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Trick of the Trade: Cut IV extension tubing for 2-person ultrasound guided nerve block

illustration nerve block ultrasound guided needle

Ultrasound-guided procedures are difficult enough just identifying the anatomy. Performing a nerve block with the ultrasound in one hand and the needle in the other hand adds extra challenges. The simplest 1-person approach involves attaching a syringe with local anesthetic directly to the end of the procedural needle. A 2-person approach involves attach the syringe to a custom tubing-needle setup such as below. However, this custom setup may not be readily available.

IV and extension tubing attached to needle

Trick of Trade: Cut Standard IV Extension Tubing

Required equipment:

  • Ultrasound linear probe
  • 10 cc syringe
  • IV tubing
  • Procedural needle
  • Shears

IV extension injection port

Almost all standard IV extension tubing that connects IV fluid bags to a peripheral IV have an injection port near the downstream end.

  1. Clamp the IV tubing just upstream from the injection port and cut off all the unused upstream IV tubing.
  2. Attach a 10 cc syringe with local anesthetic to the injection port.
  3. Attach the other end of this IV tubing (Luer lock attachment) to the procedural needle.
  4. Prime the IV line with the anesthetic.
  5. Perform the nerve block with one person advancing the needle under ultrasound guidance, while the other person aspirates and injects the anesthetic when needed.

Video: 2-person ultrasound-guided nerve block with cut IV tubing

Bonus Tip: This approach is applicable to many procedures requiring aspiration or instillation of anesthetic, such as peritonsillar abscess aspiration.

Read more from the Tricks of the Trade series.

By |2024-10-23T07:23:46-07:00Oct 23, 2024|Neurology, Tricks of the Trade, Ultrasound|
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SAEM Clinical Images Series: Doubly Double Vision

palsy

A 52-year-old female with a past medical history of hypertension and prediabetes presented to the emergency department with double vision that started one day prior to arrival. She stated that her double vision improved when she closed one eye. She denied trauma, headache, neck pain, dizziness, dysphagia, numbness, tingling, weakness, or gait instability.

 

Vitals: BP 181/119; HR 76; RR 18; T 98.4°F; O2 saturation 96% on room air

General: No acute distress, well-appearing

Neurologic: AOx3; Following commands. Speech without dysarthria. PERRLA. EOM: incomplete abduction of the L and R eye. No facial asymmetry. Tongue protrudes midline. No pronator drift. 5/5 strength in all extremities. Sensation is intact throughout. Finger to nose is normal. Gait is narrow and steady.

None

Cranial nerve 6 (CN VI), also known as the abducens nerve, is responsible for ipsilateral eye movement. CN VI palsy presents clinically with the inability to abduct the eye resulting in horizontal diplopia. Patients often present complaining of double vision that is worse with lateral gaze. Other symptoms on presentation may include headache, nausea, vomiting, hearing loss, and recent viral symptoms. CN VI is typically diagnosed clinically by an inability to abduct the eye. It is the most common oculomotor palsy in adults and can be caused by damage anywhere along the course of the abducens nerve. Etiologies in adults include ischemia, trauma, neoplasm, demyelinating lesions, increased intracranial pressure, and infection. Risk factors include microvascular disease such as hypertension and inflammatory conditions. Bilateral CN VI nerve palsy without associated intracranial abnormalities is rare. Importantly, abducens nerve palsy is the second most common oculomotor palsy in children and a frequent presenting sign of an intracranial tumor. Children with CN VI palsy should be evaluated for ataxia and other gait disturbances which may indicate a brainstem glioma.

Depending on the presenting symptoms and medical history, the workup should include an MRI/MRA brain to evaluate for microvascular ischemia and cerebrovascular accident. Treatment of CN VI palsy should be targeted at the underlying cause. In cases of CN VI palsy due to microvascular ischemia, symptoms often self-resolve. In children, treatment includes alternating patching of the eyes, but this has not been shown to be effective in adults.

