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

Atypical Antipsychotic Overdose

History & Physical

38M, unknown medical history, brought in after being found unresponsive next to an empty bottle of Seroquel. Presenting vital signs notable for blood pressure of 96/43, heart rate 103. Examination reveals tentatively protected airway (GCS E2 M5 V3, SpO2 100%, RR 14), normal pupil diameter and reactivity, dry mucous membranes with thick vomitus in oral cavity.

Laboratory evaluation was unremarkable, and there was no evidence of aspiration on chest radiography. ECG showed sinus tachycardia without QT prolongation. Blood pressure increased to normal range with fluid resuscitation. The patient’s mental status progressively improved and he was discharged after six hours of uneventful continuous cardiac monitoring.

Toxidrome Summary1

Class Vital Signs Mental Status Pupils Skin Other Examples
Anti-cholinergic T
HR
BP
Delirium
Agitation
Coma
Mydriasis Dry Urinary retention
BS
Anti-histamines
Anti-parkinson
Anti-psychotic
Anti-depressant
Sympathomimetic T
HR
BP
Agitation
Hallucination
Paranoia
Mydriasis Diaphoresis Tremor
Hyperreflexia
Cocaine
Amphetamine
Ephedrine
Opioid/Sedative HR
RR
BP
CNS depression
Coma
Miosis   Hyporeflexia
Needle marks
Opioids
Benzo
Barbiturates

Evaluation1,2

  • POC Glucose
  • ECG (QT interval)
  • Serum acetaminophen, salicylate, EtOH level
  • Serum drug levels if known (anti-epileptics)
  • Urine toxicology screen
  • Chemistry (metabolic acidosis, electrolytes, renal function)
  • LFT (hepatotoxicity)
  • CK (rhabdomyolysis)
  • Serum osmolarity (osmolar gap)
  • UA with microscopy (crystals in ethylene glycol poisoning)
  • ABG (carboxyhemoglobin, methemoglobin)

Pharmacology, Toxicity and Management of Second Generation Antipsychotic (SGA) Overdose3

Pharmacology, Toxicity and Management of Second Generation Antipsychotic (SGA) Overdose

References

  1. Kulig, K. (2013). General Approach to the Poisoned Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 1954-1959). Elsevier Health Sciences.
  2. Wittler, M., & Lavonas, E. (2013). Antipsychotics. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 2047-2051). Elsevier Health Sciences.
  3. Levine M, Ruha A-M. Overdose of atypical antipsychotics: clinical presentation, mechanisms of toxicity and management. CNS Drugs. 2012;26(7):601–611.
  4. WikEM: Antipsychotic toxicity

Back Pain

Causes of Back Pain

Causes of Back Pain

Key Historical Findings

Onset
Acute onset with associated activity suggests mechanical process
Acute onset without trigger, particularly if severe pain may suggest vascular process
Progressive onset without trigger suggests non-mechanical process (i.e. malignancy)
Aggravating/Alleviating Factors
Worsening with cough/valsalva suggests herniated disk
Relief with flexion associated with spinal stenosis
Location/Radiation
Radicular pain typically extends below knee, associated with nerve root involvement
Radiation to/from chest or abdomen suggests visceral source
Flank location suggests retroperitoneal source
History/Associated Symptoms
Fever
Medications (particularly anti-coagulants)
Hematuria
Malignancy
IVDA
Vascular disease

Key Physical Findings

  • Abnormal vital signs

    • Fever: abscess, osteomyelitis, discitis
    • Hypertension: dissection
    • Shock: AAA
  • Localize point of greatest tenderness
  • Examine abdomen for pulsatile mass
  • Perform thorough neurological examination including rectal tone and perianal sensation
  • Positive straight leg raise associated with sciatic nerve root irritation and is sensitive (but not specific) for disk disease.

References

  1. Mahoney, B. (2013). Back Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 278-284). Elsevier Health Sciences.
  2. WikEM: Lower back pain

Acute Pelvic Pain

Evaluation of Acute Pelvic Pain

Acute Pelvic Pain

Key Historical Findings

Location
Lateralized: suggests process related to tube or ovary, consider unilateral urinary tract process. On right, add appendicitis to differential; on left, add diverticulitis (particularly if age >40.
Central: suggests process involving uterus, bladder or bilateral adnexa
Diffuse: suggests PID
Radiation
Radiation to rectum suggests pooling of fluid or blood in cul-de-sac
Onset
Abrupt: suggests acute intrapelvic hemorrhage (from ruptured ectopic or ovarian cyst), ovarian torsion, urolithiasis
Gradual: inflammatory process such as PID
Chronic/recurrent: suggests endometriosis, recurrent ovarian cyst, ovarian mass
Associated Symptoms
Fevers/chills: suggests infectious process
Nausea/vomiting: suggests process involving gastrointestinal tract, though may accompany pregnancy or severe pain associated with ovarian torsion, urolithiasis.
Dysuria: suggests process involving urinary tract, though may be associated with local vulvar/vaginal process
Urinary urgency: more specific for bladder or urethral irritation
Obstetric History
History of recurrent spontaneous abortions or prior ectopic pregnancy increases likelihood of recurrence.
Ongoing fertility treatments increase likelihood for ectopic/heterotopic (occurs in 1:100 with assisted reproduction compared to 1:8000 in general population)
Vaginal Bleeding
In non-pregnant: suggests PID, DUB, cervical or uterine cancer
In early pregnancy: may be associated with ectopic pregnancy, non-viable IUP, or subchorionic hemorrhage
In late pregnancy: may be associated with placental pathology (previa, abruption)

Key Physical Findings

  • Pelvic examination: assists with localization of lateralized process. Should be preceded by ultrasound if >20 weeks.
  • Abnormal vaginal discharge: suggests vaginitis, cervicitis, PID, or retained foreign body.
  • Cervical motion tenderness: suggests reproductive tract inflammation or irritation of adjacent structures (appendicitis, cystitis)
  • Unilateral adnexal mass/tenderness: associated with ovarian cyst/mass, TOA, ectopic, or ovarian torsion.

