Wellens Syndrome

Case Presentation

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.

Presentation ECG
Presentation ECG

Presentation ECG

Biphasic T-wave in V2, deep and symmetric T-wave inversions in V3-V4

Post-Catheterization ECG
Post-Catheterization ECG

Post-Catheterization ECG

Resolution of biphasic T-wave and T-wave inversions

History1

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

Criteria2,3

  1. History of chest pain
  2. Normal or slightly-elevated cardiac enzymes
  3. No precordial Q-waves
  4. Isoelectric or <1mm ST-segment elevation
  5. Pattern present in pain-free state
  6. Type A (25%): Biphasic T-wave in V2/V3
  7. Type B (75%): Deep, symmetrically inverted T-waves in V2/V3

Clinical Significance3

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.

Case Summary

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).

References:

  1. 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.
  2. Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. YMEM. 1999;33(3):347-351.
  3. 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.
  4. 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.
  5. Kannan L, Figueredo VM. Images in clinical medicine. Wellens’ syndrome. N Engl J Med. 2015;372(1):66. doi:10.1056/NEJMicm1400946.

Palpitations

Brief H&P

48F with a history of Grave disease (off medications for 4 months), presenting with palpitations. Noted gradual onset of palpitations while at rest, describing a pounding sensation lasting 3-4 hours and persistent (though improved) on presentation. Symptoms not associated with chest pain, shortness of breath, loss of consciousness, nor triggered by exertion. She reported a history of 8-10 episodes in the past for which she did not seek medical attention. Review of systems notable only for heat intolerance.

On physical examination, vital signs were notable for tachycardia (HR 138bpm). No alteration in mental status, murmur, tremor or hyperreflexia appreciated.

Labs

  • Hb: 14.7
  • Urine hCG: negative
  • TSH: <0.01
  • Total T3: 311ng/dL
  • Free T4: 2.64ng/dL

ECG

Palpitations - Sinus Tachycardia

Sinus Tachycardia

Impression/Plan

Palpitations due to sinus tachycardia from symptomatic hyperthyroidism secondary to medication non-adherence. Improved with propranolol, discharged with methimazole and PMD follow-up.

Differential Diagnosis of Palpitations1, 2

Differential Diagnosis of Palpitations

Evaluation of Palpitations

History and Physical

Subjective description of symptom quality
Rapid and regular beating suggests paroxysmal SVT or VT. Rapid and irregular beating suggests atrial fibrillation, atrial flutter, or variable conduction block.
Stop/start sensation: PAC or PVC
Rapid fluttering: Sustained supraventricular or ventricular tachycardia
Pounding in neck: Produced by canon A waves from AV dissociation (VT, complete heart block, SVT)
Onset and offset
Random, episodic, lasting instants: Suggests PAC or PVC
Gradual onset and offset: Sinus tachycardia
Abrupt onset and offset: SVT or VT
Syncope
Suggests hemodynamically significant arrhythmia, often VT
Examination
Identify evidence of structural, valvular heart disease

ECG1

ECG Finding Presumed etiology
Short PR, Delta waves WPW, AVRT
LAA, LVH Atrial fibrillation
PVC, BBB Idiopathic VT
Q-waves Prior MI, VT
QT-prolongation VT (polymorphic)
LVH, septal Q-waves HCM
Blocks  

Algorithm for the Evaluation of Palpitations3

Algorithm for the Evaluation of Palpitations

References

  1. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med. 1998;338(19):1369-1373. doi:10.1056/NEJM199805073381907.
  2. Probst MA, Mower WR, Kanzaria HK, Hoffman JR, Buch EF, Sun BC. Analysis of emergency department visits for palpitations (from the National Hospital Ambulatory Medical Care Survey). The American Journal of Cardiology. 2014;113(10):1685-1690. doi:10.1016/j.amjcard.2014.02.020.
  3. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician. 2005;71(4):743-750.

Nonsustained Ventricular Tachycardia

Case 1

64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.

In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.

Evaluation and Management:

  • NSVT with known (severe) ischemic heart disease
  • For repetitive monomorphic ventricular tachycardia: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)1

ECG’s

ECG 1
ECG 1

ECG 1

Non-specific IVCD, LAA, VPC

ECG 2
ECG 2

ECG 2

VT initiated by fusion complex

Case 2

31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.

In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.

Evaluation and Management:

  • NSVT progressing to VT
  • Initially attributed to electrolyte disturbances. However, serial ECG’s continued to show prolonged QTc (possibly acquired, home medications included metoclopramide and erythromycin). Early echocardiography demonstrated global hypokinesis with EF 30-35% attributed to severe sepsis and recurrent defibrillation. Cardiac CT after resolution of acute illness showed persistently depressed ejection fraction without coronary atherosclerosis. The presence of NICM associated with malignant dysrhythmias warranted ICD placement.
  • Cardioversion for hemodynamic compromise (I, B), B-blockade (I, B), amiodarone if no LQTS (I, C), urgent angiography if ischemia not excluded (I, C)1
  • Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.2

ECG’s

ECG 1
ECG 1

ECG 1

Ventricular bigeminy

ECG 2
ECG 2

ECG 2

Long-QT

VT on Telemetry
VT on Telemetry

VT on Telemetry

Non-sustained ventricular tachycardia noted on telemetry monitoring

Definition3,4

  • > 3-5 consecutive beats originating below the AV node
  • Rate > 100bpm
  • Duration <30s

Epidemiology3,5

  • Occurs in 0-4% of ambulatory patients
  • Increased frequency in males and with increasing age
  • In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.6,7,8

Evaluation

In all patients:
History: including arrhythmogenic medications/substances, pertinent family history
Physical examination
ECG/CXR
TTE
In selected patients:
Exercise testing
Advanced imaging (CT/C-MR)
Electrophysiologic studies
Genetic testing

NSVT in the absence of structural heart disease

NSVT in Idiopathic Ventricular Tachycardia

Ventricular outflow arrhythmias:
RVOT: 70-80%, LBBB pattern
LVOT: 20-30%, RBBB pattern
Mechanism:
Adrenergically mediated
Occur during exercise, resolve as heart-rate increases, recur during recovery
Management:
Exclude arrhythmogenic right ventricular cardiomyopathy (imaging, myocardial biopsy)
If symptomatic, beta-blockade, ± IC anti-arrhythmic, CCB (verapamil) for ILVT
Prognosis:
Good, rare tachycardia-induced cardiomyopathy, rare SCD

