Chest Pain

An 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

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

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

Imaging

CXR: Negative acute.
CT Head: Negative acute.
CT Cardiac: NICM, EF 35%.

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

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

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

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

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

Altered Mental Status Applied

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:

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.
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

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

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

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

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
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.

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

Management of Seizures

Medications for Treatment of Seizures

Medication	Dose (adult)	Dose (peds)	Comment
1^st 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
2^nd Line
Fosphenytoin	20mg PE/kg IV
Phenytoin	20mg/kg IV		May cause hypotension
3^rd 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

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
WikEM: Seizure

Simplified ACLS Algorithms

Cardiac Arrest

Tachycardia

Bradycardia

References

Hazinski, M., Samson, R., & Schexnayder, S. (Eds.). (2010). 2010 Handbook of Emergency Cardiovascular Care for Healthcare Providers. Dallas, TX: American Heart Association.
WikEM: Adult pulseless arrest
WikEM: ACLS: Tachycardia
WikEM: ACLS: Bradycardia

Altered Mental Status

Components of Consciousness

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

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

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

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

Weakness

View Algorithm
There is a ddxof algorithm for the evaluation of weakness. View it here.

Motor Neuron Signs

Upper Motor Neuron:: Spasticity; Hyperreflexia; Pronator drift; Babinski
Lower Motor Neuron:: Flaccidity; Hyporeflexia; Fasciculation; Atrophy

Causes of Weakness

Lesion	Critical	Emergent
Non-neurological	Shock (VS, clinical assessment) Hypoglycemia (POC glucose) Electrolyte derangement (BMP) Anemia (POC Hb, CBC) MI (ECG, troponin) CNS depression (Utox, EtOH)
Cortex	Stroke	Tumor Abscess Demyelination
Brainstem	Stroke	Demyelination
Spinal Cord	Ischemia Compression (disk, abscess, hematoma)	Demyelination (transverse myelitis)
Peripheral	Acute demyelination (GBS)	Compressive plexopathy
Muscle	Rhabdomyolysis	Inflammatory myositis

Weakness Syndromes

Unilateral weakness, ipsilateral face: Lesion: Contralateral cortex, internal capsule; Causes: Stroke (sudden onset), demyelination/mass (gradual onset); Symptoms: Neglect, visual field cut, aphasia; Findings: UMN signs; Key features: Association with headache suggests hemorrhage or mass
Unilateral weakness, contralateral face: Lesion: Brainstem; Causes: Vertebrobasilar insufficiency, demyelination; Symptoms: Dysphagia, dysarthria, diplopia, vertigo, nausea/vomiting; Findings: CN involvement, cerebellar abnormalities
Unilateral weakness, no facial involvement: Lesion: Contralateral medial cerebral cortex, discrete internal capsule; Causes: Stroke; Rare Cause: Brown-Sequard if contralateral hemibody pain and temperature sensory disturbance
Unilateral weakness single limb (monoparesis/plegia): Lesion: Spinal cord, peripheral nerve, NMJ; UMN signs: Brown-Sequard if contralateral pain and temperature sensory disturbance; LMN signs: Radiculopathy if associated sensory disturbance; Normal reflexes, normal sensation: Consider NMJ disorder
Bilateral weakness of lower extremities (paraparesis/plegia): Lesion: Spinal cord, peripheral nerve; UMN signs: Anterior cord syndrome (compression, ischemia, demyelination) if contralateral pain and temperature sensory disturbance; Cauda equina: Loss of perianal sensation, loss of rectal tone, or urinary retention; GBS: If no signs of cauda equina and sensory disturbances paralleling ascending weakness (with hyporeflexia)
Bilateral weakness of upper extremities: Lesion: Central cord syndrome; Causes: Syringomyelia, hyperextension injury; Findings: Pain and temperature sensory disturbances in upper extremities (intact proprioception)
Bilateral weakness of all four extremities (quadriparesis/plegia): Lesion: Cervical spinal cord; Findings: UMN signs below level of injury, strength/sensory testing identifies level
Bilateral weakness, proximal groups: Lesion: Muscle; Causes: Rhabdomyolysis, polymyositis, dermatomyositis, myopathies; Findings: Muscle tenderness to palpation, no UMN signs, no sensory disturbances
Facial weakness, upper and lower face: Lesion: CNVII; Causes: Bell’s palsy, mastoiditis, parotitis; Other CN involvement suggests brainstem lesion, multiple cranial neuropathies, or NMJ