Take-Home Points

  • CN VI palsy is the most common oculomotor palsy in adults and presents with an inability to abduct the eye.
  • Treatment of CN VI palsy should target the underlying pathology which may include infection, trauma, neoplasm, or increased intracranial pressure.
  • CN VI palsy in children may indicate an intracranial tumor and workup should include a full neurologic examination and intracranial imaging when appropriate.

  • Graham C, Gurnani B, Mohseni M. Abducens Nerve Palsy. 2023 Aug 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 29489275.

    Merino P, Gómez de Liaño P, Villalobo JM, Franco G, Gómez de Liaño R. Etiology and treatment of pediatric sixth nerve palsy. J AAPOS. 2010 Dec;14(6):502-5. doi: 10.1016/j.jaapos.2010.09.009. PMID: 21168073.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-09-28T21:34:14-07:00Oct 7, 2024|Neurology, SAEM Clinical Images|
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PEM Pearls: Approach to Spontaneous Intracranial Hemorrhage in Pediatric Patients

pediatric intracranial hemorrhage on MRI

Case:

A 6-year-old female with a past medical history of immune thrombocytopenia presents to the Emergency Department (ED) for concerns of dysarthria that started the day prior to arrival. The patient’s mother denies any recent trauma, including head injury.

Vitals and Physical Exam

  • Blood pressure 109/80
  • Pulse 121 beats/minute
  • Respiratory rate 22 breaths/minute
  • Oxygen saturation 100% on room air
  • Temperature 36.8ºC

Her physical exam is remarkable for a mild right-sided facial droop with forehead sparing and dysarthria.

Initial Work-Up

The patient’s ED workup shows the following:

  • Point-of-care glucose: Normal
  • Platelet count: 0 platelets/liter
  • Hemoglobin: 9.8 g/dL
  • Head CT: Frontal lobe hemorrhage

Background

Although rare, pediatric intracranial hemorrhage (ICH) contributes to almost half of all childhood strokes and can cause lifelong disability and death [1]. One 3-center prospective study on pediatric ICH noted a 9% mortality rate with ⅓ of survivors having “significant disability” at 2-year follow-up [2]. Primary predictors of adverse outcomes from pediatric ICH involve the following [2-4]:

  • Hemorrhagic lesion volume
  • Presence of hydrocephalus and/or herniation
  • Altered mental status

Multiple studies consistently point to vascular causes such as arteriovenous malformation as a leading risk factor for spontaneous pediatric ICH followed by hematological pathologies including coagulation deficiencies [5-7].  No matter the cause, the sequelae of pediatric ICH can be devastating making early detection and immediate intervention essential for better outcomes. Unfortunately, given children often present with vague and non-specific symptoms, there is often a delay in presentation to care and in diagnosis [8]. Unfortunately, in contrast to adults, there are no set guidelines for the management of pediatric ICH despite its associated morbidity and mortality.

Clinical Findings

Although headache is the most common presenting symptom, other symptoms can vary [6,8,9]. In one study, children <6 years old were more likely to present with symptoms such as seizures and altered mental status, while children ≥6 years presented more with focal deficits, headache, vomiting, and altered mental status [9].

Presenting Symptom/FindingIncidence
Headache46-80%
Vomiting21-64%
Altered mental status37-50%
Seizures37-54%
Focal deficits (hemiparesis and aphasia)16-50%
Table 1. Incidence rates of common symptoms and findings in pediatric patients with a spontaneous intracranial hemorrhage (adapted from Boulouis G, et al [7].) 

Differential Diagnosis

Given how rare pediatric ICH is, consider other diagnoses when a patient presents with focal deficits, altered mental status, and/or vague symptoms such as headache and weakness.

  1. Bell’s palsy
  2. Cerebral venous thrombosis
  3. Complicated migraines
  4. Drug intoxication/exposure
  5. Inborn error of metabolism
  6. Intracranial mass
  7. Ischemic stroke
  8. Metabolic derangements (hypoglycemia, hyponatremia)
  9. Non-accidental trauma
  10. Posterior Reversible Encephalopathy Syndrome (PRES)
  11. Seizures with Todd’s paralysis

Approach for the ED Provider

Key history questions:

  1. When did the symptoms start?
  2. Does the child or anyone in the family have any history of bleeding disorder?
  3. Have you noticed excessive bruising from minimal trauma?
  4. Has the child had any recent illnesses?