References:

  1. Hart, D., & Lipsky, A. (2013). Acute Pelvic Pain in Women. In Rosen's Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 266-272). Elsevier Health Sciences.
  2. WikEM: Pelvic pain

Gastrointestinal Bleeding

Evaluation and Management of Gastrointestinal Bleeding

Evaluation and Management of Gastrointestinal Bleeding

Key Historical Features

Quantity
Patient’s estimate
Symptoms suggestive of anemia/volume depletion: (pre)syncope, dyspnea
Appearance/Location
Distinguish upper from lower GI bleding
PMH
Prior episodes and source
History of aortic aneurysm graft
Comorbidities: presence of CAD, CHF, liver disease or diabetes increases mortality
Medications/substance use
Gastrotoxic, anti-coagulants, anti-platelet agents
Alcohol abuse

Key Physical Findings

Vital signs
Tachycardia or hypotension
Eyes
Conjuntival pallor suggests anemia
Scleral icterus suggests liver disease
Abdomen
Hyperactive bowel sounds may be present in UGIB (blood is cathartic)
Epigastric tenderness to palpation suggests PUD
Diffuse tenderness suggests bowel ischemia, obstruction/ileus, or perforation
Rectal (digital, anoscopy)
May reveal fissures, hemorrhoids or polyps

Labs/Diagnostic Tests

  • CBC: consider transfusion for Hb <8-10g/dL particularly in elderly or those with CAD
  • BMP: BUN:creatinine > 36 in the absence of renal failure suggests UGIB
  • PT/PTT/INR: coagulopathy
  • Lactate: elevated in bowel ischemia or systemic hypoperfusion
  • T&S or T&C
  • ECG: screen for myocardial ischemia

Blatchford Scoring System

Item Value Points
BUN 18-22 2
22-28 3
28-70 4
>70 6
Hb (male) 12-13 1
10-12 3
<10 6
Hb (female) 10-12 1
<10 6
SBP 100-109 1
90-99 2
<90 3
Other HR > 100 1
Melena 1
Syncope 2
Liver disease 2
Heart failure 2

References:

  1. Goralnick, E., & Meguerdichian, D. (2013). Gastrointestinal Bleeding. In Rosen's Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 248-253). Elsevier Health Sciences.

Aortic Dissection

Imaging

Prominent cardiomediastinal silhouette, which may be due to patient position.

Prominent cardiomediastinal silhouette, which may be due to patient position.

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CT Angiography Aorta

Highly complex type B aortic dissection originating at the distal arch (just distal to the left subclavian artery) and terminating at the level of diaphragm. The dissection contains multiple false lumens containing blood products of differing ages (thrombus and contrast-opacified blood). No apparent involvement of the left common carotid or left subclavian artery.

Mediastinum Anatomy

Mediastinal Masses

Anterior
Retrosternal goiter
Thymoma
Germ-cell tumor
Lymphadenopathy (lymphoma)
Middle
Aortic arch aneurysm
Dilated pulmonary artery
Tracheal lesion
Posterior
Esophageal lesions
Hiatal hernia
Descending aortic aneurysm
Paraspinal abscess

References:

  1. Faiz, O., & Moffat, D. (2002). Anatomy at a glance. Malden, MA: Blackwell Science.
  2. Whitten CR, Khan S, Munneke GJ, Grubnic S. A diagnostic approach to mediastinal abnormalities. Radiographics. 2007;27(3):657–671. doi:10.1148/rg.273065136.
  3. WikEM: Widened mediastinum

Nausea and Vomiting

Pathophysiology of Nausea and Vomiting

Pathophysiology of Nausea and Vomiting

Complications of Nausea and Vomiting

  • Hypovolemia: activates RAAS
  • Metabolic alkalosis: loss of hydrogen ions in vomitus
  • Hypokalemia: RAAS promotes sodium retention and potassium excretion
  • Esophageal injury: Mallory-Weiss tear, Boerhaave syndrome
  • Aspiration

Key Historical Findings

Duration of vomiting
Acute: Episodic and occurring for <1 week. Suggestive of obstructive, toxic/metabolic, infectious, ischemic or neurologic process.
Chronic: Episodic and occurring for >1 month. Suggestive of partial obstruction, motility disorder or neurologic process.
Onset
Acute onset: suggests pancreatitis, gastroenteritis, or cholecystitis.
Timing
Post prandial: delayed >1 hour suggests gastric outlet obstruction or gastroparesis.
Contents
Bile: presence of bile suggests patent connection between duodenum and stomach (no GOO)
Undigested food: suggests upper GI tract process (achalasia, esophageal stricture, Zenker)
Feculent: suggests distal bowel obstruction
Associated symptoms
Headache: suggests elevated ICP

Causes of Nausea and Vomiting

Causes of Nausea and Vomiting

References

  1. Zun, L. (2013). Nausea and Vomiting. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 238-247). Elsevier Health Sciences.

