Category Archives: CORE EM

EM@3AM – Acute Cholecystitis

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 41-year-old obese female presents for evaluation of severe right upper quadrant pain and nausea without emesis. The patient reports post-prandial pain of one months duration, acutely worsening prior to presentation following the consumption of a bacon cheeseburger. ROS is negative for sick contacts, foreign travel, and changes in bowel habits. The patient denies a surgical history.

Triage VS: T101.6°F Oral, HR 134, BP 147/99, RR 24, SpO2 98% on room air

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Acute Cholecystitis1-4

  • Risk Factors: oral contraceptives or estrogen replacement therapy (alters cholesterol and bile salt metabolism leading to gallstone formation and gallbladder hypomotility1), diseases of the terminal ileum (e.g. Crohns; secondary to poor bile salt reabsorption), cirrhosis (decreased bile acid secretion), hemolytic diseases (pigmented gallstones), pregnancy, obesity, TPN
  • Presentation: RUQ or epigastric pain, postprandial pain, nausea +/- emesis, +Murphy’s sign (+LR: 2.8; 95% CI, 0.8-8.62), +/- fever
  • Evaluation:
    • US (Sensitivity 95%, Specificity 98%3): sonographic Murphy’s, pericholecystic fluid, gallstones/biliary sludge, gallbladder wall thickening > 3mm.
    • CBC, LFTs
      • CBC: often demonstrates leukocytosis
      • LFTs: transaminitis; allows for evaluation of choledocolithiasis
  • Treatment:
    • Antimicrobials:
      • Mildly ill: ciprofloxacin 400 mg IV + metronidazole 500 mg IV
      • Critically ill: vancomycin 20 mg/kg (up to 2 g) IV + piperacillin/tazobactam 4.5 g IV
    • Fluid Resuscitation
    • Pain control
    • Anti-emetic PRN
    • Surgical Consultation – cholecystectomy
  • Pearls:
    • Diabetes is a risk factor for emphysematous cholecystitis:3 initiate antibiotic therapy directed against Gram-negative rods and anaerobes, and consult surgery.
    • Include acalculous cholecystitis in your differential diagnosis of the critically ill: RUQ pain, epigastric pain, and nausea are absent upon initial evaluation in up to 75% of these patients.1



  1. Welch J, Chike V, Bowens N, Arnell T, Ferri F. Acute Cholecystitis. First Consult. 2011. Elsevier, Philadelphia, PA.
  2. Trowbridge R, Rutkowski N, Shojania K. Does this patient have acute cholecystitis? JAMA. 2003; 289(1): 80-86.
  3. Glasgow R, Mulvihill S. Treatment of Gallstone Disease. In: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Philadelphia: Saunders Elsevier, 2016:1134-1151.e5.
  4. Senturk S, Miroglu T, Cilici A, Gumua H, Tekin R, et al. Diameters of the common bile duct in adults and postcholecystectomy patients: a study with 64-slice CT. Eur J Radiol. 2012; 81(1): 39-42.

EM@3AM – Acute Limb Ischemia

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 62-year-old male with a history of paroxysmal a.fib (CHADS2: 0; daily ASA1) presents for evaluation of left lower extremity (LLE) numbness and weakness. The patient reports the onset of his symptoms five hours prior to arrival, during his granddaughter’s dance recital. He denies slurred speech, visual changes, facial and upper extremity sensory and motor deficit. He denies right lower extremity symptoms.  HPI is negative for back pain, recent trauma, joint pain, and joint redness prior to symptom onset. ROS is unremarkable. Surgical history is significant only for remote inguinal hernia repair.

 Triage VS: T99.7°F Oral, HR 82, BP 129/76, RR 24, SpO2 98% on room air

Physical exam:

Neuro: LLE: weakness of plantarflexion and dorsiflexion; decreased sensation L4-S2 dermatomes below the knee

Cardiac: irregularly irregular

Vascular: Cool, mottled LLE; femoral pulse palpable, popliteal pulse non-palpable, dorsalis pedis and posterior tibial pulses non-palpable. Doppler confirms the absence of popliteal, dorsalis pedis, and posterior tibial pulses.

EKG: NSR, 82 bmp, axis WNL, no ST-T wave changes, QT WNL

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Acute Limb Ischemia1-4

  • Risk Factors: Conditions that pre-dispose to thrombosis (hypercoagulable state, arterial aneurysms, peripheral arterial disease (atherosclerotic plaque rupture), etc.) or embolism (atrial fibrillation, post MI, left ventricular dysfunction, mechanical cardiac valve with sub therapeutic anticoagulation, etc.).
    • Trauma is an uncommon etiology: limb ischemia may occur secondary to direct vessel injury and subsequent thrombosis.2
  • Clinical Presentation: Classically taught as the six Ps: pain, paresthesia, pallor, poikilothermia, pulselessness, and paralysis. Patients may also report claudication.
    • Considered to be acute in onset if symptoms began within 2 weeks of presentation 2
  • Evaluation:
    • Assess limb: appearance, temperature, pulses (including by Doppler), sensation, and strength
    • Lower extremities: ABI < 0.3 = subcritical acute ischemia2
  • Treatment:
    • Consult vascular surgery:
      • The Society for Vascular Surgery publishes classification standards based upon clinical and Doppler findings (limb viable vs. threatened vs. irreversibly damaged) which direct management and treatment.4
    • Discuss initiation of heparin bolus 80 U/kg, then 18 U/kg/hr + ASA PO.2
  • Pearls:
    • Palpable pulses in the contralateral extremity suggests embolism as the underlying etiology.3
    • Morbidity and mortality rates are high in patients with acute limb ischemia: 10-15% undergo limb amputation during hospitalization.2