Review of Spinal Cord Anatomy

Dorsal Column – Medial Lemniscus (fine touch, proprioception)
1. Afferent sensory fibers with cell body in DRG
2. Ascend in ipsilateral posterior column
3. Synapse in medulla, decussate, ascend in contralateral medial lemniscus
4. Synapse in thalamus (VPL)
5. Synapse in sensory strip of post-central gyrus
Spinothalamic Tract (pain, temperature)
1. Afferent sensory fibers with cell body in DRG
2. Ascends 1-2 levels
3. Synapse in ipsilateral spinal cord, decussate, ascend in contralateral lateral spinothalamic tract
4. Synapse in thalamus (VPL)
5. Synapse in sensory strip of post-central gyrus
Lateral Corticospinal Tract (motor)
1. Efferent cell body in motor strip of pre-central gyrus
2. Descends through internal capsule
3. Decussates in pyramid of medulla, descends in contralateral lateral corticospinal tract
4. Synapse in anterior horn, lower motor neuron to muscle fiber

References

Morchi, R. (2013). Weakness. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 124-128). Elsevier Health Sciences.

Fever

Causes of Fever

Key Features

Morbidity and mortality increase with age and comborbidities
Most common sources in elderly: respiratory, genitourinary, skin/soft-tissue
Atypical presentations: functional decline, altered mental status

Immediate Evaluation and Management

Critical Findings
- Altered mental status
- Respiratory distress
- Hemodynamic instability
Critical Interventions
- Airway management, supplemental O2
- Cardiac monitoring
- Fluid resuscitation
- Empiric antibiotics
- Cooling measures (T>41.0°C)

Pathophysiology of Fever

Production of endogenous or exogenous pyrogens
Increase temperature set point in hypothalamus: Patient experiences chills when core temperature < set point
Vasoconstriction, shivering causes fever: Patient experiences euthermia, though may feel malaise, fatigue
Resolution: Patient experiences sweats until core temperature returns to normal set point

References

Blum, F., & Biros, M. (2013). Fever in the Adult Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 119-123). 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

Axis

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

Downsloping ST-segment depression
Asymmetric T-wave inversion

Bundle Branch Blocks

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

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

Hemiblocks

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

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

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

Diplopia

History and Physical

38F with no medical history, presenting with double vision. The patient reported six weeks of intermittent diplopia for which she had presented to this hospital previously. She was briefly admitted for evaluation of possible cranial nerve IV palsy. Extensive imaging was unremarkable, without mass lesion, infarction, vascular malformation, or meningeal enhancement. She was discharged with outpatient follow-up including ophthalmology clinic and further imaging.

The patient represented due to persistent diplopia that is worse with right gaze. The diplopia is predominantly vertical, alleviated by head tilt. Now associated with three days of right ptosis as well as two weeks of progressive weakness and fatigue – most notable when climbing stairs.

Examination notable for right hypertropia increased on right or downward gaze suggestive of isolated inferior rectus weakness. Pupils were equal and reactive. There was marked fatigable ptosis with 2mm right palpebral fissure compared to 10mm on contralateral side. Symmetrical muscle weakness was noted, 4/5 neck flexion, elbow extension, wrist flexion/extension, shoulder abduction, hip flexion. Gait was wide-based. Application of ice for 5 minutes improved right palpebral fissure opening to >7mm.

Further evaluation included CXR and CT chest with intravenous contrast which did not identify a mediastinal mass. The patient’s respiratory status remained stable throughout hospitalization as assessed by measurements of forced vital capacity. On hospital day one, an edrophonium test was performed which was positive. The patient was started on pyridostigmine, completed a course of IVIG and was discharged with outpatient neurology follow-up.

Evaluation of Diplopia ¹

History

Onset/cadence
Direction of gaze with worst diplopia
Orientation (vertical/horizontal)
Associated symptoms (headache, vertigo, dysarthria, eye pain)

Terms Describing Eye Position

Tropias are always present, phorias are identified by cross-cover testing (break fusion)

