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Working up SAH Core content
Subarachnoid hemorrhage is a big deal. In my mind, there are two reasons why it is a big deal:
That is a bad combination. If you remember our conversation on posterior circulation CVA, a morbid disease process with a presentation that can mimic benign and common conditions is a recipe for disaster.
But recent literature investigating presentation features and diagnostics have made the SAH less of a lurking monster. Let’s dive in.
Define Your Disease
The subarachnoid space is the area in between the arachnoid matter and the pia matter. Remember that the three meninges or “skins” to the brain include the following: the dura matter, arachnoid matter, and pia matter from outward to inward. The dura is closely adherent to the inner lining of the skull (hence why epidurals cannot cross suture lines). The subdural space is largely a potential space that often fills with venous blood when old people fall down. The arachnoid matter is our next layer of meninges and below it is the subarachnoid space, a true space filled with a network of connective tissue fibers called trabeculae and following between these trabeculae is the cerebrospinal fluid (CSF). Below the subarachnoid space is the pia matter, which is a thin layer coating the brain itself.
A subarachnoid hemorrhage therefore is a bleeding event into the subarachnoid space. This most commonly occurs secondary to an aneurysm, usually a berry or saccular aneurysm. It is estimated that ~80% of SAHs are from a saccular aneurysm.3,4 It is important to note that while saccular aneursyms are the most common cause of SAHs, most aneursyms do not rupture. The prevalence of aneurysms is thought to be somewhere around 5%, which is significantly higher than that of SAH.5
Other cause of SAH include vascular malformations such as ateriovenous malformation (AVM), intracranial dissection, cerebral venous thrombosis, anticoagulant use/poisoning, sickle cell disease, among others.6 There is also the entity of the perimesemphalic bleed, which is a non-anuersymal SAH that is discussed as a separate disease entity given its generally benign course requiring only observation and have a good prognosis.13
The presentation for subarachnoid hemorrhage as classically been taught to be a “thunderclap headache” which has been loosely defined as the worst headache of the patient’s life with an abrupt onset. Other concerning historical elements that raise the concern for SAH include association with exertion, nausea and vomiting, and loss of consciousness. Meningismus on physical exam is also classically taught but may be a delayed finding.7
Recent efforts have been made to outline a decision rule and highlight key features of the history and physical exam that evidence to support their association with SAH. Most notably the Ottawa SAH rule was created in 2013 and has gotten some press, both good and bad.
The Ottawa SAH rule was initially published in JAMA in 2013 by Jeff Perry and colleagues.8 In the study they prospectively analyzed some proposed decision rules crafted from a prior patient data set. They had three prior rules they analyzed, and found sensitivies as high as 98.5% but added additional elements to create the final Ottawa SAH rule with a sensitivity of 100%. This had the downside of a specificity of 15%. Here is the rule:
The study does have some external validation (albeit retrospective) out of the Mayo clinic.9 Researchers there applied the Ottawa SAH rule to all patients presenting with a chief complaint of headache during the time period from January 2011 to November 2013, two months after the publication by Perry. In this chart review study, 5000+ patients with headache were reviewed. Of them, ~1500 met exclusion criteria (paragraph 2 in the figure above) and ~3000 had headache reach maximum intensity at >/= 1 hour. This left 454 patients, or 9% of initial headache complaint charts. Of these, 9 cases of SAH were found, yielding an incidence of 2% (compared to 6.2% for Perry’s study). This external validation also had a sensitivity of 100% with an abysmal specificity 7.6%. Interestingly in this article they reference a low clinical applicability given the 9% utilization rate, but fail to see that this likely means only 9% of patients with HA have characteristics concerning for SAH.
While I appreciate the work of Perry and others in developing decision rules that can help us risk stratify patients into lower or higher risk buckets, there are many flaws in the Ottawa SAH rule. I certainly am not doing a head CT in all those over-the-hill headache patients simply because they are 40+. I am also not selectively using the rule for “negative only” patients. The selective application of a rule only when it suits you, ie when its negative (PERC, Ottawa SAH, Canadian Head CT, etc), I think is poor practice as well. What I take away from this decision rule and its validations are the high yield elements of the history and physical exam. These are now evidence based data elements you can use in risk stratifying your patient.
So you think you have a patient who has a subarachnoid hemorrhage. Or might have one. Or, really, if we are being realistic/pessimistic about the disease, the data, and the probabilities most likely does not have one but has enough high risk elements in their history and/or exam to necessitate further work up. What do you do now?
