We discuss a case of ataxia in children and how to approach the evaluation of these pts.

Hosts:
Ellen Duncan, MD, PhD
Brian Gilberti, MD

Introduction

• The episode focuses on ataxia in children, which can range from self-limiting to life-threatening conditions.
• Pediatric emergency medicine specialist shares insights on the topic.

The Case

• An 18-month-old boy presented with ataxia, unable to keep his head up, sit, or stand, and began vomiting.
• Previously healthy except for recurrent otitis media and viral-induced wheezing.
• The decision to take the child to the emergency department (ED) was based on acute symptoms.

Differential Diagnosis

• Common causes include acute cerebellar ataxia, drug ingestion, Guillain-Barre syndrome, and basilar migraine.
• Less common causes include cerebellitis, encephalitis, brain tumors, and labyrinthitis.

Importance of History and Physical Examination

• A detailed history and physical exam are essential in diagnosing ataxia.
• Key factors include time course, recent infections, signs of increased intracranial pressure, and toxic exposures.
• Look for signs such as bradycardia, hypertension, vomiting, and overall appearance.

Diagnostic Workup

• Initial tests include point-of-care glucose and neuroimaging for concerns about trauma or increased intracranial pressure.
• MRI is preferred for posterior fossa abnormalities, but non-contrast head CT is commonly used due to accessibility.
• Lumbar puncture may be needed if meningismus is present.

Treatment Approach

• Treatment depends on the underlying cause:
  • Acute cerebellar ataxia is self-limiting and typically resolves with time.
  • Antibiotics are required for meningitis or encephalitis.
  • Steroids may be useful for cerebellitis and acute disseminated encephalomyelitis (ADEM).
  • Specialist consultations are necessary for severe diagnoses like intracranial masses.

Outcome of the Case Study

• The child had a normal fast T2 MRI and improved during the ED stay.
• Diagnosed with a combination of cerebellar ataxia and labyrinthitis.
• Received myringotomy tubes and experienced no further neurologic changes or otitis media episodes.

Take-Home Points

1. Diverse Etiologies:  Ataxia in children can have various causes that range from self-limiting to life-threatening
2. Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures.
3. Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting.
4. Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities.
5. Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention.

We discuss the approach to diagnosing and managing hypernatremia in the emergency department.

Hosts:
Abigail Olinde, MD
Brian Gilberti, MD

Episode Overview:

• Introduction to Hypernatremia
• Definition and basic concepts
• Clinical presentation and risk factors
• Diagnosis and management strategies
• Special considerations and potential complications

Definition and Pathophysiology:

• Hypernatremia is defined as a serum sodium level over 145 mEq/L.
• It can be acute or chronic, with chronic cases being more common.
• Symptoms range from nausea and vomiting to altered mental status and coma.

Causes of Hypernatremia based on urine studies:

• Urine Osmolality > 700 mosmol/kg
  • Causes:
    • Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses
    • Unreplaced GI Losses: Vomiting, diarrhea
    • Unreplaced Insensible Losses: Burns, extensive skin diseases
    • Renal Water Losses with Intact AVP Response:
    • Diuretic phase of acute kidney injury
    • Recovery phase of acute tubular necrosis
    • Postobstructive diuresis
• Urine Osmolality 300-600 mosmol/kg
  • Causes:
    • Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea
    • Partial AVP Deficiency: Incomplete central diabetes insipidus
    • Partial AVP Resistance: Nephrogenic diabetes insipidus
• Urine Osmolality < 300 mosmol/kg
  • Causes:
    • Complete AVP Deficiency: Central diabetes insipidus
    • Complete AVP Resistance: Nephrogenic diabetes insipidus
• Urine Sodium < 25 mEq/L
  • Causes:
    • Extrarenal Water Losses with Volume Depletion: Vomiting, diarrhea, burns
    • Unreplaced Insensible Losses: Sweating, fever, respiratory losses
• Urine Sodium > 100 mEq/L
  • Causes:
    • Sodium Overload: Ingestion of salt tablets, hypertonic saline administration
    • Salt Poisoning: Deliberate or accidental ingestion of large amounts of salt
• Mixed or Variable Urine Sodium
  • Causes:
    • Diuretic Use: Loop diuretics, thiazides
    • Adrenal Insufficiency: Mineralocorticoid deficiency
    • Osmotic Diuresis with Renal Water Losses: High glucose, mannitol

Risk Factors:

• Patients with impaired thirst response or those unable to access water (e.g., altered or ventilated patients) are at higher risk.
• Important to consider underlying conditions affecting thirst mechanisms.

Diagnosis:

• Initial assessment includes history, physical examination, and laboratory tests.
• Key tests: urine osmolality and urine sodium levels.
• Lab errors should be considered if the clinical picture does not match the lab results.

Management Strategies:

• Calculate the Free Water Deficit (FWD) to guide treatment. 

• Administration routes include oral, NGT, G-tube, or IV with D5W for larger deficits.
• Safe correction rate is 10-12 mEq/L per day or 0.5 mEq/L per hour to avoid cerebral edema.
• Address hypovolemia with isotonic fluids before correcting sodium.

Monitoring and Follow-Up:

• Monitor sodium levels every 4-6 hours.
• Assess urine output and adjust free water administration as needed.
• Admission to ICU for symptomatic patients or those with severe hypernatremia (sodium >160 mEq/L).
• Decision to discharge vs admit is a complicated one that factors in symptoms, etiology, degree of hypernatremia, patient preference, access to follow up, etc.

Take Home Points:

• Hypernatremia is a serum sodium level over 145 mEq/L, with symptoms ranging from nausea to coma.
• It is primarily caused by water loss exceeding intake due to various factors like sweating, vomiting, diarrhea, and renal issues.
• Correcting hypernatremia too quickly can lead to cerebral edema, so a safe correction rate is essential.
• Initial treatment involves calculating the Free Water Deficit and selecting the appropriate administration route.
• Monitor sodium levels frequently and decide on admission or discharge based on symptoms, sodium levels, and patient’s ability to follow up.

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)

Hosts:
Brian Gilberti, MD
Jonathan Kobles, MD

Introduction

1. Background

• • Physiology:
    • Normal range and the significance of deviations (>5.5 mEq/L)
  • Epidemiology:
    • Prevalence of hyperkalemia in the ER
    • ESRD missed HD → ECG, monitor

Causes / Risk Factors

• • Causes
    • Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia

• • High-Risk Medications:

• • • Antibiotics: Bactrim, antifungals

• • • Calcineurin inhibitors

• • • Beta-blockers

• • • ACE/ARB

• • • K+ Sparing diuretics

• • • NSAIDs

• • • Digoxin

• • • SUX – high risks in neuromuscular disease

• • Lab errors, hemolysis in samples
    • VBG vs Chem accuracy 
    • When to repeat a hemolyzed sample 
    • 2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).

