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
Diverse Etiologies: Ataxia in children can have various causes that range from self-limiting to life-threatening
Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures.
Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting.
Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities.
Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention.
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.
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.
Episode 95.0 – Local Anesthetic Systemic Toxicity (LAST)
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.
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)
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
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.
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.
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.
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
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
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.
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.
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.
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
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
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