The go-to standard test for someone with concern for SAH is a non-contrast head CT. Until recently, and actually still even today, the value of the CT head to rule in or out a SAH was a topic of hot debate. Luckily, this is another area where recent literature has shed some light:
Perry Article 2011
Perry’s back at it again looking at the sensitivity of CT for SAH, particularly within 6 hours. The clinical setting for this prospective cohort study was 11 tertiary care hospitals in Canada from November 2000 to December 2009 (sound familiar?). They looked at 3132 adult patients with new acute headache with <1 hour to peak symptoms. Overall, CT for SAH had a 92.9% sensitivity and 100% specificity. In the 953 patients in whom the CT was preformed within 6 hours of symptom onset, they had a 100% sensitivity and specificity. In this group there were 121 SAHs, an incidence of 12.9%!
In this article they were highlighting the difference in detection rate for new, third generation CT scanners over the prior generations and studies assessing them. It is important to note, however, that this is a cohort study and treating physicians were not asked to deviate from their standard care. Therefore, many of the patients with negative head CTs did NOT get lumbar puncture. The study authors did 6+ month follow up, referral to neurosurgical centers, and coroner record assessment to verify no SAH in patients. Take this for what you will. It is, interestingly, the “index test” or gold standard to diagnose SAH (CT or LP and clinical follow up). What the study does not show which I would love to see is the % of patients with a negative head CT at <6 hours who got LPs.
At >6 hours from headache onset, CT had an 85.7% sensitivity.
Dubosh Meta-analysis 2016
The work of Perry was combined with 5 others studies in a meta-analysis published in Stroke in January 2016.11 It was this publication that really got people (at least social media people) talking about CT head as a true “rule out” for SAH at < 6 hours. With a pooled sample of 8907 patients and a sensitivity of 98.7% with confidence intervals of 97.1 to 99.4%, this article concluded that “normal brain CT within 6 hours of headache is extremely sensitive in ruling out aneurysmal SAH.” Let’s look at this a little more closely:
The meta-analysis was composed of the study by Perry detailed above and studies by Backes, Stewart, Mark and Blok. Perry contributed 3136 patients and was the only prospective study. The other studies combined contributed 1309 and were quite heterogeneous in their designs, but all did meet the index (gold standard) test for follow up. Given that the Mark and Blok studies reported on CT negative patients, some extrapolation had to be used to arrive at the true positive and negative rate in these studies. Amazingly, because incidence is vital to determining the positive and negative predictive values of a test, the incidence of the Perry study was applied to the Blok study to generate a full data set. It is also worth noting that of the 8907 total patients there were seemingly 13 missed SAHs, and 11 of the 13 were from the Mark study.
In the end, after much extraplotation that frankly somewhat escapes me, the authors did find a worst case scenario sensitivity of 98.7%.
So from the above data it has been widely accepted (though not universally) that a negative head CT completed with a 16-slice, 3rd generation or greater machine and read by an attending level radiologist is adequate to rule out SAH. Pheeww.
THE LUMBAR PUNCTURE
So what if your patient presents at >6 hours? Or you don’t believe the above data is convincing enough? What’s your next step? As we discussed initially, the lumbar puncture is the next branch point in the work up and rule out of SAH.
The reason this study is completed is to look for a) red blood cells in the CSF or b) xanthrochromia in the CSF. For those not in the know, xanthrochromia is the discoloration of CSF caused by the breakdown of blood products. Interestingly, the breakdown of RBCs in the CSF causes two things- first you see oxyhemoglobin, which can happened within 2-4 hours but can occur in vivo (in the person) and in vitro (in the test tube). Secondly you see bilirubin production which is formed only in vivo. Xanthrochromia cannot come from another place. RBCs in the CSF break down and cause the discoloration. Importantly, spectrophotometry is needed to truly recognize the bilirubin signal in xanthrochromia and distinguish it from oxyhemoglobin.
As you can tell, RBCs will be seen in the CSF immediately upon SAH, but xanthrochromia can take time. Because sticking a needle into someone’s spine can cause bleeding in and of itself (surprise, surprise), the differentiation between a traumatic tap and a true positive SAH can be difficult. Luckily, some more recent literature helps us tell between the two, and guess who it’s by.
Jeff Perry and his crew got one more bit of useful data out of those Canadian academic EDs from 2000-2009. The group looked at the same patient populations as the Ottawa SAH rule group with the same inclusion/exclusion criteria and definitions. If you remember, LPs were performed at the discretion of the treating physician. Data were collected on the CSF gathered and CSF was considered abnormal is xanthrochromia was present (5 of 6 sites using visual analysis) or if RBC was >1 x 106. An aneurysmal SAH was defined as +CT, or xanthrochromia, or RBCs in final tube with CT angio + for aneurysm.
In this study, 1739 patients underwent LP. Of these, 641 had >1×106 RBCs or xanthrochromia in their CSF. Of these, only 15 were found to have a SAH, 7 by xanthrochromia, 8 by RBC + CT angio results.13
The meat of this article then comes in the analysis of the RBC #s for the 8 patients with SAH signaled by RBCs in CSF and the remainder of the 641 patients. Generally, patients not diagnosed with SAH had significantly lower numbers of RBCs in the CSF. In looking at the number of RBCs in the fourth tube, the investigators found that a cut point of 2000 x 106 included all of the patients with SAH, creating a sensitivity of 100%.