Key physical exam findings:

  1. Is there any bruising, gum bleeding, or signs of non-accidental trauma?
  2. In infants, is the fontanelle bulging or flat?
  3. Are there any focal neurologic findings such as facial droop, pupil asymmetry, etc?
  4. Are there any signs of increased intracranial pressure (i.e., papilledema)?

Workup to initiate:

Emergency medicine physicians should have strong suspicion for ICH particularly in the setting of a pediatric patient presenting with acute onset of headache, vomiting, altered mental status, seizure, and/or focal deficits.

  1. Emergent neuroimaging: CT or MRI is essential in order to distinguish between ischemic versus hemorrhagic causes. CT is often the first imaging study completed due to ease of access. If no acute intracranial process is noted, MRI is warranted to evaluate for ischemic stroke or other etiology.
  2. Laboratory studies:
    • Point-of-care glucose
    • Comprehensive metabolic panel
    • Ammonia (if concerned for inborn error of metabolism)
    • Comprehensive blood count
    • Prothrombin time with INR, partial thromboplastin time
    • Urine drug screen (if concerned for drug exposure contributing to symptoms)

Management:

If a patient has a confirmed ICH, consultation with neurosurgery is required. Immediate transfer may be necessary if your facility does not have neurosurgical services. Further management includes:

  1. Reversing coagulopathy [7,10,11]:
    • If the patient has an underlying coagulopathy, consider intravenous vitamin K and/or fresh frozen plasma.
    • Pediatric patients with hemophilia require immediate factor replacement (factor VIII or IX).
    • Patients on anticoagulation need anticoagulation reversal with the appropriate reversal agents.
  2. Neuroprotective supportive measures (prevent worsening brain injury): 
    • Monitor the patient closely with frequent neurologic checks for any signs of deterioration.
    • Maintain euglycemia as hyperglycemia is associated with worse outcomes [7].
    • Maintain normothermia. Use external cooling measures or antipyretics to manage hyperthermia [10].
    • Treat clinical and subclinical seizures with antiepileptics. Consider EEG monitoring to detect subclinical status [7].  The benefits of prophylactic administration of antiepileptics is unknown in this population [10].
    • Avoid hypotension [7, 10]. There are no established guidelines for hypertension management in pediatric ICH; blood pressure goals should be discussed with the neurosurgical team and blood pressure variability should be avoided.
  3. Treatment of increased intracranial pressure:  If the patient has a change in mental status or develops focal deficits, an increase in intracranial pressure should be suspected [10,11].
    • Treat hypotension, hypercapnia, and hypoxia.
    • Elevate the head of the bed to 30 degrees.
    • Ensure appropriate pain control.
    • Sedation may be necessary but be wary of resultant hypercapnia and consider intubation if patients require a lot of sedation or become too somnolent following medication.
    • In patients with acute deterioration or concern about impending herniation, consider hyperventilation if the patient is intubated and/or treatment with a hyperosmolar agent like mannitol or hypertonic saline.
    • Some patients may need acute interventions such as an external ventricular drain or operative decompression with clot removal.
    • Steroids have not been shown to be beneficial [10].

Case Resolution

The patient was transferred to a tertiary care center. Further imaging confirmed an intraparenchymal hemorrhage in the left frontal lobe and right parietal lobe with midline shift. No underlying lesions or vascular malformation were seen.

Management: The patient was admitted to intensive care and received tranexamic acid and a platelet transfusion. She was monitored by neurosurgery but no surgical interventions were needed. For her idiopathic thrombocytopenia, she received steroids and IV immunoglobulin.

Hospital Course: Her deficits and platelet count improved during her stay, and she was discharged on hospital day 5 with outpatient neurology and hematology follow-up.

