All posts by Anand Swaminathan

CORE EM: Compartment Syndrome

Originally published at CoreEM.net, 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.

Epidemiology:

  • 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

Causes:

  • 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)

Pathophysiology:

  • 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).

Diagnosis 

  • 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 (emcurious.com)

Stryker Kit (emcurious.com)

Management:

Basics:

  • 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)

Fasciotomy

  • 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

References:

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 CoreEM.net, 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 - What-when-how.com

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.

References

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 CoreEM.net, 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

Definition:

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.

Epidemiology:

  • 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

Classification:

  • 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 (radiopaedia.org)

    CT Chest: Aortic Dissection (radiopaedia.org)

  • 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 (ultrasoundcases.info)

      TEE: Aortic Dissection (ultrasoundcases.info)

    • 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)

Management

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

References

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.

R.E.B.E.L. EM – Xanthochromia Detection: Visual Inspection vs. Spectrophotometry

Originally published at R.E.B.E.L. EM on January 25, 2016. Reposted with permission.

Follow Dr. Salim R. Rezaie on twitter @srrezaie and Dr. Anand Swaminathan at @EMSwami

Xanthochromia-765x573

Background: Although non-contrast head CT (NCHCT) has near perfect sensitivity (98-100%) in detecting aneurysmal subarachnoid hemorrhage (SAH) when performed within 6 hours of headache onset, sensitivity declines after 6 hours. As a result of declining sensitivity, lumbar puncture (LP) continues to be part of the workup in suspected SAH. An LP gives providers the ability to perform CSF analysis for red blood cells and detect xanthochromia by visual inspection or spectrophotometry. In most of the world, including the United States, the predominant approach to identifying xanthochromia is visual detection. However, this technique is subjective and considered unreliable by many. Spectrophotometry is a more objective test but, has lower specificity, carries a higher cost and is unavailable in the majority of hospitals.

In patients with SAH diagnosed by NCHCT or suspected based on LP results, angiography (CTA or MRA) is typically performed to investigate for an aneurysm that requires neurosurgical intervention. Angiography is considered to be the “gold standard” test for looking for aneurysmal SAH although it is not without it’s own limitations (a small minority of the population will have benign aneurysms and these increase with age).

Clinical Question: What are the test performance characteristics of visual inspection and spectrophotometric assessment and how do they compare?

Article: 

Chu K et al. Spectrophotometry or visual inspection to most reliably detect xanthochromia in subarachnoid hemorrhage: systematic review. Ann Emerg Med 2015. PMID: 24635988

Population: English language studies including patients presenting with headache who had LPs and CSF was evaluated for xanthochromia by either visual inspection or spectrophotometry.

Design: Systematic Review

Critical Findings

  • Spectrophotometry
    • Sensitivity: 86.5% (I2 = 26.1%)
    • Specificity: 85.8% (I2 = 95.5%)
    • (+) LR: 6.6
    • (-) LR: 0.29
  • Visual Inspection
    • Sensitivity: 83.3% (I2 = 51.9%)
    • Specificity: 95.7% (I2 = 76.0%)
    • (+) LR: 14.1
    • (-) LR: 0.35

In the included studies, the criteria standard for the diagnosis of aneurysmal SAH was angiography (either CTA or MRA) or clinical follow-up.

Strengths:

  • First systematic review investigating this question
  • QUADAS-2 tool used to assess methodological quality of included studies

Limitations:

  • Only Medline, Embase and Cochrane libraries were searched for relevant articles
  • Non-English studies were not included
  • Grey literature search was not performed
  • Only three of the studies found directly compared spectrophotometry and visual inspection
  • Included studies used various outcomes to define subarachnoid hemorrhage
  • Moderate to high heterogeneity between included studies prohibiting meta-analysis of the results
  • The “criteria standard” for diagnosis was angiography or follow-up if angiography wasn’t performed. All patients did not receive angiography.

Authors Conclusions: The heterogeneity in the underlying studies, combined with significant overlap in pooled confidence limits, makes it impossible to provide a definite conclusion about the diagnostic accuracy of spectrophotometry versus visual inspection.”

Our Conclusions: This systematic review highlights the nuances in the workup of SAH. The existing data on this topic demonstrates that neither spectrophotometry nor visual inspection is optimal diagnostic methods for detecting SAH in patients with normal NCHCT. It is unclear from the available evidence which method is superior.