Clinical Presentation / eval 

• Symptomatic vs. Asymptomatic:
  • “First symptom of hyperkalemia is death” 
  • If severe, ascending muscle weakness → paralysis 
    • Point at which patients experience symptoms depends on chronicity
      • >7 mEq/L if chronic and can be lower if acute
  • Hyperkalemia can be a cause of non-specific GI symptoms
• EKG Changes:
  • ECG findings may be the first marker the ER doc gets that something is wrong
  • Typical changes: 
    • Peaked T-waves, shortened QT
    • Lengthening of PR interval and QRS duration 
    • Bradycardia / Junctional rhythm
      • Hyperkalemia can produce bradycardia without other ECG findings
    • Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017)
  • Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG
    • Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998)
  • ECG changes are not linear, there is no exact association between K+ levels and ECG changes
  • ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs)
    • Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms
  • BRASH Syndrome
    • Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels. 
• Labs
  • Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice)
  • Consider evaluation for adrenal insufficiency
  • Waiting for labs may not be an option
    • Renal dysfunction + consistent ECG findings → prompt treatment before chem results
    • Realistically 2 hours to get back chemistry in most settings ≈ eternity

Management in the ER

• Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia

• A. Acute Management Strategies:
  • Cardiac protection with calcium
    • 1g over 5-10 mins
      • Lasts 30-60 mins, may have to redose 
      • Dose considerations if on digoxin 
      • AEs: Calciphylaxis and hypercalcemia
        • Fast pushes can result in hypotension, arrhythmia
    • Calcium chloride vs calcium gluconate
    • Caution in patients taking Digoxin
  • IVF choice – NS vs LR
    • Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL
  • Shifting potassium: 
    • insulin/glucose
      • 5 units vs 10 units 
        • 5 similar effect, less hypoglycemic episodes (LaRue 2017)
        • If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume 
      • Decrease but about 0.5-1.2 mEq/L
      • Effect starts 10-20 mins after administration and can last 4-6 hours
    • Albuterol
      • 10-20 mg over 10 mins (NB: higher dose than for asthma)
      • Peak effect at 90 mins
      • Decreases by 0.5 – 1.0 mEq/L alone
        • With insulin, ~1.2 mEq/L, additive effect 
    • Bicarbonate
      • Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue 
        • May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss
      • Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift.
  • Removal: 
    • Lokelma (Sodium Zirconium cyclosilicate)
      • Luckily residents have never had to use Kayexalate
      • Can start working in 1-2 hours of administration 
      • 0.37 mEq/L reduction at 4 hours after 10 g
      • Not a magic bullet in patients who need dialysis
    • Diuretics
      • No studies that demonstrate effectiveness in this ED setting
        • May be effective in patients with normal renal function
      • If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K
      • Nephron BOMB
        • Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex)
        • Thiazide (500-1000 mg IV chlorothiazide or 5-10 mg metolazone)
        • +/- Acetazolamide
        • +/- Fludrocortisone
          • May help stimulate the kidneys to secrete potassium
          • Primarily helpful in patients with mineralocorticoid deficiencies
    • Dialysis
      • Involve renal early because it takes a while to call in an HD nurse sometimes 
      • If no access and emergent HD is required → HD catheter placement
  • Strategies for suspected Brash syndrome
    • Epinephrine/Levo (if hypotensive/bradycardic)
    • Calcium gtt 
• Disposition/wrap up
  • Many factors at play here – patient preference, access, degree of hyperkalmia, identifiable / corrected cause 

Take Home points

• • Hyperkelamia causes can be put into three categories, pseudohyperkalemia, due to redistribution, and due to total body increase in potassium. Check out the show notes for a more complete list
  • Hyperkalemia can be difficult to pick up on before the labs come back because it can lurk without symptoms or even ECG changes
  • If a patient does have ECG changes, they may not follow that linear pattern that is traditionally taught and ECGs can be poorly sensitive. Now, if you do see changes, the ones that are more commonly associated with adverse events are QRS widening, junctional rhythm, and bradycardia
  • Treatment is a numbers game, calcium for cardiac stabilization can last just 30-60 minutes, insulin will be the fastest way to shift potassium back into cells, but be mindful that 10 units is associated with increased episodes of hypoglycemia whereas 5 units may have the same effect in reducing potassium. And albuterol is at a much higher dose than what is given for asthma 
  • Lokelma is now a pillar of treatment for removal of potassium. 
  • Diuretics with the goal of kiuresis may have a role in the oliguric patient, and increased doses along with other agents may buy time in patients with severe hyperK when HD is not readily available 
  • Involve renal early if you think that the patient will require HD

This week we discuss 3 articles recently reviewed in our conference - LOV-ED study, Validation of Step-By-Step and Therapeutic Hypothermia.

Take Home Points

1. The step-by-step approach to managing febrile infants is a reliable decision instrument to identify patients at low risk for invasive bacterial infections. Caution in the group of patients 22-28 days of age.
2. The LOV-ED study shows an association between employing a lung-protective ventilation strategy in the ED and decreased complications from mechanical ventilation. Best available evidence says that we should embrace this approach in the ED.
3. Cooling to 33 degrees is no better than cooling to 36 degrees. However, shooting 36 degrees is more difficult than we may have thought. We have to continue to be vigilant about maintaining patients in the target temperature range and avoiding fever.

The Step-By-Step Algorithm

Lung-Protective Ventilation Protocol (LOV-ED Study)

Read More

The SGEM: SGEM #171: Step-by-Step Approach to the Febrile Infant

REBEL EM: The Benefit of Lung Protective Ventilation in the ED Should Be LOV-ED

Taming the SRU: A Crack in the Ice? An In-Depth Breakdown of the TTM Trial

References

Gomez B et al. Validation of the Step-by-Step Approach in the Management of Young Febrile Infants. Pediatrics. 2016 Aug.  PMID: 27382134

Fuller BM et al. Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial. Ann Emerg Med 2017. PMID: 28259481

Bray JE et al. Changing target temperature from 33oC to 36oC in the ICU management of out-of-hospital cardiac arrest: a before and after study. Resuscitation 2017; 113: 39-43. PMID: 28159575

This week we delve into the argument for cardioversion in recent-onset AF as well as the logistics of getting it done.

Read More

Core EM: Podcast 64.0 – Rate Control in AF

Core EM: Recent Onset Atrial Fibrillation

Core EM: 30-Day Outcomes After Aggressive AF Management in the ED

The SGEM: SGEM#88: Shock Through the Heart (Ottawa Aggressive Atrial Fibrillation Protocol

References

Nuito I et al. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA 2014; 312(6): 647-9. PMID: 25117135

Stiell IG et al. Association of the Ottawa aggressive protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation and flutter. Can J Emerg Med 2010; 12(3): 181-91. PMID: 20522282

Stiell IG et al. Outcomes for Emergency Department Patients with Recent-Onset Atrial Fibrillation and Flutter Treated in Canadian Hospitals. Ann Emerg Med 2017. PMID: 28110987

This week we discuss the rare but life-threatening methemoglobinemia with a focus on recognition and use of the antidote.

Take Home Points

• MetHb –emia occurs as a results of various medications including amyl nitrite, dapsone, nitroprusside, phenazopyridine, sodium nitrite and topical anesthetics like benzocaine
• Patients will present with cyanosis, short of breath, fatigue, dizziness, weakness and ultimately CNS depression and death at higher concentrations.
• If you have a cyanotic/hypoxic patient that does not respond to supplemental oxygen, be concerned for MetHb and send a co-oximetry panel.
• If the level is <25% and the patient is asymptomatic you can observe, but if the level is >25% or the patient is symptomatic, you will treat with the antidote methylene blue given as a bolus of 1-2 mg/kg over 5 minutes
• And as always, make sure to call your local poison center to get your toxicologists involved. They can help with dosing, and they are also an important player of the public health component in cases such as these, to make sure this is an isolated incident and we don’t have a repeat of the 11 blue men situation.

Price DP. Chapter 127. Methemoglobin Inducers. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 9e New York, NY: McGraw-Hill; 2011. Accessed April 19, 2017.

Methemoglobinemia Signs and Symptoms

Methemoglobinemia Treatment

This week we do a brief review on recognizing CO monoxide poisoning and expertly managing it.