It is important to note that while this is not the only study on the topic, it is one of the most methodologically sound with an appropriately high sample size.
So there we have it. Subarrachnoid hemorrhage from soup to nuts, as they say. In our talk we have gone all the way from the diagnosis and the important historical elements as well as the physical exam findings, best outlined in the Ottawa SAH rules. Let’s not forget the limitations and issues with this rule as well.
We then looked at the initial diagnostic modalitiy of choice- the modern non-contrast head CT. We see with the best data available the sensitivity of this test is ~99% and most find this to safely rule out the disease to the best degree that modern medicine is able.
Finally we looked at the LP and its use, especially if the timeframe is > 6 hours. What we find from Perry again is that a cut point of 2000 x 106 is appropriately sensitive to rule out SAH as well.
Post-CVA Show Notes
Strokes are bad. It doesn’t take a medical professional to know this. Bleeding or ischemia into the brain is something we all want to avoid and as the care takers of the general population we want to be able to recognize and (when able) treat patients with cerebral vascular accidents (CVAs).
But there is an entity lurking out there that can often confound even the most astute pracitioners- the posterior circulation CVA. As a resident I knew of this disease and knew enough to fear it, but it took some time before I became comfortable with the disease process, its symptoms, the physical exam of the post-CVA patient, and how to diagnose it. That is what we are talking about today.
Now if you’re new to EMsandbox, let me welcome you to the educational process. I am a firm believer that true understanding of a disease requires a strong understanding of its anatomy and pathology. So, like in all EMsandbox podcasts, we are going to start with some anatomy.
The Posterior Circulation
The posterior circulation of the brain is that which is fed by the vertebrobasilar system. This circulation originates from the vertebral arteries which originate from the subclavian arteries on either side. They branch off and quickly find refuge in the transverse foramen of the vertebral bodies. This occurs at C6 typically. They then course up and enter the skull through the foramen magnum, the same opening through which the spinal cord enters/exits the skull. The two vertebral arteries come together to form the basilar artery, hence the name vertebrobasilar system. The basilar artery forms the meat of the circle of willis (remember med school?). The basilar artery itself sits primary along the pons, but the whole system lies along the brainstem.
From here the system produces many branches. The important ones for this discussion are the posterior cerebral artery PCA, which feds much of the occipital lobe of the brain, the medial temporal lobe and the thalamus, the superior cerebellar artery, which feds the superior cerebellum and some midbrain, the anterior inferior cerebellar artery, which feds the inferolateral pons and anteroinferior cerebellum, and finally the posterior inferior cerebellar artery, which is the most variable of the bunch but feds the under surface of the cerebellum and some medulla. Now it should be noted that the supplies in this area are often variable and not finite. Diagnosing the location of the clot/bled is often difficult on physical exam findings alone.1,2
What these brain parts do/how to test
Occipital lobe, cerebellar, and brainstem function is a difficult area to grasp. Let’s start with the occipital lobe.
The occipital lobe is the smallest of the four lobes of the brain and is involved primarily with visual processing. Again, it is supplied by the PCA. While it is supplied by elements of the posterior circulation, it does not have the same complications as many of the other regions because of some cranial anatomy we will get into later.
The cerebellum- which translates to “the little brain” is the coordination center of the brain. It receives sensory information from the body, spinal cord, and other areas of the brain and helps regulate voluntary movements like coordination, speech, and balance. It is primarily supplied by the SCA, but there are also some regions supplied by the AICA and the PICA.3
The brainstem- Discussing the brainstem is a big fish to fry. With the large collection of cranial nerves running through it, the roles of the brainstem get complicated. Know that it is broken down into three component parts: the midbrain, pons, and medulla from cephalad (toward the head) to caudad (toward the feet). One way of thinking about the brainstem and its functions are to think of the involved cranial nerves (CN). As there are 12 cranial nerves, breaking them down into 4 CNs per section
Midbrain: the “highest up” of the brainstem parts, the midbrain possess CNs 3 and 4. It is therefore best thought of as involved in eye movement. An easy way to test the midbrain is in pupillary reactivity. This does require function of CN 2, the optic nerve as well.4,5
Pons: The pons possess CNs 5-8. It therefore has roles in facial movement and expression. There are also roles in hearing and equilibrium. An easy test of the pons includes the corneal reflex in which the eye is lightly touched to induce a blink response (motor of the face as we said).6,7 It is supplied by the basilar artery itself as well as some SCA.