Algorithm for the Evaluation of Diplopia ²

Causes of Diplopia ^3,4,5,6

Finding	EOM	Causes	Features
Mechanical orbitopathy	Variable. Abrupt restriction of movement	Orbital cellulitis	Pain, erythema
		Orbital pseudotumor	Autoimmune
		Trauma	History
		Thyroid eye disease	Bilateral
Isolated CN III	Limited adduction/upgaze/downgaze	Microvascular ischemia	Pain, risk factors, pupil-sparing
		Aneurysm	Pupil involvement
		Demyelination	MRI
Isolated CN IV	Limited downgaze (hypertropia)	Trauma	May be mild
		Microvascular ischemia	Less common than CN III
		ICP	Fundoscopy, imaging
		Demyelination	MRI
Isolated CN VI	Limited abduction (esotropia)	ICP	Fundoscopy, imaging
		Demyelination	MRI
		Microvascular ischemia	Less common than CN III
INO	Limited adduction (exotropia)	Demyelination	MRI
INO	Limited adduction (exotropia)	Stroke	Dysarthria, ataxia, facial weakness
Multiple CN involvement (III, IV, VI)	Variable	Cavernous sinus process	Retroorbital pain, conjunctival injection or chemosis
Brainstem deficits	Variable	Brainstem stroke	Weakness, dysmetria, tremor
		Basilar artery occlusion	Vertigo, slurred speech
		Wernicke	AMS, ataxia, nystagmus
		Basilar meningitis	Fever, photophobia, meningismus
		Miller-Fisher	Ataxia, areflexia
Neuromuscular process	Variable	Myasthenia gravis	Fatigability, ice test

References

Alves, M., Miranda, A., Narciso, M. R., Mieiro, L., & Fonseca, T. (2015). Diplopia: a diagnostic challenge with common and rare etiologies. The American journal of case reports, 16, 220–223. doi:10.12659/AJCR.893134
Borooah, S., Wright, M., & Dhillon, B. (2011). Pocket Tutor Ophthalmology. JP Medical Limited. Retrieved from https://books.google.com/books?id=z\_CfWj8-ftoC
Dinkin, M. (2014). Diagnostic approach to diplopia. Continuum (Minneapolis, Minn.), 20(4 Neuro-ophthalmology), 942–965. doi:10.1212/01.CON.0000453310.52390.58
Rucker, J. C., & Tomsak, R. L. (2005). Binocular diplopia. A practical approach. The neurologist, 11(2), 98–110. doi:10.1097/01.nrl.0000156318.80903.b1
Friedman, D. I. (2010). Pearls: diplopia. Seminars in neurology, 30(1), 54–65. doi:10.1055/s-0029-1244995
Guluma, K. (2013). Diplopia. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 176-183). Elsevier Health Sciences.
WikEM: Diplopia

Anemia

HPI

70M with a history of dementia presenting with 3 days of fatigue. The patient was unable to provide detailed history, however family members reported worsening fatigue with the patient requiring assistance with ambulation for several days. The patient was referred from an outside clinic after point-of-care hemoglobin of 6.7. No reported history of anemia, and no history suggestive of obvious external bleeding.

Vital signs stable, tachycardia and tachypnea noted with minimal exertion but saturating well on ambient air and in no acute distress. Examination notable for conjunctival pallor without scleral icterus, systolic flow murmur, brown stool guaiac negative.

CBC with hemoglobin of 7.5 , MCV 80.3 , RDW 22.4 , no leukocytosis and normal platelets. Also noted was an alkaline phosphatase of 828 , normal total and direct bilirubin, and undetectable serum troponin. Chest x-ray showed a possible pleural-based mass.

The patient was transfused two units of PRBC’s and admitted for further evaluation. CT chest/abdomen/pelvis revealed sternal and rib-based pleural soft-tissue mass, prostate mass, pelvic and retroperitoneal lymphadenopathy as well as extensive bony metastatic disease consistent with primary prostate cancer with diffused metastasis. Serum PSA was 2,087 . Iron studies suggested anemia of chronic disease. Reticulocytes were not obtained but may have suggested inadequate production index given extensive bony metastases and possible associated myelosuppression. The patient was symptomatically improved after transfusion and discharged with outpatient follow-up for discussions regarding possible biopsy and treatment.

Images

Areas of pleural thickening. Possible pleural based mass in left mid lung.

CT Chest: Lung Window

Rib-based pleural soft tissue masses.
Large 5.6 x 4.4cm anterior sternal soft-tissue mass.

CT Body: Bone Window

Extensive bony metastatic disease.
Prostate mass, large pelvic and retroperitoneal lymphadenopathy.
Consistent with primary prostate cancer with diffuse metastasis.