Potential to Impact Current Practice: Based on the available literature, there is not convincing evidence to embrace one of these diagnostic tests over the other.

Bottom Line: In patients who are NCHCT negative for SAH, neither spectrophotmetry nor visual inspection for xanthochromia are perfect tests. The absence of an established “gold-standard” CSF assay limits the utility of lumbar puncture after negative NCHCT in these patients due to the issues with result interpretation.

Post Peer Reviewed By: Salim Rezaie (Twitter: @srrezaie)

CORE EM: Pharmacology of Insulins

Originally published at CoreEM.net, 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: Anand Swaminathan, MD // Edited by: Mary Ann Howland, PharmD

Background:

Insulin was first licensed for human use in 1922. Since then, numerous formulations with various similar names have been produced and marketed. Because the names of the different drugs are often very similar (novolin vs novalog) it can difficult for emergency providers to keep all of the agents straight. In this post, we discuss the categories of insulins, the nomenclature and the pharmacokinetics of the most commonly used agents.

Thank you to the St. John’s pharmacy students for their incredible work in compiling the information shared below.

Insulin Categories

  • Rapid Acting – AnaLOGs
    • Aspart, lispro, glulisine
  • Short Acting
    • Regular (NovoLIN or HumuLIN)
  • Intermediate Acting
    • NPH, protamine combined
  • Long Acting (Basal)
    • Glargine (Lantus), detemir (Levemir)

Insulin Nomenclature

  • Novo Products – Novo Nordisk company
  • Hum Products – Eli Lilly company
  • Suffixes
    • Log – Rapid acting (i.e. NovoLog, HumaLog)
    • Lin R – Short acting (NovoLin R, HumuLin R)
    • Lin N – Intermediate acting (NovoLin N, HumuLin N)
Insulin Name Onset Peak Duration
Rapid Acting
Lispro (Humalog) < 15 minutes 0.5 – 3 hours 3-5 hours
Aspart (Novolog) < 15 minutes 0.5 – 3 hours 3-5 hours
Glulsine (Apidra) < 15 minutes 0.5 – 3 hours 3-5 hours
Short Acting
Regular (Novolin R or Humulin R) 0.5 – 1 hour 2-4 hours 4-8 hours
Intermediate Acting
NPH (Novolin N or Humulin N) 2-4 hours 4-10 hours 10-18 hours
Long Acting
Glargine (Lantus) 4-6 hours Same action throughout the day 24 hours
Detemir (Levemir) 2-3 hours 6-8 hours Dose dependent (5.7 – 23.3 hours)
Combinations
Hululin or Novolin 70/30 0.5 – 1 hour 2-10 hours 10-18 hours
Novolog Mix 70/30, Humalog Mix 75/25 or 50/50 < 15 minutes 1-2 hours 10-19 hours
Kennedy M. Pancreatic hormones and antidiabetic drugs. In: Katzung B & Masters S, eds. Basic & Clinical Pharmacology. 12th ed. NY, NY: McGraw-Hill; 2012:748.

Kennedy M. Pancreatic hormones and antidiabetic drugs. In: Katzung B & Masters S, eds. Basic & Clinical Pharmacology. 12th ed. NY, NY: McGraw-Hill; 2012:748.

Reasons for Hypoglycemia in Patients on Insulins

  • Caloric intake inadequate for insulin dose
    • Reduced intake, increased exercise, catabolic stress (infection, myocardial infarction etc.)
    • Decreased gluconeogenesis
  • Reduced insulin elimination
    • Insulins primarily renal excreted
    • Patients with CKD, ESRD or AKI at risk for reduced elimination
  • Increased insulin dose
    • Unintentional (medication error)
    • Intentional (self harm, homicide)

Disposition

  • Regular Insulin – short acting enough for ED observation + discharge home
  • Kinetics of large insulin overdose unpredictable – admit to high monitored setting

Core EM: Spinal Epidural Abscess

Originally published at CoreEM.net, 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

Definition: Suppurative infection enclosed within the epidural space spinalepidural1

Epidemiology

  • Incidence: 2-3 cases per 10,000 hospitalized patients (Sendi 2008).Rate is increasing given the rise in number of spinal procedures and anesthesia techniques
  • Mortality is low at 5%, however, if untreated paralysis may occur
  • Can occur at any age but most patients are between 50 and 70 years old.