NSVT in Polymorphic Ventricular Tachycardia

Mechanism
LQTS (acquired or inherited)
Familial catecholaminergic polymorphic VT
Management
Symptomatic (ex. syncope, cardiac arrest): ICD
Asymptomatic QTc > 550ms: consider ICD
Prognosis
Increased risk SCD

Arrhythmogenic Right Ventricular Cardiomyopathy

Mechanism
Fibrosis, fibro-fatty replacement of myocardium in RVIT/RVOT/RV apex
May occur with only subtle structural abnormalities of the right ventricle
LBBB morphology
Management
Anti-arrhythmics of limited utility
Catheter ablation, ICD backup
Prognosis
Increased risk SCD

NSVT with apparent structural heart disease1

Hypertension and LVH

Mechanism
Stretch-induced abnormal automaticity
Fibrotic tissue
Presence of NSVT correlates with degree of hypertrophy and subendocardial fibrosis
Management
Evaluation for ischemic heart disease
Aggressive medical management of hypertension (including beta-blockade)
Prognosis
Unclear

Valvular Disease

Mechanism
High incidence in AS, severe MR (25%)
Mechanical stress from dysfunctional valvular apparatus
Management
Beta-blockade if symptomatic
Prognosis
No evidence that NSVT is an independent predictor of SCD.

Ischemic Heart Disease9-14

Mechanism
Monomorphic VT associated with re-entry at the borders of ventricular scars
Ischemia induces polymorphic NSVT/VF
Management
Revascularization, beta-blockade, statin, ACE/ARB
MADIT I, MUSTT: ICD for ICM LVEF <40%, NSVT, EPS inducible VT
MADIT II, SCD-HeFT: ICD for moderate-to-severe LV dysfunction irrespective of NSVT or EPS findings
Prognosis
NSTEMI with NSVT >48h after admission 2x risk SCD (MERLIN-TIMI 36)
STEMI with NSVT common, not as predictive of ACM or SCD as LVEF (CARISMA)
NSVT <24h after admission for NSTEMI/STEMI not of prognostic significance.

Hypertrophic Cardiomyopathy

Mechanism
Genetic myocardial disease
Myocyte disarray, fibrosis, ischemia result in arrhythmogenic substrate
Management
Restriction of physical activity
ICD (NSVT, LV thickness, FH SCD, syncope, abnormal BP response to exercise)
Beta-blockade, anti-arrhythmic for symptoms
Prognosis
Increased risk SCD (1% annual)

Other Conditions

  • Non-ischemic dilated cardiomyopathy
  • Giant-cell myocarditis
  • Repaired TOF
  • Amyloidosis
  • Sarcoidosis
  • Chagas cardiomyopathy

Algorithm for the Evaluation of NSVT1

Algorithm for the Evaluation of Nonsustained Ventricular Tachycardia

References

  1. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death–executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(17):2099–2140. doi:10.1093/eurheartj/ehl199.
  2. Higham PD, Adams PC, Murray A, Campbell RW. Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study. Q J Med. 1993;86(9):609–617.
  3. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol. 2012;60(20):1993–2004. doi:10.1016/j.jacc.2011.12.063.
  4. Katritsis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J. 2004;25(13):1093–1099. doi:10.1016/j.ehj.2004.03.022.
  5. Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.
  6. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890. doi:10.1056/NEJM199912163412503.
  7. Jouven X, Zureik M, Desnos M, Courbon D, Ducimetière P. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med. 2000;343(12):826–833. doi:10.1056/NEJM200009213431201.
  8. Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.
  9. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989;321(6):406–412. doi:10.1056/NEJM198908103210629.
  10. Goldstein S. Propranolol therapy in patients with acute myocardial infarction: the Beta-Blocker Heart Attack Trial. Circulation. 1983;67(6 Pt 2):I53–7.
  11. Moss AJ. MADIT-I and MADIT-II. J Cardiovasc Electrophysiol. 2003;14(9 Suppl):S96–8.
  12. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996;335(26):1933–1940. doi:10.1056/NEJM199612263352601.
  13. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890. doi:10.1056/NEJM199912163412503.
  14. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225–237. doi:10.1056/NEJMoa043399.
  15. WikEM: Nonsustained Ventricular Tachycardia

Low Voltage ECG

Definition

  • QRS in limb leads <5mm
  • QRS in precordial leads <10mm

General Causes

  • Fluid, fat or air attenuating signal
  • Myocardial infiltration
  • Loss of viable myocardium

Example

Low Voltage ECG
Low Voltage ECG

Low Voltage ECG

ECG of patient with pericardial effusion

Baseline ECG
Baseline ECG

Baseline ECG

Old ECG from same patient

Differential Diagnosis of Low Voltage ECG

Differential Diagnosis of Low Voltage ECG

References

  1. Madias JE. Low QRS voltage and its causes. J Electrocardiol. 2008;41(6):498–500. doi:10.1016/j.jelectrocard.2008.06.021.
  2. WikEM: Low ECG voltage

Chest Pain

Evaluation of Chest Pain

Evaluation of Chest Pain

References

  1. Brown, J. (2013). Chest Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 214-222). Elsevier Health Sciences.

Dyspnea

Causes of Dyspnea

Causes of Dyspnea

Findings in Selected Causes of Dyspnea

Condition History Symptoms Findings Evaluation
Anaphylaxis Exposure to allergen Abrupt onset, facial swelling Stridor, wheezing, hives  
PE Immobilization, malignancy, prior DVT/PE, surgery, OCP Abrupt onset, pleuritic chest pain Tachycardia, hypoxia ECG (RV strain)
CT PA, D-dimer
LE US (DVT)
Pneumonia Exposure, tobacco use Fever, productive cough Focal rales CXR
CBC
Blood/respiratory cultures
Pneumothorax Trauma, thin male Abrupt onset, chest pain Decreased BS, subQ emphysema, JVD and tracheal deviation if tension CXR
US
Fluid overload Dietary indiscretion, medication non-adherence Orthopnea, PND JVD, S3/S4, peripheral edema CXR
US
ECG
BNP
COPD/Asthma Tobacco use, personal/family history Progressive Retractions, accessory muscle use, wheezing CXR
US (distinguish from fluid overload)
Malignancy Tobacco use, weight loss Hemoptysis   CXR
CT Chest

References

  1. Braithwaite, S., & Perina, D. (2013). Dyspnea. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 206-213). Elsevier Health Sciences.