Abdominal Pain

Pathophysiology of Abdominal Pain

  1. Visceral: distension of hollow organs or capsular stretch of solid organs.
  2. Somatic: parietal peritoneal irritation
  3. Referred

    • Extra-abdominopelvic

      • Epigastric: inferior MI
      • Pelvic: hip
      • Abdominal: lower lobe pneumonia/infarction
    • Abdominopelvic

      • Shoulder: diaphragmatic irritation (ex. perforated duodenal ulcer, splenic pathology)
      • Mid-back: aortopathy, pancreatitis
      • Flank: renal pathology
      • Low back: uterus, rectum

Concerning Historical Features

  • Elderly: increased probability for severe disease with poor clinical diagnostic accuracy
  • Immunocompromised: HIV/AIDS, uncontrolled diabetes, chronic liver disease, chemotherapy, other immunosuppression
  • Pain preceding nausea/vomiting: increased likelihood of surgical process
  • Abrupt onset, duration <48h, constant timing
  • Prior abdominal surgical history: consider bowel obstruction
  • No prior episodes of similar pain
  • Recent antibiotic or steroid use: may mask signs of infection
  • Cardiac risk factors (HTN, vascular disease, atrial fibrillation: increased risk for mesenteric ischemia or aortic aneurysm
  • Heavy NSAID use or anticoagulation: increase concern for gastrointestinal bleeding

Imaging

  • Plain film reserved for those who would otherwise not undergo CT. XR abdomen for bowel obstruction or radiopaque foreign body.
  • CT abdomen/pelvis with IV contrast, particularly if elderly or immunocompromised.
  • Ultrasound preferred for hepatobiliary pathology
  • Bedside ultrasound for identification of IUP, free intraperitoneal fluid, cholecystitis, CBD dilation, ascites, hydronephrosis, aortopathy, volume status.

Causes of Abdominal Pain

Causes of Abdominal Pain

References

  1. Budhram, G., & Bengiamin, R. (2013). Abdominal Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 223-231). Elsevier Health Sciences.

Chest Pain

An Algorithm for the Evaluation of Chest Pain

Algorithm for the Evaluation of Chest Pain

NOTE: Algorithm revised in November, 2017. The prior version is no longer supported but remains available here.

Guided Lecture

EM Ed
Watch “Chest Pain: It’s Giving Me Angina” from EM Ed. In this lecture Dr. Celedon reviews the critical differential diagnosis for chest pain and how to safely and effectively work up patient’s with this challenging chief complaint.

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.

Endocrine Emergencies

HPI

30 year-old female with a history of autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), polysubstance use, brought to the emergency department by ambulance with reported chief complaint of fever. On presentation, the patient reported fever for one day, associated with cough. She was lethargic and confused, answering yes/no questions but unable to provide detailed history. She states that she has been taking her home medications as prescribed, which include hydrocortisone, fludrocortisone, synthroid and insulin. No collateral information was immediately available.

Additional history was obtained from chart review upon discharge. The patient was hospitalized two weeks prior with pneumonia and discharged after two days. For 2-3 days prior to presentation, she reported the following symptoms to family members: nausea/vomiting, cough, decreased oral intake, fevers, and palpitations – she did not take her home medications during this time.

Physical Exam

VS: T 38.6 HR 112 RR 18 BP 149/82 O2 90% RA
Gen: Alert, fatigued, slow responses.
HEENT: No meningeal irritation, dry mucous membranes.
Pulmonary: Tachypnea, inspiratory wheezing and faint crackles at left and right inferior lung fields, appreciated anteriorly as well.
Neuro: Alert, oriented to self, situation, not month/year. PERRL, EOMI, facial muscles symmetric, tongue protrudes midline without fasciculation. Peripheral sensation grossly intact to light touch and moves all extremities on command.

Labs

  • VBG: alkalemia, primary respiratory
  • CBC: no leukocytosis, normal differential, normocytic anemia
  • BMP: 131, 2.5 , 94, 28, 11, 1.6, 115
  • Mg: 1.3
  • Lactate: 1.0
  • TSH: 17 , T4: 1.03
  • Troponin: 0.129

ECG

ECG 1
ECG 2

Imaging

  • CXR: Negative acute.
  • CT Head: Negative acute.
  • CT Cardiac: NICM, EF 35%.
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CT Chest non-contrast

  • Diffuse patchy GGO (pulmonary edema, atypical pneumonia, alveolar hemorrhage, others).
  • Multiple bilateral pulmonary nodules.
  • Possible pulmonary arterial hypertension.

Hospital Course

The patient’s evaluation in the emergency department was concerning for severe sepsis secondary to suspected pulmonary source (given association of fever with cough, hypoxia and abnormal chest imaging findings). The patient had persistent alteration in mental status concerning for CNS infection. While preparing for lumbar puncture, cardiac monitoring revealed sustained polymorphic ventricular tachycardia without appreciable pulse. CPR was initiated, amiodarone 150mg IV push administered and at first pulse check a perfusing sinus rhythm was noted with immediate recovery of prior baseline mental status. Amiodarone load was continued and additional potassium sulfate (PO and IV) was administered. Review of telemetry monitoring revealed preceding 30-45 minutes of non-sustained ventricular tachycardia. The patient had two more episodes of sustained ventricular tachycardia requiring defibrillation. The patient was admitted to the medical intensive care unit for continued management.

#Sustained Ventricular Tachycardia
Initially attributed to critical hypokalemia and hypomagnesemia. However, after appropriate repletion serial ECG’s continued to demonstrate prolonged QT interval (possibly acquired secondary to medications, later review revealed multiple promotility agents for treatment of gastroparesis which could contribute to QT-prolongation including erythromycin and metoclopramide, also associated with endocrinopathies). Early echocardiography demonstrated global hypokinesis with estimated EF 30-35%. This was initially attributed to severe sepsis, as well as recurrent defibrillation. However, cardiac CT after resolution of acute illness showed persistent depressed ejection fraction, no evidence of coronary atherosclerosis. The presence of non-ischemic cardiomyopathy (may be attributable to chronic endocrine dysfunction or prior history of methamphetamine abuse) associated with malignant dysrhythmias warranted ICD placement for secondary prevention which the patient was scheduled to receive.