Outpatient: Repeat imaging 3 weeks after discharge showed resolution of the midline shift and decrease in hemorrhage size.

Pearls

  • Consider pediatric ICH in patients presenting with focal deficits, altered mental status, and/or generalized symptoms such as headache, seizures, and weakness.
  • Management of pediatric ICH is focused on maintaining physiological homeostasis and preventing further brain injury.
  • Call your neurosurgical team early for consultation and evaluation or transfer your patient to the appropriate tertiary care center.

Read more pediatric EM blog posts in the PEM Pearls series.

References

  1. Baldovsky MD, Okada PJ. Pediatric stroke in the emergency department. J Am Coll Emerg Physicians Open. 2020;1(6):1578-1586. Published 2020 Oct 6. doi:10.1002/emp2.12275. PMID: 33392566
  2. Porcari GS, Beslow LA, Ichord RN, Licht DJ, Kleinman JT, Jordan LC. Neurologic Outcome Predictors in Pediatric Intracerebral Hemorrhage: A Prospective Study. Stroke. 2018;49(7):1755-1758. doi:10.1161/STROKEAHA.118.021845 PMID: 29895534
  3. Guédon A, Blauwblomme T, Boulouis G, et al. Predictors of Outcome in Patients with Pediatric Intracerebral Hemorrhage: Development and Validation of a Modified Score. Radiology. 2018;286(2):651-658. doi:10.1148/radiol.2017170152 PMID:29023219
  4. Jordan LC, Kleinman JT, Hillis AE. Intracerebral hemorrhage volume predicts poor neurologic outcome in children. Stroke. 2009;40(5):1666-1671. doi:10.1161/STROKEAHA.108.541383 PMID: 19286576
  5. Ciochon UM, Bindslev JBB, Hoei-Hansen CE, et al. Causes and Risk Factors of Pediatric Spontaneous Intracranial Hemorrhage-A Systematic Review. Diagnostics (Basel). 2022;12(6):1459. Published 2022 Jun 13. doi:10.3390/diagnostics12061459 PMID: 35741269
  6. Al-Jarallah A, Al-Rifai MT, Riela AR, Roach ES. Nontraumatic brain hemorrhage in children: etiology and presentation. J Child Neurol. 2000;15(5):284-289. doi:10.1177/088307380001500503 PMID: 10830193
  7. Boulouis G, Blauwblomme T, Hak JF, et al. Nontraumatic Pediatric Intracerebral Hemorrhage. Stroke. 2019;50(12):3654-3661. doi:10.1161/STROKEAHA.119.025783 PMID: 31637968
  8. Yock-Corrales A, Mackay MT, Mosley I, Maixner W, Babl FE. Acute childhood arterial ischemic and hemorrhagic stroke in the emergency department. Ann Emerg Med. 2011; 58:156–163. doi: 10.1016/j.annemergmed.2010.10.013 PMID: 21310508
  9. Lo WD, Lee J, Rusin J, Perkins E, Roach ES. Intracranial Hemorrhage in Children: An Evolving Spectrum. Arch Neurol. 2008;65(12):1629–1633. doi:10.1001/archneurol.2008.502 PMID: 19064750
  10. Ferriero DM, Fullerton HJ, Bernard T, et al. Management of stroke in neonates and children. A scientific statement from the American Heart Association/American Stroke Association. Stroke. 2019;50:e51-e96. doi: 10.1161/STR.0000000000000183 PMID: 30686119
  11. Tsze D and Steele D. Neurosurgical Emergencies, Nontraumatic. In: Fleisher G and Ludwig S,. eds. Textbook of Pediatric Emergency Medicine, 6e. Lippincott Willimas and Wilkins. 2010. Accessed online 5/23/2024.
By |2024-06-19T23:59:23-07:00Jun 20, 2024|Expert Peer Reviewed (Clinical), Neurology, Pediatrics, PEM Pearls|
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SAEM Clinical Images Series: Seeing Double

ophthalmoplegia

A 53-year-old woman with no significant past medical history presented to the emergency department with a 3-day history of double vision on leftward gaze. She initially presented to urgent care with a chief complaint of chest heaviness and concern that her blood pressure was too high, but was sent to the emergency department for further cardiac and neurological evaluation after her urgent care provider noticed abnormal eye movement. She endorsed mild, intermittent headaches associated with diplopia when looking to the left. However, she denied any blurry vision when looking forward. She denied any trauma or falls.