Syncope

Causes of Syncope

Causes of Syncope

History

  • Rate of onset
  • Position at onset
  • Duration, rate of recovery
  • Preceding features

    • Obstruction: associated with exertion
    • Neurocardiogenic: associated with emotion, micturition, bowel movement, emesis, neck movement
  • Following features

    • Seizure: Postictal confusion
    • Hypotension: Initial VS
    • Associated trauma

Physical Examination

  • VS: rhythm, BP, temperature
  • HEENT: mucous membranes (laceration, dry), trauma, papilledema
  • CV: murmur (AS), rub (pericarditis), bruit (cerebrovascular disease), JVD (obstruction)
  • Lungs: crackles (CHF)
  • Abdomen: pulsatile mass (AAA)
  • Extremities: pulse discrepancy (dissection)
  • Neuro: focal findings (stroke, mass, seizure)

Evaluation

  • ECG: arrhythmia (PR, QT, Brugada, unanticipated hypertrophy, RV strain, pericarditis)
  • Orthostatic VS
  • CBC: anemia
  • BMP: electrolyte abnormalities (hyponatremia, hyper/hypokalemia)
  • Glucose: hypoglycemia
  • Troponin: ischemia
  • B-hCG: ectopic
  • Utox: drugs
  • CXR: dissection
  • CT head: focal neurological findings
  • CT PA: concern for PE
  • US abdomen: AAA

San Francisco Syncope Rules (CHESS)

  • CHF
  • Hematocrit <30%
  • ECG abnormality
  • SBP <90mmHg
  • SOB

References

  1. De Lorenzo, R. (2013). Syncope. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 135-141). Elsevier Health Sciences.

ECG Guide

The format of this article is atypical for the structure and concept of the website – but it’s always been about learning. Here is a simplified guide to ECG interpretation with a focus on the aspects I find more challenging to understand or recall.

Grid and Leads

The ECG grid
Limb leads
Precordial Leads

Axis

ECG axes

Atrial Enlargement

Atrial enlargement

Normal:
First portion of deflection is RA, second is LA
Right Atrial Enlargement:
P-wave amplitude > 2.5mm in inferior leads
Normal duration P-wave
Left Atrial Enlargement:
P-wave duration increased (terminal negative portion >0.04s)
Amplitude of terminal negative component >1mm below isoelectric line in V1

Ventricular Hypertrophy

Right Ventricular Hypertrophy:
Right axis deviation
Abnormal R-wave progression

  • Increased R-wave amplitude in leads overlying the right ventricle (V1)
  • Increased S-wave amplitude in leads overlying the left ventricle (V6)
Criteria

  • V1: R>S
  • V6: S>R
Left Ventricular Hypertrophy:
Left axis deviation
Increased R-wave amplitude in leads overlying the LV (I, aVL, V5, V6)
Increased S-wave amplitude in leads overlying the RV (V1)
Criteria:

  • Precordial Leads
    • R-wave in V5/V6 + S-wave in V1/V2 > 35mm
    • R-wave in V5 > 26mm
    • R-wave in V6 > 20mm
  • Limb Leads
    • R-wave in aVL > 11mm
    • R-wave in aVF > 20mm
  • Combined
    • R-wave in aVL + S-wave in V3 > 20mm (F), 28mm (M)

Secondary Repolarization Abnormalities

Secondary repolarization abnormality

  • Downsloping ST-segment depression
  • Asymmetric T-wave inversion

Bundle Branch Blocks

Left Bundle Branch Block

Left bundle branch block

  • QRS duration > 0.12s (3 boxes)
  • Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
  • Associated ST-segment depression and T-wave inversion
  • Reciprocal changes in V1, V2 (deep S-wave)
  • Possible LAD

Right Bundle Branch Block

Right bundle branch block

  • QRS duration > 0.12s (3 boxes)
  • RSR’ in V1, V2
  • Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Hemiblocks

His-Purkinje system and hemiblocks (anterior fascicular block, posterior fascicular block)

Other Blocks

  • Non-specific intraventricular conduction delay: QRS >0.10s without BBB
  • Incomplete BBB: LBBB/RBBB pattern with non-prolonged QRS
  • Bifascicular block: RBBB + LAFB/LPFB (by axis deviation)

Ischemia and Infarction

ECG changes associated with ischemia and infarction

  1. Hyperacute T-waves
  2. T-wave inversion: Symmetric, compared to TWI associated with repolarization abnormalities
  3. ST-elevation: Unlike J-point elevation, ST-segment merges with T-wave
  4. Q-waves
    1. Duration > 0.04s
    2. Amplitude > 1/3 R-wave
    3. Normal in aVR

Coronary Artery Territories

Coronary artery territories

Distribution Coronary Artery Leads Reciprocal Changes
1. Inferior RCA, PDA II, III, aVF Anterior, Lateral
2. Lateral LCx I, aVL, V5, V6 Inferior
3. Anterior LAD V1-V6 Inferior
4. Posterior RCA Posterior Anterior (esp. V1)

External Links

Lactic Acidosis

HPI:

59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.

She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.

On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.

In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.

PMH:

  • Congestive heart failure

PSH:

  • None

FH:

  • Mother with diabetes
  • Father with MI at age 65

SHx:

  • 4-5 drinks of alcohol/day
  • No tobacco or drug use

Meds:

  • None

Allergies:

NKDA

Physical Exam:

VS: T 37.4 HR 106 RR 18 BP 145/82 O2 100% RA
Gen: Morbidly obese female, lying in bed, in no acute respiratory distress, speaking in complete sentences.
HEENT: Dry, cracked lips, slightly erythematous, otherwise moist mucous membranes, poor dentition. Mild scleral icterus. No cervical lymphadenopathy.
CV: Rapid rate, regular rhythm, normal S1/S2, II/VI systolic ejection murmur at LUSB, no radiation appreciated. No jugular venous distension.
Lungs: Clear to auscultation in posterior lung fields bilaterally, no crackles appreciated.
Chest: Well-circumscribed erythematous patch in folds beneath left breast, no underlying fluctuance, no significant tenderness to palpation. On contralateral breast, some hyperpigmentation but no erythema.
Abdomen: Obese, non-tender, non-distended. Patch of erythema below pannus, mildly tender to palpation.
Ext: Bilateral lower extremities with marked edema and overlying scaly plaques, some slightly ulcerated weeping serous fluid. Peripheral pulses are difficult to palpate, capillary refill difficult to assess.