Take Home Points

• CO poisoning happens most often from common are accidental exposures from faulty home heaters, camp stoves and indoor use of gas powered generators, structure fires and intentional exposure like in suicide attempts.
• Patients with a mild exposure will present with symptoms like headache, nausea, vomiting, dizziness, vision blurring, palpitations, confusion or myalgias.  More severe exposures may produce Altered mental status. seizures, coma, dysrythmias, myocardial ischemia, metabolic acidosis, syncope and vital sign abnormalities including hypotension and, eventually, cardiac arrest.
• To help distinguish the vague symptoms of a patient who may have chronic exposure ask about things like whether symptoms improve in different environments or whether they have sick pets, as human viral illness generally don’t affect our dogs and cats.
• If you’re concerned about CO send a co-ox panel.  City dwellers may have a baseline carboxyhemoglobin of 1-2% and smokers around 6-10% but others should really have no carboxyhemoglobin.
• Treatment is supplemental O2 which can be stopped when symptoms improve.  For severe symptoms and for pregnant patients, consider hyperbarics to prevent long term sequelae and to protect the fetus.  As always, consider discussing the case with your local poison center to help decide whether a patient warrants transfer for hyperbarics.

LITFL: Carbon Monoxide Poisoning

EMCrit: Podcast 122 – Cardiac Arrest after the Toxicology of Smoke Inhalation with Lewis Nelson

FOAMcast: Episode #1: EMCrit Episode #122 – Cyanide and Carbon Monoxide Toxicity

Nelson LS, Hoffman RS: Inhaled Toxins, 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) 159: p 2036-2045.

Tomaszewski C. Chapter 125. Carbon Monoxide. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 9e New York, NY: McGraw-Hill; 2011. Accessed April 19, 2017.

This week we discuss the identification, prevention and treatment of local anesthetic systemic toxicity.

LITFL: Local Anesthetic Toxicity

Wiki EM: Local Anesthetic Systemic Toxicity

References:

Schwartz DR, Kaufman B. Local Anesthetics. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. eds. Goldfrank’s Toxicologic Emergencies, 10e New York, NY: McGraw-Hill; 2015. Link

Neal JM et al, American Society of Regional Anesthesia and Pain Medicine. American Society of Regional Anesthesia and Pain Medicine checklist for managing local anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med 2012;37:16–8. PMID: 22189574

Cao D et al. Intravenous lipid emulsion in the emergency department: a systematic review. J Emerg Med 2015; 48(3): 387-97. PMID: 25534900

This week we talk about mammal bites - dogs, cats and humans - with a focus on wound closure, antibiotics and rabies prophylaxis.

EM:RAP: Animal Bites – A Short Board Review

EM:RAP: Episode 107 Mammalian Bites

Rebel EM: Medical Myths in the Management of Dog Bites

CDC: Rabies Info

References

Chen E et al. Primary Closure of Mammalian Bites. Acad EM 2000; 7(2): 157- 162. PMID: 10691074

Paschos NK et al. Primary closure versus non-closure of dog bite wounds. A radomised controlled trial. Injury 2014 45(1): 237-40. PMID: 23916901

Medeiros IM, Saconato H. Antibiotic prophylaxis for mammalian bite (Review). Cochrane Database of Systematic Reviews 2008 (3); PMID: 11406003

This week we cover a workshop from our conference on CNS infections focusing on meningitis.

CSF Analysis (LITFL)

EM Lyceum: Viral Meningitis “Answers”

EM RAP: Meningitis

LITFL: Bacterial Meningitis

LITFL: CSF Analysis

The NNT: Glucocorticoid Steroids for Bacterial Meningitis

References

Attia J et al. Does this adult patient have acute meningitis. JAMA 1999; 281(2): 175-81. PMID: 10411200

Brouwer MC et al. Corticosteroids for acute bacterial meningitis (review). Cochrane Database Syst Rev 2015. PMID: 26362566

Cooper DD, Seupaul RA. Is adjunctive dexamethasone beneficial in patients with bacterial meningitis? Ann Emerg Med 2012; 59(3): 225-6. PMID: 22088494

de Gans J et al. Dexamethasone in adults with bacterial meningitis. NEJM 2012; 347(20): 1549-57. PMID: 12432041

Hasbun R et al. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. NEJM 2001; 345(24): 1727-34. PMID: 11742046

Sakushima K et al. Diagnostic accuracy of cerebrospinal fluid lactate for differentiating bacterial meningitis from aseptic meningitis: a meta-analysis. J Infection 2011; 62: 255-62. PMID: 21382412

Tunkel AR et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis 2004; 39: 1267-84. PMID: 15494903

This week we discuss some of the many dialysis-related emergencies we frequently see in the ED.

Take Home Points

1. On any dialysis patient, make sure to do a good assessment of their access site.  If it’s a fistula, assess for a thrill, for any warmth/induration/erythema and make sure they have distal sensation and perfusion.  If it’s a catheter, evaluate for any signs of infection—so warmth, erythema or discharge.
2. Bleeding is a big concern. If the patient is bleeding from their access, start with direct pressure to the bleeding site, then move on to topical thrombotic agents and if needed throw a figure 8 stitch with a 5-0 proline on a non-cutting needle.
3. Peritoneal dialysis patients are at risk for bacterial peritonitis.  In a PD patient that appears infected, get a peritoneal fluid sample and start antibiotics
4. Dialysis patients are susceptible to dialysis disequilibrium syndrome which can present as altered mental status, focal neurological deficits or even frank coma or seizures after dialysis.  Make sure to consider a broad differential in these patients and start with a solute load such as an amp or two of D50 while starting your work up.

Core EM: Hyperkalemia

Core EM: Episode 7.0 – Hyperkalemia + Rate Control in AFib

Al Sacchetti: ED Repair of Bleeding Dialysis Shunt

EM: RAP: Episode 107 – Dialysis Emergencies

EMBlog Mayo Clinic: How to Stop a Post-Dialysis Site Bleeding

emDocs: Managing Fistula Complications in the Emergency Department

This week we discuss a recent article in Annals of EM on contrast induced nephropathy and whether the phenomena is real or dogma.

ACR Table on CIN – FOAMCast

FOAMCast: Episode 65 – Contrast Induced Nephropathy and Genitourinary Trauma

REBEL EM: Contrast Induced Nephropahty: Fact or Myth

Core EM: Acute Kidney Injury is not Associated with IV Contrast Use in the ED

EM Lit of Note: Punching Holes in CIN

EMCrit: Do CT Scans Cause Contrast Nephrophathy?

EM Lit of Note: Punching Holes in CIN

EM Docs: Contrast-Induced Nephropathy – Confounding Causation

This week we dive into acute rhinosinusitis focusing on diagnosis and discussing the absence of utility for antibiotics in most patients.

Take Home Points

1. Sinusitis is a clinical diagnosis. Patients typically present with purulent nasal discharge and facial pain or other URI symptoms.
2. The vast majority of patients with acute rhino sinusitis will be viral in nature and will not benefit from antibiotics
3. Patients with prolonged symptoms, more than 7-10 days, without improvement or continued fevers past 2-3 days should be considered for antibiotic treatment as should those who are immunocompromised.

Show Notes

Melio FR, Berge LR. Upper Respiratory Tract Infections, 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) 75: p 965-79.

The NNT: Antibiotics for Clinically Diagnosed Acute Sinusitis in Adults

The NNT: Antibiotics for Radiologically-Diagnosed Acute Maxillary Sinusitis

Lemiengre MB et al. Antibiotics for clinically diagnosed acute rhinosinusitis in adults. Cochrane Database Syst Rev. 2012. PMID: 23076918

Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev. 2008. PMID: 18425861

We go over the essential and complex topic of vasopressors in the ED.