  1. Hart R, Pearce L, Rothbart R, McAnulty J, Asinger R, et al. Stroke with intermittent atrial fibrillation: incidence and predictors during aspirin therapy. Stroke prevention in atrial fibrillation investigators. J Am Coll Cardiol. 35(1):183-187.
  2. Creager M, Kaufman H, Conte M. Clinical Practice. Acute limb ischemia. N Engl J Med. 2012; 366(23):2198-2206.
  3. Earnshaw J. Acute Ischemia: Evaluation and Decision Making. In: Rutherford’s Vascular Surgery. 8th ed. Philadelphia: Saunders Elsevier, 2014: 2518-2527.e1.
  4. Rutherford D, Baker J, Ernst C, Johnston K, Porter J, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg. 1997; 26(3): 517-538.

EM@3AM – Acute Angle Closure Glaucoma

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 62 year-old female with a PMHx of hypertension presents for evaluation of severe left eye pain associated with blurred vision, headache, and nausea.  The patient reports the sudden onset of her symptoms as occurring 30 minutes prior to arrival while entering a movie theater. ROS is negative for sick contacts, ocular discharge, and foreign body sensation. The patient wears glasses that she is “unable to see without.”

Triage VS: HR 122, BP 132/91, RR 18, SpO2 98% RA
Corrected: OD 20/20, OS 20/200, OU 20/40

Ocular examination:
-No evidence of foreign body
-Fluorescein stain without uptake
-IOP 15 mmHg

-EOMI, pupil (5mm) mid-position and fixed, conjunctival injection, hazy cornea
-No evidence of foreign body
-Fluorescein stain without uptake
-IOP 34 mmHg

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Acute Angle Closure Glaucoma1-3

  • Risk Factors: hyperopia, age >60, female sex
  • Presentation: sudden onset, severe eye pain +/- blurred vision, +/- nausea or emesis, +/- headache, pupil mid-positioned +/- fixed or sluggish, IOP >20mmHg
  • Precipitating factors:
    • Transition to dim lighting
    • Medications
      • Anticholinergics (topicals: cyclopentolate, tropicamide, etc., or systemic: antihistamines, antipsychotics, anticonvulsants, anti-parkinsonian medications, atropine, etc.)
      • Adrenergic agents (vasoconstrictors, bronchodilators, appetite depressants, etc.)
    • Emotional stress/pain (mydriasis secondary to increased sympathetic tone)
  •  Treatment:
    • Consult ophthalmology
    • Decrease production of aqueous humor:
      • Beta blockade: timolol 0.5% gtt
      • Alpha-2 agonists: apraclonidine 1% gtt or brimonidine 0.2% gtt
      • Carbonic anhydrase inhibitors:
        • Acetazolamide gtt or dorzolamide 2% gtt + 500 mg PO or IV acetazolamide
    •   Improve outflow of aqueous humor:
      • Cholinergic agent: pilocarpine 2% gtt
    • Decrease volume of aqueous humor:
      • Osmotic diuretic: mannitol 1-2g/kg IV
  •  Pearls:  
    • Obtain a thorough medical history:
      • B-blockade: caution with heart blocks, history of severe bronchospasm
    • Carbonic anhydrase inhibitors: avoid in sickle cell patients
    • Pilocarpine therapy should not be initiated until one hour following the instillation of an aqueous humor reducing agent:
      • Pilocarpine constricts the ciliary muscle causing miosis and increasing the axial thickness of the lens. While this allows for increased outflow of aqueous humor, it may also paradoxically worsen the condition by reducing the depth of the anterior chamber.2
    •  Suspect medication induced acute angle closure glaucoma if elevated IOP is present bilaterally.4


  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 60, Aneurysmal Disease.
  2. Jovina S, Aquino M, Chew P. Angle-Closure Glaucoma. In Ophthalmology. 4th ed. Philadelphia, Elsevier 2014; 10.12: 1060-1069.e2.
  3. Day A, Nolan W, Malik A, Viswanathan A, Foster P. Pilocarpine induced acute angle closure. BMJ Case Rep. 2012; 2012.
  4. Aminlari A, East M, Wei W, Quillen D. Topiramate induced acute angle closure glaucoma. Open Ophthalmol J. 2008; 2:46-47.

EM@3AM – Acute Chest Syndrome

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

 A 4-year old male with a history of sickle cell anemia presents to the ED for evaluation of fever of two days duration (Tmax 103.2) and progressively worsening shortness of breath. The patient’s parents report 48-hour hospitalization 6 months prior secondary to a vaso-occlusive crisis (pain localized to the extremities). ROS is negative for sick contacts. Medications include penicillin prophylaxis. Immunizations are up to date.

VS: HR 127, BP 97/64, RR 32, SpO2 91% on room air.

