Idiopathic Intracranial Hypertension: Review the essentials of this "can't miss" diagnosis before it's too late!

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Idiopathic Intracranial Hypertension (IIH), previously known as ‘Psuedotumor Cerebri’ or ‘Benign Intracranial Hypertension’ that is actually NOT benign is a disorder characterized and defined by the clinical symptoms of increased intracranial pressure (ICP) not due to any other cause. IIH is, in some ways, a diagnosis of exclusion, as you must have negative neuroimaging and a normal CSF composition to rule out other causes of increased ICP prior to making this diagnosis. However, this is not your average “diagnosis of exclusion” since disease progression can lead to significant morbidity.

So, why must you not miss this diagnosis?  Transient vision changes, which is the second most common presenting complaint (after headaches), can lead to permanent vision loss.  And since this is primarily a disease of young, otherwise healthy individuals, you can understand why this is kind of a big deal.

Who gets it?

This is a disorder primarily of overweight females of childbearing age. However, it can affect individuals of all ages and males. Rapid weight gain over a short period of time is potentially a greater risk factor than obesity itself. Classically implicated medications include tetracyclines (doxycycline and minocycline), growth hormone, retinoids and OCPs.

How do these patients present?

The most common complaint: Headache, often diffuse and of gradual onset, which progresses in severity over time. It is frequently accompanied by transient visual changes, which may be precipitated by positional changes (usually standing, sometimes bending forward or lying down), Valsava, eye movement or bright lights. Photopsias (a fancy term for seeing ‘brief sparkles’ or ‘flashing lights’) are frequently described. Pulsatile tinnitus, retrobulbar pain, and back pain round out the list of most frequently seen complaints.

Every complaint listed above is fairly non-specific, so this is where things get a little tricky, right? Keep this in mind: Pulsatile tinnitus (often described as hearing rushing water or wind) in the setting of new headaches is very suggestive of IIH.

Symptoms tend to wax and wane for weeks-to-months, or even years before a diagnosis is made. However, a minority of patients will have a more fulminant course with resulting rapid vision loss.

The most common abnormal findings on exam are papilledema, visual field deficits and sixth nerve palsy.

How is it diagnosed?

You MUST get neuroimaging and send CSF analysis to exclude other causes of increased ICP. And if you are considering IIH, then venous sinus thrombosis should also be on your differential—there is significant overlap in terms of presentation and risk factors.

Once you have excluded all other causes, diagnosis is made via an elevated opening pressure on that LP that you performed (lateral recumbent position).**

**Before the LP, this is the PERFECT opportunity to break out your ultrasound and measure the optic nerve diameter.

In summary, the full list of diagnostic criteria (per the Dandy criteria) are:

  • Symptoms of increased ICP
  • No other neurological abnormalities or impaired level of consciousness
  • Elevated ICP with normal CSF composition
  • Normal neuroimaging
  • No other apparent cause of increased ICP

How is it treated?

For in-service: therapeutic lumbar puncture. Obviously, discontinue any potential offending agents. Weight loss, carbonic anhydrase inhibitors (acetazolamide), diuretics (furosemide) and CSF shunting are all traditionally utilized therapies. Recent data suggests that acetazolamide combined with a low-sodium, weight reduction diet may be the most effective option.

Want to learn more?

https://emedicine.medscape.com/article/1214410-overview

https://www.uptodate.com/contents/idiopathic-intracranial-hypertension-pseudotumor-cerebri-clinical-features-and-diagnosis?search=idiopathic%20intracranial%20hypertension&source=search_result&selectedTitle=1~148&usage_type=default&display_rank=1

https://www.aao.org/eyenet/article/managing-idiopathic-intracranial-hypertension-evid

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Headache and nausea after a night out on the town: Just a hangover? Or a "can't miss" diagnosis?

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It’s In-Service season, people! Let’s review the essentials of carbon monoxide poisoning. And before you start with your “Ugh, really? How many times do we have to—“, let me cut you off and have you gimme the full list of indications for hyperbaric oxygen therapy…. EXACTLY. Are you ready to review now?

1)  How do these patients present?

HISTORY, HISTORY, HISTORY. The classic example goes something like: A family of five presents from home in the dead of winter complaining of headaches associated with a myriad of vague, nonspecific complaints.

Later on, you overhear mom mention, out of frustration, that she had to pay for an Uber XL to get the whole fam to the ED tonight, since dad’s Camero was ‘on empty.’   Turns out, upon arriving home from the bars last night, dad accidentally left his car keys in the ignition before passing out in the doorway connecting the garage to the kitchen. (Ok, so maybe you won’t see that last part on the boards, but it’s my favorite real-life example).

The most common complaints: (1) HEADACHE, (2) nausea, (3) dizziness, and mental status changes with more severe toxicity (memory disturbances commonly manifested as amnesia, decreased cognition, stupor, coma, gait disturbances, etc). Keep in mind that the list of potential associated complaints is broad and encompass nearly every organ system.

Don’t count on the physical exam to nail the diagnosis. Remember that pulse oximetry is not affected. Know the traditional buzz words “cherry red” lips and skin for the boards; but also know that these are rarely seen in clinical practice.