Hosts:
Brian Gilberti, MD
Catherine Jamin, MD

Introduction

• Host: Brian Gilberti, MD
• Guest: Catherine Jamin, MD
  • Associate professor of Emergency Medicine at NYU Langone Health
  • Vice Chair of Operations
  • Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine
• Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED

What Are Vasopressors and When to Use Them

• Two primary mechanisms to increase blood pressure:
  1. Increasing systemic vascular resistance via vasoconstriction
  2. Increasing cardiac output via augmenting inotropy and chronotropy
• Indicators for vasopressor use:

• • MAP <65, systolic BP <90, or significant drop from baseline BP
  • Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate
  • Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients)

Commonly Used Vasopressors in the ED

• Norepinephrine
• Epinephrine
• Vasopressin
• Phenylephrine

Norepinephrine

• Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy)
• Starting Dose: 10 mcg/min, titrate to MAP >65
• Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min
• Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic)
• Pros: Can be infused peripherally via large bore IV

Vasopressin

• Mechanism: Activates V1a receptors causing vasoconstriction
• Dose: Fixed, non-titratable dose of 0.04 units/min
• Situational Preference: Second-line in septic shock
• Concerns: Potential for peripheral ischemia

Phenylephrine

• Mechanism: Stimulates alpha-1 receptors causing vasoconstriction
• Starting Dose: 100 mcg/min, titrate to MAP >65
• Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation
• Concerns: Increases afterload, can worsen low cardiac output states

Epinephrine

• Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors
• Starting Dose: 5-10 mcg/min, titrate to MAP >65
• Situational Preference: Anaphylactic shock, septic cardiomyopathy
• Limitations: Can induce tachycardia, may elevate lactate levels

Escalation Strategy in Refractory Shock

• Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine
• Consider POCUS, lactate, central venous saturation, and acid-base status

Peripheral Pressors

• Can safely be administered peripherally via large bore IVs in proximal upper extremity
• Sites: Cephalic or basilic veins
• Adverse Events: Low at 1.8% based on meta-analysis
• Actions in case of extravasation: Phentolamine injection, nitroglycerin paste

Push-Dose Pressors

• Primarily Phenylephrine (peri-intubation, during procedures)
• Also Epinephrine for peri-code situations
• Doses: Epi – 5-20 mcg every 2-5 min

Take-Home Points

• Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine.
• Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65
• Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock.
• Vasopressin is commonly the second we reach for in most of these scenarios
• Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock
• Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output
• The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access
• Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient

Additional References

• Importance of RUSH (Rapid Ultrasound in SHock) exam for diagnosis and treatment planning: https://emcrit.org/rush-exam/

This week we discuss the ED management of anterior and posterior epistaxis.

Take Home Points

1. The first step is managing epistaxis is solid pressure.  This means holding a tight pinch just distal to the nasal bones and hold, without peaking, for at least 5 minutes.  This will stop a good deal of the bleeding.
2. If you need to do more, start by soaking gauze in either oxymetazoline or epinephrine, mix in some lidocaine to help with anesthesia, pack the nare with that and add on some compression.  Hope fully this stops the bleeding enough that you can see a good bleeder and perform cautery.
3. Third line of treatment would be to try some soaked gauze, but this time with TXA. Can’t hurt to try!
4. And then last resort is of course packing. Here make sure the patient is anesthetized with some lidocaine, lubricate the packing well and apply horizonally, no vertically as we are often tempted.

Epistaxis Tray

Show Notes

LITFL: Epistaxis

Core EM: Podcast 18.0 – Influenza Testing and Epistaxis

REBEL EM: Do Patients with Epistaxis Managed by Nasal Packing Require Prophylactic Antibiotics

EM Lyceum: Epistaxis, “Answers”

Zahed R et al. A new and rapid method for epistaxis treatment using injectable form of tranexamic acid topically: a randomized controlled trial. Am J Emerg Med 2013; 31: 1389-92. PMID: 23911102

This week, we review a simplified approach to determining the rhythm on an EKG with a tachydysrhythmia.

Take Home Points

1. When looking at a tachy rhythm that isn’t sinus tach, quickly differentiate by determining if the QRS complexes is narrow or wide and then determine if the rhythm is regular or irregular. This approach quickly drops the rhythm into 1 of 4 boxes and makes rhythm determination much easier
2. Each of those 4 categories has a small set of rhythms included. Narrow and irregular – AF, Aflutter with variable block or MFAT. Narrow and regular – SVT or Aflutter. Wide and irregular – Torsades, VF, AF with aberrancy or a BBB. Wide and regular – VTach, SVT with aberrancy or SVT with a BBB.
3. If you see wide and regular, the top 3 diagnoses are VT, VT and VT. Assuming VT and treating for that will almost never send you astray

Read More

EM: RAP: Episode 84 – Tachycardia

Core EM: A Simplified Approach to Tachydysrhythmias

Core EM: Atrioventricular Nodal Reentry Tachycardia

Core EM: Ventricular Tachycardia

Core EM: Recent-Onset Atrial Fibrillation

Simplified Approach to Tachydysrhythmias Diagnosis

Tachydysrhythmias Therapeutic Algorithm

Torsades de Pointes

Torsades de Pointes

This week we discuss two recent journal articles - the POKER trial and the ketorlac analgesic ceiling

Take Home Points

1. The POKER trial examined the difference between propofol and ketofol when it comes to adverse respiratory events.  They found no significant difference between the groups.  Given the increased risk of medication errors using two medication instead of one, you may want to avoid the mixture.
2. Ketorolac has an analgesic ceiling effect lower than you may have thought.  When comparing IV doses of 10mg, 15mg and 30mg they found no difference in analgesic effect.  Given the risks of side effects may increase with higher doses, you may want to stick to the lower 10mg dose.

RebelEM: The POKER Trial: Go All in on Ketofol?

St. Emlyn’s: JC: Is Ketofol with the hassle?

Core EM: Propofol vs. Ketofol in PSA

EM: RAP: Just Enough Ketorlac

RebelEM: The Ketorolac Analgesic Ceiling

Core EM: Parenteral Ketorlac Dosing

Propofol or Ketofol for Procedural Sedation and Analgesia in Emergency Medicine-The POKER Study: A Randomized Double-Blind Clinical Trial. PubMed ID: 27460905

Comparison of Intravenous Ketorolac at Three Single-Dose Regimens for Treating Acute Pain in the Emergency Department: A Randomized Controlled Trial. PubMed ID: 27993418

Do patients with 1st trimester bleeding need to get anti-D immunoglobulin if they're Rh negative? We dive into the topic this week.

Take Home Points

1. An Rh negative woman can become alloimmunized to Rh antigen if exposed to blood from an Rh positive fetus. Theoretically, this alloimmunization can occur even in early pregnancy
2. While anti-D immune globulin has clearly been shown to be beneficial in preventing alloimmunization in 2nd and 3rd trimester pregnancy, there is no evidence supporting use specifically in the 1st trimester
3. Despite the absence of evidence, RhoGam administration has become routine in many places. At this time, it’s advisable to follow local practice patterns regarding which patients should be given RhoGam.

References

ACOG Practice Bulletin. Prevention of Rh D Alloimmunization. Int J Gynaecol Obstet 1999; 66(1): 63-70. PMID: 10458556 Recommendations reaffirmed in 2016

Hahn SA et al. Clinical Policy: Critical Issues in the Initial Ealuation and Management of Patients Presenting to the Emergency Department in Early Pregnancy. Ann Emerg Med 2012; 60(3): 381-419. PMID: 22921048

Hannafin B et al. Do Rh-Negative Women with First Trimester Spontaneous Abortions Need Rh Immune Globulin. Am J Emerg Med 2006; 24: 487-9. PMID: 16787810

Visscher RD, Visscher HC. Do Rh-Negative Women with an Early Spontaneous Abortion Need Rh Immune Prophylaxis? Am J Obstet Gynecol 1972; 113(2): 158-65. PMID: 4623673

This week we discuss three common complications of delivery: cord prolapse, nuchal cord and shoulder dystocia.