Physical examination:
Neuro: GCS 15
HEENT: PERRLA, TMs clear bilaterally, nasal mucosa unremarkable, oropharynx clear and moist, no lymphadenopathy
CV: Tachycardia, cap refill 2 secs
Pulm: End-expiratory wheezing
Abdomen: ND, NT, no guarding or rebound
GU: Without findings
Derm: No rashes

CXR demonstrates multi-lobar infiltrate.

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Acute Chest Syndrome (ACS)1-3

  • Presentation: fever (>38.5°C or 101.3°F), tachypnea, cough, +/-chest pain, +/- wheezing and new infiltrate on CXR
  • Evaluation:
    • CXR, CBC, reticulocyte count, VBG, blood cultures, sputum culture2
    • Consider underlying etiologies and evaluate as appropriate:
      • Sepsis
      • PNA
      • PE
      • Fat embolism
  •  Treatment:
    • Bronchodilators – improve peak expiratory flow2
    • Incentive spirometry and analgesia – prevent development/worsening of atelectasis
    • Empiric antibiotic therapy following procurement of culture samples (target Chlamydia, Mycoplasma, and Streptococcus)
    • Oxygen therapy to maintain SpO2 >92%
    • Fluid resuscitation targeting euvolemia (avoid iatrogenic pulmonary edema)
    • Exchange transfusion (in consultation with heme/onc) for:
      • Severe hypoxemia
      • Multi-lobar involvement
      • Worsening course
  •  Pearls:
    • Acute chest syndrome is the leading cause of death in sickle cell patients in the U.S. (12% mortality).2
    • Infection is most common cause of ACS ( C. Pneumoniae and RSV).
    • A normal pulmonary exam is most frequently associated with ACS.2
    • ACS rapidly progresses to ARDS = admit to ICU level care


  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 236, Sickle Cell Disease and Hereditary Hemolytic Anemias.
  2. Vichinsky E, Neumayr L, Earles A, Williams R, Lennette E, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. N Engl J Med. 2000; 342:1855-1865.
  3. Traill L and Barton M. Focus On: Acute Chest Syndrome – The Critical Cough. American College of Emergency Physicians Clinical and Practice Management. 2008. Available from:—Practice-Management/Focus-On–Acute-Chest-Syndrome—The-Critical-Cough/

CORE EM: Vertebral Osteomyelitis

Originally published at, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Written by: Latrice Triplett, MD // Edited By: Anand Swaminathan, MD


  • Inflammation of the vertebrae due to a pyogenic, fungal or mycobacterial organism.

    MRI Images - Vertebral Osteomyelitis (The Lancet)
    MRI Images – Vertebral Osteomyelitis (The Lancet)
  • Classified as either acute (days), subacute (weeks) or chronic (months)
  • Spondylodiscitis: a term encompassing osteomyelitis, spondylitis and discitis. Often used interchangeably with osteomyelitis.


  • 1 to 2.4 cases per 100,000 people (Zimmerli 2010)
  • More common in males with M:F of 3:1
  • Rate is also increasing due to increased number of spinal procedures
  • Typically affects adults, with most cases occurring in patients over 50 years old.


  • Infection occurs by three routes:
    • Hematogenous spread – secondary to infections of the GU, skin, soft tissue and respiratory system, indwelling catheters or endocarditis
      • Due to the bifurcated structure of the arterial supply, generally presents as infection of 2 contiguous vertebrae and the intervertebral disc
    • Direct inoculation during trauma or spinal surgery
    • Spread from adjacent soft tissue infection
  • Organism
    • Most cases in the United States are pyogenic.
      • Most common organism is Staph Aureus (36-67% of cases) (Boody 2015).
      • Other pathogens include: E. Coli, Pseudomonas Aeruginosa and Group B and G hemolytic Strep
    • Other pathogens to consider:
      • Fungal – blastomycosis, coccidiomycosis, histoplasmosis, aspergillosis
      • Brucellosis
      • Mycobacterial
    • Location: lumbar (48%) most common, followed by thoracic (35%) and cervical (6.5%)

History and Physical

  • Risk Factors:
    • Diabetes Mellitus (most common)
    • Immunosuppression: HIV, Malignancy, chronic steroids or immunosuppressant medication use
    • Spinal fracture, trauma or recent procedure
    • Substance Abuse: Alcoholism and IVDU
    • Presence of an indwelling vascular device
    • Elderly
  •  Symptoms
    • Back pain – often described as dull, may be present for weeks to months
    • Neurologic symptoms (paresthesias, weakness or radiculopathy) present in approximately one-third of patients
    • Most patients lack systemic symptoms
  • Exam
    • Tenderness over affected vertebrae
    • Paraspinal tenderness or spams may be present which may mislead the clinician towards a musculoskeletal diagnoses


  • Labs
    • Leukocytosis and Neutrophilia are poorly sensitive and highly non-specific (Gouliouris 2010). The degree of elevation does not predict disease severity.
    • ESR and CRP are sensitive, yet not specific.
      • CRP concentration rise and fall quicker than ESR, often used to guide treatment
    • Blood Cultures – an important element in management and treatment
      • Blood culture positivity often decides whether a patient will require a bone biopsy.
      • Cultured specimen narrows antibiotic coverage
    • Urinalysis/Urine Culture –UTI is a frequent missed source of bacteremia (especially in diabetic patients).
  • Imaging
    MRI Images (

