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.

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%.
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
IM-0001-0054
IM-0001-0054
IM-0001-0058
IM-0001-0058
IM-0001-0062
IM-0001-0062
IM-0001-0066
IM-0001-0066
IM-0001-0070
IM-0001-0070

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

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.

Fever

Causes of 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

  1. 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

The ECG grid
Limb leads
Precordial Leads

Axis

ECG axes

Atrial Enlargement

Atrial enlargement

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

Ventricular Hypertrophy

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

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

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

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

Secondary Repolarization Abnormalities

Secondary repolarization abnormality

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

Bundle Branch Blocks

Left Bundle Branch Block

Left bundle branch block

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

Right Bundle Branch Block

Right bundle branch block

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

Hemiblocks

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

Other Blocks

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

Ischemia and Infarction

ECG changes associated with ischemia and infarction

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

Coronary Artery Territories

Coronary artery territories

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

External Links

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

Chest x-ray with pleural-based mass

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

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CT Chest: Lung Window

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

Algorithm for the Evaluation of Anemia

References:

  1. 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.
  2. 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.
  3. WiKEM: Anemia

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

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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.
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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 Injury1,2

Algorithm for the Management of Severe Traumatic Brain Injury

References

  1. 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
  2. Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
  3. 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

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

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

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

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

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

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

Assessment/Plan:

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

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

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

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

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

Differential Diagnosis of Elevated Serum Lactate 1,2

Differential Diagnosis of Elevated Serum Lactate

Algorithm for Evaluation of Acidemia 3,4

Algorithm for Evaluation of Acidemia

Algorithm for Evaluation of Alkalemia 3,4

Algorithm for Evaluation of Alkalemia

References:

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

Pleural Effusion

HPI:

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

Hospital Course:

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

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

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

PMH:

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

PSH:

  • TAH-BSO

FH:

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

SHx:

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

Meds:

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

Allergies:

  • Shellfish
  • Physical Exam:

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

    Labs/Studies:

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

    Imaging

    CXR

    CXR: Pleural Effusion

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

    CT Chest (High-Resolution):

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

    TTE:

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

    Assessment/Plan:

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

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

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

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

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

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

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

    Case 2: Malignant Pleural Effusion

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

    Case 3: Traumatic Thoracentesis

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

    Case 4: Pneumonia

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

    Etiology of Pleural Effusions: 1

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

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

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

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

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

    Differential Diagnosis of Pleural Effusions

    References:

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

    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

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

    CT Abdomen/Pelvis

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    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 Criteria1,2

    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

    Fever in Systemic Lupus Erythematosus

    HPI:

    48F with a history of SLE presenting with two weeks of fevers and joint pain. The patient reports progressive development of these symptoms associated with malaise and muscle aches. She also reports two days of cough productive of yellow sputum, but denies chest pain, shortness of breath or hemoptysis. She states that these symptoms are comparable to prior lupus flares but have persisted longer than usual. She has not travelled or been hospitalized recently and has no sick contacts.

    PMH:

    • SLE
    • AVN left hip

    PSH:

    • Total hip arthroplasty

    FH:

    Non-contributory

    SHx:

    • Denies tobacco, alcohol or drug use.
    • Works as an accountant.
    • No history of TB exposure.

    Meds:

    • Methotrexate 50mg p.o. weekly
    • Plaquenil 400mg p.o. daily
    • MVI

    Allergies:

    NKDA

    Physical Exam:

    VS: T 39.4 HR 138 RR 19 BP 97/61 O2 98% 2L NC
    Gen: Alert, responsive and in no acute distress.
    HEENT: PERRL, dry mucous membranes, no oropharyngeal lesions or erythema, TM intact bilaterally, no cervical lymphadenopathy, neck supple.
    CV: Tachycardia, regular rhythm without additional heart sounds.
    Lungs: Clear to auscultation bilaterally.
    Abd: +BS, soft, non-tender, non-distended, no rebound/guarding.
    Ext: No peripheral edema, extremities warm and well-perfused, diffuse tenderness to palpation and resisted range of motion of joints with particular involvement of bilateral shoulders, elbows, knees and ankles. No effusion noted, no erythema or warmth.
    Neuro: Alert, oriented to self, location and time. PERRL, EOMI, facial sensation intact, facial muscles symmetric, palate rises symmetrically, tongue protrudes midline without fasciculation, peripheral sensation and motor strength grossly intact with normal gait.