Medulla: the most caudad of the brainstem segments, the medulla houses CNs 9-12. It is involved in tongue and pharyngeal movements; it is therefore tested via the gag reflex. It is supplied primarily by the PICA, anterior spinal artery, and the vertebral arteries themselves.8
Cranial Anatomy and Divisions
This is a surprisingly important concept to grasp and part of what makes the posterior CVA an important diagnosis to make early. The brain within its skull has several internal divisions of fibrous tissue. The cerebral hemispheres are separated by the falx cerebri. The brainstem and cerebellum lie below the tentorium cerebelli. This creates a bit of a space issue- bordered above by the tentorium cerebelli, and laterally and inferiorly by the skull base, these structures don’t have a lot of room to move when edema becomes an issue… and herniation through the foramen magnum is the path of least resistance.
Again, as noted above, the occipital lobe is part of the conversation in that it has posterior circulation blood supply, but is not constrained by the tentorium.
Now the pathology…
So now let’s talk about strokes. Cerebral vascular accidents come in a few flavors; the big categories divide into infarction, or lack of blood supply, and hemorrhage. Infarcts constitute ~80% of the CVAs we see. These can be thrombotic or embolic. The risk factors for these are similar, with thrombotic having a stronger association with dyslipidemia, smoking, and diabetes and embolic having the strongest association with Afib, but this disease itself is correlated highly with atrial fibrillation.9
Hemorrhagic CVAs are again the less common of the two and has the strongest asscociation with hypertension. African American ethnicity and chronic renal disease have also been seen to be correlated.10
Of the strokes, it is estimated that 1 in 5 are posterior circulation.11
Because the posterior circulation supplies many parts of the brain with many different functions, presentation can be variable. Again, this is not a neurology podcast, and because our goal is to make you think of the posterior circulation infarct clinically, we are not going to get weighed down in the details. So, what is the posterior circ cva patient look like?
Generally, your patient is going to be older with the risk factors we just outlined above. As you will see, because so much of what can be infarcted is involved in the processes of balance, coordination, vision and movement, patients will often complain of one or more of the following: dizziness/vertigo, nausea/vomiting, visual disturbances (classically diplopia), gait instability/falling (classically to one side), and poor coordination.
To break this down by vascular territory:
Posterior cerebral artery– a major supplier to the occipital lobe so visual complaints will often predominate.
Superior cerebellar artery– an important vessel for the cerebellum, patients affected in this artery experience Ipsilateral limb ataxia, vertigo, nystagmus, dysarthria, and gait ataxia.
Anterior inferior cerebellar artery– Ipsilateral dysmetria, hearing loss, Horner’s syndrome.
Posterior inferior cerebellar artery– vertigo, nausea, vomiting.12
Posterior Circ CVA vs peripheral vertigo
Vertigo is a common ED presentation and only about 1-3% of cases are thought to have a central cause, meaning originating from the brain or brainstem as opposed to the periphery (most notably the inner ear). Misdiagnosis rates, however, for central causes are high as 35%.13 The peripheral disease processes that cause syndromes of vertigo are benign paroxisymal peripheral vertigo, Meniere’s disease, and vestibular neuritis.
A common presentation with a rare but lurking serious etiology is never a fun situation to be in as a diagnostician. There are many tables out there that are supposed to help differentiate peripheral vertigo from central.14 These I find unreliable, given the number of “variable” or “depends” categories they hold. The important elements are as follows:
Sequella of post circ CVA
The number of patients who develop space occupying edema after a cerebellar/posterior circ infarct is not entirely clear. The most recent literature compiled on the topic from Neugebauer 2013 sites numbers from 17% to 54%.18 Additionally complicating the picture is the fact that only 50% of patients with mass effect on imaging develop clinical deterioration.
A smaller study19 reported on personal experience in 52 patients with space occupying cerebellar infarcts and found Babinski’s sign and horizontal gaze deficits to be the most frequent predictors of badness. They also report a <24 hour timeframe from first sign of compression to significant decompensation.
So when your patient starts to show signs of herniation on imaging, the first question to ask is what is the clinical exam? If the patient has the physical exam findings to suggest progression to herniation (babinski’s sign and horizontal gaze palsys), then treatment is necessary. From our standpoint, we can intervene with hyperventilation (user beware rebound spike) and osmotic agents (mannitol, hypertonic saline). Most importantly though, this patient needs and neurointensivist. Obstructive hydrocephalus and brain edema with mass effect are most definitely treated with ventriculostomy and suboccipital decompressive craniectomy.
Superficial Thrombophlebitis- CORE CONTENT
While typically thought of as a benign, self-limited condition, superficial thrombophlebitis (STP) has some caveats to work up and treatment, which are often not fully understood. We will review these here.
First, let’s start with some simple definitions. Superficial thrombophlebitis is composed of thrombosis– clot within a blood vessel, and phlebitis– inflammation of the walls of a vein.