    MRI Images –

    • Gadolinium enhanced MRI – modality of choice, highly sensitive and specific (Mylona 2009).
      • Although MRI with and without contrast is preferred, a non-contrast MRI can evaluate for inflammatory processes.
      • If a patient requires premedication or has renal failure, obtain the non-contrast MRI first. A contrast MRI can be done later to delineate subtle findings.
      • Findings include: enhancement (hypointense on T1 and hyperintense on T2) of vertebral endplates and adjacent disc space (Image 1)
    • CT Scan with IV contrast – use only if MRI contraindicated
      • Inferior in evaluation of disc spaces and neural tissues
        • Less sensitive than MRI and may be falsely negative in early disease
        • Used primarily by surgeons for biopsy of spine
      • Findings include loss of end plate definition and narrowing of disc space (Image 2)
      • Previously used CT Myelogram now out of favor due to potential for intradural spread of infection.
    • Plain Radiographs – often done to evaluate other causes (masses, fracture) however not recommended for diagnosis
      • Poorly sensitive and findings typically present in advanced disease (10-14 days after onset), once significant bone demineralization has already occurred
    • Radionuclide studies – (including: Tech 99m Bone scan, Gallium -67)
    • Sensitive but not specific, long acquisition time and difficult to obtain in the emergent setting


  • Pathogen directed therapy – Antibiotics tailored towards cultured organism
    • Given the dependence on blood culture results to guide therapy, current recommendations (IDSA 2015 Guidelines) suggest holding empiric antibiotics in medically stable patients (non-septic, hemodynamically stable, neurologically intact) until cultures grow out.
      • Note: this is a weak recommendation based on low quality evidence and patients should be managed on a case by case basis in conjunction with the inpatient treatment team
    • Empiric coverage:
      • Vancomycin 15-20 mg/kg/dose every 8-12 hrs PLUS
      • 3rd Generation Cephalosporin: Cefotaxime (2 g IV every 6 hrs), Ceftriaxone (1 to 2 g IV daily) or Ceftazidime (1 to 2 g IV every 8 -12 hrs)
      • Alternate: Cefepime 2 g IV every 12 hours
      • Duration: 6 weeks (occasionally 12 weeks if advanced disease) of IV antibiotics followed by 1-2 months of oral antibiotics
  • Surgical Consult – although most patients are successfully treated with antibiotics alone, some may require surgical intervention if there is concern for vertebral instability or spinal cord compromise.
    • Indications for surgical intervention include: associated abscess formation, spinal cord compression, progression of disease despite antimicrobial treatment
    • Obtain consult (Neurosurgery or Orthopedics) early, since patients may require bone biopsy for detection of organism

Take Home Points

  • Clinical presentation is very nonspecific; evaluate all patients presenting with back pain for infectious risk factors.
  • Baseline labs should not guide diagnosis, but may assist in later management.
  • MRI is key to diagnosis, obtain this imaging in all patients who raise clinical suspicion
  • Patients with hemodynamic instability and neurologic compromise warrant empiric antibiotics. The initiation of empiric antibiotics in hemodynamically stable, neurologically intact patients should be done on a case-by-case basis.


Berbari EF, Kanj SS, et al. Executive Summary: 2015 Infectious Disease Society of America (IDSA) Clinical Practice Guidelines for the Diagnosis and Treatment of Native Vertebral Osteomyelitis in Adults. Clin Infect Dis 2015 Sept 15;61(6):859-63. PMID: 26316526

Boody B, et al. Vertebral Osteomyelitis and Spinal Epidural Abscess: An Evidence-based Review. J Spinal Disord Tech. 2015 Jul;28(6):E316-27 PMID: 26079841

Chowdhury V, Gupta A, Khandelwal N. Diagnostic Radiology: Musculoskeletal and Breast Imaging. 3rd ed. New Delhi: JP Brothers Medical Ltd; 2012

Della-Guistina, D. Evaluation and Treatment of Acute Back Pain in the Emergency Department. Orthopedic Emergencies 2015 May; 33(2) 311-26. PMID: 25892724

Gouliouris T, et al. Spondylodiscitis: update on diagnosis and management. J Antimicrob Chemother. 2010 Nov;65 Suppl 3:iii 11-24 PMID: 20876624

Mylona E, et al. Pyogenic Vertebral Osteomyelitis: A Systematic Review of Clinical Characteristics. Semin Arthritis Rheum. 2009 Aug; 39(1):10-7. PMID: 18550153

Pruitt CR, Perron AD. Specific Disorders of the Spine. In: Sherman SC eds. Simon’s Emergency Orthopedics. 7th ed. New York, NY: McGraw-Hill; 2014

Winters ME, Kluetz P et al. Back Pain Emergencies. Med Clin North Am, 2006 May;90(3):505-23. PMID: 16473102

Zimmerli W. Vertebral Osteomyelitis. N Engl J Med 2010 Mar; 362(11)1022-9. PMID: 20237348

CORE EM: Compartment Syndrome

Originally published at, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Definition: Increased pressure within a closed space that compromises circulation and, thus, function of the tissues (i.e. muscle, nerve, bone) within the space. Sequelae include neurological deficit, Volkmann’s contracture, limb amputation and crush syndrome.