#Severe Sepsis
Attributed to pulmonary source given CT findings, healthcare associated and covered broadly. Mental status gradually improved and returned to baseline. CT head was negative, lumbar puncture deferred.

#Hypokalemia
Unclear etiology. Adrenal insufficiency commonly associated with hyperkalemia and no history of surreptitious fludrocortisone use. Possibly secondary to GI losses. Improved with repletion.

#Autoimmune Polyglandular Syndrome
Started on stress-dose steroids in emergency department. Transiently developed DKA which was reversed appropriately and hydrocortisone was tapered to home regimen. Home levothyroxine was resumed.

Endocrine Emergencies: Hyperthyroidism

Symptoms

Constitutional Weight loss, heat intolerance, perspiration
Cardiopulmonary Palpitations, chest pain, dyspnea
Neuropsychiatric Tremor, anxiety, double vision, muscle weakness
Neck Fullness, dysphagia, dysphonia
Musculoskeletal Extremity swelling
Reproductive Irregular menses, decreased libido, gynecomastia

Signs

Vital signs Tachycardia, widened pulse pressure, fever
Cardiovascular Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur
Ophthalmologic Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze
Neurologic Tremor, hyperreflexia, proximal muscle weakness
Dermatologic Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia
Neck Enlarged or nodular thyroid

Thyroid Storm

Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).

Precipitants
Medical: Sepsis, MI, CVA, CHF, PE, visceral ischemia
Trauma: Surgery, blunt, penetrating
Endocrine: DKA, HHS, hypoglycemia
Drugs: Iodine, amiodarone, inhaled anesthetics
Pregnancy: post-partum, hyperemesis gravidarum

Scoring (Burch, Wartofsky)

Fever
99-100 5
100-101 10
101-102 15
102-103 20
103-104 25
>104 30
Tachycardia
90-110 5
110-120 10
120-130 15
130-140 20
>140 25
Mental Status
Normal 0
Mild agitation 10
Extreme lethargy 20
Coma, seizure 30
CHF
Absent 0
Mild (edema) 5
Moderate (rales, atrial fibrillation) 10
Pulmonary edema 15
GI
None 0
Nausea/vomiting, abdominal pain 10
Jaundice 20
Precipitating Event
None 0
Present 10
  • >45: thyroid storm
  • 25-44: impending thyroid storm
  • <25: unlikely thyroid storm

Management

Supportive measures
Volume resuscitation and cooling
Benzodiazepines for agitation
Beta-blockade
Propranolol 60-80mg PO q4h
Propranolol 0.5-1.0mg IV, repeat q15min then 1-2mg q3h
Esmolol continuous infusion
Endocrinology consultation
PTU, SSKI

Endocrine Emergencies: Hypothyroidism

Symptoms

Constitutional Weight gain, cold intolerance, fatigue
Cardiopulmonary Dyspnea, decreased exercise capacity
Neuropsychiatric Impaired concentration and attention
Musculoskeletal Extremity swelling
Gastrointestinal Constipation
Reproductive Irregular menses, erectile dysfunction, decreased libido
Integumentary Coarse hair, dry skin, alopecia, thin nails

Signs

Vital signs Bradycardia, hypothermia
Cardiovascular Prolonged QT, increased ventricular arrhythmia, accelerated CAD, diastolic heart failure, peripheral edema
Neurologic Lethargy, slowed speech, agitation, seizures, ataxia/dysmetria, mononeuropathy, delayed relaxation of reflexes
Musculoskeletal Proximal myopathy, pseudohypertrophy, polyarthralgia
Gastrointestinal Ileus

Myxedema Coma

Precipitants
Critical illness: sepsis (especially PNA), CVA, MI, CHF, trauma, burns
Endocrine: DKA, hypoglycemia
Drugs: amiodarone, lithium, phenytoin, rifampin, medication non-adherence
Environmental: cold exposure
Recognition
History: hypothyroidism, thyroidectomy scar and acute precipitating illness
Hypothermia: temp <95.9°F (or normal in presence of infection)
AMS: lethargy, confusion, coma, agitation, psychosis, seizures
Hypotension: refractory to volume resuscitation and pressors
Bradypnea: with hypercapnia and hypoxia
Hyponatremia

Management

  • Airway protection
  • Fluid resuscitation
  • Thyroid hormone replacement
    • Young, otherwise healthy patients: T3 10ug IV q4h
    • Elderly, cardiac compromise: 300ug IV x1
  • Hydrocortisone: 50-100mg IV q6-8h
  • Treat precipitating illness

Interpretation of Thyroid Function Tests

Condition TSH T4
None Normal Normal
Hyperthyroidism Low High
Hypothyroidism High Low
Subclinical hyperthyroidism Low Normal
Subclinical hypothyroidism High Normal
Sick euthyroid Low Low

Endocrine Emergencies: Adrenal Insufficiency

Either primary due to adrenal gland failure (often secondary to autoimmune destruction), or secondary most often due to exogenous glucocorticoid administration (usually requiring more than 30mg/day for > 3wks).

