Conventional teaching for treatment of confirmed or suspected tension pneumothorax in an unstable patient is immediate chest decompression with a large bore angiocatheter [1]. New generation angiocaths feature blood control technology, which allows a flash of blood to rise into the hub but will not transmit that blood out the end, which increases safety and decreases messes. Half of the departments I work in now stock blood control angiocaths; since this device is more expensive than its predecessors, you can expect all american hospitals will soon move to them.

Notice the blood control valve, which adds length to the hub compared to the same catheter without this feature.

BC Valve

 

2016-04-21 06.47.58

 

The blood control valve prevents blood from flowing out the hub but also prevents any other fluid from flowing through the catheter, including air. So stabbing your pneumothorax patient with this device will not decompress the chest.

Fortunately the valve opens permanently when it is pushed down by IV tubing, or by attaching a syringe.

valve is closed

attach syringe

now valve is opened

 

So place the angiocath as usual, then take a syringe, pull out the plunger, and twist it firmly onto the hub, until you hear your rush of air.

There are all sorts of problems with using any needle or angiocath to decompress pneumothorax, especially if you use the usual anterior approach, and you are better off in most cases performing a finger thoracostomy or quickly placing a chest tube. But if you do use an angiocath, be mindful of blood control technology, because if you place a catheter thinking you’ve relieved tension but you haven’t, now you’ve made a real mess.

BC angiocath in package

 

[1] See chapter ten of the sixth edition of Roberts and Hedges.

[2] I’ve pictured the Becton Dickinson device but many angiocath manufacturers offer the same feature under a variety of names.

Avoid Alcohol Withdrawal Admissions

January 28th, 2016
by reuben in tox

 

NAAW

 

Alcoholic patients are predisposed to many dangerous conditions and present an array of management challenges for emergency providers, however at many centers, some of these patients present with uncomplicated alcohol intoxication and end up admitted for alcohol withdrawal. This serves no one’s interests because alcohol withdrawal is a condition that generally does not benefit from inpatient management; detoxification proceeds over several days and the patient is discharged, unfortunately often to resume drinking, no better off than before.

Though some alcoholics present in advanced withdrawal, requiring aggressive management and an ICU or step-down bed, many (most?) patients admitted for alcohol withdrawal present to the ED intoxicated and develop withdrawal in the department. Admitting this group is at best pointless and usually avoidable. There’s a lot of literature and discussion around treating alcohol withdrawal, but very little on how to prevent it, which perhaps is part of the problem.

The first step is to identify patients at risk for withdrawal. The most obvious risk factor is a history of alcohol withdrawal, especially prior admission for alcohol withdrawal; ideally these patients would be flagged at triage. Anyone who drinks every day is at risk, though. Most at-risk patients arrive to the ED drunk, but if a daily drinker presents not drunk (i.e. comes with some other concern) or is in early withdrawal, promptly dose librium and reassess.

Intoxicated alcoholics at risk for withdrawal should be reassessed frequently for alertness. Once the sobering alcoholic is alert he is at risk for withdrawal and the most pressing concern is whether he can be safely discharged. If yes, discharge.*  If he cannot be discharged for whatever reason (requires sutures, psychiatry, social work, an xray, etc.), dose librium and reassess (and re-dose) every hour or two, until he can be discharged or needs to be admitted for some other reason.

Librium dosing. I see librium dosed at 25 or 50 mg, which works as part of a taper in mild withdrawal, but is often inadequate in the severe alcoholic whose last drink was 8 hours ago. You can succeed with small doses if you’re able to keep a very close eye and redose frequently as needed, but in most busy ED’s, you’re better off with a bigger dose, which will give you more time to circle back to reassess. For patients at risk to withdraw but without signs/symptoms, I use 100 mg. If early withdrawal has already developed, I write for 200 mg, yes that’s eight tabs, thank your nurse for making sure you meant it. 200 mg is outside the guidelines, but oral chlordiazepoxide is very safe; I have used this dose on hundreds of patients without running into trouble with respiratory depression or excessive somnolence.

Caveat 1: Many alcoholics suffer with a host of comorbid medical, psychiatric, and substance problems beyond alcohol dependence. If these problems can be even partially addressed in a sustainable way during an inpatient stay, that admission is of benefit, even if the patient goes right back to drinking. My impression is that severe alcoholism so completely dominates the patient’s function that their accompanying problems cannot be meaningfully addressed unless and until the patient stops drinking. I am aware of no way to move severe alcoholics to sobriety other than high-intensity case management; if your hospital can set this up during an inpatient stay, by all means, admit.