  • Most commonly seen after a traumatic injury to an extremity
  • Can occur in the absence of fracture
  • Occur in 1-10% of tibial fractures (Elliott 2003)
  • 75% of traumatic compartment syndrome accounted for by long-bone fractures (Carter 2013)
  • Most common sites: lower leg, upper leg, forearm, gluteal/thigh and hand


  • Fracture
  • Bleeding into compartment (i.e. vascular injury)
  • External compression (i.e. cast, crush injury)
  • Iatrogenic (infiltration of IV infusion, surgical complication)

Causes of Compartment Syndrome (Roberts + Hedges)

Causes of Compartment Syndrome (Roberts + Hedges)


  • Increased compartment pressure -> increased venous pressure -> compromised local circulation and hypoxia
  • Three general etiologies
    • Increased compartment contents (bleeding, infiltrated infusion)
    • Decreased compartment volume
    • External pressure
  • Tissue threshold for ischemia
    • Muscle – 4 hours
    • Nerve – 8 hours
    • Fat – 12 hours
    • Skin – 24 hours
    • Bone – 72-96 hours

Signs + Symptoms:

  • Classic “5Ps”
    • Pain disproportionate to injury or exam findings (hallmark finding)
    • Paresthesias
    • Pallor
    • Pulselessness
    • Paralysis
  • Pain with passive stretch of muscles within specific compartment

Clinical Evaluation for Compartment Syndrome (Roberts + Hedges)

  • Limitations of examination
    • Examination only potentially useful in patients who are alert. Often, patients at risk for compartment syndrome have polysystem trauma and may be obtunded
    • Pallor, pulselessness and paralysis are late findings
    • Motor weakness evaluation may be limited by pain (Frink 2010)
  • A review article in 2013 looks at all of the above clinical signs and symptoms and concludes that there is limited quality investigations to determine the performance of any of them (Nelson 2013).


  • Unconscious patient
    • Signs and symptoms will not be evaluable in this group
    • If the patient has a high-risk injury for compartment syndrome (tibial fracture, crush injury etc) direct compartment pressure measurement should be performed
    • Consider repeat measurement every 4 hours as compartment syndrome is a progressive disease (Wall 2010)
  • Compartment Pressure Measurement
    • Diagnostic Threshold
      • Absolute pressure > 30 mm Hg
      • Perfusion pressure (DBP – Compartment Pressure): < 30 mm Hg
    • Pressure Measurement Pearls
      • Single compartment pressure measurements have been shown to have low specificity leading to over-diagnosis and over-treatment (Nelson 2013, Whitney 2014)
      • Serial Pressure Measurement: Patents with high clinical suspicion of compartment syndrome but normal initial measurements should have serial measurements performed
      • Continuous Pressure Monitoring: A single study out of Scotland demonstrated a sensitivity of 94% and specificity of 98% for continuous compartment pressure monitoring (McQueen 2013)
      • At risk extremities have multiple compartments. It is critical to measure the compartment pressure in every compartment.

Compartment Syndrome Algorithm (Wall 2010)

Compartment Syndrome Algorithm (Wall 2010)

  • Mercury Manometer System (Whitesides method)
    • In vitro, measurements found to be both inaccurate and inconsistent (Ullasz 2003, Boody 2005)
    • Technique overestimates pressure leading to increased false positives (Boody 2005)
    • Can be assembled from teams typically found in the ED

Mercury Manometer System Final Image (Roberts + Hedges)

Mercury Manometer System Final Image (Roberts + Hedges)

  • Arterial Line System 
    • In vitro studies demonstrate excellent correlation between actual pressure and measured pressure by this system (Boody 2005)
    • Can be assembled from teams typically found in the ED

Arterial Line System (Roberts + Hedges)

Arterial Line System (Roberts + Hedges)

  • Styker® device
    • In vitro studies demonstrate excellent correlation between actual pressure and measured pressure by this system (Boody 2005)
    • Video reviewing setup and use of Styker® device can be found here

Stryker Kit (

Stryker Kit (



  • Immediate surgical consultation
  • Patient with compartment syndrome often have polytrauma so make sure to perform a complete trauma evaluation.
  • Restore circulating volume to increase perfusion to the extremity
  • Remove any external compressive devices (casts, splints, tourniquets). Removal of casts (or bi-valving) can reduce pressure by up to 65-90%
  • Maintain limb at level of heart or keep slightly dependent (maximize arterial perfusion without decreasing venous drainage)
  • Don’t forget to look for concomitant rhabdomyolysis and crush syndrome (reperfusion injury occurring after traumatic rhabdomyolysis characterized by extensive muscle death, hyperkalemia, metabolic acidosis and myoglobinuric acute renal failure)


  • Optimal therapeutic approach is immediate fasciotomy in the operating room. Delay of surgical intervention can result in irreversible muscle damage, nerve death and bone infarction
  • Indications (Wall 2010)
    • Clinical signs of acute compartment syndrome
    • Absolute compartment pressure > 30 mm Hg
    • Perfusion pressure < 30 mm Hg
  • Regardless of the specific compartment involved, all compartments in the affected extremity should have fasciotomy performed

Take Home Points

  1. Compartment syndrome is a life and limb threatening emergency that requires early recognition, prompt diagnosis and immediate management with fasciotomy
  2. While clinical evaluation is flawed, pain out of proportion to injury and pain with passive stretch of muscles within the compartment are the best screening tools.
  3. Do not wait for the development of pallor, absence of pulse or paralysis to consult surgery. These are late findings that may only arise once the limb is non-salvageable.
  4. In unconscious patients, there should be a low threshold to measure compartment pressure in patients who are at risk as clinical signs cannot be evaluated
  5. When measuring compartment pressures, look for an absolute pressure > 30 mm Hg and perfusion pressure (DBP – compartment pressure) of < 30 mm Hg. All patients with a clinical suspicion and normal pressures should have repeat pressures measured.

