A young child, otherwise healthy, is brought to the pediatric emergency department after a fall. The parents report a fall from approximately 2 feet after which the patient cried immediately and without apparent loss of consciousness. Over the course of the day, the patient developed an enlarging area of swelling over the left head. The parents were concerned about a progressive decrease in activity and interest in oral intake by the child, and they were brought to the emergency department for evaluation. Examination demonstrated a well-appearing and interactive child – appropriate for age. Head examination was notable for a 5x5cm hematoma over the left temporoparietal skull with an underlying palpable skull irregularity not present on the contralateral side. Non-contrast head computed tomography was obtained.
Fracture of the left temporal and parietal bone with overlying scalp hematoma.
Algorithm for the Evaluation of Pediatric Head Trauma (PECARN)1,2,3
- Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374(9696):1160-1170. doi:10.1016/S0140-6736(09)61558-0.
- Brenner D, Elliston C, Hall E, Berdon W. Estimated risks of radiation-induced fatal cancer from pediatric CT. American Journal of Roentgenology. 2001;176(2):289-296. doi:10.2214/ajr.176.2.1760289.
- Schonfeld D, Bressan S, Da Dalt L, Henien MN, Winnett JA, Nigrovic LE. Pediatric Emergency Care Applied Research Network head injury clinical prediction rules are reliable in practice. Archives of Disease in Childhood. 2014;99(5):427-431. doi:10.1136/archdischild-2013-305004.
A 62 year-old male with no significant medical history, presented to the emergency department with several days of vomiting. Examination showed suprapubic fullness with tenderness to palpation and a bedside ultrasound was performed:
Ultrasound revealed moderate bilateral hydronephrosis with a relatively non-distended bladder. Labs were notable for new renal failure and the patient was admitted for continued evaluation. He was ultimately diagnosed with idiopathic retroperitoneal fibrosis with bilateral distal ureteral obstruction requiring stenting.
Anatomy of Acute Urinary Retention:
Differential Diagnosis of Acute Urinary Retention:1,2,3
A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.
Free air is seen diffusely in the non-dependent portions of the abdomen: in the anterior abdomen and pelvis, inferior to the diaphragm, and in the perisplenic region. There is complex free fluid in the abdomen.
Algorithm for the Evaluation of Hypotension1
This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.
- The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
- The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
- If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
- Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
- Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.
- Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.
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
|Acute ||Chronic |
- 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
|Stage ||Signs/Symptoms ||Incubation Period |
|Primary ||Chancre, reginal lymphadenopathy ||3 weeks |
|Secondary ||Rash, fever, malaise, generalized lymphadenopathy, mucous membrane lesions, condyloma lata, headache, meningitis ||2-12 weeks |
|Latent ||Asymptomatic ||Early (<1 year) |
Late (>1 year)
|Tertiary ||Cardiovascular: |
Aortic aneurysm, aortic insufficiency, coronary artery ostial stenosis
|<2 years |
|CNS: || |
|Acute syphilitic meningitis: headache, confusion, meningeal irritation ||<2 years |
|Meningovascular: cranial nerve palsy ||5-7 years |
|General paresis: headache, vertigo, personality changes, vascular event ||5-7 years |
|Tabes dorsalis: dementia, ataxia, Argyl-Robertson, [arrow-down] proprioception ||10-20 years |
Local tissue destruction
|1-46 years |
- 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.