Vitals: Temp 36.7°C; Heart rate 86 beats/min; Respirations 18 breaths/min; BP 150/82 mmHg; O2 Saturation: 100%

General: No acute distress and appears comfortable. She is alert and oriented.

Eyes: Equal, round and reactive pupils and severely limited adduction of the right eye, all other extraocular movements are normal.

Neuro: All other cranial nerves are intact, normal tone in bilateral upper and lower extremities, normal sensation bilaterally to light touch and pinprick except for mildly decreased sensation to pinprick over right ulnar distribution.

CBC, CMP, EKG, and Troponins were normal.

Lipid panel: Cholesterol 241 (H)

CSF: No oligoclonal bands, Protein 197 (H), Albumin 57 (H), IgG 16.3 (H)

Internuclear ophthalmoplegia (INO) is defined as the inability to adduct the eye due to a lesion in the medial longitudinal fasciculus (MLF) and can be accompanied by nystagmus in the same eye. The two main causes of internuclear ophthalmoplegia are demyelination of the medial longitudinal fasciculus (MLF) from multiple sclerosis (MS) and ischemic cranial nerve damage from stroke. However, a comprehensive list of causes of INO includes: infarction (ischemic stroke), demyelination (MS), tumor, encephalitis, hemorrhage, hydrocephalus, Chiari malformation, infection (Lyme Disease), and trauma. Usually, MS is seen in younger patients where both eyes are affected whereas strokes occur more often in older patients and only one eye is affected.

The therapeutic approach focuses on treating the underlying cause and hence determining the etiology is of immense importance. A brain MRI should be ordered to evaluate for ischemia and demyelination. Proton density imaging is beneficial in identifying MLF lesions in multiple sclerosis. A lumbar puncture can also help rule out infections. A kappa-free light chain antibody test is a faster and less expensive way to test for multiple sclerosis than looking for oligoclonal bands in the CSF.

Given this patient’s relatively young age and vascular risk factors, stroke is highest on the differential. Her brain MRI showed areas of restricted diffusion in the right dorsal medial pons correlating with her exam. It also showed periventricular and subcortical white matter changes which is a non-specific finding in chronic small vessel ischemic changes vs underlying demyelinating disease. This was followed up with an MRI of her spine that demonstrated C5-6 stenosis with associated cord edema and an additional enhancing C3-4 lesion concerning for demyelinating disease. Her lumbar puncture revealed 3 nucleated cells and a protein of 197 but was deemed a traumatic tap. There were no oligoclonal bands. The initial brain MRI findings favored stroke for which she underwent a stroke work-up and was ultimately discharged on aspirin and atorvastatin for secondary prevention. However, due to concern for demyelinating disease, she was also treated with a 3-day course of IV methylprednisolone. Ultimately, she was discharged and asked to come back for a follow-up for repeat brain imaging and evaluation. A recent study showed that patients with unilateral or bilateral INO who experienced symptomatic diplopia were commonly managed by uniocular occlusion. Another case report showed that a young man who presented with acute INO responded rapidly to treatment with IV alteplase when administered within 2 hours of the onset of symptoms and resolution within 15 minutes. A case series revealed that 1 in 5 patients failed to recover from an INO. Hence, it is critical that a definitive workup is carried out to determine the etiology of the INO.

Take-Home Points

  • Brain MRI including DWI is a useful diagnostic tool for INO.
  • Unilateral INO is more frequently related to ischemic/vascular causes whereas bilateral INO is associated with MS.