Read More:

Plastsurgproj’s YouTube Channel: Compartment pressure measurement


Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg. – British Volume 2003; 85: 625–32.

Carter MA: Compartment Syndrome Evaluation in Roberts JR, Hedges JR, Custalow CB, et al (eds): Clinical Procedures in Emergency Medicine, ed 6. Philadelphia, Saunders, 2013, Ch 54:p 1095-1124.

Frink M et al. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res 2010;468:940–50. PMID: 19472025

Nelson JA. Compartment pressure measurements have poor specificity for compartment syndrome in the traumatized limb. J Emerg Med 2013; 44(5): 1039-44. PMID: 23321294

Wall CJ et al. Clinical practice guidelines for the management of acute limb compartment syndrome following trauma. ANZ J Surg 2010; 80: 151-6. PMID: 20575916

Whitney A et al. Do one-time intracompartmental pressure measurements have a high false-positive rate in diagnosing compartment syndrome. Acute Care Surg 2014; 76: 479-83. PMID: 24458053

McQueen MM et al. The estimated sensitivity and specificity of compartment pressure monitoring for actue compartment syndrome. J Bone Joint Surg Am 2013; 95: 673-7. PMID: 23595064

Ullasz A et al. Comparing the methods of measuring compartment pressures in acute compartment syndrome. Am J Emerg Med 2003; 21: 143-5. PMID: 12671817

Boody AR, Wongworawat MD. Accuracy in the measurement of compartment pressures: a comparison of three commonly used devices. J Bone Joint Surg 2005; 87: 2415-2422. PMID: 16264116

CORE EM: Peri-Mortem C-Section

Originally published at, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Written by: Allie Boyd, MD // Edited By:  Salil Bhandari, MD

Definition: A cesarean section preformed either during maternal cardiac arrest or during impending maternal cardiac arrest the primary goal of which is to increase the chance of successfully resuscitating the mother and, potentially, improving fetal survival.

Physiological Changes in Late Pregnancy

  • Blood volume and cardiac output increase by 30-40% above the nonpregnant state by 28 weeks
    • This hypervolemic state is protective for the mother, as fewer red cells are lost during hemorrhage
    • Clinical signs of maternal shock manifest only after 40% of maternal blood volume is lost
  • Late pregnancy is very susceptible to hypotension from compression of the inferior vena cava (IVC) in the supine position by the enlarged uterus
  • The enlarged uterus causes elevation of the diaphragm by about 4 cm, and results in a decrease in the functional residual capacity by about 20%

General approach to the pregnant trauma patient

  • Overall same general approach as in non-pregnant patients. Focus must always be on resuscitating the mother, not the fetus.
  • Special considerations in primary survey
    • Airway: There is physiologic narrowing of the upper airways in the third trimester
      • Use an endotracheal tube 1 size smaller.
      • Intubation medications are the same.
      • RSI is the preferred method of intubation for any indication in the third trimester due to the increased risk of aspiration.
    • Breathing: Pregnant patients are predisposed to rapid falls in Pa02 during apnea
      • Supplemental O2 should be provided for any pregnant patient being resuscitated regardless of saturation.
    • Circulation: Hypovolemia should be suspected before clinical signs of hypotension in trauma patients, as the state of hypervolemia and resulting hemodilution may mask underlying significant blood loss.
      • Aggressive volume resuscitation is encouraged regardless of blood pressure.
      • Resuscitation of the pregnant patient should include uterine displacement to relieve compression of the IVC and thus improve cardiac output and restore circulation.
        • Perform in any patient in whom the uterus could potentially cause compression regardless of gestational age or lack of knowledge of gestational age.
        • Traditional teaching: This can be done by tilting the backboard up a 30 degree angle to the left, but may be difficult to perform effective chest compressions while patient tilted
        • New model: It is more effective to manually move the uterus to the patient’s left with one or two hands during ongoing chest compressions, while patient remains flat on their back.

Decubitus Position -

Purpose of Peri-Mortem C-Section (PCS):

  • Primary goal is improvement of maternal, not fetal, resuscitation
  • PCS decreases uterine compression on the IVC thus increasing venous return, resulting in improved maternal cardiac filling pressure.
  • PCS also allows for improved respiratory mechanics, as the diaphragm is lowered after the procedure

When to perform a PCS:

  • Traditional teaching: perform a PCS at 24 weeks in a peri-arrest or arresting mother, as a fetus is generally
    Size of Uterus in Pregnancy

    Size of Uterus in Pregnancy

    considered viable at 24 weeks gestational age.

