UMEM Educational Pearls - By Danya Khoujah

Given the similarity in pathophysiology, pharmacologic treatments for ischemic stroke have been modeled after those for acute myocardial infarction, such as the use of antiplatelets and thrombolytic agents. Have you ever wondered, why don't we give glycoprotein IIb/IIIa inhibitors (GPIs) as well?
A Cochrane review answers this question; GPIs increase morbidity in acute ischemic stroke (in the form of intracranial hemorrhage), with no evidence of benefit (improvement in Rankin Scale).
The systematic review looked at randomized clinical trials of GPIs in patients with ischemic stroke of 6 hours or less, alone or in combination with thrombolytics.

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We all dread performing lumbar punctures on the obese patient. The traditional standard length spinal needle (9 cm) is becoming increasingly inadequate in reaching the subdural space in our overweight society.

Abe et al developed a formula for selecting the proper needle length to reach the middle of the spinal canal from the skin using retrospective CT data from 178 patients.

Length of needle (cm) = 1+ 17 x Weight (kg)/ Height (cm)

Given the average height of the American woman (163 cm or 5’4’’) our standard length spinal needle will FAIL to reach the mid-thecal space if a woman weighs more than 170 lb (75 kg)!!!

Paul Blart Mall Cop, and King of Queens star Kevin James (5’8’’, 285 lb) would require a 13.7 cm spinal needle. This means even our long spinal needles (12.7 cm) would FAIL by 1 cm.

Note that this formula resulted in selection of needles too small (6%) and too long (31%) of the time. Abe’s linear correlation had an R value of 0.81, (p<.001)

Bottom-Line: Consider use of a long spinal needle (12.7 cm) or IR guided LP in overweight /obese patients and the above formula to guide your depth of insertion

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Some medical issues arise in patients with brain tumors:

// Steroids are used to decrease vasogenic edema, especially preop or during radiation therapy. Patients are ideally gradually weaned off steroids. Dexamethasone is most commonly used. 1-2% of patients are at risk for adrenal suppression.

// Infections: Post-op wound infections can be delayed up to months, especially in patients on steroids.

// Antiepileptics: Although technically not recommended in patients with brain tumors who have not had seizures (American Academy of Neurology 2010), many surgeons continue to prescribe antiepileptics preoperatively and then discontinue them by 1 month postop if the patients remain seizure-free. Levetiracetam is emerging as the drug of choice due to favorable side effect profile.

// Thromboembolism: Brain tumors are considered very high risk for venous thromboembolism. Low-molecular-weight heparin is the treatment of choice, with warfarin being an acceptable substitute.

// Arterial thrombosis and ischemic stroke: Risk is increased with certain medications, and thrombolysis is contraindicated.

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Elsberg syndrome is sacral radiculitis caused by a viral infection, most commonly herpes simplex virus type 2 (HSV-2) - whether a primary infection or a reactivation. The typical patient is a young sexually active woman presenting wtih acute transient urinary retention and sensory lumbosacral symptoms, such as dull pain in anorectal region, paresthesias, loss of sensation or flaccid paresis of leg muscles. Patients can also have constipation or erectile dysfunction.

The presence of inguinal lymphadenopathy and/or anogenital rash can be important clues but are not necessary for diagnosis. CSF may show mild to moderate pleocytosis, with a mild elevation in proteins. Herpes PCR in the CSF may be positive as well. The MRI may show varying degrees of root or lower spinal cord edema with hyperintensity of T2-weighted images.

In immunocompetent patient, the disease usually self limiting, usually resolving in 4-10 days, but can be progressive and ascending in patients with immunocompromise, such as HIV or cancer. Antiviral treatment may shorten the duration of illness in cases with confirmed herpes, either oral or IV.

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Cauda Equina Syndrome is a true neurologic and surgical emergency. Unfortunately, no constellation of symptoms or exam findings is 100% sensitive. In fact, no single symptoms predicts the radiographic finding of cauda equina syndrome with an accuracy greater than 65%.

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Patients with myasthenia gravis (MG) may be seen in the emergency department for symptoms that are not related to their MG, such as an upper respiratory tract infection or chest pain, for example.

The emergency physician should be careful in prescribing new medications to patients with MG, as that can precipitate a myasthenic crisis (and therefore cause significant morbidity and mortality). Below is a list of medications that are commonly implicated; an extensive list can be found on www.myasthenia.org/docs/MGFA_medicationsandmg.pdf)

• Iodinated IV contrast
• Fluoroquinolones
• Aminoglycosides
• Macrolides
• IV magnesium replacement
• Beta blockers (metoprolol and labetalol)

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Delirium has long been recognized as a common disorder of the geriatric ED population (seen in up to 20% of patients above the age of 65 years), but how good are we at detecting it?

Studies show that the diagnosis of delirium is made in the ED in only 11-46% of patients, which means that more than half go undiagnosed. The problem is, the risk of death at 3 months increases by 11% for every 48 hours of delirium the patient experiences, and so does their length of stay and functional decline. It is mostly missed in patients who have a baseline cognitive dysfunction, such as dementia.

So what can we do about that?

Treat delirium as a neurolgical emergency; be vigilant about diagnosing it and treating it. There are a lot of neurocognitive tests that can be used for diagnosis (such as the mini-mental status exam), but they are usually too cumbersome to use in an ED setting. The CAM (Confusion Assessment Method) has been extensively studied and has a sensitivity and specifity of about 95% to diagnose delirium. It includes the acuity of onset, fluctuant course, inattention (the hallmark), disorganized thinking and/or altered level of consciousness.