  • Kim SS, Lee MH, Ji C. Unilateral Internuclear Ophthalmoplegia Following Minor Head Injury. Korean J Neurotrauma. 2022 Oct 24;18(2):329-334. doi: 10.13004/kjnt.2022.18.e64. PMID: 36381451; PMCID: PMC9634317.
  • Mahawish KM, Aravind A. Acute onset internuclear ophthalmoplegia responsive to treatment with intravenous alteplase. N Z Med J. 2020 May 22;133(1515):119-121. PMID: 32438384.
  • Simmons J, Rhodes M. Conservative and Surgical Management of Unilateral and Bilateral Internuclear Ophthalmoplegia (INO)-A Retrospective Analysis. Br Ir Orthopt J. 2022 Nov 7;18(1):152-158. doi: 10.22599/bioj.280. PMID: 36420121; PMCID: PMC9650975.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-03-16T21:53:50-07:00Mar 22, 2024|Neurology, Ophthalmology, SAEM Clinical Images|
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SAEM Clinical Images Series: Intracranial Abnormality

mega cisterna magna

A 26-year-old male with no significant past medical history presented to the ED after slipping on wet pavement and hitting his head on the ground three hours prior. He endorsed a constant, achy 7/10 headache accompanied by nausea and photophobia. He denied vomiting, dizziness, diplopia, loss of consciousness, or seizures. Nothing made it better or worse.

 

Vitals: BP 101/63; HR 76; RR 14; T 36.7°C

General: Alert and oriented, no acute distress

HEENT: Normocephalic, atraumatic, tenderness elicited over right occipital bone, PERRLA, + photophobia

Neurologic: WNL with no focal motor or sensory deficits appreciated other than photophobia; deep tendon reflexes 2+ throughout, steady gate

Non-contributory

This patient has a classic presentation of Mega Cisterna Magna (MCM). MCM is a rare cystic posterior fossa malformation characterized by a 10 mm or larger cisterna magna on midsagittal planes, absent hydrocephalus, and an intact cerebellar vermis. Most cases of MCM are found during prenatal ultrasonography. Adults with isolated MCM are typically asymptomatic and found incidentally on radiographic imaging. No follow-up or treatment is needed.

More than 90% of patients with isolated MCM (such as our patient) have a favorable prognosis and normal development. However, there are multiple conditions that have been found to be associated with MCM. Developmental or cognitive delay occurs in about 8% of patients with MCM, and patients with MCM scored slightly lower than controls when comparing memory, executive functioning, and language fluency. MCM is also associated with other central nervous system (CNS) anomalies; the most common being ventriculomegaly, cerebellar hypoplasia, and arachnoid cysts. Renal defects, such as a horseshoe kidney, are the most common extra-CNS anomalies.

Take-Home Points

  • Mega Cisterna Magna is a cystic posterior fossa malformation typically found on perinatal ultrasonography or incidentally on cranial imaging in asymptomatic patients. MCM is a benign condition with no need to follow up or initiate treatment.
  • Mega Cisterna Magna is associated with developmental and cognitive delay, inferior memory, executive functioning, and verbal fluency, renal defects, and other CNS anomalies.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-10-26T20:58:31-07:00Oct 27, 2023|Neurology, SAEM Clinical Images|
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SAEM Clinical Images Series: A Man with Blurry Vision

cranial nerve

A middle-aged man with a past medical history of hypertension and tobacco use disorder presented to the Emergency Department after evaluation by an ophthalmologist.  He complained of ten days of a right-sided headache and three days of diplopia. He denied eye pain, pain with eye movements, photophobia, and vision loss.

Vitals: Temp 98.4 °F (36.9 °C); BP 122/72; Pulse 90; Resp 16; SpO2 100%

Neuro: Ptosis, “down and out” deviation and pupil dilation of the right eye were noted. Extraocular movements were intact and pupils were reactive to light bilaterally. No other neurologic deficits were observed.