    • At 24 weeks gestation, there is a 20-30% chance of extrauterine fetal survival if neonatal facilities are available.
  • New model: PCS is resuscitative hysterotomy for the mother
    • 24 week guideline is flawed
      • You will likely not have this information in this clinical setting.
      • Even the best ultrasound dating criteria is subject to 1-2 weeks of uncertainty.
      • PCS is primarily resuscitative for mother – best chance of saving the fetus is to save the mother.
    • Counter argument to new model: before 24 weeks gestation, the fetus is small and PCS will not have significant effect on maternal hemodynamics.
    • Alternate guide to perform PCS
      • There is a reported gestational age anywhere near viability
      • The abdomen is large, specifically if fundal height is above umbilicus
      • If baby looks big on ultrasound (may not have time to measure biparietal diameter, but can get a general sense of the size of the fetus)

How long after arrest do you have to perform a PCS?

  • Perform a PCS as soon as possible after maternal cardiac arrest.
  • After 4 minutes of maternal arrest there is a precipitous decline in fetal neurologic outcome and survival.
  • Despite decreased utility after 4 minutes for fetal survival, resuscitative hysterotomy will continue to hold benefits to the mother.

How to perform a PCS:

  • Make a vertical incision from xiphoid to the pubis using a scalpel (ideally #10 Blade)
  • Cut through subcutaneous tissue to get to peritoneal wall
  • Use fingers to bluntly dissect to the peritoneum
  • Cut through peritoneum vertically (ideally with scissors or use a scalpel to initiate an opening inferiorly)
  • Deliver the uterus, then cut into the lower half of the uterus vertically to avoid the placenta and then use scissors to extend the incision upwards until you reach the baby
  • Deliver the baby (neonate will likely need resuscitation)
  • Clamp and cut the umbilical cord
  • Place packing/towels in the opened uterus and abdomen

Below is a short blast talk on the Peri-Mortem C-Section from Core EM Faculty Salil Bhandari

Take home points:

  1. Think of PCS as a resuscitative hysterotomy primarily aimed at saving the life of the mother
  2. If you think PCS will improve maternal resuscitation, act quickly to start and complete the procedure
  3. The optimal surgical approach for a PCS is via a large vertical incision.


Ramanathan S, Porges RM. Anesthetic Care of the Injured Pregnant Patient. In Capan LM, Miller SM, Turndorf H Editors, Trauma Anesthesia and Intensive Care; J.B. Lippincott Company; 1991; 599-628.

Pimentel L. Mother and Child: Trauma in Pregnancy. Emerg Med Clin North Am. 1991 Aug;9(3):549-63. PMID: 2070767

Drost TF, Rosemurgy AS, Sherman HF, Scott LM, Williams JK. Major Trauma in Pregnant Women: Maternal/fetal Outcome. J Trauma. 1990 May;30(5):574-8. PMID: 2342141

Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S829. PMID20956228

O’Connor RL, Sevarino FB. Cardiopulmonary arrest in the pregnant patient: a report of a successful resuscitation. J Clin Anesth. 1994;6(1):66. PMID 8142104

Cordero DR, Toffle RC, McCauley CS. Cardiopulmonary arrest in pregnancy: the role of caesarean section in the resuscitative protocol. W V Med J. 1992;88(9):402. PMID: 1462532

Additional resources:

EMCrit: Peri-Mortem C-section

St. Emlyn’s: Peri-mortem C-section

JAMIT: Perimortem Caesarian Section

CORE EM: Aortic Dissection

Originally published at, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Written by: Alexandra Ortega, MD // Edited by: Anand Swaminathan, MD


A tear in the innermost layer of the aorta (the intima) allowing for blood to dissect between layers of the aortic wall, which may lead to end-organ damage or death.


  • 10,000 deaths in the US annually
  • Incidence 16/100,000 for men, 9/100,000 for women (Milewicz 2011)
  • Ratio of Aortic Dissection (AD) to Acute Coronary Syndrome is 1:600
  • 22% of cases undiagnosed prior to death (Cline 2012)

Predisposing Factors:

  • History of prior dissection
  • Hemodynamic Stessors (HTN, cocaine use)
  • Connective Tissue Disorders (Marfan Syndrome, Ehlers-Danlos Syndrome)
  • Anatomic Abnormalities that cause abnormal flow (bicuspid aortic valve)
  • Questionable predisposing factors: PCOS, Pregnancy, Family History


  • Stanford (More commonly used)
    • Type A- Any involvement of the ascending aorta
    • Type B- Descending aorta only (distal to the left subclavian artery)
  • DeBakey
    • Type 1: Involves ascending aorta, aortic arch, and descending aorta
    • Type 2: Ascending aorta only
    • Type 3: Descending aorta only

AD Variants

  • Intramural thrombus- an infarction in the aortic media, most often due to an injury to the vaso vasorum, results in a thrombus within the aortic wall, which may extend or resolve spontaneously. Often a precursor to dissection
  • Perforating ulcer- ulcer formation due to atherosclerosis which can lead to intramural thrombus, dissection or aortic perforation (Cline 2012)