*Caveat 2: An at-risk inebriate who sobers in the ED and is discharged must of course be able to acquire alcohol to avoid withdrawal. Though alcoholics are astonishingly capable of accomplishing this regardless of circumstance, it may not be safe to discharge a brittle alcoholic at the cusp of withdrawal at 4am. Have an honest conversation with him, if he won’t be able to get booze for a few hours, dose librium and observe for a few hours.

 

help me help you

 

 

Thanks to Lewis Nelson and Anand Swaminathan for their insights. 

Face Mask Capnography

December 28th, 2015
by reuben in resus

Guest post by Terrance McGovern

End-tidal capnography is frequently used in the ED for monitoring patients at risk for hypoventilation.  Some departments stock the luxury oral/nasal sampling devices, but many of us have to make due with a nasal-only apparatus or fashion our own using a nasal cannula; these will not capture CO2 exhaled from the mouth. You can easily use a conventional face mask to build a capnometer that will continuously sample nasal and oral exhaled breaths, and provide supplemental oxygen. 

Screenshot 2015-12-28 06.14.12

Screenshot 2015-12-28 06.14.20

 

If you use a non-rebreather mask with both exhalation valves activated, you must keep the reservoir insufflated with oxygen. To deactivate the exhalation valves, peel off the rubber gasket pictured most prominently in step 4.

If you provide high-flow oxygen, this will dilute the exhaled CO2 and the ETCO2 number will be artificially low, but the waveform is intact–if the wave amplitude is too small, change the monitor scale from max of 50 (default on most monitors) to max of 20.

Thanks to Brendan Milliner for his assistance/face.

 

addendum: similar setup described by an obscure author in the air medical journal.

The Causes of Cardiac Arrest

November 23rd, 2015
by reuben in .cardiac arrest

It has been repeatedly demonstrated that the use of drugs empirically does not work in cardiac arrest. Despite this, ACLS often feels like an algorithmic march down a menu of pharmaceuticals, one drug after the next, hold compressions, ok still asystole, have we tried bicarb? Until everyone has had enough and the patient is pronounced.

There are three things you can do to benefit your patient in cardiac arrest. The first is good chest compressions, which serves mostly to buy time. The second is shocking shockable rhythms, and the third is identifying and treating the cause of cardiac arrest. The use of a vasopressor in the right dose probably offers some benefit; unfortunately we can’t figure out what the right dose is and epinephrine 1 mg every few minutes is almost certainly way too much.

Which drug is next keeps you busy and is the focus of how ACLS is taught, which is why it’s so dangerous: it feels right but not only does not benefit the patient, which drug is next distracts you from the most important task in cardiac arrest, which is figuring out why the patient in front of you just died, so you can offer a treatment to address it.

Causes of CA

Dysrhythmia is a central cause of cardiac arrest; as soon as a cardiac monitor is available, check a rhythm and if shockable, shock immediately. If you’re not sure if the rhythm is shockable, shock. The harm caused by an unindicated shock is trivial compared to the harm of untreated pulseless vtach or vfib.

Acute coronary syndrome is a hugely important cause of cardiac arrest, but causes cardiac arrest predominantly by dysrhythmia, which you will fix by checking the rhythm early and often. ACS can also cause cardiac arrest by pump failure, these patients may benefit from emergent reperfusion and would ideally be in a cath lab, if we knew that acute coronary artery occlusion was the problem. If you think ACS is the cause of arrest, cath lab is not an option, and the patient seems salvageable, give a thrombolytic. The data is equivocal in this context but I think the majority of resuscitationists would offer it for hearts too good to die.

Any sufficiently severe insult to airway or breathing can cause cardiac arrest, fortunately they are all treated at once with 100% FiO2 through an endotracheal tube. If the cause of cardiac arrest is unlikely to be primarily A or B, intubation can be deferred in favor of a supraglottic device; however, if A or B is the problem, all efforts should be directed at establishing oxygenation, usually via endotracheal intubation. Diverting your finite cognitive powers to ACLS drugs in respiratory arrest is particularly poor care.