Pathogenesis

  • Classified as either primary or secondary:
    • Primary: Hematogenous spread from a distant focus to the epidural space
      • Usually from skin and soft tissue infections
      • Often located in the posterior/dorsal aspect of the spinal canal due to the presence of infection prone adipose tissue.
    • Secondary: Direct inoculation from recent spinal procedure, trauma or contiguous spread from adjacent discitis or osteomyelitis
      • Typically develops in the anterior/ventral epidural space
    • Organism: Most commonly Staph Aureus (MSSA and MRSA) with Coagulase-negative Staph and gram negative bacilli as the second and third most common, respectively
    • Enlarging abscess may lead to spinal cord compromise via direct compression or interruption of blood supply

History and Physical

  • Risk Factors – The presence of certain comorbidities places patients at increased risk for developing disease. However, 20% of patients with SEA will have no predisposing factors. Risk factors include:
    • Immunocompromised: DM, HIV, Malignancy, chronic steroids or immunosuppressant medication use
    • Spinal Abnormality: trauma, surgery, arthritis
    • Substance Abuse: Alcoholism, IVDU
    • Presence of an indwelling catheter
    • Elderly
  • Spinal epidural abscess is known for its nonspecific presentation, and can be easily missed. Adding it to the differential is often the critical step in making the diagnosis.
    • Classic triad of fever, back pain and neurologic symptoms is only present in 15% of patients. (Darouiche 2006)
      • Back pain is the most common symptom (75% patients).
        • Described as localized, severe and midline with tenderness to percussion.
      • Fever is an inconsistent finding (50% of patients). Normothermia should not deter further workup.
      • Neurologic symptoms (33% of patients) may indicate spinal cord compromise. These patients require rapid work-up and management. Once paralysis develops, it is often irreversible.
    • 4 Stages of Progression (Heusner 1948) – stepwise symptomatology of spinal epidural abscesses
      • Pain: back pain at the spinal level affe3cted (however, lesions may be distant to location of pain)
      • Radiculopathy: nerve root pain radiating from involved spinal region
      • Weakness: motor weakness, sensory deficit, bladder and bowel dysfunction (retention or incontinence)
      • Paralysis
    • Skip lesions – lesions present in noncontiguous vertebrae.
      • Increased risk if patient has 2 or 3 of the following symptoms (Ju 2015):
        • Delay in presentation (symptoms for ≥7 days)
        • Concomitant area of infection outside the spine and paraspinal region
        • ESR >95 mm/h at presentation.
    • If a patient displays symptoms not localized to a certain spinal level, consider imaging the entire spine.

Diagnostics

  • MRI Image of Spinal Epidural Abscess (http://d3gef7ppmbvsns.cloudfront.net/)Labs – routine labs are unhelpful in diagnosis but are drawn to assist inpatient management
    • CBC: Leukocytosis is present in 66% of cases (Davis 2004), however a normal WBC count is insufficient to rule out SEA.
    • ESR/CRP: sensitive, however very nonspecific.
      • ESR normal values vary by age, and are frequently elevated in patients with neoplastic disease, regardless of the presence of infection.
      • CRP normalizes quicker than ESR, and may be used in post-op patients or trended as an indicator of treatment success.
      • Recently, a treatment guideline suggested incorporating ESR/CRP elevation in the decision to pursue imaging (Davis 2011). It is important to note that this treatment guideline was based on a small set (n =86) of patients. Currently, neither the presence nor the degree of elevation should be used to rule-in or rule-out SEA
    • Blood Cultures
      • Provides assistance in tailoring antibiotic therapy
      • Isolates have excellent correlation with the organism later found during surgical drainage
  •  Imaging
    • Gadolinium enhanced MRI: gold standard for diagnosis, over 90% sensitive (Darouiche 2006). MRI is able to detect an abscess in early disease, show the extent of inflammatory changes and identify thecal sac compression.
    • CT with IV contrast – indicated only when MRI is contraindicated
      • Cannot readily distinguish early findings of infection from typical soft tissue, disk and osseous changes