Labs/Studies:

  • CBC: 11.1/11.1/34.5/212 (MCV 114.2)
  • BMP: 140/4.5/97/20/10/1.14/64
  • Anion Gap: 23
  • LFT: AST: 73, ALT: 26, AP: 300, TB: 4.6, DB: 2.1, Alb: 3.0, INR 1.3
  • BNP: 158
  • Troponin: 1.284
Sinus tachycardia, LVH, secondary repolarization abnormalities

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.

CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.

CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.

TTE:
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.

US Abdomen:
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.

Assessment/Plan:

The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.

Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.

One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.

Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.

Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.

Differential Diagnosis of Elevated Serum Lactate 1,2

Differential Diagnosis of Elevated Serum Lactate

Algorithm for Evaluation of Acidemia 3,4

Algorithm for Evaluation of Acidemia

Algorithm for Evaluation of Alkalemia 3,4

Algorithm for Evaluation of Alkalemia

References:

  1. Fall, P. J., & Szerlip, H. M. (2005). Lactic acidosis: from sour milk to septic shock. Journal of intensive care medicine, 20(5), 255–271. doi:10.1177/0885066605278644
  2. Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
  3. Ingelfinger, J. R., Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological Approach to Assessment of Acid–Base Disturbances. The New England journal of medicine, 371(15), 1434–1445. doi:10.1056/NEJMra1003327
  4. Ingelfinger, J. R., & Seifter, J. L. (2014). Integration of Acid–Base and Electrolyte Disorders. The New England journal of medicine, 371(19), 1821–1831. doi:10.1056/NEJMra1215672

Pleural Effusion

HPI:

64F with a history of CAD, MI, CHF, CLL and rheumatoid arthritis who presented to the emergency department after transfer from a rehabilitation facility for respiratory distress. The patient reported several days of progressive shortness of breath with dyspnea on exertion. She also noted some associated orthopnea and lower extremity edema. The patient was recently hospitalized for similar symptoms and was diagnosed with CHF at the time. At the rehab facility, the patient became hypoxemic and hypertensive, reporting shortness of breath and chest pain prior to presentation.

Hospital Course:

The patient was initially managed with BiPAP and nitroglycerin continuous infusion, but was then stable on supplemental O2 via nasal cannula and was transitioned to long-acting nitrates and anti-hypertensives. The patient’s hypoxemic respiratory failure was initially attributed to acute exacerbation of left-ventricular heart failure, and the patient was managed with spot diuresis. However, there was no symptomatic improvement and the patient became hypernatremic so diuresis was held as alternative diagnoses were explored.

A transthoracic echocardiogram showed preserved LVEF (50-55%), but some diastolic dysfunction and elevated PAP/RAP. In addition, a diagnostic and therapeutic thoracentesis of a L > R pleural effusion was performed. Pleural fluid studies were suggestive of a transudative process, though with some abnormal characteristics (including lymphocyte predominance, as well as presence of signet cells).

Rheumatology and pulmonology services were consulted for input and recommendations for further evaluation were appreciated. Per rheumatology, the patient’s diagnosis of rheumatoid arthritis may not be consistent with her presentation or prior serologic studies. Her pleural fluid analysis was also not consistent with rheumatoid disease. According to pulmonary consult, the patient’s hypoxemia remains most consistent with left ventricular dysfunction though primary pulmonary processes cannot be excluded (and would warrant further evaluation with imaging and pulmonary function testing).

PMH:

  • CHF
  • CAD
  • CVA
  • Myocardial Infarction
  • HTN
  • Hypothyroidism
  • CLL
  • Anemia

PSH:

  • TAH-BSO

FH:

  • No family history of autoimmune disease.
  • Mother: DM

SHx:

  • Denies tobacco/EtOH/drug use
  • Lives at home, at SNF since discharge

Meds:

  • Furosemide 20mg p.o. daily
  • Gabapentin 300mg p.o. t.i.d.
  • Hydralazine 50mg p.o. t.i.d.
  • Hydrochlorothiazide 25mg p.o. b.i.d.
  • Hydroxychloroquine 200mg p.o. daily
  • Levothyroxine 25mcg p.o. daily
  • Minoxidil 2.5mg p.o. b.i.d.
  • Pantoprazole 40mg p.o. daily
  • Prednisone 15mg p.o. daily

Allergies:

  • Shellfish
  • Physical Exam:

    VS: T 37.2 HR 84 RR 15 BP 147/75 O2 97% 4LNC
    Gen: Elderly female, alert and oriented to self and place, responding appropriately to questions.
    HEENT: Mucous membranes moist, sclera anicteric, no cervical lymphadenopathy.
    CV: Regular rate and rhythm, normal S1/S2, no additional heart sounds. III/VI mid-systolic murmur heard best at LLSB with diastolic component, no radiation appreciated. Non-displaced PMI. JVP measured to 14cm.
    Lungs: Decreased breath sounds in left lung field to inferior 2/3 with crackles above, on right crackles to inferior 1/2 of lung fields posteriorly. Dullness to percussion of inferior left lung field posteriorly.
    Abdomen: Soft, non-tender, non-distended, no hepatosplenomegaly, no appreciable fluid wave.
    Ext: Bilateral lower extremities with 2+ pitting edema to knees, some hyperpigmentation to right lower extremity.

    Labs/Studies:

    • CBC: 11.2/10.2/32.7/179
    • BMP: 141/3.9/103/30/15/0.85/107
    • INR: 0.9
    • BNP: 1857
    • UA: WBC 4, RBC 29 , +Bacteria, UCr 90, UPr 14
    • Rheum: CCP <16, ANCA neg, RF 936
    • Pleural Fluid: LDH 98 (serum 237), Protein 2.8 (serum 6.0), Glucose 107
    • Cytology: Reactive mesothelial cells, histiocytes, lymphocytes, signet cells

    Imaging

    CXR

    CXR: Pleural Effusion

    There is a large left pleural effusion obscuring the lower half of the left hemi thorax. The cardiac silhouette is also obscured. There is pulmonary venous vascular congestion. There is also a right pleural effusion with fluid tracking into the minor fissure. Pulmonary interstitial edema is also noted.

    CT Chest (High-Resolution):

    • Bilateral, left greater than right, pleural effusions with adjacent atelectasis and collapse versus consolidation of the left lower lobe.
    • Prominent main pulmonary artery measuring 3.3 cm in diameter, which can be seen with pulmonary arterial hypertension.