The term superficial and its associated confusion as lead to actual changes in anatomical nomenclature within the leg. In years passed, the two deep veins of the leg were termed the deep and superficial femoral veins. This lead to confusion, as these are deep venous structures. Hence the superficial femoral venin (a deep vein) was renamed simply the femoral vein. There are, therefore, two deep veins of the leg: the deep femoral vein and the femoral vein. The true superficial veins of the leg you can think of as any vessel that comes through the saphenous opening, or the popliteal fossa. They are all, essentially, tributaries off the axial veins- the great saphenous and small saphenous vein.
Noted distinction: Superficial thrombophlebitis vs superficial vein thrombosis.
Some text makes a distinction between an inflamed clot in the tributaries to the great and small saphenous veins (called superficial thrombophlebitis) and an inflamed clot in these vessels themselves (called superficial vein thrombosis [SVT]). We will discuss these entities collectively initially but then make distinctions in them when it comes to management.
What causes this?
Given this is a clotted vessel with associated inflammatory changes, Virchow’s triad (stasis, endothelial injury, hypercoagulable state) comes into play. Anything that increases a person’s risk for these pathologic states will also increase their risk of superficial thrombophlebitis and superficial vein thrombosis.
The #1 cause of STP is varicose veins. This condition is involved in nearly 90% of cases. In these varicosities there is venous stasis; there is often then an associated trauma to these superficial veins that leads to the thrombosis and resultant inflammation.
The other causes/risk factors for these conditions are the same as those for DVT: malignancy, IV cannulation, estrogens & pregnancy, smoking, and prior history to name a few. Interesting, STP is particularly common in the post-partum period.
How do I diagnose this?
The diagnosis of STP is more or less clinical, with correlation of bedside or formal ultrasonography. A streak of erythema overlying a superficial vessel with a “palpable cord” usually seen. Ultrasound is helpful in both quantifying the size and location of the thrombosis.
Do I have to look for a DVT too?
In cases of superficial venous thrombosis, which again is a thrombosis/erythema in the axial veins (the great and small saphenous veins), there has been shown a clear association with concurrent DVT. The rates vary depending on the study cited, but most cite a rate somewhere between 6 and 40%, with a few going as high as 65%.2,3,4 Generally, it has been found that the more proximal the thrombus the more likely a concurrent DVT will be found. This is most true in the great saphenous vein.3
Therefore, in text that makes a distinction between STP and SVT, they recommend duplex US in cases of SVT to assess for concurrent DVT. When text use the blanket term STP, an ultrasound is recommended for confirming length of thrombus and assessment for concurrent DVT. BMJ best practices makes this recommendation.4
How do I treat this badboy?
Treatment recommendations have been evolving over the last decade. Collectively, it is agreed that any patient with a concurrent DVT be treated with anti-coagulation. The other uniformly recommended treatment include heat and compression stocking therapy.5 Essentially, there was a Cochrane review in 2007 that showed similar efficacy of low molecular weight heparin (LMWH) to NSAIDs.6 Then the Calisto trial came out.
The CALISTO Trial was a larger study completed in 2010 trying to answer the question of whether or not patients with superficial vein thrombosis were at increased risk of developing DVTs and PEs. With 3000 patients enrolled, they showed a strong association with reduced DVT (18% in placebo v 3% in anticoagulated), PE (5% vs 0%) and extension of clot (51% vs 4%) at 47 days.7 Patients in this study had clots of > 5 cm and were excluded if < 3 cm from saphenofemoral junction.
This has led to a change in societal recommendations, practice patterns, and of course some controversy. The most widely held societal recommendation followed is probably the American College of Chest Physicians who recommend anticoagulation treatment in patients with clot burden > 5 cm.8 Others have included additional high risk elements such close proximity to the saphofemoral junction (<5 cm) and significant hypercoagulable state (ie cancer) to the list of indications for anticoagulation.1
There is controversy regarding the treatment in this area, as large randomized studies are lacking. Wichers et al, for example, did a systematic review assessing various forms of treatment. His study showed similar prevention of propogation in patients using NSAIDs compared to anticoagulants, but the authors went on to recommend more aggressive anticoagulation.9
In this regard, it will have to come down to the patient in front of you and their clot burden/location. The important take homes here are some SVT are more likely to propogate than others, with risk factors being large clots, proximity to the femoral vein, involvement above the knee, prior clots, and medical risk factors.
The pros and cons of full anticoagulation above NSAIDs must be weighed in each patient’s case. With significant benefit from anticoagulation included decreased extension rates, lower rates of DVT and PE, and less need for surgical intervention (to name a few), there is good argument for starting these medications, but as always the risk of anticoagulation must be considered.
Airway Adjuncts Core Content Show Notes
Before the Devices
Lets not forget the basics. The first and most valuable resources at your disposal are your own two hands. In a patient with an occluded airway or concern for airway compromise, a simple maneuver can re-establish patency and buy you time to assemble, measure and deploy your airway adjuncts.