Symptoms

Constitutional Weakness, fatigue
Gastrointestinal Anorexia, nausea, cramping
Neuropsychiatric Depression, apathy
Reproductive Amenorrhea, decreased libido
Musculoskeletal Myalgia, arthralgia

Signs

General Hyponatremia, orthostatic hypotension, low-grade fever
Primary Hyperpigmentation, hyperkalemia, hyperchloremia, acidosis
Secondary Hypoglycemia

Management

Maintenance
Hydrocortisone 20mg qAM, 10mg qPM
Fludrocortisone 50-100ug daily
Minor illness (x2)
Hydrocortisone 40mg qAM, 20mg qPM
Fludrocortisone 50-200ug daily
Adrenal Crisis
Dexamethasone 4mg IV or hydrocortisone 100mg IV
2-3L 0.9% NaCl
Treat precipitating illness

Life-Threatening Electrolyte Abnormalities3

Critical Hypokalemia

Causes
GI losses (diarrhea, laxative use)
Renal losses (hyperaldosteronism, diuretics)
Cellular shifts (alkalosis)
ECG changes
U-waves 4
T-wave flattening
Ventricular arrhythmias (exacerbated with digoxin use)
Treatment
Maximum rate 10-20mEq/h with ECG monitoring
If malignant ventricular arrhythmias or arrest imminent, consider more rapid administration (10mEq over 5 minutes)

 

Critical Hypomagnesemia

Causes
GI, renal losses
Thyroid dysfunction
Treatment
1-2g IV over 5-60 minutes or IVP for Torsades

Conclusion

Unfortunately, this patient’s comprehensive clinical picture does not fit neatly into a particular category of endocrinologic pathology. Her underlying autoimmune disorder manifests both primary adrenal and thyroid dysfunction. Components of the patient’s presentation are suggestive of critical hypothyroidism (myxedema coma) including alteration in mental status, QT-prolongation and hyponatremia as well as possible precipitant of pneumonia. However, despite elevated TSH, the patient’s free T4 level was within normal range. Also absent was hypoventilation (the patient was appropriately tachypneic for degree of hypoxia and with resultant respiratory alkalosis) or bradycardia/hypothermia.
Similarly, adrenal insufficiency is typically associated with hyperkalemia, whereas our patient had critical hypokalemia that was determined to be at least a contributory factor to her ventricular dysrhythmia. The etiology of the patient’s hypokalemia remained unexplained.

References:

  1. Sharma, A., & Levy, D. (2009). Thyroid and Adrenal Disorders. In Rosen’s Emergency Medicine (8th ed., Vol. 2, pp. 1676-1692). Elsevier Health Sciences.
  2. Savage MW, Mah PM, Weetman AP, Newell-Price J. Endocrine emergencies. Postgrad Med J. 2004;80(947):506–515. doi:10.1136/pgmj.2003.013474.
  3. ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112(24 Suppl):IV1–203. doi:10.1161/CIRCULATIONAHA.105.166550.
  4. Levis JT. ECG diagnosis: hypokalemia. Perm J. 2012;16(2):57.

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.

Altered Mental Status Applied

H&P

58 year-old female with no known past medical history, brought to emergency department by husband due to fatigue and weakness. The patient does not speak and cannot provide history. Her husband describes a progressive decline from normal baseline two weeks ago, noting lethargy/fatigue. Noted decreased speech and attention one week ago, and absent speech and requiring assistance with ambulation for the past two days. Thorough review of systems unremarkable excepting vomiting with decreased oral intake (tolerating fluids) and prior headache which resolved.

On examination, vital signs were normal, the patient was lying in bed and in no acute distress. The patient was non-verbal and did not follow commands (GCS E4-M5-V2). She was unable to comply with a thorough neurological examination, however pupils were equal and reactive, eyes tracked without nystagmus, no facial asymmetry noted, reflexes 1+ and symmetric in UE/LE, cannot participate in strength/sensory testing. Abdominal examination notable for infraumbilical and left-sided mass which elicits groans with palpation, though no rigidity or guarding. Mucous membranes moist, no skin tenting.

Labs

  • CBC: 13.5 (97% neutrophils) , 12.9, 38.2, 240
  • BMP: 107, 2.4, 70, 28, 9, 10, 0.44, 102
  • Serum osmolarity: 224
  • Urine osmolarity: 239
  • UNa: 20

Imaging

IM-0001-0022
IM-0001-0022
IM-0001-0024
IM-0001-0024
IM-0001-0026
IM-0001-0026
IM-0001-0028
IM-0001-0028
IM-0001-0032
IM-0001-0032
IM-0001-0036
IM-0001-0036
IM-0001-0040
IM-0001-0040
IM-0001-0044
IM-0001-0044
IM-0001-0048
IM-0001-0048
IM-0001-0052
IM-0001-0052
IM-0001-0056
IM-0001-0056
IM-0001-0060
IM-0001-0060
IM-0001-0064
IM-0001-0064
IM-0001-0068
IM-0001-0068
IM-0001-0072
IM-0001-0072
IM-0001-0076
IM-0001-0076
IM-0001-0080
IM-0001-0080
IM-0001-0084
IM-0001-0084
IM-0001-0088
IM-0001-0088
IM-0001-0092
IM-0001-0092
IM-0001-0010
IM-0001-0010
IM-0001-0014
IM-0001-0014
IM-0001-0018
IM-0001-0018
IM-0001-0022
IM-0001-0022
IM-0001-0026
IM-0001-0026
IM-0001-0030
IM-0001-0030
IM-0001-0034
IM-0001-0034
IM-0001-0038
IM-0001-0038
IM-0001-0042
IM-0001-0042
IM-0001-0046
IM-0001-0046
IM-0001-0050
IM-0001-0050

CT abdomen/pelvis with intravenous contrast

  • Large, 15 cm cystic mass in the left abdomen, which likely arises from the mesentery. This mass is suspicious for neoplasm.
  • Multiple low-density cystic lesions in the liver, which measure up to 4.5 cm in diameter and are concerning for metastatic disease. Alternatively, these may represent benign hepatic cysts which are unrelated to the mesenteric mass.
  • Massively distended bladder, with moderate bilateral hydronephrosis and mild hydroureter.