2) How is it diagnosed?

Send a co-oximetry panel. Don’t get tripped up on details- you can send either a venous or arterial blood sample. If your clinical suspicion is high, do not delay treatment pending results.

A CO level >3% in non-smokers, or >10% in smokers, is diagnostic.

The actual percentages weakly correlate with associated symptoms and overall prognosis.  That being said, in the proper clinical setting, you can make the diagnosis and treat presumptively with normal or borderline CO levels.

3) How is it treated?

ABC’s- Intubate if the patient is altered and unable to protect his/her airway. Administer 100% oxygen via NRB. Keep this patient on a cardiac monitor. If for no other reason, CO binds to cardiac myoglobin with an even greater affinity than to hemoglobin, resulting in cardiac ischemia, ventricular arrhythmias, and cardiovascular collapse in severe cases. Finally, know your indications for Hyperbaric Oxygen (HBO).**

**note: this list is variable (and debatable) depending on the source, but generally accepted indications include: anyone who is pregnant, anyone who has signs of cardiac ischemia, history of prolonged LOC, or presence of neurological deficits.

  • Focal neurological deficits, coma, h/o transient LOC (transient LOC = independent risk factor for increased morbidity)
  • Pregnancy (with CO > 15%)
  • Evidence of cardiac ischemia, usually on EKG (or h/o CAD with CO >20%)
  • Basically any symptoms with CO >40%
  • Symptoms that don’t resolve after 6 hrs of 100% O2 via NRB

KEEP IN MIND: Clearance of CO via:

Room air: ~300 minutes

100% NRB: ~90 minutes

HBO: ~15-30 minutes

IDEALLY, TRANSFER FOR HBO SHOULD BE MADE ON A CASE-BY-CASE BASIS, AND SHOULD TAKE INTO CONSIDERATION THE STABILITY OF THE PATIENT FOR TRANSFER AND THE TIME INVOLVED FOR THE TRANSFER PROCESS ITSELF, AMONG OTHER THINGS.

The reason we transfer patients for HBO therapy = prevention of long-term neurologic sequelae.  

 

Want to learn more?

https://lifeinthefastlane.com/ccc/carbon-monoxide-poisoning/

https://lifeinthefastlane.com/ccc/hyperbaric-oxygen-and-carbon-monoxide-poisoning/

https://emedicine.medscape.com/article/819987-treatment#d12

https://emcrit.org/racc/cardiac-arrest-after-smoke-inhalation/

 

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Can you ID the active ingredient in the Cyanokit?

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1) Name the active ingredient in the Cyanokit. The Cyanokit contains hydroxocobalamin (HCN), which is essentially Vitamin B12 + an extra hydroxyl group. It is one of two main antidote kits in circulation for treatment of cyanide poisoning. The other most commonly distributed kit is aptly named the Cyanide Antidote Kit. It contains amyl nitrite and sodium thiosulfate.

2) Why does this matter?

One of these two kits is contraindicated in patients with cyanide poisoning in whom there is a concomitant concern for carbon monoxide poisoning (ie: patients involved in home/commercial fires or smoke inhalation victims-- the most common presentation for cyanide toxicity).

And why is this so? These two kits contain two completely different active compounds that work to clear cyanide by two completely different mechanisms.

Cyanokit: Cyanide displaces the extra hydroxyl group on B12 to form cyanocobalamin, which is excreted by the kidneys.

Cyanide Antidote Kit: sodium nitrite (or any other kit utilizing nitrites) reacts with hemoglobin to form methemoglobin (met-hgb). Cyanide, which throws a wrench in oxidative metabolism by binding with cytochrome oxidase via the electron transport chain, preferentially binds to Met-Hgb over cytochrome oxidase.

Stay with me, people, we’re almost done…. We know that Met-Hgb shifts the oxygen dissociation curve to the left, causing decreased oxygen delivery to the tissues. And increased tissue hypoxia via the production of Met-Hgb compounded by carbon monoxide -induced tissue hypoxia = BAD.

 

3) Quick! How is the Cyanokit administered?

Each kit contains a vial with 5 g of hydroxocobalamin in powdered form, IV tubing, transfer spike and instruction card. You will need to grab a bag of 0.9% normal saline.

Inject 200ml of NS into the vial. Rock (do not shake) the vial back and forth for 60 seconds to mix. Hang and infuse over 15 minutes.  The standard 5 g dose should be sufficient without needing to re-dose.

Don’t forget to draw labs BEFORE starting the infusion, since hydroxocobalamin will interfere with the results of labs that rely on the use of colorimetric probes, which includes your carboxyhemoglobin level, as well as lactate and certain LFTs.

 

Want to learn more?

https://lifeinthefastlane.com/tox-library/toxicant/inhalation/cyanide/

http://www.thepoisonreview.com/2009/12/18/hydroxocobalamin-vs-sodium-nitrite-cyanide-antidote-smackdown/

http://www.thepoisonreview.com/2010/04/10/cyanide-antidote-smackdown-hydroxocobalamin-vs-sodium-nitrite/

https://emcrit.org/racc/cardiac-arrest-after-smoke-inhalation/

 

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