Non-contributory

This patient has a partial cranial nerve (CN) III (oculomotor nerve) palsy. CN III is composed of: (a) internal somatic motor fibers that innervate the levator palpebrae superioris (which elevates the upper eyelid) and the medial recti, superior recti, inferior recti, and inferior oblique extraocular muscles, and (b) external parasympathetic fibers innervating the ciliary muscles (involved in accommodation) and sphincter pupillae (involved in pupillary constriction). The presentation of complete isolated CN III palsy generally involves ipsilateral ptosis (due to levator palpebrae paralysis) and “down and out” ocular deviation (due to preservation of superior oblique and lateral rectus function).

The most common etiology of CN III palsy is ischemia of the nerve fibers secondary to diabetes mellitus or hypertension, which preferentially affects the internal somatic fibers that surround the blood supply. This etiology classically results in a pupil-sparing palsy due to preserved function of the external parasympathetic fibers. However, the most feared etiology is an intracranial aneurysm, most commonly a posterior communicating artery aneurysm. This source of external compression classically affects both the internal somatic motor fibers and external parasympathetic fibers, resulting in asymmetric pupil dilation.

Take-Home Points

  • CN III palsy etiologies include ischemia secondary to diabetes mellitus or hypertension, and structural causes, most commonly a posterior communicating artery aneurysm.
  • On exam, complete CN III palsies will present with ipsilateral ptosis, “down and out” ocular deviation, and pupillary dilation. Partial CN III palsies may have a more subtle presentation.
  • New-onset CN III palsy should be evaluated with a CTA to rule out an aneurysm.

  • Biousse V, Newman NJ. Third nerve palsies. Semin Neurol. 2000;20(1):55-74. doi: 10.1055/s-2000-6833. PMID: 10874777. 2. Singh A, Bahuguna C, Nagpal R, Kumar B. Surgical management of third nerve palsy. Oman J Ophthalmol. 2016 May-Aug;9(2):80-6. doi: 10.4103/0974-620X.184509. PMID: 27433033; PMCID: PMC4932800.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-08-14T14:10:25-07:00Aug 18, 2023|Neurology, SAEM Clinical Images|
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Phenobarbital as First-Line Medication for Alcohol Withdrawal: Have You Switched From Benzodiazepines Yet?

phenobarbital first line monotherapy for alcohol withdrawal

Are you using phenobarbital instead of benzodiazepines as the first-line monotherapy for patients in alcohol withdrawal in the Emergency Department (ED)? If not, you probably should be. Another old drug for a new indication, right? Well not exactly. Phenobarbital is indeed an older and relatively cheap drug (less than $20 per loading dose) that has gained some press recently for the treatment of acute alcohol withdrawal [1-3].

Why should you consider using phenobarbital as monotherapy rather than benzodiazepines?

Phenobarbital used to be one of the standard treatments for ethanol (EtOH) withdrawal prior to the introduction of benzodiazepines. However, there are key advantages over benzodiazepines.

  1. Phenobarbital has a dual mechanism of action, binding both the GABA receptor and glutamate receptors in the CNS [3]. This helps EtOH withdrawal symptoms by up-regulating GABA activity and down-regulating excitatory glutamate activity.
  2. Phenobarbital has a predictable metabolization with a long half-life of approximately 3-5 days, which allows the drug to self-taper after the initial loading dose and symptom control in the ED [1, 2]. This contrasts the relatively shorter half-life of many available benzodiazepines, which often require more frequent redosing.

Is phenobarbital safe for the treatment of EtOH withdrawal in the ED?

In short, yes. Several studies have indicated that dosing with phenobarbital (PO or IV) is safe and effective at decreasing the need for escalating doses of benzodiazepines for EtOH withdrawal [1-6]. In comparison to benzodiazepines, it demonstrated:

  • Fewer episodes of hypotension and apnea [1-6]
  • Decreased hospital and ICU stay duration in admitted patients [1]
  • Decreased requirement for ICU level care [1]