Hospital Course

The patient was admitted to the medical intensive care unit. The following problem list details findings from the extensive inpatient evaluation.

#Altered Mental Status: The patient’s dramatically depressed level of consciousness improved gradually with correction of hyponatremia and the patient was alert, oriented and at baseline at the time of discharge. Evaluation included MRI brain which showed only chronic microvascular changes. A lumbar puncture was notable for isolated elevation of CSF protein. The patient was treated empirically for HSV encephalitis until CSF HSV PCR resulted negative. Neurology was consulted and identified increased CSF oligoclonal bands of unclear significance.

#Hyponatremia: Nephrology consulted, presumed SIADH based on urine studies (secondary to infection or malignancy). Corrected upon discharge.

#Pelvic Mass: Initially thought to arise from small bowel on CT abdomen/pelvis, after bladder decompression and transvaginal ultrasound, thought to arise from adnexa. Gynecology consulted, cyst characteristics (homogenous, fluid-filled) suggest benign process and tumor markers within normal limits. No acute intervention, drainage or biopsy warranted.

#Bladder distension: Unclear etiology, associated with mild/moderate hydronephrosis. Thought to be secondary to bladder outlet obstruction secondary to pelvic mass. Indwelling catheter placed, discontinued prior to discharge with successful spontaneous voiding trial and normal post-void residual.

Hyponatremia Applied

Hyponatremia Applied

Altered Mental Status Applied

Altered Mental Status Applied

Sore Throat

Evaluation of Sore Throat

Evaluation of Sore Throat

Physical Examination:

Neck
Stiffness, limitation of extension suggestive of retropharyngeal abscess.
Jaw
Trismus associated with peritonsillar cellulitis or abscess.
Oral Cavity
Dry mucous membranes suggest dehydration (from odynophagia) and indicates severity of symptoms.
Tongue elevation, sublingual/submental induration, poor dentition (particularly of mandibular molars) associated with Ludwig Angina.
Unilateral tonsillar enlargement with contralateral uvular deviation suggests peritonisllar abscess. Fluctuance may be palpated.
Tonsilar exudates suggest infectious pharyngitis (non-specific).
Palatal petechiae suggest bacterial pharyngitis.
Ulcerations of the anterior oral cavity are associated with herpes infection, lesions on the soft palate are suggestive of coxsackievirus infection.
Rarely, a grey membrane in the posterior pharynx will suggest diphtheria.
Lymphadenopathy
Tender anterior cervical lymphadenopathy may suggest bacterial pharyngitis.
Posterior cervical lymphadenopathy is associated with infectious mononucleosis.
Large, firm, non-mobile lymph nodes may suggest malignancy.
Eyes
Presence of conjunctivitis (also rhinorrhea, exanthema) associated with viral pharyngitis.
Skin
Ulcers involving the hands, feet, in addition to pharyngeal lesions suggest coxsackievirus infection.
Scarlatiniform rash associated with pharyngitis (particularly in school-age children) suggests streptococcal pharyngitis.
Abdomen
Splenomegaly is associated with infectious mononucleosis.

Centor Criteria (Modified)

  • +1: Fever
  • +1: Tonsillar Exudate
  • +1: Tender anterior cervical lymphadenopathy
  • +1: Absence of cough
  • -1: Age >45yo

Incidence of GABHS by Centor Criteria

  • 0, -1: 1%
  • 1: 10%
  • 2: 17%
  • 3: 35%
  • 4: 51%

References:

  1. Newman, D., & Shreves, A. (2013). Sore Throat. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 198-202). Elsevier Health Sciences.
  2. King, B. R., & Charles, R. A. (2004). Pharyngitis In The ED Diagnostic Challenges And Management Dilemmas. Emergency medicine practice, 6(5), 1–24.

Dizziness and Vertigo

Types of Dizziness

Types of Dizziness

Distinguishing Central vs. Peripheral Vertigo

Characteristic Peripheral Central
Onset Sudden Gradual
Intensity Severe Mild
Duration Minutes Weeks
Timing Intermittent Continuous
Nystagmus Horizontal Vertical, bidirectional
Exacerbation with head movement +
Auditory symptoms +
Neurological findings +

Causes of Vertigo

Causes of Vertigo

Characteristics of common causes of vertigo

Cause Mechanism Onset Symptoms Findings
Peripheral
BPPV Otolith Brief, positional episodes Nausea, vomiting, absent auditory symptoms. Dix-Hallpike positive
Vestibular neuronitis Viral, post-viral inflammation of vestibular portion of CNVIII Acute and severe, subsiding over days. Nausea, vomiting, absent auditory symptoms. Head thrust abnormal
Meniere Endolymphatic hydrops Recurrent, lasting hours Tinnitus, hearing loss. SNHL
Central
Vertebrobasilar insufficiency Atherosclerosis (vascular risk factors) Acute onset, recurrent episodes if TIA Headache, gait impairment, diplopia, absent auditory symptoms. Neurologic deficits
Cerebellar stroke Atherosclerosis (vascular risk factors) Acute and severe Headache, dysphagia, gait impairment Dysmetria, dysdiadochokinesia, ataxia, CN palsy
Brainstem stroke Atherosclerosis (vascular risk factors), dissection Acute and severe Dysphagia, dysphonia, gait impairment, sensory disturbances Loss of pain/temperature on ipsilateral face, contralateral body, palatal/pharyngeal paralysis
MS Demyelination Subacute onset History of other, variable symptoms INO