    TTE:

    • LVEF is 50-55%.
    • Impaired left ventricular relaxation, which is associated with grade I/IV or mild diastolic dysfunction.
    • Moderate aortic stenosis with mild regurgitation (AVA 1.4 cm3, mean gradient 14mmHg, peak velocity 2.4 m/s).
    • Severe pulmonary hypertension (est PASP 52-62mmHg).
    • The inferior vena cava appeared dilated and decreased <50% with respiration (RAP 10-20 mmHg).
    • Minimal pericardial effusion without echocardiographic evidence of tamponade.

    Assessment/Plan:

    64F with history of CAD (prior MI), CHF, hypertension, CLL, hypothyroidism presented from a SNF with progressive shortness of breath, orthopnea and LE swelling, found to have bilateral (L>R) pleural effusion now s/p thoracentesis with transudative fluid.

    #Acute hypoxic respiratory failure: Large pleural effusions, s/p thoracentesis with pleural fluid suggestive of transudative process. Most likely secondary to left ventricular diastolic dysfunction. Improved after thoracentesis and diuresis. High-resolution CT chest performed without evidence of autoimmune-related pulmonary fibrosis or ILD (though persistent pleural effusions, pulmonary vascular congestion).

    #Pleural fluid signet cells: Identified on cytology, potentially related to history of untreated CLL or alternative primary malignancy.

    #Left ventricular diastolic dysfunction, decompensated: Associated with pleural effusions and hypoxemic respiratory failure. Management with diuresis.

    #Pulmonary Hypertension: Severe, noted on transthoracic echocardiography, may be secondary to hypoxemia associated with pleural effusions, consider repeat imaging once euvolemic or right-heart catheterization.

    #Microscopic Hematuria: No evidence of infection, no symptoms suggestive of nephrolithiasis. No casts identified or significant proteinuria. Plan for renal ultrasound.

    #Rheumatoid Arthritis: History of rheumatoid arthritis, on prednisone and hydroxychloroquine. Imaging without evidence of inflammatory arthropathy, RF elevated but CCP negative. Per rheumatology, the patient’s symptoms are not consistent with RA, continuing home medications while evaluation is ongoing. Pleural effusions unlikely associated with RA as transudative, and without monocyte predominance or low glucose.

    Case 2: Malignant Pleural Effusion

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    Within the lungs there are ground-glass opacities bilaterally, and a left pleural effusion with adjacent consolidation vs compressive atelectasis.
    • Protein: 2.6 (serum: 4.9)
    • LDH: 1275 (serum: 219)
    • Cytology: Malignant cells

    Case 3: Traumatic Thoracentesis

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    Moderate right pleural effusion, some fluid in non-dependent portions suggestive of loculation. Diffuse nodules and opacification in right lung with compressive atelectasis. Left pleural effusion with high density material at the posterior costophrenic angle. Left chest tube.
    • Protein: 2.7 (serum 6.4)
    • LDH: 344 (serum 236)
    • Cell count: 100,000 RBC

    Case 4: Pneumonia

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    Loculated right pleural effusion with foci of atelectasis and consolidative changes concerning for pneumonia. Minimal left-sided pleural effusion with consolidative changes. Enlarged mediastinal lymph nodes, possibly reactive.
    • Protein: 4.3 (serum 6.7)
    • LDH: 377 (serum 108)
    • pH: 7.46
    • Glucose: 153
    • Neutrophils: 84%

    Etiology of Pleural Effusions: 1

    Etiology Frequency (%)
    CHF 35
    Pneumonia 22
    Malignancy 15
    Pulmonary Embolism 11

    Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: 1,2

    Pleural effusions can be easily identified on chest radiography, physical examination findings include dullness to percussion, decreased tactile fremitus and decreased (or absent) breath sounds.

    • Hemoptysis: Malignancy, PE, TB
    • Weight Loss: Malignancy, TB
    • Ascites: Cirrhosis, ovarian cancer
    • Unilateral Leg Swelling: PE
    • Bilateral Leg Swelling: CHF, cirrhosis, nephrotic syndrome
    • Jugular Venous Distension: CHF

    Differential Diagnosis of Pleural Effusions: 1,2,3,4

    Differential Diagnosis of Pleural Effusions

    References:

    1. Light, R. W. (2002). Clinical practice. Pleural effusion. The New England journal of medicine, 346(25), 1971–1977. doi:10.1056/NEJMcp010731
    2. McGrath, E. E., & Anderson, P. B. (2011). Diagnosis of pleural effusion: a systematic approach. American journal of critical care : an official publication, American Association of Critical-Care Nurses, 20(2), 119–27– quiz 128. doi:10.4037/ajcc2011685
    3. Thomsen, T. W., DeLaPena, J., & Setnik, G. S. (2006). Videos in clinical medicine. Thoracentesis. The New England journal of medicine (Vol. 355, p. e16). doi:10.1056/NEJMvcm053812
    4. Wilcox, M. E., Chong, C. A. K. Y., Stanbrook, M. B., Tricco, A. C., Wong, C., & Straus, S. E. (2014). Does this patient have an exudative pleural effusion? The Rational Clinical Examination systematic review. JAMA : the journal of the American Medical Association, 311(23), 2422–2431. doi:10.1001/jama.2014.5552
    5. WikEM: Pleural effusion

    Pericardial Effusion

    HPI:

    43F with a history of HTN and diastolic heart failure presenting with two days of shortness of breath. Reports that symptoms are worse at night when lying down to sleep and associated with a cough productive of white sputum. She also reports intermittent left-sided chest pain, described as sharp and exacerbated by cough or deep inspiration. She denies fevers/chills, nausea/vomiting, sick contacts or recent travel.
    m

    PMH:

    • Hypertension
    • Diabetes Mellitus (Type II)
    • Hyperlipidemia
    • Diastolic heart failure

    PSH:

    • Cesarean section

    FH:

    • Father with MI at 76 years-old

    SHx:

    • Lives at home.
    • Denies tobacco, alcohol or drug abuse.

    Meds:

    • Lasix 40mg p.o. daily
    • Lisinopril 20mg p.o. daily
    • Atenolol 50mg p.o. daily
    • Omeprazole 20mg p.o. daily
    • Lantus 14 units daily
    • Novolin 6 units t.i.d

    Allergies:

    NKDA

    Physical Exam:

    VS: T 98.2 HR 81 RR 19 BP 219/91 O2 95% RA
    Gen: Adult female in no acute distress, alert and responding appropriately to questions.
    HEENT: PERRL, EOMI, mucous membranes moist.
    CV: RRR, no murmurs appreciated, no JVD.
    Lungs: Crackles at right lung base.
    Abd: Soft, non-tender, non-distended, without rebound/guarding.
    Ext: 1+ pitting edema in bilateral lower extremities to knee.
    Neuro: AAOx4, grossly normal peripheral sensation and motor strength.