Head tilt chin lift: Simply press down on the forehead and raise the jaw upward.
Jaw thrust: used in patients with concern for cervical spine fracture. Place thenar eminence on the zygomatic arc of the patient and place fingers behind the angle of the mandible. Pull up on the mandible, causing the jaw to be pushed forward.
Spectrum of Use
Airway adjuncts have a spectrum of purposes, from assisting a patient in maintaining airway patency to esophageal occlusion and assisted ventilation with positive pressure breaths.
When discussing the following airway adjuncts, it is important to think first about what you are trying to fix or correct. Start by asking yourself wheres the problem?
Does your patient have a brain stem issue and lack of respiratory drive? Or are they medically suppressed (opioids), with an intact respiratory drive but less interest in keep their oropharynx open? Is it simply an oral issue with tongue swelling? Or have they aspirated significant quantities of stomach content and no amount of airway stenting going to save their abused lungs?
Thinking about where the problem is and what it is will help you select the right adjunct.
Indications: Patients with concern for upper airway obstruction. Can be used in patients with intact gag reflex or clenched teeth (if appropriately sized).
Contraindications: Concern for significant skull base fracture or midface fracture.
Measuring: Measure larger nare diameter and estimate NPA on this. Measure from the edge of the nare to the angle of the mandible.
Insertion: Lubricate the tip of the NPA and insert with the bevel directed toward the nasal septum.
Indications: Patients with concern for upper airway obstruction. No gag reflex and relaxed jaw musculature.
Contraindications: Gag reflex.
Measuring: Measure from the commissure (edge of the mouth) to the angle of the mandible.
Insertion: Insert airway “upside down” (or some say rotated 90 degrees) with tip running along the hard palate. When you feel soft palate rotate 180 degrees until phalange hits the teeth.
Indications: Patients with compromised airway, depressed respiratory drive, or at risk for aspiration. No gag reflex and relaxed jaw musculature.
Measuring: Adjunct dependent.
Insertion: Adjunct dependent.
A dual lumen device inserted blindly
Size: Available in two sizes: 37 Fr (for patients 4 to 6 ft or 122 to 183 cm tall) and 41 Fr (for patients more than 5 ft or 152 cm tall)
Size: sized by ideal body weight of the patient.
Insertion: Sniffing position, partially inflated cuff, lubricate mask rim, insert with aperture facing along the tongue line. Run the back aspect of the LMA along the hard palate to help avoid displacing the tongue posteriorly.
Size: sized by patient’s height (similar to ideal body weight).
Insertion: With consciousness not to displace the tongue posteriorly, run the tip of the King along the hard palate, much like the LMA. Insert fully to base of connector is aligned with the teeth. Inflate the cuff with the mLs of airway outlined for King size.
While not technically an airway adjunct, the process of ramping deserves discussion. With the ever growing size of the American patient, consideration of positioning is important. When the patient loses their airway reflexes or ventilator drive, the obsess patient is very likely to occlude their own airway. While good mask seal is important in all BVM use, it will not overcome the soft palate and pharyngeal obstruction. Couple this with minimal submental space and lots of anterior chest wall, intubating the supine obese patient becomes an often insurmountable task.
Enter ramping. This is simply the process of elevating the upper thorax, shoulder, neck and head of the obese patient to allow an ear to sternal notch anatomic alignment. This helps keep the airway open in the RSI process and allows for optimal view of the vocal cords during tube passage.
Core Content Show Notes:
Here we review three major antihypertensive- Beta Blockers, Calcium Channel Blockers, and Clonidine- who share a similar toxidrome. The way these meds with present in overdose is bradycardia and hypotension.
Basics of neurotransmission: There really are only 3 components you need to know about this complex biochemical process to understand meds. These are the presynaptic cell, the neurotransmitter, and the post-synaptic cell. Here we apply this to how the body maintains blood pressure and cardiac output:
Now let’s talk about the specific agents.
Mechanism of Action: blocks the first step in this chain reaction. Stimulating α2 receptors in the CNS affects the presynaptic cell. This decreases the output of Epi/NE into the blood stream.
Distinguishing clonidine from BBs and CCBs: As we said, all these agents will have bradycardia and hypotension. The non-BP related effects are where you see the difference in the agents. Clonidine also hits the locus coeruleus (don’t need to remember this) in the brain, and causes an opioid-like syndrome of miosis, lethargy and respiratory depression
Beta Blockers (BBs)
Mechanism of Action: blocks the β1 receptors on our myocytes. The Epi/NE are in the blood stream, but do not get to have their post-synaptic effect.
Distinguishing BBs from others: Because they work on β receptors, there can be cross-reactivity in toxicity (at what level depends on medications selectivity β1 vs β2). The β2 effects are seen as bronchospasm, especially in patients with reactive airways. Blocking Epi in the liver with also result in decreased gluconeogenesis and can hypoglycemia.