    Labs/Studies:

    • 0h:
    • CBC: 6.0/7.7/23.5/259
    • BMP: 138/2.8/116/18/12/0.66/71
    • Ca: 5.0 (corrected for hypoalbuminemia: 6.9)
    • Mg: 1.1
    • Lactate: 0.7
    • ESR: 81 (0-20)
    • CRP: 7.99 (0-0.74)
    • C3: 60 (79-152)
    • C4: 13 (16-38)
    • 12h:
    • BMP: 142/4.6/113/26/15/0.75/128
    • Ca: 7.8

    Imaging:

    • CXR: Negative for acute cardiopulmonary process.

    Assessment/Plan:

    48F with a history of SLE presenting with fever and polyarticular arthralgia.

    #SIRS: Fever and tachycardia in the setting of immunosuppression. The differential diagnosis includes pneumonia (bacterial, viral, less-likely fungal), which would be community-acquired. Association with polyarticular arthralgia suggests symptoms may represent lupus flare given no leukocytosis and elevated CRP.

    #Hypocalcemia: Asymptomatic, likely due to hypoalbuminemia and hypomagnesemia. Improved after IV fluids and correction of hypokalemia, hypomagnesemia.

    Hospital Course:

    The patient was admitted and completed a 7-day course of ceftriaxone and azithromycin. Rheumatology was consulted for management of lupus flare, which included resuming home medications and a prednisone taper upon discharge.
    The patient was admitted ten days later, presenting with fevers, productive cough and pleuritic chest pain. Found to have a left lower lobe sub-segmental pulmonary embolus and antiphospholipid syndrome. She was also treated empirically for healthcare-associated pneumonia with cefepime and vancomycin given fever and productive cough though there were no imaging findings suggestive of consolidation and sputum cultures were negative.

    Differential Diagnosis of Hypocalcemia: 1,2

    Differential Diagnosis of Hypocalcemia

    Laboratory Evaluation of Hypocalcemia: 1,2

    Laboratory Evaluation of Hypocalcemia

    Clinical Manifestations of Hypocalcemia: 1

    • Neuromuscular
      • Hyperexcitability
      • Perioral paresthesias
      • Muscle weakness, cramps, fasciulations, tetany
    • CNS
      • Depression
      • Irritability
      • Confusion
      • Seizure
    • Cardiac
      • Decreased contractility/conduction
      • QT prolongation

    Management of Symptomatic Hypocalcemia: 1

    • 10mL 10% Calcium Gluconate
    • Dilute in 100mL D5W

    Fever in SLE:

    It is important to differentiate whether fever in a patient with SLE is due to disease activity (flare) or active infection.

    Risk Factors for Infection:3

    • Neutropenia/Lymphopenia
    • Hypocomplementemia
    • Immunosuppressive therapy (especially Azathioprine4)

    Laboratory Studies:3

    • CRP: sensitivity 100%, specificity 90% >1.35mg/dL 5
    • PCT: sensitivity 75%, specificity 75% 6

    References:

    1. Cooper, M. S., & Gittoes, N. J. L. (2008). Diagnosis and management of hypocalcaemia. BMJ (Clinical research ed.), 336(7656), 1298–1302. doi:10.1136/bmj.39582.589433.BE
    2. Hannan, F. M., & Thakker, R. V. (2013). Investigating hypocalcaemia. BMJ (Clinical research ed.), 346(may09 1), f2213–f2213. doi:10.1136/bmj.f2213
    3. Cuchacovich, R., & Gedalia, A. (2009). Pathophysiology and clinical spectrum of infections in systemic lupus erythematosus. Rheumatic diseases clinics of North America, 35(1), 75–93. doi:10.1016/j.rdc.2009.03.003
    4. Zhou, W. J., & Yang, C.-D. (2009). The causes and clinical significance of fever in systemic lupus erythematosus: a retrospective study of 487 hospitalised patients. Lupus, 18(9), 807–812. doi:10.1177/0961203309103870
    5. Kim, H.-A., Jeon, J.-Y., An, J.-M., Koh, B.-R., & Suh, C.-H. (2012). C-reactive protein is a more sensitive and specific marker for diagnosing bacterial infections in systemic lupus erythematosus compared to S100A8/A9 and procalcitonin. The Journal of rheumatology, 39(4), 728–734. doi:10.3899/jrheum.111044
    6. Scirè, C. A., Cavagna, L., Perotti, C., Bruschi, E., Caporali, R., & Montecucco, C. (2006). Diagnostic value of procalcitonin measurement in febrile patients with systemic autoimmune diseases. Clinical and experimental rheumatology, 24(2), 123–128.