    Labs/Studies:

    • Troponin: 0.15
    • Procalcitonin: 0.15
    • CBC: 10.9/9.1/26.4/296
    • BMP: 134/4.6/104/22/56/2.87/214

    Imaging:

    Pericardial Effusion

    Pericardial Effusion

    Measured in the largest dimension, suggestive of a moderate to large pericardial effusion.

    E-Point Septal Separation

    E-Point Septal Separation

    E-Point Septal Separation (EPSS), estimated here is the smallest distance between the anterior leaflet of the mitral valve and intraventricular septum. Values > 12mm are suggestive of depressed ejection fraction.

    Left Ventricular Hypertrophy

    Left Ventricular Hypertrophy

    Thickened left ventricular wall.

    Pericardial Effusion - Subxiphoid

    Pericardial Effusion - Subxiphoid

    Pericardial Effusion - Parasternal Long

    Pericardial Effusion - Parasternal Long

    Pericardial Effusion - Parasternal Short

    Pericardial Effusion - Parasternal Short

    • CXR: Consolidation involving the majority of the right lung, cardiomegaly.
    • Bedside Echo: LVEF 55%, concentric LVH, no wall motion abnormality, moderate pericardial effusion noted, RV not collapsed.

    Assessment/Plan:

    43F with a history of HTN, diastolic heart failure presenting with SOB.

    #SOB: CXR finding of right-sided consolidation with history of productive cough, evidence of leukocytosis with neutrophil predominance, and relative hypoxemia suggestive of community-acquired pneumonia. No evidence of systemic inflammatory response. PE unlikely, patient is not bed-bound and alternative diagnosis more likely.
    – Start empiric antimicrobial therapy ceftriaxone 1g IV q24h, azithromycin 500mg IV q24h.

    #Pericardial Effusion: Noted on bedside echo, no evidence of RV collapse to suggest cardiac tamponade. Also, no JVD and pulsus paradoxus measured at 8mmHg.
    – Obtain formal transthoracic echocardiogram to evaluate effusion.
    – Consult cardiology if worsening hemodynamics

    #Elevated Troponin: No ECG changes suggestive of acute ST-elevation MI. May represent NSTEMI though historical features not consistent with ACS.
    – Trend troponin/EKG q.8.h. x3
    – Give aspirin 325mg, consider anti-coagulation.
    – Consider stress echo prior to discharge

    #Elevated Creatinine: Baseline unknown, likely acute component with or without chronic kidney disease.
    – Volume resuscitation as tolerated, follow repeat chemistry.

    #Hypertension: Asymptomatic, resume home medications.

    Physiology of Cardiac Tamponade 1

    • Intrapericardial pressure (IPP) normally reflects intrathoracic pressure (ITP).
    • Inspiration: low ITP → low RAP → increased RA filling.
    • Expiration: high ITP → low LAP → increased LA filling.
    • Increased pericardial fluid → increased IPP → increased LA/RA filling pressures (diastolic dysfunction) → increased variation with respiration.
    • Earliest hemodynamic change in cardiac tamponade is JVD or IVC dilation.

    IVC variation as marker for RAP 1

    IVC Diameter (cm) Change with Respiration (%) RAP (mmHg)
    <2.1 >50% 0-5
    <2.1 <50% 5-10
    >2.1 >50% 5-10
    >2.1 <50% >15

    Grading Pericardial Effusions 1

    Grade Echo-free space (mm) Size (mL)
    Small <10 100
    Moderate 10-20 100-500
    Large >20 >500

    Differential Diagnosis of Pericardial Effusion 2,3

    Differential Diagnosis of Pericardial Effusion

    History and Physical Exam in Patients with Acute Pericarditis 2,3

    Symptom/Sign ACS Pericarditis PE
    Quality Pressure Sharp Sharp
    Pleuritic No Yes Yes
    Positional No Yes (worse when supine) No
    Duration Minutes to hours Hours to days Hours to days
    Improves with NG Yes No No
    Friction Rub No Yes No
    S3 Maybe No No

    References:

    1. Schairer, J. R., Biswas, S., Keteyian, S. J., & Ananthasubramaniam, K. (2011). A Systematic Approach to Evaluation of Pericardial Effusion and Cardiac Tamponade. Cardiology in Review, 19(5), 233–238. doi:10.1097/CRD.0b013e31821e202c
    2. Khandaker, M. H., Espinosa, R. E., Nishimura, R. A., Sinak, L. J., Hayes, S. N., Melduni, R. M., & Oh, J. K. (2010). Pericardial Disease: Diagnosis and Management. Mayo Clinic Proceedings, 85(6), 572–593. doi:10.4065/mcp.2010.0046
    3. Lange, R. A., & Hillis, L. D. (2004). Clinical practice. Acute pericarditis. The New England journal of medicine, 351(21), 2195–2202. doi:10.1056/NEJMcp041997

    Lower Extremity Edema

    HPI:

    51 year-old male with a history of HTN, DM and chronic alcohol abuse presenting with lower extremity swelling. He notes one month of progressive, bilateral lower extremity swelling, in the past two weeks associated with increasing pain and redness and is now no longer able to ambulate due to pain. He denies fevers/chills, chest pain or shortness of breath. He also denies orthopnea and paroxysmal nocturnal dyspnea. He states that he has not had these symptoms prior to one month ago. On review of systems he denies nausea/vomiting, abdominal pain, and changes in bowel or urinary habits. He has a history of GI bleeding (unknown treatment) but denies hematemesis, hematochezia or melena. He has previously experienced alcohol withdrawal, which manifested as tremors, but no hallucinations or seizures.

    PMH:

    • HTN
    • DM
    • Chronic EtOH abuse

    PSH:

    None

    FH:

    Unknown

    SHx:

    • Drinks 1-2 pints of alcohol daily, last drink this morning.
    • Denies current tobacco or drug abuse, no prior IVDA.