Calcium Channel Blockers (CBBs)
Mechanism of Action: blocks the Ca2+ channel, that last step in the cascade where increased concentration of Ca2+ in the myocyte leads to increased inotropy.
Distinguishing CCBs from others: CCBs affect the same Ca2+ channel on other organs, including the pancreas. Blocking these channels in the pancreas decreased insulin secretion, leading to hyperglycemia.
Generally, in terms of symptom severity it goes from clonidine < Beta Blocker < Calcium Channel Blocker in terms of severity.
General principles of toxicology apply, which include: decontamination, enhanced elimination, and antidotes. For our antihypertensives, you can use activated charcoal and whole bowel irrigation, depending on the time frame. There are no real means of eliminating these agents more quickly.
Again, generally a “mild” overdose, clonidine often does not have the severe bradycardia or hypotension of the others. Interestingly, atropine is not a good agent in this overdose. This is because atropine works by decreasing parasympathetic (vagal mediated) tone, with the hopes of unopposed sympathetic tone leading to increased heart rate and blood pressure. But as we know, the sympathetic system is being blocked at the level of the brain stem, so no dice.
But if you move down the cascade, you arrive at Epi/NE which still have open, normal β1 receptors and downstream effects. Giving some exogenous Epi/NE gets the cascade back on track. You can also try to increase the calcium gradient at the level of the Ca2+ channel simply by giving calcium. This can work, but the effect is moderate at best.
Now, if we go off what we’ve learned, we no atropine isn’t going to help much. Epi/NE work for clonidine, but we are blocked one step further down the cascade, at the β1 receptor, so Epi/NE can be given in heaps but there is no receptor to act on. Giving calcium to increase the transcellular gradient still works, and is still with limited benefit.
But wait! There is another receptor on our myocytes that also increases cAMP, just like β1!! It’s the glucagon receptor. cAMP is cAMP and works on the Ca2+ channel just the same, no matter where it came from. So by giving glucagon you can bypass the β1 receptor and still get your Ca2+ into the cell.
Calcium Channel Blockers (CCBs)
Now we’re at the end of the line. The Ca2+ channel is blocked and no amount of atropine, Epi/NE, calcium, or glucagon is going to open it. So, what do we do?
Hyperinsulinemia-Euglycemia (HIE): why this stuff works is complicated/not fully understood. Maybe it’s because the heart in a stressed state uses carbohydrates more, and HIE increased carbs available. Maybe it’s that insulin can sneak more Ca2+ into the myocyte. Maybe it’s magic. Maybe it’s Maybelline. Either way, it works. And all you need to remember is 1 U/kg. That is the bolus and hourly rate.
Intravenous Lipid Emulsion (ILE): Putting a bunch of lipids in the blood seems to work. Why? Maybe it’s a lipid sink, absorbing the CCB, removing it from the active site. Maybe it’s an alternative form of myocyte energy. Again, the physiology is unclear. To use this call your pharmacist, but generally is 1.5 ml/kg bolus and 0.5 ml/kg. The efficacy and safety of this treatment for CCB is not as well established as HIE, so use this with caution.
Cunningham Shoulder Reduction- Core Content
Shoulder reductions and the various techniques can get confusing. Everyone and their mother has come up with some way they think is best to reduce this dislocated joint. Here we discuss a new(ish) type of reduction that does not require procedural sedation- the Cunningham technique. First, a little review.
The shoulder is the most commonly dislocated joint. It has evolved to have insane range of motion in multiple planes. But with this mobility comes instability. The dome of the Humerus sits in a very shallow cup of the glenoid. Lets review some anatomy quickly.
The shoulder joint in its brass tax is composed of the humeral head sitting in the glenoid fossa of the scapula. The scapula has two other important boney prominences involved in the shoulder’s architecture- the coracoid and the acromion. The acromion articulates with the clavicle the (technically) third bone of the shoulder. Along this U shaped articulation the deltoid and trapezius muscles attach. The coracoid has a strong coraco-acromion ligament as well as a coracoclavicular ligament. It also is the insertion point for the biceps brachii and the pec minor.
When the humeral head dislocates from the glenoid, the shoulder often takes a classic “step off” appearance with a flattening of the deltoid. The patient will often keep that arm fully adducted against the body with the forearm across the abdomen.
The shoulder can dislocate in three directions- anteriorly, posteriorly, and inferiorly. The anterior dislocation is by far the most common- representing >90% of all dislocations. Mechanistically, it is often with the arm abducted and externally rotated. Think of a quarter back about to throw a pass. This is the most vulnerable position. Posterior dislocations are classically taught to occur after seizures or electrocutions, where there is abnormal muscular contraction, but practically this is often a fall on an internally rotated outstretched arm. The inferior dislocation, the white whale of shoulder dislocations, occurs in 0.5% of dislocations and is the result of an axial load on the shoulder. This is also called luxatio erecta and presents with the arm stuck in abduction.