Management

  • Empiric Antibiotics: directed against Staphylococcus and Gram Negative Bacilli.
    • Vancomycin (30-60 mg/kg divided into two daily doses) PLUS
    • 3rd Generation Cephalosporin: Cefotaxime (2 g IV every 6 hrs), Ceftriaxone (2 g IV every 12 hours) or Ceftazidime (2 g IV every 8 hours)
  • Operative drainage: Not all epidural abscesses are surgically drained. Decision is determined by:
    • Neurologic deficits
      • Those with developing neurologic deficits are often drained given risk of rapid development to paralysis.
      • Patients whom have already progressed to paralysis with low likelihood of improvement are often treated with antibiotics alone.
    • Presence of a drainable abscess versus a phlegmon on imaging
      • A phlegmon is granulomatous-thickened tissue without a significant purlent collection. It is noted as a homogenously enhancing lesion on MRI.
      • A liquid abscess is displayed as a central hypointense region with hyperintense peripheral enhancement.
    • Location – given small amount of epidural space, and thus increased risk of developing neurologic sequelae, cervical or thoracic epidural abscesses are more likely to be surgically drained

Take Home Points

  • Spinal Epidural Abscess may present insidiously and patients often lack the classic triad of fever, back pain and neurologic symptoms
  • Empiric Antibiotics should cover Staphylococcus (including MRSA) and Gram negative Bacilli
  • All patients with clinical suspicion require rapid evaluation with MRI as the diagnostic study of choice
  • Although not all patients will go to the operating room, surgical consult (Neurosurgery or Orthopedics) should be obtained emergently

References

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

Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006; 355; 2012-2020 PMID: 17093252

Davis DP, et al. The Clinical Presentation and Impact of Diagnostic Delays on Emergency Department Patients with Spinal Epidural Abscess. J Emerg Med. 2004 Apr;26(3):285-91. PMID:15028325

Davis DP, et al. Prospective Evaluation of a Clinical Decision Guideline to Diagnose Spinal Epidural Abscess in Patients who Present to the Emergency Department with Spine Pain. J Neurosurg Spine. 2011 Jun;14(6):765-70. PMID: 21417700

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

Heusner A, Nontuberculosis Spinal Epidural Infections. N Engl J Med. 1948 Dec; 239(23) 845-54. PMID: 18894306

Ju K, et al. Predicting patients with concurrent noncontiguous spinal epidural abscess lesions. Spine J. 2015 Jan 1; 15(10):95-101. PMID: 24953159

Sendi P, et al. Spinal epidural abscess in clinical practice. QM. 2008 Jan; 101(1)1-12. PMID: 17982180

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

R.E.B.E.L. EM – Epistaxis Myths Part I – Do Patients with Epistaxis Managed by Nasal Packing Require Prophylactic Antibiotics?

Originally published at R.E.B.E.L. EM on May 30, 2015. Reposted with permission.

Follow Dr. Salim R. Rezaie on twitter @srrezaie and Dr. Anand Swaminathan at @EMSwami

Epistaxis1Epistaxis is a common Emergency Department (ED) complaint with over 450,000 visits per year and a lifetime incidence of 60% (Gifford 2008, Pallin 2005). Posterior epistaxis is considerably less common than anterior epistaxis and represents about 5-10% of all presentations. Many patients with posterior epistaxis will be managed with a posterior pack and admitted for further monitoring. Traditional teaching argues that:

  1. Patients with nasal packs should be given prophylactic antibiotics to prevent serious infectious complications.
  2. Patients with posterior packs should be admitted to the ICU for cardiac monitoring as they are at risk for serious bradydysrhythmias.

Objective: To review the literature behind the traditional teaching and use the evidence to guide our management. In this post, we’ll take on the first dogmatic teaching of prophylactic antibiotics.

One important note, the literature base is scant on all topics regarding epistaxis. Randomized Double-Blind Control Trials (RDCT) are rare and study quality is overall very poor.Antibiotics

Dogma #1: Prophylactic antibiotics are necessary for patients with nasal packing.

The concern is that patients with packing in place are at a high risk of developing infectious complications including acute otitis media (AOM), sinusitis and toxic shock syndrome (TSS). A deep dive into the archives resulted in four studies that look at the question (1 on posterior packs, 2 on anterior packs and one non-specified).


Derkay CS et al. Posterior nasal packing. Are Intravenous antibiotics really necessary?Arch Otolaryngol 1989; 115: 439-41. PMID: 2923686

Population: RDCT of 20 patients with posterior packs (all packs were impregnated with antibiotics)
Intervention: Intravenous cefazolin
Control: Placebo (exact content not specifiec)
Outcome: Neither group had any infectious complications. The packing in the placebo group was noted to be foul smelling and 8/10 had heavy growth of multiple organisms. In the cefazolin group, 8/10 packing had light growth of a single organism.