Take Home Points

1. If you have a patient with a cord prolapse, elevate the presenting part to take pressure off the cord, place the patient in trendelenburg and fill the bladder. Then, redline it to the OR for a c-section.
2. Nuchal cord is common but likely not too dangerous. Just gently unwrap the umbilical cord and the fetus should be just fine
3. Shoulder dystocia isn’t common but it’s a true emergency as the fetus can suffer severe hypoxia or death. You’ve got a bout 5 minutes to deliver. Immediately call for help from OB, place a foley catheter to drain the bladder and place the mom’s legs so that her knees are pressed into her chest. This helps to open up the pelvis and give more room for the shoulder to be delivered. If that doesn’t work, you can try the wood’s screw maneuver or place the mom on all 4s. If you’ve got an OR ready, pushing the head back in is also an option but only if you have an OR available

Read More

Core EM: Shoulder Dystocia

emDocs: The Complicated Delivery: What You Can Do

Del Portal DA et al.  Emergency department management of shoulder dystocia.  J Emerg Med. 2014 Mar;46(3):378-82. PMID: 24360351

This week we look at TBI and discuss some of the pitfalls and pearls in early management of traumatic ICH.

Take Home Points

1. If you get a heads up from EMS on an incoming trauma, take the lead time you get to clearly delineate everyone’s roles to help ensure the resuscitation runs smoothly.
2. In the severe TBI patient, the key is in preventing secondary injury to the brain. We do this by guarding against hypoxia, hypercarbia, hypotension and aspiration. Max your pre-ox, get the ETT in quickly to prevent oxygenation and ventilation issues and keep the head up if possible
3. Hypotension is rarely seen in isolated head trauma. If the patient is or becomes hypotensive, reassess for any sources of hemorrhagic shock that may have been missed and consider whether the meds you gave may have caused the problem.
4. Hypertension is much more common and despite extensive research, we haven’t shown that dropping the patient to normal levels is beneficial. Keeping the SBP < 180 seems reasonable but check your local protocol as well.
5. If the patient’s ICP spikes or your concerned about herniation, administer mannitol or hypertonic saline and get your neurosurgeon to the bedside since the patient is gonna need decompression
6. Finally, make sure to reverse any anticoagulant the patient may have on board as this will hopefully prevent hematoma expansion.

Read More

emDocs: Roc Rocks and Sux Sucks! Why Rocuronium is the Agent of Choice for RSI

Core EM: Podcast 31.0 – Rocuronium vs. Succinylcholine

Core EM: Intensive Blood Pressure Lowering in Intracerebral Hemorrhage (ATACH-2 Trial)

PulmCCM: Hyperosmolar Therapy for Increased Intracranial Pressure (Review)

EM Cases: Episode 89 – DOACs Part 2: Bleeding and Reversal Agents

Hopper AH. Hyperosmolar therapy for raised intracranial pressure. NEJM 2012; 367(8): 746-52. PMID: 22913684

Wang X et al. Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials. J Anesth 2014; 28(6): 821-7. PMID: 24859931

Zeiler FA et al. The ketamine effect on ICP in traumatic brain injury. Neurocrit Care 2014; 21(1): 163-73. PMID: 24515638

This week we discuss a bit about back pain and specifically, lumbar radiculopathy with a focus on causes and red flags.

Read More

St. Emlyn’s: Back to Basics: Back Pain in the ED

Edlow JA. Managing nontraumatic acute back pain. Ann Emerg Med 2015; 66: 148-53. PMID: 25578887

Goldberg H et al. Oral steroids for acute radiculopathy due to a herniated lumbar disk: a randomized clinical trial. JAMA 2015; 313 (19): 1915-23. PMID: 25988461

Friedman BW et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: a randomized clinical trial. JAMA 2015; 314 (15): 1572-80. PMID: 26501533

This week we discuss the ED management of seizures focusing on treatment and workup particularly of a 1st seizure episode.

Take Home Points

1. Get a detailed history to tease out whether the patient had a seizure or a syncopal event. Regardless, get an EKG on 1st time seizures in case it was actually syncope.
2. BZDs are first line therapy for seizure termination. If you don’t have IV access, go with 10 mg of midazolam or 2-4 mg of lorazepam IM
3. Always review the 5 main categories for causes of seizures in order to make sure you’re not missing anything. Those categories once again are vital sign abnormalities, CNS infections, toxic/metabolic issues, CNS space occupying lesions including masses and bleeds and finally epilepsy.
4. In patients with a first time seizure without a particular cause and return to baseline neurologic status, there’s unlikely to be any benefit to a NCHCT or to starting an AED. Scheduling close follow up with a neurologist is very reasonable. The key is to do a thorough examination and make sure you’re not missing a subtle abnormality.
5. Finally, in status epilepticus hit the patient with 2-3 hefty doses of BZDs and if the seizure is still ongoing, strongly consider moving to propofol and intubation in order to rapidly control the seizure activity.

Read More

Core EM: Parenteral Benzodiazepines

LITFL: Seizure

EMCrit: Podcast 155 – Status Epilepticus with Tom Bleck

First10EM: Management of Status Epilepticus in the Emergency Department

Huff SJ et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Seizures. Ann Emerg Med 2014; 43(5): 605-25. PMID: 15111920

This week, the podcast features a talk on Visualization given at the All NYC EM conference in October 2016.

Read More

EMCrit: EHPR Part 5: Using Mental Practice and Visualization Exercises by Mike Lauria

This week we feature a short primer on penetrating chest trauma focusing on circulation first over airway and breathing.

Take Home Points

1. Don’t rush to the airway. In most situations, you have some time so resuscitate before you intubate. Give blood products and get the BP up a bit to give yourself a little better physiologic situation in which to intubate.
2. Start your massive transfusion immediately if the patient is shocked. There’s always a delay in getting products but the earlier you start, the shorter the delay.
3. Include US in your primary survey. Your E-FAST should start with the cardiac window, then go to the lungs and then, finally, the abdomen. This order focuses on finding pathology you can fix immediately.
4. If the patient is shocked and peri-arrest or recently lost vitals, open the chest and look for a fixable injury. Start with opening the pericardium to relieve tamponade, identify and repair cardiac wounds and cross clamp the aorta.

Read More

Larry Mellick: Open Thoracotomy Video

EMCrit: Podcast 081 – An Interview on Severe Trauma with Karim Brohi

LITFL: Penetrating Chest Trauma

EM:RAP: How to Crack the Chest

EM: RAP: Stabbed in the Chest

We discuss the diagnosis and management of septic arthritis in the pediatric population.

Hosts:
Brian Gilberti, MD
Ellen Duncan, MD

• General

  • Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis

  • Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition.

  • Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint.

• Workup

  • Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain.

  • Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation.

  • Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach.

  • The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000.

1 criterion met = 3% probability of septic arthritis

2 criteria met = 40% probability of septic arthritis

3 criteria met = 93% probability of septic arthritis

4 criteria met = 99+% probability of septic arthritis

• If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available.

• Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies.

• Management

  • Empiric antibiotic therapy should target the most likely organisms and should not be delayed. Antibiotics may be narrowed once culture results are obtained.

  • The choice of antibiotics is dependent on the age group, with specific combinations suggested for neonates, children between 1 month and 4 years, and children aged 5 and older.

  • Cultures are only positive in 50-60% of cases. Synovial fluid PCR studies can help narrow antibiotic treatment.

• Take Home Points

  • Limp in the pediatric population can commonly be transient synovitis but we should always consider septic arthritis

  • Some clues in the history and physical that would point you towards septic arthritis include fever, refusal to bear weight, and limited range of motion on exam

  • We are going to have to get labs, including CBC, inflammatory markers, and preoperative labs, along with an XR and possibly an ultrasound

  • Kocher criteria is one tool that can help us determine if this is a patient that requires a joint tap.