Algorithm for the Evaluation of Anemia ^1,2

References:

Zaiden R, Rana F. Evaluation of Anemia. BMJ Best Practice. Oct 2014. http://us.bestpractice.bmj.com/best-practice/monograph/93/overview.html. Last accessed 15 May 2015.
Janz, T. G., Johnson, R. L., & Rubenstein, S. D. (2013). Anemia in the emergency department: evaluation and treatment. Emergency medicine practice, 15(11), 1–15– quiz 15–6.
WiKEM: Anemia

Conjunctivitis and the Red Eye

Differential diagnosis of Conjunctivitis ^1,2,3

Condition	Pain	Visual Acuity	Photophobia	Discharge	Conjunctiva	Lymphadenopathy	Laterality	Associated Features
Viral conjunctivitis	None	Unaffected	None	+ watery	++ follicular pattern	Pre-auricular	Unilateral, spreads bilateral	Viral URI
Bacterial conjunctivitis	None	Unaffected	None	++ purulent	+++ papillary pattern	Occasional	Unilateral, spreads bilateral	Otitis media
Allergic conjunctivitis	None	Unaffected	None	+ mucoid	+	None	Bilateral	Atopy

Differential Diagnosis of Red Eye ^4,5

Condition	Comment	Hyperemia	Pupil	Pain	Visual Acuity	Cornea
Subconjuntival hemorrhage	Associated with trauma, coagulopathy, hypertension.	Unilateral, sharply circumscribed	Unaffected	None	Unaffected	Clear
Blepharitis	Acute/chronic inflammation of eyelid.	Diffuse	Unaffected	Foreign body sensation	Unaffected	Clear
Epislceritis	Recurrent, self-limited episodes, possible autoimmune association.	Engorged, radially-oriented vessels	Unaffected	Mild	Unaffected	Clear
Scleritis	Vascular or connective tissue disease.	Focal or diffuse, pink sclera	Unaffected	Moderate	Reduced	Clear
Acute angle-closure glaucoma	Mydriasis leading to decreased outflow of aqueous humor.	Circumcorneal injection	Semi-dilated	Severe	Reduced	Hazy
Acute anterior uveitis	Inflammation of iris or ciliary body.	Circumcorneal injection	Constricted	Moderate	Reduced	Hazy
Keratitis	Inflammation of corneal epithelium. Caused by infection, contact lenses, UV exposure.	Multiple punctate erosions, stain with fluorescein	Unaffected	Moderate	Reduced	Hazy

Algorithm for the Evaluation of the Red Eye ⁶

References

Teoh, D. L., & Reynolds, S. (2003). Diagnosis and management of pediatric conjunctivitis. Pediatric emergency care, 19(1), 48–55.
Azari, A. A., & Barney, N. P. (2013). Conjunctivitis. JAMA: the journal of the American Medical Association, 310(16), 1721. doi:10.1001/jama.2013.280318
Cronau, H., Kankanala, R. R., & Mauger, T. (2010). Diagnosis and management of red eye in primary care. American family physician, 81(2), 137–144.
Leibowitz, H. M. (2000). The red eye. New England Journal of Medicine, 343(5), 345–351. doi:10.1056/NEJM200008033430507
Richards, A., & Guzman-Cottrill, J. A. (2010). Conjunctivitis. Pediatrics in review / American Academy of Pediatrics, 31(5), 196–208. doi:10.1542/pir.31-5-196
Borooah, S., Wright, M., & Dhillon, B. (2011). Ophthalmology. JP Medical Limited.

Severe Traumatic Brain Injury

HPI:

34 year-old male brought in by ambulance s/p assault. Field GCS reportedly 7, in trauma bay assessed as E2-V4-M6. Witnessed seizure in CT scanner, resolved with lorazepam. Intubated for airway protection, underwent external ventricular drain placement and transferred to surgical ICU.

Initial imaging revealed bifrontal subdural hematomas and right temporal hemorrhagic contusion with generalized edema. Repeat imaging one hour later showed interval development of large extra-axial hemorrhage overlying the right occipital and parietal lobes (2.2cm), representing subdural or epidural hematoma.

The patient’s ICU course was complicated by continued seizures and refractory elevation in intracranial pressure. A pentobarbital infusion was started and titrated to adequate burst suppression and hyperosmolar therapy with both mannitol and hypertonic saline continued. Additional imaging revealed stable hemorrhage but continued diffuse cerebral edema evidenced by sulcal effacement.

On hospital day 5, examination revealed bilateral fixed and dilated pupils. Imaging revealed effacement of basilar cisterns, pre-pontine cistern, and cisterna magna suggestive of impending/ongoing transtentorial and tonsillar herniation. Pentobarbital was weaned and conventional cerebral angiography as well as cerebral perfusion studies were consistent with brain death.