Pepper C et al. Prospective study of the risk of not using prophylactic antibiotics in nasal packing for epistaxis. J Laryng Otology 2012: 257-9. PMID: 22214602

Population: Before and after, non-randomized, non-blinded study of 149 patients requiring packing for epistaxis.
Intervention: Amoxicillin/Clavulanic Acid in first 78 patients
Control: No antibiotics in 71 patients
Outcome: Neither group had an infectious complication


 

Lily PackingBiswas D, Mal RK. Are systemic prophylactic antibiotics indicated with anterior packing for spontaneous epistaxis. Acta Oto-Laryngologica 2009; 129: 179-81. PMID: 18607977

Biggs TC et al. Should prophylactic antibiotics be used routinely in epistaxis patients with nasal packs? Ann R Coll Surg Engl 2013; 95: 40-2. PMID:23317726

Unlike the prior two studies, the Biswas and Biggs articles are more difficult to interpret due to their methodologies. In the Biswas study, 21 patients had anterior packing of which 9 received antibiotics. The investigators sent swabs from the packed and unpacked nares and found no difference in bacterial growth in the antibiotic and no antibiotic group.

In the Biggs study, 57 patients in total were enrolled in a before and after study. 38 were enrolled prior to the institution of an algorithm, which called for limited use of antibiotics. In the before group, > 70% of patients were given prophylactic antibiotics versus just 12% in the after group. Neither group had any infectious complications despite the change in antibiotic prescription rate.


Summary: Although the three identified studies are of varying quality and methods, overall it appears that administration of IV, oral or topical antibiotics was no different than placebo in terms of infectious outcomes. It is important to note that in all studies, packing was removed after 24-48 hours.

No AntibioticsIn the Derkay study, the presence of single organism growth in the antibiotic group raises the concern of selecting out resistant organisms. Additionally, antibiotics have a number of known nasty side effects including diarrhea (in up to 1 in 8 patients), allergic reactions and severe anaphylaxis (in up to 0.024%).

Bottom Line: The available evidence does not defend the routine use of prophylactic antibiotics in patients who require nasal packing for epistaxis. In patients with immunosuppression, they should be considered.

Post Peer Reviewed By: Salim Rezaie, MD (Twitter: @srrezaie)


References:

  1. Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am.
  2. 2008;41:525-536. PMID: 18435996
  3. Pallin DJ, Chng YM, McKay MP, et al. Epidemiology of epistaxis in US emergency departments, 1992 to 2001. Ann Emerg Med. 2005;46:77-81. PMID: 15988431
  4. Derkay CS et al. Posterior nasal packing. Are Intravenous antibiotics really necessary? Arch Otolaryngol 1989; 115: 439-41. PMID: 2923686
  5. Pepper C et al. Prospective study of the risk of not using prophylactic antibiotics in nasal packing for epistaxis. J Laryng Otology 2012: 257-9. PMID: 22214602
  6. Biswas D, Mal RK. Are systemic prophylactic antibiotics indicated with anterior packing for spontaneous epistaxis. Acta Oto-Laryngologica 2009; 129: 179-81. PMID: 18607977
  7. Biggs TC et al. Should prophylactic antibiotics be used routinely in epistaxis patients with nasal packs? Ann R Coll Surg Engl 2013; 95: 40-2. PMID: 23317726

Core EM: Ventricular Tachycardia

Originally published at CoreEM.net, 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: Anand Swaminathan, MD (@EMSwami) // Edited by: Reuben Strayer, MD (@emupdates)

Definition: A wide-complex (QRS complex > 120 msec) tachydysrhythmia that originates within or below the bundle of His.

  • Nonsustained VT: Short episodes of VT lasting < 30 seconds
  • Sustained VT: prolonged episodes of VT lasting > 30 seconds

Differential to Consider

  • SVT (or atrial flutter) with aberrancy (i.e. WPW)
  • Sinus tachycardia with a bundle branch block

Mimics (typically, wide with rate < 110 bpm) (Hollowell 2005)

  • Hyperkalemia
  • Na Channel Blocking Agent Overdose
  • Accelerate Idioventricular Rhythm (AIVR)

Brugada Algorithm - Rosen's

Diagnosis

There are a number of algorithms that can be used to diagnose VT with the Brugada criteria being the most widely used. The derivation study of this algorithm found a sensitivity of 98.7% and specificity of 96.5%. (Brugada 1991). However, the study was not performed under ED circumstances (patients were taken off cardiac meds prior to EKG, not acute presentations etc). There is no algorithm that has 100% sensitivity or specificity.