History

  • Onset, duration, timing, severity, exacerbating factors
  • Vascular risk factors: age, male, HTN, CAD, DM, atrial fibrillation
  • Vestibulotoxic medications: aminoglycosides, AED

Key Physical Examination Findings

  • VS: Presence of hypotension suggests presyncope
  • Head: Examine for evidence of trauma
  • Neck: Auscultate for carotid bruit
  • Ear: Effusion or perforation suggests peripheral process (possible perilymphatic fistula)
  • Eye: Examine for pupillary defects (CNIII), papilledema, extraoccular muscles
  • Neuro: Cerebellar testing

Positional Testing

Dix-Hallpike
Turn head 45°
Upright sitting → supine (head overhanging bed)
Positive: nystagmus + symptoms on one side
Roll
Supine
Turn head 90°
Positive: nystagmus + symptoms on both sides, more severe on affected

HINTS1

Normal head impulse, direction-changing nystagmus, or skew deviation suggests stroke.

Head impulse
Focus on examiner’s nose
Rapidly turn head 10° in horizontal plan
Presence of corrective saccade suggests defect of peripheral vestibular nerve
Nystagmus
Peripheral: Horizontal, unidirectional. Increases on gaze in direction of fast phase (decreases or resolves opposite)
Central: Direction changing
Skew deviation
Cross cover
Presence of vertical disconjugate gaze suggests brainstem dysfunction

HINTS Gallery

Positive Head Impulse Test
Central Changing Nystagmus
Skew Deviation

Labs

  • Glucose
  • CBC/Chemistry
  • ECG

Imaging

  • Warranted if findings concerning for central process
  • MRI preferred

Management

Specific etiologies
Vestibular neuronitis: steroids
Meniere: dietary changes
BPPV: canalith repositioning
Symptomatic relief
Promethazine (Phenergan) 12.5-25mg PO
Ondansetron (Zofran) 4mg IV
Lorazepam (Ativan) 1-2mg PO/IV
Meclizine (Antivert) 25mg PO q6-8h PRN

References

  1. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y.-H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke; a journal of cerebral circulation, 40(11), 3504–3510. doi:10.1161/STROKEAHA.109.551234
  2. Chang, A., & Olshaker, J. (2013). Dizziness and Vertigo. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 162-169). Elsevier Health Sciences.

Headache

Pathophysiology of Headache (“cephalalgia”)

  • Sensation via meninges and blood vessels, mediated via CN V.

High-Risk Historical Features (indications for imaging)

  • Sudden onset (seconds/minutes), patient recalls activity at onset
  • Worst in life or change in character from established headache
  • Fever, neck pain/stiffness
  • Altered mental status
  • Malignancy
  • Coagulopathy: iatrogenic, hepatopathy, dialysis
  • Immunocompromised
  • Rare: CO exposure, jaw claudication, PCKD

Location of Pain

Headache Location

  1. Unilateral: migraine
  2. Periorbital: glaucoma, CVT, optic neuritis, cluster
  3. Facial/maxillary: trigeminal neuralgia, sinusitis
  4. Temporal: GCA
  5. Occipital: cerebellar stroke
  6. Nuchal: meningitis

Evaluation of Headache 2

Evaluation of Headache

Characteristics of Primary Headaches

Type Location Duration Quality Associated symptoms Comment
Migraine Unilateral Hours to days Throbbing Photophobia, phonophobia Atypical migraines with neurological findings (basilar, ophthalmoplegic, ophthalmic, hemiplegic)
Tension Bilateral Minutes to days Constricting None
Cluster Unilateral, periorbital Minutes to hours Throbbing Conjunctival injection, lacrimation, rhinorrhea, miosis, eyelid edema Males 90%, triggered by EtOH.

Physical Examination Findings

Vital Signs
Fever: present in 95% of patients with meningitis
Head
Trauma: signs of basilar skull fracture
Temporal artery tenderness/induration: GCA
Pericranial muscle tenderness: tension headache
Trigger point, Tinnel sign: occipital neuralgia
Eyes
Pupillary defects: aneurysm with CN III compression
Papilledema, absence of spontaneous venous pulsations: elevated intracranial pressure
EOM abnormalities: ICH, mass lesion, neuropathy (DM, Lyme)
Horner syndrome (ptosis, miosis, anhidrosis): carotid dissection
Visual field defect: stroke, atypical migraine
Conjunctival injection: glaucoma (fixed, mid-size pupil, elevated intraocular pressure), cluster headache
Mouth
Thrush: immunocompromise
Sinuses
Tenderness to palpation, abnormal transillumination: sinusitis
Neck
Resistance to supine neck flexion: meningitis
Kernig: supine position, hip flexed, knee flexed, resistance to knee extension
Brudzinski: supine position, neck flexion results in knee flexion
Jolt accentuation: patient rotates head side-to-side, 2-3 times/sec exacerbates headache

CSF Analysis 4

Test Bacterial Viral Fungal/TB
Opening pressure >15cm H20 Normal Normal
WBC (cells/mm3) >1,000 <100 Variable
Differential PMN Lymphocytes Lymphocytes
Protein (mg/dL) >250 >50 >50
Glucose (mg/dL) <10 Normal <45

References:

  1. Russi, C. (2013). Headache. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 170-175). Elsevier Health Sciences.
  2. Godwin SA, Villa J. “Acute headache in the ED: Evidence-Based Evaluation and Treatment Options.” Emerg Med Pract 2001; 3(6): 1-32.
  3. Edlow, J. A., Panagos, P. D., Godwin, S. A., Thomas, T. L., & Decker, W. W. (2008). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 52(4), 407–436. doi:10.1016/j.annemergmed.2008.07.001
  4. Seehusen, D. A., Reeves, M. M., & Fomin, D. A. (2003). Cerebrospinal fluid analysis. American family physician, 68(6), 1103–1108.
  5. WikEM: Headache