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.6 HR 86 RR 16 BP 128/84 O2 99% RA
    Gen: Adult, non-obese male, lying in bed. Tremors noted in upper extremities.
    HEENT: PERRL, EOMI, no scleral icterus. Mucous membranes moist.
    CV: RRR, normal S1/S2, no additional heart sounds, JVP 3cm above sternal angle at 30°.
    Lungs: CTAB, no crackles.
    Abd: Soft, non-distended, with normoactive bowel sounds. Liver edge palpated 1cm below costal margin at mid-clavicular line, non-tender. No rebound/guarding.
    Ext: Warm, well-perfused with 2+ distal pulses (PT, DP). 3+ pitting edema symmetric in bilateral lower extremities to knee. Erythema and warmth bilaterally extending from ankles to mid-shin. Mild tenderness to palpation. No pain with passive dorsiflexion. 3x3cm shallow ulceration below medial malleolus on right lower extremity without underlying fluctuance or expression of purulent material. No venous varicosities noted. Decreased sensation to light touch below knee bilaterally.
    Rectal: Normal rectal tone, brown stool, guaiac negative.
    Neuro: Alert and oriented, CN II-XII intact, gait intact, normal FTN/RAM.

    Labs/Studies:

    • CBC: 7.4/13.1/39/180
    • Creatinine: 0.84
    • Albumin: 4.3
    • BNP: 28

    Imaging:

    Venous Lower Extremity Ultrasound

    1. No DVT.
    2. Pulsatile flow in bilateral EIV (external iliac veins) suggestive of elevated right heart pressure.

    Assessment/Plan:

    51M with HTN, DM, EtOH abuse presenting with lower extremity edema. Chronic bilateral lower extremity edema likely secondary to chronic venous insufficiency perhaps related to OSA given ultrasound findings of pulsatile flow in EIV’s. Doubt systemic cause: no evidence of heart failure on exam and normal BNP, no stigmata of cirrhosis and normal albumin, normal creatinine. Also, no evidence of DVT on ultrasound though bilateral DVT unlikely. Bilateral cellulitis also unlikely as the patient is afebrile without leukocytosis, however the patient was started on antibiotics including ceftriaxone and TMP/SMX given erythema, warmth and tenderness to palpation. The patient received benzodiazepines which eased withdrawal symptoms and he was admitted for continued treatment.

    Mechanisms of Lower Extremity Edema: 1

    Mechanisms of Lower Extremity Edema

    Differential Diagnosis of Lower Extremity Edema: 1,2

    Differential Diagnosis of Lower Extremity Edema

    Evaluation:

    History 1,2

    • Duration: acute (<72h) vs. chronic
    • Pain: DVT, CRPS, less severe in venous insufficiency
    • Systemic Disease
      • Cardiac: orthopnea, PND
      • Renal: proteinuria
      • Hepatic: jaundice, ascites
    • Malignancy: lymphedema
    • Improvement with elevation/recumbency: venous insufficiency
    • OSA: snoring, daytime somnolence
    • Medications: B-blocker, CCB, hormones, NSAID’s

    Physical Exam 1,2

    • Distribution: unilateral, bilateral, generalized
    • Quality: pitting, non-pitting
    • TTP: DVT, cellulitis
    • Varicose veins: venous insufficiency
    • Kaposi-Stemmer: inability to pinch dorsum of foot at base of 2nd toe (lymphedema)
    • Systemic Disease
      • Cardiac: JVD, crackles
      • Hepatic: ascites, scleral icterus, spider angiomas
    • Brawny, medial maleolar involvement: venous insufficiency

    Key Features Distinguishing Cellulitis: 3

    • Typically unilateral and acute
    • Often with systemic symptoms (fever, leukocytosis)
    • Risk Factors: immunosuppression, previous episodes, DM, PVD

    References:

    1. Trayes, K. P., Studdiford, J. S., Pickle, S., & Tully, A. S. (2013). Edema: diagnosis and management. American family physician, 88(2), 102–110.
    2. Ely, J. W., Osheroff, J. A., Chambliss, M. L., & Ebell, M. H. (2006). Approach to leg edema of unclear etiology. Journal of the American Board of Family Medicine : JABFM, 19(2), 148–160.
    3. Keller, E. C., Tomecki, K. J., & Alraies, M. C. (2012). Distinguishing cellulitis from its mimics. Cleveland Clinic journal of medicine, 79(8), 547–552. doi:10.3949/ccjm.79a.11121
    4. WikEM: Pedal edema

    Seizure

    HPI:

    Seizure - 2.2cm rim-enhancing lesion in the right occipital lobe.

    2.2cm rim-enhancing lesion in the right occipital lobe.

    26M with a history of retroperitoneal embryonal carcinoma (IIIC, known liver/lung metastases) presenting with new-onset “seizures” for one week. The patient reports the first episode occurred 6 days ago, he noted progressive loss of vision on the left side (over 1-2min), followed by loss of consciousness and awoke in an ambulance. He denies any urinary/fecal incontinence, tongue biting, or post-spell confusion, and he awakes spontaneously and is able to get up under his own power. Episodes are not associated with palpitations, nausea or diaphoresis. An episode of identical character occurred 4 days later and triggered his presentation today. He otherwise denies fevers/chills, headaches, nausea/vomiting, changes in vision outside of episodes.

    A witness, the father, described the patient reporting vision loss, followed by collapse and tensing of trunk and limb muscles for 1-2 minutes (without rhythmic shaking) during which the patient was unresponsive. The patient then awoke but was confused, unaware of what had happened and unable to recognize his father.

    The patient was initially diagnosed with his malignancy several months ago, presenting with flank pain, weight loss and hemoptysis and recently completed a third cycle of chemotherapy (VIP: etoposide, ifosfamide, cisplatin).

    PMH:

    • Retroperitoneal embryonal carcinoma. Stage IIIC

    PSH:

    • None

    FH:

    • Relative with testicular malignancy.

    SHx:

    • No t/e/d use
    • Lives at home with family

    Meds:

    • Norco 5/325mg p.o. q.4.h. p.r.n. pain

    Allergies:

    NKDA

    Physical Exam:

    VS: T 98.4 HR 67 RR 17 BP 116/67 O2 98% RA
    Gen: Well-appearing, no acute distress
    HEENT: PERRL, MMM, no lesions, discs sharp b/l
    CV: RRR, normal S1/S2, no M/R/G
    Lungs: CTAB, no crackles/wheezing, no focal consolidation
    Abd: +BS, soft, NT/ND, no hepatosplenomegaly
    GU: Testes descended b/l, no masses, non-tender
    Ext: Warm, well-perfused, no rashes/ecchymoses
    Neuro: AAOx4, CN II-XII intact, OS 20/40 OD 20/70, normal visual fields to confrontation, no dysmetria/dysdiadochokinesia, normal gait

    Labs/Studies:

    • CBC: 7.8/14.4/43.3/179
    • BMP: 138/4.0/105/25/7/0.66/94
    • AFP: 3.5
    • B-hCG: 4222
    • MRI Brain: 2.2 cm rim-enhancing heterogeneous lesion in the right occipital lobe concerning for a metastatic focus.

