperparathyroidism causes decreased ionized calcium binding to albumin and increases ionized calcium levels
Causes of Hypocalcemia1,2,3
- Carpopedal spasm
- QT prolongation
- Heart failure
- Basal ganglia calcifications
- Severe (symptomatic, QT prolongation)
- Calcium gluconate 1-2g IV in 50mL of D5W over 10-20min followed by slow infusion of additional 2g over 2 hours.
- Calcium gluconate 1g PO q6h
- Calcitriol 0.2mcg PO BID
- Yu, AS. Relation between total and ionized serum calcium concentrations. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on October 6th, 2016.)
- Cooper MS, Gittoes NJL. Diagnosis and management of hypocalcaemia. BMJ. 2008;336(7656):1298-1302. doi:10.1136/bmj.39582.589433.BE.
- Hannan FM, Thakker RV. Investigating hypocalcaemia. BMJ. 2013;346(may09 1):f2213-f2213. doi:10.1136/bmj.f2213.
A young male with a history of HIV (untreated for the last year, with unknown CD4 count), and syphilis (reportedly treated with an intramuscular injection 1 year ago), presents with 4 months of a painful rash on the palms and soles and diplopia. Examination revealed the rash pictured below, ocular examination with minimal papilledema and anterior chamber inflammation.
Labs were unremarkable. CSF sampling was notable for 34 WBC’s with lymphocyte predominance (92%), and elevated protein (56mg/dL). The patient was admitted for syphilis with presumed neurosyphilis. Serum RPR titer was elevated at 1:64, FTA-ABS and CSF VDRL were reactive. The patient was treated with intravenous penicillin and anti-retroviral therapy was reinitiated.
- Sexual contact (estimated transmission probability 60% per partner)
- African-American, Hispanic
- Male > Female
- Male (primary syphilis), female (secondary syphilis) – lesion visibility
- Urban > rural
||Chancre, reginal lymphadenopathy
||Rash, fever, malaise, generalized lymphadenopathy, mucous membrane lesions, condyloma lata, headache, meningitis
||Early (<1 year)
Late (>1 year)
Aortic aneurysm, aortic insufficiency, coronary artery ostial stenosis
|Acute syphilitic meningitis: headache, confusion, meningeal irritation
|Meningovascular: cranial nerve palsy
|General paresis: headache, vertigo, personality changes, vascular event
|Tabes dorsalis: dementia, ataxia, Argyl-Robertson, [arrow-down] proprioception
Local tissue destruction
- Non-treponemal (screening)
- RPR, VDRL
- Limitations: sensitivity, false positive (age, pregnancy, drugs, malignancy, autoimmune, viral infections)
- Treponemal (confirmatory)
- Indications for CSF sampling: neurologic/ophthalmologic symptoms, tertiary syphilis (aortitis, gumma, iritis), HIV coinfection with elevated RPR titer (> 1:32)
- CSF: leukocytosis (predominantly lymphocytes), protein
- CSF VDRL reactive
- Negative CSF FTA-ABS may rule out neurosyphilis
Syphilis in HIV-infected Individuals2
- Primary: larger and more lesion, multiple ulcers
- Secondary: genital ulcers more common, higher RPR/VDRL titers
- Tertiary: possibly more rapid progression to neurosyphilis
- Singh AE, Romanowski B. Syphilis: review with emphasis on clinical, epidemiologic, and some biologic features. Clin Microbiol Rev. 1999;12(2):187-209.
- French P. Syphilis. BMJ. 2007;334(7585):143-147. doi:10.1136/bmj.39085.518148.BE.
An approximately 40 year-old male with a history of aortic stenosis s/p mechanical aortic valve replacement (on Coumadin) as well as hypertension presented to the emergency department with a chief complaint of severe headache. The patient was in severe distress on arrival and was unable to provide detailed history, he complained of two days of severe left-sided headache while clutching his head and groaning. Examination was notable for sensory localization with directed movements of right hemibody, and no apparent response on the left. He was taken to emergently for CT head non-contrast.
CT Head non-contrast
57 mm right posterior parenchymal hemorrhage with intraventricular component. Moderate edema, mass effect and 9 mm of midline shift.
Admission INR was 2.9, the patient received 25 units/kg of PCC as well as vitamin K 10mg IV x1. Neurosurgery was consulted and the patient was taken to the operating room for management.
Management of Supratherapeutic INR and Complications of Anti-Coagulation
- Ansell J, Hirsh J, Hylek E, et al. Pharmacology and management of the vitamin K antagonists: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; (6 Suppl):160s