Seizure

Definition

Seizure
Pathologic neuronal activation leading to abnormal function
Epilepsy
Recurrent unprovoked seizures

Classification

  • Cause
    • Primary: Unprovoked
    • Secondary: Provoked, caused by trauma, illness, intoxication, metabolic disturbances, etc.
  • Effect on mentation
    • Generalized: involvement of both hemispheres with associated loss of consciousness (tonic-clonic, absence, atonic, myoclonic)
    • Focal: Involving single hemisphere with preserved level of consciousness
  • Status epilepticus
    • Witnessed convulsions lasting >5min
    • Recurrent seizure without recovery from postictal period

Causes of Seizures

Causes of Seizures

Management of Seizures

Management of Seizures

Medications for Treatment of Seizures

Medication Dose (adult) Dose (peds) Comment
1st Line
Lorazepam 4mg IV <13kg: 0.1mg/kg (max 2mg)
13-39kg: 2mg

>39kg: 4mg
Repeat in 10min
Midazolam 10mg IM 0.2mg/kg IM (max 5mg) Repeat in 10min
Midazolam 10mg buccal 0.5mg/kg buccal (max 5mg) Repeat in 10min
2nd Line
Fosphenytoin 20mg PE/kg IV    
Phenytoin 20mg/kg IV   May cause hypotension
3rd Line
Midazolam 0.05-2mg/kg/hr    
Propofol 1-2mg/kg bolus then 20-200mcg/kg/min    
Pentobarbital 5-15mg/kg bolus then 0.5-5mg/kg/hr    
Special Conditions
Glucose 50mL D50/W   Hypoglycemia
MgSO4 6g IV over 15min   Eclampsia (20wks gestation to 6wks post-partum)
Pyridoxine 0.5g/min until seizures stop, max 5g   INH ingestion
3% saline 100-200mL over 1-2h   Confirmed hyponatremia

History

Points suggestive of seizure over alternative process
Abrupt onset
Duration < 120s
LOC
Purposeless activity: automatisms, tonic-clonic
Provocation: fever in children, substance withdrawal
Postictal state
Retrograde amnesia
Incontinence, oral trauma (buccal maceration, tongue laceration)
Rapidly resolving lactic acidosis
Important historical points for patients with seizure history
Recent illness
Medications (adherence, changes, interactions)
Substance use
Ictogenic factors
Recent/remote head trauma
Developmental abnormalities
Substance use
Sleep deprivation
Pregnancy

Key Physical Examination Findings

  • Vital sign abnormalities persisting beyond immediate postictal state (may suggest drug/toxin exposure, CNS lesion)
  • Nuchal rigidity
  • Signs of IVDA
  • Sequela

    • Head trauma
    • Tongue laceration
    • Shoulder dislocation (posterior)
  • Neurological exam

    • Stroke
    • Elevated ICP
    • Failure to note improvement in postictal confusion (encephalopathy, subclinical seizures)

Labs

  • Glucose
  • BMP (Na, Ca, Mg)
  • AED levels
  • CBC (leukocytosis and bandemia common post-seizure)
  • CSF
  • B-hCG
  • LFT (hepatic dysfunction, alcoholic hepatitis)
  • Lactate (rapidly resolves on repeat)

Indications for Imaging

  • New seizures
  • History of trauma
  • History of malignancy
  • Immunocompromised
  • Headache
  • Anti-coagulation
  • Focal neurological exam
  • Persistent AMS

References

  1. McMullan, J., Davitt, A., & Pollack, C. (2013). Seizures. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 156-161). Elsevier Health Sciences
  2. WikEM: Seizure

Altered Mental Status

Components of Consciousness

Components of Consciousness

Causes of Altered Mental Status

Causes of Altered Mental Status

History

Rate of onset
Abrupt: CNS
Gradual: Systemic

Physical Examination

  • Vital Signs

    • Blood Pressure: low (shock), high (SAH, stroke, ICP)
    • Heart Rate: low (medication overdose, conduction block), high (hypovolemia, infection, anemia, thyrotoxicosis, drug/toxin)
    • Temperature: low/high (infection, drug/toxin, environmental)
    • Respiratory Rate: low/high (CNS, drug/toxin, metabolic derangement)
  • Eyes

    • Unilateral dilation: CNS/structural cause
    • Papilledema: ICP
    • EOM: cranial nerve dysfunction
    • Oculocephalic: brainstem function
  • Head: trauma
  • Mucous membranes: hydration, laceration
  • Neck: meningeal irritation
  • Pulmonary: respiratory effort
  • CV: murmur, arrhythmia, CO
  • Abdomen: pulsatile mass, sequelae of liver failure
  • Skin: rash, needle tracks

Labs

  • Glucose
  • ECG: arrhythmia, ischemia, electrolyte abnormalities
  • BMP: electrolytes, renal failure, anion gap
  • ABG: hypoxemia, hypercarbia
  • Urinalysis: infection, SG
  • Utox
  • CBC: leukocytosis, leukopenia, severe anemia, thrombocytopenia
  • Ammonia: hepatic encephalopathy
  • TFT: thyrotoxicosis, myxedema coma
  • CSF: meningitis, encephalitis

Imaging

  • CT head: Non-contrast sufficient to identify ICH. Use contrast if mass/infection suspected
  • CTA head/neck: If aneurysm, AVM, venous sinus thrombosis or vertebrobasilar insufficiency suspected
  • CXR: PNA

References

  1. Bassin, B., & Cooke, J. (2013). Depressed Consciousness and Coma. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 142-150). 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.