  • Arthrocentesis is the gold standard for diagnosis, but antibiotics should be started promptly if the diagnosis is suspected.

  • The choice of antibiotics is dependent upon age group.

    • Neonates get vanc/cefepime, kids 1-4 yo get vanc / ceftriaxone

    • Older than 5 yo get vancomycin

      • Add ceftriaxone to them if patient has sickle cell disease, are immunocompromised, or Lyme or STI are suspected

  • Always cross check with institutional preferences / guidelines when choosing antibiotics

This week we discuss facial trauma and the disasters it can cause to your airway management.

Take Home Points

1. In a patient with significant head and neck trauma, EACH step of the airway management can be more difficulty. BVM may be hard, LMA may be hard, RSI may be hard, so don’t be afraid to ask for help early.
2. Decide whether the patient has an actual obstruction of their airway. If they are obstructed above the larynx, don’t bother with your usual airway maneuvers, go directly to the surgical airway.
3. When you do attempt RSI, have double suction and multiple airway techniques set up. This is the time to have your friend standing at your side, scalpel in hand and ready to move directly down the difficult airway algorithm if trouble arises.
4. Finally, consider keeping the patient awake and preserving their own respiratory drive as it may give you more time to secure the airway.

Read more

LITFL: Facial Trauma

LITFL: Airway in Maxillofacial Trauma

EMCrit: Real Surgical Airway

This week we discuss the OXYGEN-ICU trial exploring the effect of excess oxygen on ICU mortality.

Read More

The Bottom Line: Normal Oxygen Versus Hyperoxia in the Intensive Care Unit (ICU) (OXYGEN-ICU)

ScanCrit: Avoid the Oxygen Reflex

REBEL EM: July 2015 REBEL Cast

References

Giradis M et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. 316(15):1583-1589. 2016. PMID: 27706466

Meyhoff CS et al. PROXI Trial Group. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA. 2009; 302(14):1543-1550. PMID: 19826023

Stub D et al. AVOID Investigators. Air versus oxygen in ST-segment-elevation myocardial infarction. Circulation. 2015;131(24):2143-2150. PMID: 26002889

This week the podcast features a talk Jenny Beck-Esmay gave at the 11th All NYC EM Conference entitled "Give TXA Now!"

Take Home Points

1. Giving TXA provides a significant mortality benefit to the any trauma patient requiring massive transfusion with an NNT = 7 for mortality
2. TXA must be given early. Give within 1 hour of injury if possible but the benefit remains up to 3 hours out
3. TXA administration: 1 gram as a bolus followed by 1 gram over the next 8 hours

Show Notes

Intensive Care Network: Karim Brohi on TXA in Trauma

EMCrit: Podcast 67 – Tranexamic Acid (TXA)

Core EM: CRASH-2 Tranexamic Acid in Major Trauma

References

CRASH-2 trial collaborators. Effects of tanexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a ransomised placebo-controlled trial. Lancet 2010; 376: 23-32. PMID: 20554319

Guerriero C et al. Cost-effectiveness analysis of administering tranexamic acid to bleeding trauma patients using evidence from the CRASH-2 trial. PLoS One 2011; 6(5): e18987. PMID: 21559279

Ker K et al. Avoidable mortality from giving tranexamic acid to bleeding trauma patients: an estimation based on WHO mortality data, a systematic literature review and data from the CRASH-2 trial. BMC Emerg Med 2012; 12:3. PMID: 22380715

Morrison JJ et al. Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) Study. Arch Surg 2012; 147 (2): 113-9. PMID: 22006852

This week we discuss Lisfranc injuries with a focus on a diagnostic pathway and management.

Take Home Points

1. A Lisfranc injury is a midfoot injury that results in displacement of one or more of the metatarsal bones from tarsus. 
2. XR will show widening of the space between the 1st and 2nd metatarsals. Getting contralateral XR may help you identify this.
3. Even if you don’t see that widening on the XR, the patient could still have a Lisfranc injury. If they cannot walk due to pain, get a weight bearing XR or CT scan to look further.
4. Once the injury is identified, the patient must be strict non-weightbearing. Place them in a posterior splint and get orthopedics involved either in the ED or for prompt follow up as the patient will probably need surgery.

Foot Bones (Google Images)

Normal Foot X-ray Series (Case courtesy of Dr Andrew Dixon, Radiopaedia.org. From the case rID: 36688)

Lisfranc Injury AP X-ray (Radiopaedia Image #1: Case courtesy of Dr Alexandra Stanislavsky, Radiopaedia.org. From the case rID: 10919)

Divergent Lisfranc Injury

Read More

LITFL: Eponymous Fractures

Radiopaedia: Lisfranc Injury

Core EM: Compartment Syndrome

This week we do a little spaced repetition on adrenal insufficiency and then discuss fluid responsiveness and resuscitation.

Read More

Marik PE. Fluid responsiveness and the six guiding principles of fluid resuscitation. Crit Care Med 2016. PMID: 26571187

LITFL: Adrenal Insufficiency

EMCrit: Podcast 64 – Assessing Fluid Responsiveness with Dr. Paul Marik

Core EM: Adrenal Crisis

Core EM: Episode 15.0 – Adrenal Crisis

References

Cavallaro F et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systemic review and meta-analysis of clinical studies. Intensive Care Med. 2010:36(9):1475-83. PMID: 20502865.

Cecconi M et al. Fluid challenges in intensive care: the FENICE study: A global inception cohort study. Intensive Care Med. 2015:41(9):1529-37. PMID: 26162676.

Landesberg G et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J. 2012:33(7):895-903. PMID: 21911341.

Lee CV et al. Development of a fluid resuscitation protocol using inferior vena cava and lung ultrasound. J Crit Care. 2016:31(1):96-100. PMID: 26475100.

Marik PE. Noninvasive cardiac output monitors: a state-of the-art review. Cardiothorac Vasc Anesth. 2013:27(1):121-34. PMID: 22609340.

This week we review some pearls in the diagnosis and management of acid reflux.

Take Home Points

1. GERD pain can mimic or co-exist with the more deadly causes of chest pain.  Be sure to consider all the serious causes of chest pain, get an EKG and maybe a chest XR while you go about symptom management.
2. Respond to a treatment doesn’t prove a diagnosis.  GERD pain may get better with nitro and ACS pain may get better with a GI cocktail.  Keep an open mind while seeing these patients.
3. Standard treatment for GERD includes an antacid and H2 blocker and maybe a PPI.  Keep in mind that a PPI takes a while to work, so be sure to give something faster acting in the ED
4. And last, for these patients, take those few extra minutes for some counseling on lifestyle modifications.  All medications come with side effects, so be sure to address things like diet, smoking and weight loss while you have a captive audience.

This week we dive into the controversies surrounding the PESIT study looking at the prevalence of PE in admitted patients with syncope

Read More

EMLit of Note: The Impending Pulmonary Embolism Apocolypse

St. Emlyn’s: JC – Prevelance of PE in Patients with Syncope

EM Nerd (EMCrit): The Case of the Incidental Bystander

Pulm CCM: PESIT Investigators: The Incidence of PE in Those Hospitalized Following First Syncope

References

Hutchinson BD et al. Overdiagnosis of pulmonary embolism by pulmonary CT angiography. Am J Rad 2015; 205(2):271-7. PMID: 26204274

This week we discuss upper GI bleeding pearls from a workshop we did in our weekly conference.