Dosing regimens

  • Common regimen: 10-15 mg/kg of IDEAL body weight (IBW) IV bolus over 30 minutes and administering 130-260 mg aliquots every 15-30 minutes for persistent symptoms [2]
    • Note that the patient’s IBW may be much lower than the actual body weight.
    • Use the MD Calc calculator for a patient’s IBW
    • Examples based on the average American height:
      • Male: 5’9” –> 71 kg IBW –> phenobarbital 710-1065 mg IV initial bolus
      • Female: 5’4” –> 55 kg IBW –> phenobarbital 550-825 mg IV initial bolus
  • Alternative lower dosing regimen: 130-260 mg IV boluses with repeated dosing as needed [3]
  • Maximum dose
    • No established maximum, but the absolute upper limit for dosing in epilepsy is 20-30 mg/kg [11]
    • Some sources recommend limiting the dose of phenobarbital in alcohol withdrawal to 15 mg/kg/day [3]
  • Adjuncts: Benzodiazepines may be added without decreasing safely [1]

Do patients need phenobarbital dosing adjustments if they have liver dysfunction?

  • Phenobarbital undergoes metabolization primarily in the liver, mostly by CYP2C9 [9].
  • “Dose adjustment” is recommended by the manufacturer in hepatic dysfunction, but no value is provided [10].
    • Since there is no recommended dosing adjustment in patients with cirrhosis and liver dysfunction, a conservative approach starting with the 130 mg boluses and titrating to the minimum effective dose would likely be the safest approach.
  • Clinical pearl: Hepatic encephalopathy is a strong contraindication to phenobarbital [9, 10].
    • Before administering a barbiturate to a cirrhotic patient for EtOH withdrawal, first ensure that hepatic encephalopathy is not the cause of the agitation or altered mental status.
    • Because patients with hepatic encephalopathy experience excess GABA stimulation, they are very sensitive to GABAergic medications (e.g., barbiturates or benzodiazepines).
    • Administration of benzodiazepines or barbiturates to these patients risk inducing a prolonged comatose state.

Is it safe to give phenobarbital to a patient who has already received benzodiazepines?

  • The concern with concurrent phenobarbital and benzodiazepine administration is oversedation. There is a paucity of evidence for this question, although preliminary data suggests that it is safe without significant mortality risk [1].
  • As a corollary, exercise caution when administering phenobarbital to patients at risk for sedation from any cause, such as hepatic encephalopathy, benzodiazepine abuse, and opioid abuse.
  • Suggested approach: If benzodiazepines have already been given, consider using the alternative, more conservative, lower dose regimen protocol (130-260 mg doses) up to 10-15 mg/kg total with close monitoring after every up-titration. Avoid giving benzodiazepines concurrently during the phenobarbital up-titration period to minimize the risk of oversedation and apnea [11].

Which patients treated with phenobarbital require admission?

There is a dearth of evidence about which patients require medical admission in the setting of phenobarbital administration. The American Society of Addiction Medicine has developed a tool to assist providers with disposition planning for patients with alcohol withdrawal syndrome for all-comers (not necessarily those treated with phenobarbital) [2]. Their recommendations are as follows:

  • Outpatient management
    • Able to follow return precautions
    • Likely to continue with alcohol use disorder treatment
    • Supportive living environment
  • Inpatient management
    • Requires frequent physician and nursing intervention
    • Heavy sedation requirements or active delirium tremens
    • Coexisting medical diagnoses that require inpatient management (severe electrolyte anomalies, infections, pancreatitis, hepatic encephalopathy, etc.)
    • History of severe withdrawals, pregnancy, or concurrent medical condition requiring treatment

Conclusion

Phenobarbital has gained significant popularity for use in EtOH withdrawal in the last few years. Several factors make it ideal for use in EtOH withdrawal, primarily its long half-life allowing for a multi-day, self-tapering effect. The most commonly recommended dosing regimen starts with a 10 mg/IBW kg bolus followed by titration every 30 minutes afterwards. Patients in the ED often can be safely phenobarbital-loaded and discharged, assuming hemodynamic stability, normal alertness, and resolution of withdrawal symptoms. More rigorous studies are needed determine dose thresholds that warrant hospital admission.

References

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By |2023-05-31T19:25:45-07:00Jun 1, 2023|Neurology, Tox & Medications|
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