Bottom Line? Don't forget to screen your elderly patients for delirium and treat them accordingly!

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There are a few available options for treatment of visual loss due to idiopathic intracranial hypertension (IIH). The Idiopathic Intracranial Hypertension Treatment Trial (IIHTT), the first randomized, prospective, placebo-controlled trial for the treatment of patients with visual loss from IIH, which results were published earlier this year, provided substantial evidence for the first 2 options.

1. Weight loss

2. Carbonic anhydrase inhibitors, such as Acetazolamide

3. Therapeutic lumbar puncture (reserved for pregnant patients or for occasional flare-ups)

4. Surgery:

a. Optic nerve sheath fenestration (ONSF): visual acuity and fields improve in most cases, but symptoms may recur. Benefit? No hardware!

b. Shunts: ventriculoperitoneal (VP) and lumboperitoneal (LP) shunts are the most frequently used. No clear benefit for one over the other. VP shunts may be programmable.

c. Cerebral venous stenting: endovascular stenting of the transverse sinus may improve the symptoms in some people.

BONUS PEARL: The headache does not correlate with the lumbar opening pressure, degree of papilledema or amount of visual loss. None of the above-mentioned management strategies is meant for the treatment of the headache alone. For that, medical management with standard symptomatic treatments, avoiding opiates and barbiturates, is recommended. Surgery is not recommended for headache alone.

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The 2013 neurosurgery guidelines mention two of the more controversial therapies used in spinal cord injuries:

- “MAP Push” (maintaining the patient’s MAP 85-90mmHg, which theoretically increases the blood flow to the penumbra): evidence for the particular MAP goal is not great, but studies show that ICU level monitoring for the first 7-14 days improves outcome as patients may have delayed cardiovascular or pulmonary instability

- Steroids are not recommended anymore (they were an “option” in the previous guidelines)

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Jolt accentuation, the exacerbation of a headache with horizontal rotation of the neck, or shaking of the stretcher in the less cooperative patient, has been promoted for the past few years as the "go-to" test to assess for meningeal irritation in patients with headache. Previous studies have quoted sensitivities as high as 97.1%. (1)

A new prospective study in AJEM challenges this belief by looking at a total of 230 patients with headaches and subsequent LPs. 197 of them had the jolt accentuation test done, which had a sensitivity of only 21% for pleocytosis (defined as greater than or equal to 5 cells/high power field in the 4th CSF tube). Kernig's and Brudzinski's signs both did even more poorly, with a sensitivity of 2% each. (2)

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Why is everyone obsessed about blood pressure management in stroke?

Greater than 60% of patients with stroke have elevated blood pressure, and 15% have a systolic blood pressure (SBP) greater than184 mmHg. That is more common in hemorrhagic stroke than ischemic stroke. 

Whether it's an acute hypertensive response or a premorbid uncontrolled hypertension, it is likely to negatively affect the clinical course and neurological outcome. 

Below is a suumary of the current guidelines for blood pressure management of stroke subtypes; for a more detailed summary of the guidelines, refer to the original article (below)

Ischemic stroke:

Lytic patients have a target SBP of <185mmHg, whereas nonlytic patients have a higher SBP target of <220mmHg

Hemorrhagic Stroke:

Non-aneurysmal hemorrhage patients with a SBP >180mmHg have a target SBP of <160 mmHg, whereas if their SBP was 150-220 mmHg then lowering it to 140 mmHg is safe. Patients with aneurysmal hemorrhage have a target SBP of <160mmHg

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Elevated intracranial pressure (ICP), defined as >20mmHg, is frequently encountered in patients with severe traumatic brain injury (TBI). A step-wise approach would include:

1.     Analgesia and sedation: frequently forgotten.

2.     Hyperosmolar agents: both hypertonic saline and mannitol can be used. Neither is superior.

3.     Induced arterial blood hypocarbia using hyperventilation (must monitor for cerebral ischemia)

4.     Barbiturates (last resort due to side effects)

5.     Surgical:

a.     CSF drain

b.     Decompressive craniectomy: benefits challenged by the DECRA study

Stocchetti N, Maas AIR. Traumatic Intracranial Hypertension. N Engl J Med 2014; 370:2121-30. 

Maybe not! A new prospective study looked at 600 adult trauma patients presenting with mild traumatic intracranial hemorrhage (with a GCS 13-15), and derived a clinical instrument that predicted the need for a “critical care intervention” (and therefore needing an ICU level of care). These interventions included intubation, neurosurgical intervention and need for invasive monitoring, among other things.

The derived instrument consisted of 4 variables:

1.     GCS less than 15

2.     Non-isolated head injury

3.     Age 65 years or older

4.     Evidence of swelling or shift on the initial head CT

The presence of at least one of these variables predicted the need for critical intervention, identifying 114 of the 116 patients who actually did require it, making it 98.3% sensitive.

This clinical decision rule is yet to be externally validated. 

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In patients presenting to the ER with a TIA (transient ischemic attack), the classic teaching has been to calculate their ABCD2 score (age, blood pressure, clinical features, duration of episode and diabetes) to determine their risk of developing a stroke.

The problem is, a moderate-to-high ABCD2 score is sensitive (86%) but not specific (35%) for a stroke in 7 days. 

The solution: Combining imaging data with the scoring system!
 

The presence of an acute infarct on a diffusion-weighted MRI (DWI) in a patient with an ABCD2 score of 4 or more carries the highest risk of stroke, at 14.9% at 7 days. On the other hand, a negative DWI predicts a 0-2% stroke risk at 7 days irrelevant of the ABCD2 score.

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