Take Home Points

1. Respect the UGIB. These patients can bleed a lot. Even if they’re not actively hemorrhagic in front of you, realize that they can open up at any time and decompensate
2. Get your consultants on board early. A skilled endoscopist is your friend as they can get control of bleeding. Don’t forget IR for TIPS in variceal bleeds and general surgery in bleeding ulcers.
3. Activate your massive transfusion protocol if the patient is unstable and give the patient PRBCs, FFP and platelets as indicated. Reverse any anticoagulants as well.
4. Give all patients with confirmed or suspected variceal bleeding antibiotics – typically, ceftriaxone. This intervention saves lives and decreases morbidity.

Read More

LITFL: EBM Upper GI Haemorrhage

EMCrit: Episode 5: Upper GI Bleed Guidelines

EMCrit: Intubating the Critical GI Bleeder

The NNT: Prophylactic Antibiotics for Cirrhotics with Upper GI Bleed

The NNT: Somatostatin Analogues (Octreotide) for Acute Variceal Bleeding

EMRAP HD: Placement of a Blakemore Tube for Bleeding Varices

This week we feature a lecture from Anand Swaminathan at our weekly conference on the ED management of acute pulmonary edema

Read More

Core EM: Acute Pulmonary Edema

EMCrit: Podcast 1 – Sympathetic Crashing Acute Pulmonary Edema

REBEL EM: Morphine Kills in Acute Decompensated Heart Failure

emDocs: Furosemide in the Treatment of Acute Pulmonary Edema

This week we discuss the rare, but life-threatening baclofen withdrawal.

Take Home Points

1. Baclofen withdrawal is a rare complication of intrathecal baclofen pumps. It’s presentation mimics sepsis and alcohol withdrawal and is characterized by hemodynamic instability, hyperthermia, increased spasticity, confusion, altered mental status and seizures. Patients can develop rhabdo from the spasticity and, eventually, can develop multi system organ dysfunction.
2. Treating baclofen withdrawal with oral baclofen is unlikely to work even at large oral doses because only a tiny amount gets into the CSF where it needs to act for withdrawal to be treated
3. Baclofen withdrawal can be emergently treated with increasing benzodiazepine doses, propofol infusions and baclofen administered via a lumbar puncture. Ultimately, these patients all need consultation with either neurosurgery or interventional pain management to interrogate the device and surgically correct the issue.

Read more

EM: RAP November 2015: Lin Sessions Intrathecal Pumps

REBEL EM: Baclofen Withdrawal

Chidester S, Smith S. Baclofen pump complications. The NYS Poison Centers Toxicology Letter 2011; 16(4): 1-12. Link

Ross J et al. Acute Intrathecal Baclofen Withdrawal: A Brief Review of Treatment Options. Neurocrit Care. 2011;14(1):103-108. PMID: 20717751

Stetkarova I et al. Procedure- and device-related complications of intrathecal baclofen administration for management of adult muscle hypertonia: a review. Neurorehabil Neural Repair. 2010;24(7):609-619. PMID: 20233964

Shirley KW et al. Intrathecal baclofen overdose and withdrawal. Pediatr Emerg Care. 2006;22(4):258-261. PMID: 16651918

A quick primer on hypocalcemia in the ED.

Hosts:
Joseph Offenbacher, MD
Audrey Bree Tse, MD

Swami’s CoreEM Post

Hypocalcemia Repletion:

• IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq
• For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours
•  For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve

References:

• Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298.
• ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209.
• Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis
• Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166.
• Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53.
• Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/
• Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163.

This week we discuss why we use antibiotics in COPD exacerbations and whether we should continue to do so.

Take Home Points

1. Most COPD exacerbations are caused by infectious etiologies. While these can be viral, there’s also a decent chance it was caused by an overgrowth of bacteria that chronically colonize these patients.
2. Strong evidence from systematic reviews demonstrates that antibiotic use reduces in-hospital mortality and decreases treatment failure
3. The GOLD group recommends antibiotics be given to patients who have increased dyspnea, increased sputum volume and increased sputum purulence or require non-invasive or invasive ventilation for their exacerbation.
4. Finally, a short course of antibiotics – either ampicillin, doxycycline or azithromycin is adequate for management.

Read More

GOLD Reports: Diagnosis, Management and Prevention 2016

Berg RMG, Plovsing RR. The hardships of being a Sith Lord: implications of the biopsychosocial model in a space opera. Adv Physiol Educ 2016; 40: 234-6. PMID: 27105743

Johannes M et al. Antibiotics in Addition to Systemic Corticosteroids for Acute Exacerbations of Chronic Obstructive Pulmonary Disease. Am J Resp Crit Care Med 2010; 181(2): 150-7. PMID: 19875685

Quon BS et al. Contemporary management of acute exacerbations of COPD: a systematic review and metaanalysis. Chest 2008; 133:756-66. PMID: 18321904

Ram FS et al. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2006:CD004403 PMID: 16625602

Rothberg MB et al. Antibiotic Therapy and Treatment Failure in Patients Hospitalized for Acute Exacerbations of Chronic Obstructive Pulmonary Disease. JAMA 2010; 303(20): 2035-2042 PMID: 20501925

Vollenweider DJ et al. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2012: CD010257 PMID: 23235687

The Podcasting Course

This week we discuss the workup and management of hiccups in the ED

Take Home Points

1. Hiccups, or singultus, are caused by a reflex arc involving the vagus nerve, CNS and phrenic nerve.  If you remember the path of these nerves, you can remember that possible bad pathologies that could cause a patient to present with prolonged hiccups.
2. Physical maneuvers are the first line for solving the hiccups.  Try things that will interrupt respiration or stimulate the vagus nerve.  We like the modified valsalva in which the patient blows on a syringe, because it’s pretty easy to get the patient to do.
3. Last, medication options for hiccups include antipsychotics, anticonvulsants, muscle relaxers and dopamine agonist.  Generally, we start with chlorpromazine 25-50 mg PO or IM.

Read More

Steger M et al.  Systemic review: the pathogenesis and pharmacological treatment of hiccups. Aliment Pharmacol Ther 2015; 42(9):1037-50. PMID 26307025

This week we review pearls from our Grand Rounds from George Willis, MD talking about feedback.

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St. Emlyn’s: #TTCNYC Resources for Feedback Talk

This week, we discuss Boerhaave syndrome focusing on making the diagnosis and managing the patient.

Take Home Points

1. Keep esophageal rupture on your differential for deadly causes of chest, epigastric or back pain.  We don’t see it often, but it’s a real thing. 
2. Boerhaave Syndrome is the spontaneous rupture of the esophagus that is caused by a sudden increase in intraesophageal pressure, as seen in forceful vomiting.  So, if the patient presents with the right symptoms and any vomiting in their history, keep this diagnosis in mind.  Other causes you might see, though less common, are childbirth, seizure, prolonged coughing or laughing, or weightlifting.
3. ED management is essentially ABCs and broad spectrum antibiotics, and maybe even antifungals.
4. As soon as you make this diagnosis, get you CT surgeon on board as the length of time to definitive treatment is directly related to mortality.

Read More

Radiopaedia: Boerhaave Syndrome

LITFL: Roast Duck and Juniper Beer

This week we discuss the diagnosis and management of pericarditis with a focus on not missing the hidden STEMI.

Read More

ECG Case of the Week (Amal Mattu): Acute STEMI vs. Pericarditis Part 1 + Part 2

REBEL EM: Colchicine for Treatment of Pericarditis

SOCMOB: Pericarditis: Treatment and Diagnosis Pocket Card

FOAMcast: Episode 54 – The Pericardium

Core EM: Pericarditis

Pericarditis PV Card (Chris Bond (socmob.org)

References

Brady W et al. Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment. Acad Emerg Med 2001;8:961–7. PMID: 11581081

Bischof JE et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2015 PMID: 26542793

This week we discuss an age-old debate: Calcium Channel Blockers or Beta Blockers for rate control in atrial fibrillation.