There are three common, crucially important obstructive causes of cardiac arrest. Pericardial tamponade and tension pneumothorax are easily excluded and should be explicitly excluded in every case of undifferentiated arrest. Massive pulmonary embolism is amenable to reperfusion therapy, usually with intravenous thrombolysis–consider risk factors, exam signs, and ultrasound the legs and RV when the context fits.

Hyperkalemia is common, immediately lethal, and readily treatable. Calcium should be given to most arrested patients with kidney disease, and hyperK is a great reason to push for point of care electrolytes testing in your shop. Hypokalemia is much less common but also easily treated and a particular consideration in malnourished patients. Likewise hypoglycemia–fingerstick testing is routine if POC blood gas not available, and empiric use of D50 is reasonable in diabetics or liver patients.

Hemorrhage is of course most relevant in trauma, which may be occult, but the peritoneum is easily sonographed and uncrossmatched blood remains one of our best therapies. Ahemorrhagic hypovolemia is even more treatable though an uncommon cause of arrest in developed countries.

There are several key antidotes to important toxins, intralipid is a rising arrest therapy to consider if a cardiotropic medication is suspected; bicarb, digibind, and hydroxocobalamin may also restore circulation in the poisoned patient.

Hyperthermia is hopefully easily identified; treatment can be tricky but should involve some form of icewater in most cases. Hypothermia is an important cause and effect of cardiac arrest and determining which can sometimes be a challenge.

Anaphylaxis as a cause of cardiac arrest will be treated by airway management and the epinephrine you’re giving anyway. Once the patient has arrested from sepsis or an aortic or intracranial catastrophe, it is unlikely that you will be able to meaningfully reverse the process.

Though excellent, step-by-step algorithms exist, it can be difficult to remember this differential while managing an arrested patient as well as your team of providers which, when large enough, invariably obstructs rather than augments care. However, once you’re used to taking care of pulseless patients, the differential can be streamlined.

Causes Highlighted

You’re not going to forget to look for and shock shockable rhythms or intubate. Hyperthermia and hypothermia announce themselves, anaphylaxis will be treated with your supportive therapies and the last three causes are more or less irreversible once the patient is dead. This just leaves eight causes which are treated with six therapies. Six is the perfect number of items for a mnemonic.

Bling

If you’ve ever been to Antwerp you know it is gloomy as hell, and you would never, ever carry bling through gloomy Antwerp. Needle, calcium, blood/fluid, thrombolytic, glucose and antidote are the six things to remind yourself to consider in the arrested patient. It’s the Hs and Ts, evolved for our post-ACLS age.

Lastly, if you are able to put arrested patients on bypass/ECMO, you are playing a different game than the rest of us and that game has a different set of rules. Come up with your own mnemonic that includes Antwerp.

Lecture is 35 minutes, then questions for 20 minutes. On Vimeo.

 

Opioids are extraordinary agents that have been used for millennia for the relief of pain and suffering; however, the history of opioids is also one of abuse and addiction. In the US, we are in the midst of a devastating iatrogenic chapter in this history, a prescription opioid epidemic that kills 15,000 Americans per year by overdose and destroys hundreds of thousands of lives and families.

In this presentation we will consider the magnitude and consequences of the current epidemic; describe how clinical organizations and clinicians were appropriated by the pharmaceutical industry so that Americans–5% of the world’s population–consume more prescription opioids than the rest of the world combined; and discuss strategies for managing patients who present to emergency departments with acute or chronic pain complaints that account for our competing mandates to palliate and protect.

These strategies center on an assessment of the likelihood that using opioids will deliver benefit or cause harm. For patients at low risk to be harmed by opioids, utilize aggressive multimodal analgesia, including opioids as needed to control acute pain, and prescribe optimal outpatient non-opioid analgesia with a small number of breakthrough opioids if indicated. For patients at high risk to be harmed by opioids, including patients with chronic pain and patients with flags for opioid misuse, avoid using opioids in the ED and outpatient settings, utilize non-opioids to manage symptoms, and, when misuse is suspected, nudge the patient to addiction treatment. The goals of optimal opioid stewardship are to provide effective symptom relief while preventing de novo cases of addiction, to control the supply of opioids in the community, and to protect existing addicts from further harm while promoting recovery.

For slides, the HELPCard treatment referral business card, and phraseology to use when managing patients at risk for opioid misuse, go to emupdates.com/help