    Electrolyte Abnormalities

    Routine laboratory studies are common in the intensive care unit; abnormalities are even more common. Typically these studies include a chemistry panel (Chem 10). The differential diagnoses of the most frequent and clinically relevant electrolyte abnormalities are detailed below.

    Differential Diagnosis and Evaluation of Hyponatremia

    Differential Diagnosis and Evaluation of Hyponatremia

    Differential Diagnosis and Evaluation of Hypernatremia

    Differential Diagnosis and Evaluation of Hypernatremia

    Differential Diagnosis and Evaluation of Hypokalemia

    Differential Diagnosis and Evaluation of Hypokalemia

    Differential Diagnosis of Hyperkalemia

    Differential Diagnosis of Hyperkalemia

    Differential Diagnosis of Hypo and Hypercalcemia

    Differential Diagnosis of Hypo and Hypercalcemia

    Differential Diagnosis of Hypo and Hypermagnesemia

    Differential diagnosis of hypo and hypermagnesemia

    Differential Diagnosis of Hypo and Hyperphosphatemia

    Differential diagnosis of hypo and hyperphosphatemia

    References:

    1. Marino, P. (2014). Marino’s the ICU book. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
    2. Fulop, M. (1998). Algorithms for diagnosing some electrolyte disorders. American Journal of Emergency Medicine, 16(1), 76–84.
    3. WikEM: Hypokalemia
    4. WikEM: Hyponatremia

    Biliary Duct Dilation

    A 45 year-old male presents with progressive jaundice over 1 month, he denies abdominal pain.

    Ultrasound

    Liver
    Common Bile Duct
    Gallbladder Wall

    CT Abdomen/Pelvis

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    • Markedly dilated intrahepatic biliary ducts, common bile duct and pancreatic duct.
    • Ill-defined fullness in the pancreatic head consistent with pancreatic adenocarcinoma vs. noncalcified obstructing biliary stone.

    Differential Diagnosis of Biliary Duct Dilation: 1,2,3

    Differential Diagnosis of Biliary Duct Dilation

    References:

    1. Kim, H. J., Lee, K. T., Kim, S. H., Lee, J. K., Lim, J. H., Paik, S. W., & Rhee, J. C. (2003). Differential diagnosis of intrahepatic bile duct dilatation without demonstrable mass on ultrasonography or CT: benign versus malignancy. Journal of gastroenterology and hepatology, 18(11), 1287–1292.
    2. Levy, A. D. (2009). Biliary Ducts – Pathology. The Radiology Assistant, 1–4. Retrieved from http://www.radiologyassistant.nl/en/p49e17de25294d/biliary-ducts-pathology.html
    3. Teefey, S. A., Baron, R. L., Schulte, S. J., Patten, R. M., & Molloy, M. H. (1992). Patterns of intrahepatic bile duct dilatation at CT: correlation with obstructive disease processes. Radiology, 182(1), 139–142. doi:10.1148/radiology.182.1.1727277

    Acute Kidney Injury

    Hospital Course:

    64 year-old female with a history of metastatic colonic adenocarcinoma was initially admitted for PO intolerance secondary to recurrent small bowel obstructions (associated with abdominal tumor burden). On hospital day six, the patient developed tachypnea, hypoxemia, hypotension and was intubated for respiratory distress. In the MICU, the patient was treated for acute hypoxic respiratory failure thought to be caused by aspiration (large volume bilious emesis prior to intubation despite NGT LCWS) vs. accumulating malignant pleural effusions vs. pulmonary embolism. Septic shock of a presumed pulmonary vs. intra-abdominal source was managed with vasopressors and broad-spectrum antimicrobials.