Common EKG Findings

  • Atrioventricular (AV) dissociation: atria and ventricles do not activate in a synchronous fashion. The EKG reveals P waves that are not conducted or linked to the QRS complexes.
  • Fusion beats: a hybrid complex resulting from the collision of a supra ventricular and ventricular impulse
  • QRS > 140 msec

Fusion Beat - LITFL

Critical Point: It is safer to assume all wide-complex, regular tachydysrhtyhmias as VT, because the treatment of SVT with aberrancy (the most common alternate diagnosis) as if it is VT is safe but misdiagnosing VT as SVT with aberrancy is potentially life-threatening.

Ventricular Tachycardia EKGs – See CORE EM Website for list

Immediate Management: The primary goal is to convert the patient back to sinus rhythm and then, to address the underlying cause (most likely ischemic heart disease)

Basics: ABCs, IV, O2, Cardiac Monitor and 12-lead EKG

Directed Management

  • Establish patient stability
    • Pulseless: If the patient has no pulse or blood pressure, proceed immediately to defibrillation and chest compressions.
    • Unstable: Evidence of end-organ (brain, heart) malperfusion or hypotension. This may manifest as altered mental status, severe shortness of breath or chest pain. If the patient is unstable, proceed directly to electrical cardioversion
    • Stable: If the patient is stable, you may pursue electrical or chemical cardioversion
  • Electrical Cardioversion
    • Synchronized cardioversion is indicated for unstable patients with VT who have a pulse.
    • Synchronized cardioversion should also be strongly considered in stable patients with VT as it is safe and both more effective and more rapid than chemical cardioversion.
    • Dose: Biphasic 100 – 200 Joules (Monophasic 200 – 360 Joules)
    • Unless patient in extremis, consider sedation /analgesia for procedure
  • Chemical Cardioversion
    • Lidocaine
      • Class 1B antidysrhythmic agent
      • Dose
        • Bolus: 1.0-1.5 mg/kg (repeat 0.5 – 0.75 mg/kg up to total of 3 mg/kg)
        • Infusion: 1-4 mg/min
  • Procainamide
    • Class 1A antidysrhythmic agent
    • Dose: 30-50 mg/min IV until dysrhythmia terminated (max of 18 mg/kg)
  • Amiodarone
    • Dose
      • Bolus: 150 mg IV over 10 min
      • Infusion: 1 mg/min IV X 6 hours then 0.5 mg/min X 18 hours

Critical Point: Although amiodarone is touted as the 1st line drug for chemical cardioversion of VT in ACLS, evidence suggests that it has poor efficacy in terminating VT. (Marill 2006, Tomlinson 2008, deSouza 2013).

Disposition: The vast majority of patients with an episode of ventricular tachycardia should be admitted to the hospital (preferably a high-acuity setting) for further workup with cardiology or electrophysiology. Patients with a properly functioning AICD may be discharged, usually after device interrogation and discussion with cardiology.

Take Home Points

  1. In the patient with a regular, wide-complex tachydysrhythmia, it is safer to treat the patient as VT.
  2. Consider VT mimics when the rate is < 120 bpm.
  3. Although chemical cardioversion is an option, electrical cardioversion should be considered in stable VT as it is safe, more effective and more rapid in returning the patient to sinus rhythm.

References

Hollowell H et al. Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supra ventricular tachycardia with aberrant conduction. Am J Emerg Med 2005; 23: 876-89. PMID: 16291445

Brugada P et al. A new approach to the diagnosis of regular wide complex tachycardia. Circulation 1991; 83: 1649-59. PMID: 2022022

Marill KA et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med 2006; 47: 217-24. PMID:16492484

Tomlinson DR et al. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J 2008; 25: 15-18. PMID: 18156531

deSouza IS et al. Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review. Emerg Med J 2013; PMID: 24042252

Yealy D, Kosowsky JM: Dysrhythmias, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 79: p 1034-63.

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