CoreEM: Recent Onset Atrial Fibrillation

ALiEM: Atrial Fibrillation Rate Control in the ED: Calcium Channel Blockers or Beta Blockers?

ALiEM: Beta Blockers vs Calcium Channel Blockers for Atrial Fibrillation Rate Control: Thinking Beyond the ED

Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. PMID 25913166

This week we discuss a recent article looking at the relevance of d/c glucose levels to patient revisits and subsequent hospitalization

Driver BE et al. Discharge glucose is not associated with short-term adverse outcomes in emergency department patients with moderate to severe hyperglycemia. Ann Emerg Med 2016. PMID: 27353284

This week we discuss the ED management of cardiac arrest with VFib and pulseless VTach.

Take Home Points

1. In cardiac arrest, the most important interventions are to deliver electricity quickly when it’s indicated and to administer good high-quality compressions with minimal interruptions to maximize your compression fraction.
2. Medications like epinephrine and amiodarone have never been shown to improve good neurologic outcomes in the ACLS recommended doses. Don’t focus on them.
3. Consider pre-charging your defibrillator to minimize pauses in CPR and maximize your chance for ROSC
4. Finally, remember that as Emergency Physicians, we are specialists in the resuscitation of cardiac arrests. ACLS is just a starting point. Push your understanding of taking care of these patients so you can deliver the best care possible

Additional Reading

Core EM: Ventricular Tachycardia

Core EM: A Simplified Approach to Tachydysrhythmias

Core EM: Amiodarone, Lidocaine or Placebo in OHCA

emDocs.net: Epinephrine in Cardiac Arrest

REBEL EM: Beyond ACLS: Pre-Charging the Defibrillator

ACLS VFib and VTach Algorithm

References

Driver BE et al. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation 2014; 85(10): 1337-41. PMID: 25033747

Kudenchuk PJ et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. NEJM. 2016; PMID: 27043165

Laina A et al. Amiodarone and Cardiac Arrest: Systematic Review and Meta-Analysis. Int J Cardiol 2016; 221: 780-8. PMID: 27434349

This week we discuss the presentation and treatment of hypokalemia.

Take Home Points

1. Hypokalemia has a wide variety of presentations ranging from generalized weakness, to paralysis, to cardiac arrhythmia or cardiac arrest.
2. When you discover hypokalemia, be sure to check and EKG. Think about underlying causes of hypokalemia, because it is rarely a solo event.
3. Treat with oral potassium supplementation of 40-60 orally every 4-6 hours for mild hypokalemia and 10-20 mEq/hour IV for severe or symptomatic hypokalemia.

Additional Reading

LITFL: Hypokalemia

LITFL: Hypokalemic Periodic Paralysis

Core EM: Hypokalemia

This week we discuss how to aggressively resuscitate patients with DKA as well as dispelling some dogmatic teachings on the topic.

Take Home Points

1. DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis.
2. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5
3. The insulin bolus isn’t necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg
4. Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient
5. Finally, don’t forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you’ve got even a hint of infection brewing

https://www.youtube.com/watch?v=P9sKk4JZmso

Additional Reading

LITFL: EBM Diabetic Ketoacidosis

Core EM: DKA

Core EM: Episode 13.0 – Diabetic Ketoacidosis: A Case

emDocs: Myths in DKA Management

REBEL EM: Is There Any Benefit to an Initial Insulin Bolus in Diabetic Ketoacidosis?

References

Aurora S et al. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med 2012; 30: 481-4. PMID: 21316179

Boyd JC et al. Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias. Clin Chem 1984; 30(5): 754-7. PMID: 6713638

Duhon B et al. Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. Ann Pharmacother 2013; 47: 970-5. PMID: 23737516

Fagan MJ et al. Initial fluid resuscitation for patients with diabetic ketoacidosis: how dry arethey? Clin Ped 2008; 47(9): 851-6. PMID:

Goyal N et al. Utility of Initial Bolus insulin in the treatment of diabetic ketoacidosis.  J Emerg Med 2010; 38(4): 422-7. PMID: 18514472

Green SM et al.  Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis.  Ann Emergency Medicine 1998; 31: 41-48. PMID: 9437340

Kitabchi AE et al. Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis?  Diabetes Care. 2008;31(11):2081. PMID: 18694978

Lebovitz HE: Diabetic ketoacidosis.  Lancet 1995; 345: 767-772. PMID: 7891491

Morris LR et al.  Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern  Med 1986;105(6):836. PMID: 3096181

Muir AB et al. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care 2004; 27(7):1541-6. PMID: 15220225

Okuda Y et al.  Counterproductive effects of sodium bicarbonate in diabetic  ketoacidosis.  J Clinical Endocrinology Metabolism 1996; 81: 314-320. PMID: 8550770

Savage MW et al.  Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011 May;28(5):508-15. PMID: 21255074

Villon A et al.  Does bicarbonate therapy improve management of severe diabetic  ketoacidosis?  Crit Care Med 1999; 27: 2690-2693. PMID: 10628611

How and when to reverse anticoagulation in the bleeding EM patient.

Hosts:
Joe Offenbacher, MD
Audrey Bree Tse, MD

Coagulation Cascade:

Algorithm for Anticoagulated Bleeding Patient in the ED:

Indications for Anticoagulation Reversal:

References: 

1. Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001
2. Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008.
3. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
4. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
5. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643
6. Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317.

This week we discuss the recognition, diagnosis and treatment of severe decompensated hyperthyroidism or thyroid storm.

Take Home Points

1. Decompensated hyperthyroidism is a rare, life-threatening condition.  It can develop in patients with long-standing untreated hyperthyroidism and is often precipitated by another event such as an infection, surgery, or trauma.
2. Patients present with tachycardia, fever, altered mental status and GI symptoms.  Keep thyroid storm in mind if a patient has a history of hyperthyroidism or if things just aren’t making sense with your patient, you can’t find a fever source, they have fever and new afib, things like that. You’re going to use a clinical scoring tool like the Burch-Wartofsky scoring system to make the diagnosis.
3. Treatment is three-fold. First treat the peripheral effects with propranolol.  Then prevent further synthesis of thyroid hormone with PTU and corticosteroids.  And last prevent the further release of thyroid hormone with iodine.  Be sure to hold off on giving the iodine until at least 1 hour after the patient receives PTU to avoid worsening the hyperthyroid.

Burch Wartofsky Scale (maryland.ccproject.com)

Additional Reading

ALiEM: Diagnosing hyperthyroidism: Answers to 7 common questions

ALiEM: Thyroid Storm – Treatment Strategies

LITFL: Thyroid Storm

WikeEM: Burch and Wartofsky Diagnostic Criteria for Thyroid Storm

Akamizu T et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid 2012; 22(7): 661-79. PMC: 3387770

This week we discuss severe hyponatremia - presentation and treatment.

EM Cases: Podcast 60: Emergency Management of Hyponatremia

References

Adrogue HJ, Maidas NE. Hyponatremia. NEJM 2000; 342(21): 1581-9. PMID: 10824078

Moritz ML, Ayus JC. 100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy. Metab Brain Dis 2010; 25: 91-6. PMID: 20221678

This week we discuss the role of phenobarbital in the management of severe alcohol withdrawal.

References

Riggan MA et al. Regarding “Phenobarbital for acute alcohol withdrawal: a prospective randomized double-blind placebo controlled study.” J Emerg Med 2016; 50 (6): 895-8. PMID: 27221017

Rosenson J et al. Phenobarbital for acute alcohol withdrawal: a prospective randomized double-blind placebo controlled study. J Emerg Med 2013; 44(3): 592-8. PMID: 2299978