Images

CT head without contrast one hour after presentation

Large extra-axial posterior hemorrhages. Hemorrhagic contusions in the right frontal and temporal lobes.
The cerebral sulci appear effaced – findings suggest diffuse cerebral edema.
S/p EVD using a right frontal approach.

CT head without contrast on hospital day 5

Interval evidence of global hypoxic/ischemic injury to the brain.
Interval apparent effacement of the basilar cisterns, pre-pontine cistern, and cisterna magna suggesting impending/ongoing downward transtentorial herniation and tonsillar herniation.
Stable supra/infratentorial subdural/epidural hematoma.

Algorithm for the Management of Severe Traumatic Brain Injury^1,2

References

Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney, N. A., & Ghajar, J. (2007). Guidelines for the management of severe traumatic brain injury. Introduction. Journal of neurotrauma, 24 Suppl 1, S1–2. doi:10.1089/neu.2007.9997
Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
WikEM: Severe traumatic brain injury

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

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

Algorithm for Evaluation of Acidemia ^3,4

Algorithm for Evaluation of Alkalemia ^3,4

References:

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
Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
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
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

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

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

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

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

References:

Light, R. W. (2002). Clinical practice. Pleural effusion. The New England journal of medicine, 346(25), 1971–1977. doi:10.1056/NEJMcp010731
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
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
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
WikEM: Pleural effusion

Pulmonary Embolism in Hospitalized Patients

Brief Progress Note

Notified by nursing of abnormal vital signs, SpO2 91%. Briefly, this patient is a 52 year-old G1P1 with no prior medical history who is post-operative day three status post total abdominal hysterectomy, bilateral salpingoophorectomy as well as tumor debulking and staging for suspected primary ovarian adenocarcinoma based on peritoneal fluid cyctology.

On evaluation, the patient denied shortness of breath, chest pain, pleuritic chest pain, cough/hemoptysis, or calf/thigh pain. She states that she had been ambulating around the ward prior to having her vital signs assessed.

Physical Exam:

VS:	T	98.9	HR	94	RR	18	BP	117/72	O2	91% RA
Gen:	No acute distress, speaking in full sentences.
HEENT:	No jugular venous distension.
CV:	RRR, normal S1/S2, no prominent P2, no additional heart sounds.
Lungs:	Decreased breath sounds at inferior 1/3 posterior lung fields bilaterally, faint crackles above, no wheezing. Dullness to percussion in inferior lung fields.
Ext:	Warm, well-perfused. Sequential compression devices on bilateral lower extremities, removed revealing trace pitting edema symmetric bilaterally, no tenderness to palpation of posterior leg, no pain with passive dorsiflexion.

Medications:

Lovenox 40mg s.q. daily
Norco 5-325mg p.o. q.4.h. p.r.n. pain
Morphine 2mg i.v. q.3.h. p.r.n. breakthrough pain
Colace 100mg p.o. b.i.d. p.r.n. constipation
Zofran 4mg i.v. q.6.h. p.r.n. nausea/vomiting

Imaging:

CXR

Bilateral pleural effusions with pleural fluid tracking along the minor fissure.

CT Chest

No evidence of pulmonary embolism, study performed 5 days prior to onset of symptoms.

CT Abdomen/Pelvis

Significant peritoneal carcinomatosis, ascites delineates peritoneal from retroperitoneal spaces.

Assessment and Plan:

52yo G1P1 with likely primary ovarian adenocarcinoma with extensive peritoneal involvement, complicated by malignant ascites and pleural effusions with hypoxemia. The primary concern in this post-operative patient with a history of malignancy is venous thromboembolism, particularly pulmonary embolism. Aside from hypoxemia, this patient had no symptoms suggestive of pulmonary embolism (denied dyspnea, chest pain, cough, or lower extremity pain). Her examination had some signs infrequently associated with pulmonary embolism which were otherwise adequately explained by known bilateral pleural effusions (including decreased breath sounds, rales, and tachypnea), she was not tachycardic, had no evidence of jugular venous distension, nor a prominent P2. In addition, she was receiving appropriate VTE prophylaxis (both pharmacological and mechanical). The application of the Modified Wells clinical decision rule suggests low likelihood of pulmonary embolism (with 2.5 points assigned for recent surgery and history of malignancy). The patient had a recent CT chest without evidence of pulmonary embolism, and given that an elevated D-dimer was virtually assured which would have necessitated repeat imaging (and the associated risks of radiation exposure and contrast injury), the episode was ascribed to ventilation/perfusion mismatch secondary to large pleural effusions. Hypoxemia resolved after several minutes at rest and no further testing was performed.