History + Physical

  • Classic presentation: sudden onset of tearing chest pain radiating to the back, however, dissection may occur anywhere along the aorta and thus the presentation may be broad and mimic other common disorders
  • Variant presentations include:
    • Patients with symptoms above and below the diaphragm
    • Chest pain or back pain + vomiting
    • Chest pain or back pain with neurologic findings (may be due to dissection into the carotid arteries)
    • Cardiac tamponade
    • Any patient that generally “looks bad”
  • Only 49% of AD patients have the classic tearing chest pain
  • Presenting blood pressure
    • Hypertension: 49%
    • Normotension: 33%
    • Hypotension: 18%
  • 4% of AD patients are women. Women diagnosed with AD tend to be older and have higher mortality
  • Classic Risk Factors (Hagan 2000)
    • 9% of patient’s have Marfan syndrome, these patients are often young
    • 72% had a history of HTN
    • 9% had prior cardiac surgery
  • Physical Examination (Hagan 2000)
    • Pulse deficit: Present in only 15%
    • Blood pressure differential19%

Presenting Symptoms + Physical Examination (Hagan 2000)

Presenting Symptoms + Physical Examination (Hagan 2000)

Diagnostic Testing

  •  EKG:
    • Most changes are non-specific (41.4%) and hard to differentiate from ACS
    • >30% of patients have no EKG changes (Hagan 2000)
  • CXR: the classic finding is a widened mediastinum (present in 62%) and over 12% of AD patients have no abnormality on x-ray (Hagan 2000)

    CT Chest: Aortic Dissection (

    CT Chest: Aortic Dissection (

  • CT: modality of choice with 100% sensitivity and 98% specificity
    • Can identify a false lumen, location of dissection flap, extension into the great vessels, signs of aortic rupture and end-organ damage
    • TEE and MRI have similar reliability
  • TTE: may be helpful in identifying cardiac tamponade in an unstable patient
    • Tamponade common cause of hypotensive presentation of AD
    • ACEP Level B guideline: Do not rely on abnormal bedside TTE result to definitely establish diagnosis of thoracic aortic dissection

      TEE: Aortic Dissection (

      TEE: Aortic Dissection (

    • ACEP Level C recommendation: Get a surgical consult or transfer to a higher level of care if TTE is suggestive of dissection (Diercks 2015)
  • D-dimer:
    • May be helpful if checked within the first 24 hours however due to overlap with other diagnoses may lead to harm (exposure to radiation and cost of imaging) if applied to a large population
    • May be negative in young patients and those with short dissection flaps
    • Likely to be negative in patients with intramural thrombus as forming clot is not exposed to circulation
    • ACEP Level C recommendation: In adult patients with suspected nontraumatic thoracic aortic dissection, do not rel on D-dimer alone to exclude the diagnosis of aortic dissection. (Diercks 2015)


Surgical Management

  • Mobilize consultants as early as possible (Cardiothoracic surgery, interventional radiology)
    • Mortality increases by 1-2% for every hour from symptom onset to definitive treatment
  • Consider pericardiocentesis if patient hypotensive

Medical Management

  • Reverse anticoagulation
  • Administer analgesia
    • Adding fentanyl for pain control can decrease endogenous catecholamines that increase HR and inotropy
  • Anti-impulse Therapy
    • Goal: Decrease blood pressure and heart rate in order to decrease shear forces on the intima and thus prevent extension of the dissection flap
    • No BP or HR goal has demonstrated a reduction in morbidity or mortality, however most sources recommend a systolic blood pressure goal of < 110 mmHg and a heart rate <60bpm
    • Medications (Greenwood 2015)
      • Beta blocker
        • Mechanism of action: negative inotrope/chronotrope
        • Esmolol ideal agent: rapid onset and easy to titrate
          • Loading Dose: 500 mcg/kg bolus over 1 min (can repeat once)
          • Infusion Dose: 50mcg/kg/min, titrate by 50mcg/kg/min q4min (max 300mcg/kg/min)
      • Dihydropyridine calcium channel blocker (nicardipine or clevidipine)
        • Mechanism of action pure arterial vasodilator (afterload reduction)
        • Nicardipine Infusion Dose: 5mg/hr titrate by 2.5 mg/hr q 5min (max 15mg/hr)

Take Home Points

  • Aortic dissection may occur in any location along the aorta and therefore the range of presentations is broad. Many AD patients do not fit the textbook presentation.
  • CT, TEE and MRI are the most reliable methods to diagnose AD
  • Once AD is diagnosed, rapid mobilization of consultant services is critical to increase the chance for survival
  • Treatment in the ED is focused on lowering blood pressure and heart rate in hypertensive patients until surgical correction can be achieved


Cline, D et. al, Tintinalli’s Emergency Medicine Manual, 7e. McGraw-Hill (2012): 160-164.

Diercks DB, et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med. 2015 Jan;65(1):32-42.e12. PMID: 25529153.

Greenwood, JC, ed. PressorDex. Irving, TX: Emergency Medicine Residents’ Association; 2015.

Hagan PG, et. al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000 Feb 16;283(7):897-903. PMID: 10685714.

Milewicz DM. Stopping a killer: improving the diagnosis, treatment, and prevention of acute ascending aortic dissections. Circulation. 2011 Nov 1;124(18):1902-4. PMID: 22042924.

Rosman HS, et al. Quality of history taking in patients with aortic dissection. Chest. 1998 Sep;114(3):793-5. PMID: 9743168.

Swaminathan A, Jones MP. Hypertensive Crises. Decision Making in Emergency Critical Care 2015 1st Edition. 208-18.

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