    On hospital day fourteen, an elevation in the serum creatinine was noted. Known nephrotoxic agents include iodinated contrast on hospital day five, and vancomycin. The patient’s vasopressor requirement had decreased to norepinephrine 6mcg/kg/min (previously requiring four vasopressors). Over the next six days, the serum creatinine continued to trend upwards associated with a decrease in urine output (0.3-0.5mL/kg/hour). Intravenous crystalloid and colloid administered liberally based on central venous pressure and ultrasound of the inferior vena cava did not impact urine output.

    Laboratory Studies

    Hospital day 19 18 17 16 15 14 3
    Creatinine 1.72 1.59 1.46 1.32 1.24 1.09 0.75
    Vancomycin 23.5 28.5 36.3 45.5 47.7 22.1

    Urine electrolytes:

    • Una: 10
    • Ucr: 180
    • Uk: 13
    • Ucl: 22
    • Uur: 265
    • FeNa: <1%

    UA: 3+LE, 1+ blood, 36WBC, 14RBC, 3+ bacteria, amorphous crystals

    Imaging:

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    CT Abdomen/Pelvis with IV contrast

    • Within the retroperitoneum, the left kidney is small and atrophic and demonstrates limited peripheral enhancement. The left renal artery is also poorly visualized.
    • Severely dilated loops of small bowel, including a segment within the left lower quadrant that may represent a closed loop obstruction.
    • There is a large (16.4 cm in largest diameter) subphrenic fluid collection in the left upper quadrant. A second large (14.2 cm in largest diameter) intraabdominal fluid collection lies inferior and anteriorly.

    Assessment:

    Oliguric acute renal failure in the setting of convincingly pre-renal urine studies which was not responsive to adequate crystalloid and colloid volume resuscitation. The patient had a normal ejection fraction on a recent echocardiogram, and while the patient was hypoalbuminemic (presumably from poor nutritional status and PO intolerance), urine output was not even transiently responsive to colloid administration. While the patient had recent administration of intravenous contrast, the elevation in serum creatinine occurred more than one week later. Further, the elevated vancomycin trough was likely a consequence rather than the etiology of worsening renal failure. AKI was likely secondary to renal artery compression from mass effect associated with abdominal metastases. There was evidence of a similar process affecting the left kidney, which was severely atrophic. The patient declined further evaluation, which would have included a renal ultrasound.

    Definition of Acute Kidney Injury: 1

    • Elevation of serum creatinine > 0.3mg/dL in 48h
    • Elevation of serum creatinine > 1.5x baseline in 7d
    • Oliguria (UOP < 0.5mL/kg/hr) > 6h

    Staging of Acute Kidney Injury: 1

    Stage Creatinine UOP
    1 1.5-1.9x <0.5mL/kg/hr for 6-12h
    2 2.0-2.9x <0.5mL/kg/hr for >12h
    3 3.0x or RRT <0.3mL/kg/hr for > 24h

    Management of Contrast-induced AKI: 2

    • Administer lowest dose
    • Use iso-osmolar, or low-osmolar contrast
    • Volume expansion (NaCl, NaHCO3)
    • PO NAC questionable benefit but likely harmless

    Differential Diagnosis of Acute Kidney Injury: 3

    Algorithm for the Evaluation of Acute Kidney Injury

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

    Evaluation of AKI: 4

    Condition Urinalysis Casts FeNa (%)
    Pre-renal Normal Hyaline <1
    Intra-renal
    ATN Mild proteinuria Pigmented granular >1
    AIN Mild proteinuria, Hb, WBC WBC casts, eosinophils >1
    GN Moderate/severe proteinuria, Hb RBC casts <1
    Post-renal Normal Crystals >1

    References:

    1. Kellum, J. A., Lameire, N., KDIGO AKI Guideline Work Group. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England), 17(1), 204. doi:10.1186/cc11454
    2. Lameire, N., Kellum, J. A., KDIGO AKI Guideline Work Group. (2013). Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Critical care (London, England), 17(1), 205. doi:10.1186/cc11455
    3. Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
    4. Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
    5. WikEM: Acute kidney injury