Signs and Symptoms of Pulmonary Embolism¹

Signs	Symptoms
Tachypnea	Dyspnea (rest/exertion)
Tachycardia	Pleurtic chest pain
Rales	Cough
Decreased breath sounds	Orthopnea
Prominent P2	Calf/thigh pain or swelling
JVD	Wheezing

Modified Wells Criteria^1,2

Feature	Points
Clinical symptoms of DVT (leg swelling, tenderness to palpation)	3.0
Pulmonary embolism most likely diagnosis	3.0
Tachycardia (HR >100)	1.5
Immobilization >3d, surgery in prior 4 weeks	1.5
Prior DVT/PE	1.5
Hemoptysis	1.0
Malignancy	1.0

>4.0 Likely
≤4.0 Unlikely

Algorithm for Evaluation of Suspected Pulmonary Embolism²

Utility of D-Dimer:²: Of limited utility in patients with high suspicion for pulmonary embolism; Decreased specificity: malignancy, hospitalized patients, pregnancy, elderly
Efficacy of DVT prophylaxis:³: LMWH prevents approximately ½ of VTE events (including PE, symptomatic and asymptomatic DVT)

References:

Kruip, M. J. H. A., Söhne, M., Nijkeuter, M., Kwakkel-Van Erp, H. M., Tick, L. W., Halkes, S. J. M., Prins, M. H., et al. (2006). A simple diagnostic strategy in hospitalized patients with clinically suspected pulmonary embolism. Journal of internal medicine, 260(5), 459–466. doi:10.1111/j.1365-2796.2006.01709.x
Tapson, V. F. (2008). Acute pulmonary embolism. The New England journal of medicine, 358(10), 1037–1052. doi:10.1056/NEJMra072753
Själander, A., Jansson, J.-H., Bergqvist, D., Eriksson, H., Carlberg, B., & Svensson, P. (2008). Efficacy and safety of anticoagulant prophylaxis to prevent venous thromboembolism in acutely ill medical inpatients: a meta-analysis. Journal of internal medicine, 263(1), 52–60. doi:10.1111/j.1365-2796.2007.01878.x

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

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

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

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

An Algorithm for the Evaluation of Chest Pain

Guided Lecture

References

HPI

Physical Exam

Labs

ECG

Imaging

CT Chest non-contrast

Hospital Course

Endocrine Emergencies: Hyperthyroidism

Symptoms

Signs

Thyroid Storm

Scoring (Burch, Wartofsky)

Management

Endocrine Emergencies: Hypothyroidism

Symptoms

Signs

Myxedema Coma

Management

Interpretation of Thyroid Function Tests

Endocrine Emergencies: Adrenal Insufficiency

Symptoms

Signs

Management

Life-Threatening Electrolyte Abnormalities3

Critical Hypokalemia

Critical Hypomagnesemia

Conclusion

References:

Causes of Dyspnea

Findings in Selected Causes of Dyspnea

References

H&P

Labs

Imaging

CT abdomen/pelvis with intravenous contrast

Hospital Course

Hyponatremia Applied

Altered Mental Status Applied

Evaluation of Sore Throat

Physical Examination:

Centor Criteria (Modified)

Incidence of GABHS by Centor Criteria

References:

Types of Dizziness

Distinguishing Central vs. Peripheral Vertigo

Causes of Vertigo

Characteristics of common causes of vertigo

History

Key Physical Examination Findings

Positional Testing

HINTS1

HINTS Gallery

Labs

Imaging

Management

References

Definition

Classification

Causes of Seizures

Management of Seizures

Medications for Treatment of Seizures

History

Key Physical Examination Findings

Labs

Indications for Imaging

References

Cardiac Arrest

Tachycardia

Bradycardia

References

Components of Consciousness

Causes of Altered Mental Status

History

Physical Examination

Labs

Imaging

References

Life-Threatening Electrolyte Abnormalities³

HINTS¹

Evaluation of Diplopia ¹

Algorithm for the Evaluation of Diplopia ²

Causes of Diplopia ^3,4,5,6

Algorithm for the Evaluation of Anemia ^1,2

Differential diagnosis of Conjunctivitis ^1,2,3

Differential Diagnosis of Red Eye ^4,5

Algorithm for the Evaluation of the Red Eye ⁶