    Assessment/Plan:

    26M w/hx retroperitoneal embryonal carcinoma with known liver/lung metastases presenting with syncope x1wk.

    # Syncope: Likely neurogenic (seizure) given imaging findings of brain mass concerning for metastasis. Location of mass correlates with seizure characteristics as likely focus of complex partial seizure with apparent secondary generalization. Currently, no evidence of significant mass effect or increased intracranial pressure (no headaches, nausea/vomiting, papilledema). Patient discussed with neurosurgery who will evaluate the patient for surgical resection of mass.  Start levetiracetam for seizure prophylaxis.

    # Retroperitoneal embryonal carcinoma: Stage IIIC with known liver/lung metastases, now with evidence of extension of disease. Consulted heme/onc who are familiar with the patient and do not plan for chemotherapy during this admission. Continue monitoring AFP, B-hCG levels which have remained stable.

    Imaging:

    CT Abdomen/Pelvis: Axial
    CT Abdomen/Pelvis: Coronal
    CT Abdomen/Pelvis: Sagittal
    MRI Brain: Axial

    Download: (.mp4)

    Differentiating Seizure and Syncope:

    The differential diagnosis of syncope is broad (and has been explored previously). This case explores the clinical features that have been shown to be most useful in differentiating syncope from seizure.1,2

    Differentiating Seizure and Syncope

    Questionnaire:

    Feature Points
    Tongue laceration 2
    Déjà vu 1
    Emotional stress associated with LOC 1
    Head turning during spell 1
    Unresponsive, unusual posture, limb movement, amnesia 1
    Confusion 1
    Lightheadedness -2
    Sweating -2
    Prolonged sitting/standing -2

    Score: >1 likely seizure, <1 likely syncope

    References:

    1. McKeon, A., Vaughan, C., & Delanty, N. (2006). Seizure versus syncope. Lancet neurology, 5(2), 171–180. doi:10.1016/S1474-4422(06)70350-7
    2. Sheldon, R., Rose, S., Ritchie, D., Connolly, S. J., Koshman, M.-L., Lee, M. A., Frenneaux, M., et al. (2002). Historical criteria that distinguish syncope from seizures. Journal of the American College of Cardiology, 40(1), 142–148.

    Quick Case: Pleuritic Chest Pain

    Image from: Maeng, C. H., Chin, S. O., Yang, B. H., Kim, S.-Y., Youn, H.-J., Cho, K. S., Baek, S. K., et al. (2007). A case of organizing pneumonia associated with rituximab. Cancer research and treatment : official journal of Korean Cancer Association, 39(2), 88–91. doi:10.4143/crt.2007.39.2.88

    30yo male presenting with forearm cellulitis, also complaining of right-sided sharp chest pain worse with deep inspiration and some movements of the ipsilateral shoulder. Found to have multiple pulmonary nodules (suggestive of metastasis) with the largest being a subpleural nodule in the superior/anterior portion of the RUL (roughly the location of the patient’s pain).

     

    Differential Diagnosis of Pleuritic Chest Pain

    Causes of Pleuritic CP

    Location of Referred Pain

    Referred Pain

     

    Syncope

    ID:

    A 50 year-old male with a reported two-year history of infrequent spells, presenting with two spells in the past two days.

    HPI:

    The patient’s spells began two years ago, he recounts that he was watching television when he lost consciousness and a friend noted he started shaking; he does not recall the event, and awoke in the hospital. The next spell occurred one year later, though the patient is unable to recall much about this episode. The patient remained spell-free until yesterday when he was on a bus, lost consciousness and awoke in a hospital. He notes that he had bit his tongue and lost control of his bladder. He was discharged hours later with a prescription for an AED which he was unable to fill. This morning, the patient had another spell while in the bathroom. His roommate heard him fall, found him on the ground, and noted that his mouth was moving but did not see any other movements.

    The patient’s episodes are all associated with loss of consciousness and are followed by 5-10 minutes of disorientation after which he recovers fully. The episodes are sometimes preceded by a feeling of “euphoria”, though this feeling sometimes occurs without subsequent LOC.

    The patient denies any associated palpitations, dizziness/LH, chest pain or muscle pain.  He has not had any recent fevers/chills, dysuria, cough, headache, changes in vision, numbness/tingling, weakness, difficulty speaking or swallowing or weight loss. He also denies any history of head trauma.

    Physical Examination:

    • VS: Stable and WNL
    • General: Well-appearing, pleasant, and in NAD.
    • HEENT: NC/AT. MMM. Small lesion on tongue.
    • Lungs: CTAB.
    • CV: RRR with occasional ectopic beats, no M/R/G.
    • Abdomen: S/NT/ND. Bowel sounds present.
    • Neurological exam: AAOx4, CN II-XII intact, motor/sensation/reflexes/coordination/gait WNL

    Imaging/Studies:

    • EKG: Occasional PAC/PVC
    • CT Brain: Unremarkable except for mild age-related cerebral atrophy

    Assessment & Plan:

    50 year-old male with a history of HTN and a reported two-year history of infrequent spells presenting with two spells in the past two days. The description of the patient’s episodes could be consistent with seizures. Aspects supporting this notion include loss of consciousness and period of confusion following each episode. One of the recent episodes was also associated with tongue-biting and loss of bladder control. Additionally, some episodes are associated with a sensation of euphoria rising from the abdomen to the head which could be indicative of an aura. Characteristics that suggest other causes include the absence of noted convulsions and non-stereotyped nature of each episode which could be due to the patient’s poor recollection of these events and absence of reliable witnesses. In the case of true seizures, the possible etiologies in this patient include a mass, metabolic abnormalities, substance use, or concomitant infection exacerbating an existing propensity for seizure activity. Other, non-seizure causes warranting evaluation include cardiogenic syncope particularly given the evidence of ectopic beats on examination and electrocardiogram.

    Differential Diagnosis of Syncope

    First, is it syncope? History is very important for distinguishing syncope from other causes (seizure, dizziness, vertigo, presyncope). Ask about precipitating events, prodromal symptoms, post-ictal confusion. Common causes of syncope and their associated symptoms are detailed in the figure below.

    References:

    1. Kapoor, W. N. (2000). Syncope. The New England journal of medicine, 343(25), 1856–1862. doi:10.1056/NEJM200012213432507