In this clinical case we present an intra-articular block/anesthesia and Cunningham reduction. Let’s discuss the shoulder block here. There are two approaches to the shoulder block: anterior and posterior.
Anterior: In this approach, you are using the coracoid process as your boney landmark. The shoulder is rotated externally and you palpate the head of the Humerus. The needle is inserted just medially to the humeral head staying slightly inferiorly and laterally to the coracoid process.
Posterior: In this approach, we are using the acromion as our boney landmark. The patient is in neutral position. The sulcus between the humeral head and the acromion is palpated. The needle is then inserted 2-3 cm the most inferio-medially part of the acromion.
Now, is using intra-articular lidocaine without procedural sedation to reduce someone’s shoulder inhumane? In short, no. As proof, Fitch et al. did a systematic review of 6 papers comparing procedural sedation to intra-articular lidocaine and found no difference in pain or reduction success rate. There were, however, more complications in the full sedation group.
A clinician can get overwhelmed with all of the possible reduction techniques out there. The ideal technique is one that is painless, requires only one practitioner, uses minimal force, and no IV sedation. Through the many attempts of proving one technique superior to the others, no one has risen to the top in the literature. The AAOS also does not endorse one technique over the others.
Today we are going to talk about the Cunningham. This is a technique that was first published on in 2003 by Dr. Neil Cunningham In the Emergency Medicine Australasia. The technique is completed by doing the following:
Have the patient sit in a comfortable position (sitting, adducted arm, elbow flexed)
Place the patient’s hand on your shoulder (if able)
Place your hand in the patient’s in elbow crease
Apply gentle downward pressure
Ask the patient to pull their shoulder blades together
Massage the shoulder/bicep musculature
Add gentle external rotation as needed
Success rates for this technique vary and this is little published literature on unselected patients. The bottom line is this is going to require a relaxed, not hyperaesthetic with a relatively thin frame (you need to over-come the muscles) and preferably not be out that long. The longer the dislocation, the more fixed the spasm.
Acad Emerg Med. 2008 Aug;15(8):703-8.
BLUNT TRAUMA ARREST
Core Content Show Notes
Henderson Paper: ‘94 California. Looked at registry of cardiac injury patients. 251 patients. Looked to find predictors of survival. Had 14% blunt injuries, but NONE underwent thoracotomy. Patients with +VS had a 62% survival, -VS had <1%. Note that not all patients underwent ED thoracotomy. 122 ED thoracotomies done, 4.9% overall survival. 110 of EDTs done on patients with PI of 20, and these had <1% survival. Paper found, like others had, that Physiologic index was the best predictor of survival and that GSW to the heart is bad for one’s health.
Durham Paper: ’92 Texas. Retrospective review of thoracotomies over a 6 year period. Specific focus was on prehospital interventions that improved survival. 389 patients, 53% GSW, 29% stab, 18% blunt. Survival: 15% for stab, 7% for GSW, 0% for blunt. Major finding among survivors was that intubated patients had a mean CPR time of 9 minutes vs 4 minutes for nonintubated patients. Basically, intubating the patient prehospital doubled your time window to preform EDT.
Lorenz Paper- ’92 California. Retrospective review of 10 years of cases from 1980-1990 with 463 total patients. Looked at the predictors of survival. They had a 22% survival for penetrating trauma (8% for GSW and 34% for stab) and a 2% survival for blunt. There were several patients with no SoL in the field who underwent EDT (remember, 1980s). None of these survived. One conclusion was that EDT should be withheld in these patients, and it now is. In dissecting the blunt arrest patients more, it turns out of the 2% survivors (3 patients), only 1 underwent EDT and the other 2 underwent operative sternotomy. Given the reported survival percentage, Lorenz concludes blunt trauma arrest is a relative contraindication to EDT. Collectively this paper reports improved survival of stabs over GSWs, and better survival in patients with higher physiologic indices.
Hunt Paper- ’05 Ohio. Site doesn’t matter here because this paper reviews the history of EDT, the pathophys of thoracic trauma, etc. Worth noting that blunt chest trauma results from deceleration or crush and results in hemothorax, heart/lung contusions, and disruption of the great vessels (bell clanger). Paper then goes into PI and cites Henderson.
Lockey Paper: ’12 UK. Essentially a paper presenting an algorithm. Lockey et al mention 18 years experience with thousands of patients, then present a skematic of how they proceed. There is an emphasis here on pre-hospital thoracotomy, as their system as physician-led EMS units. This paper does not present data supporting this. Also introduces HOT (hypovolemia, oxygenation, tension ptx) in the algorithm.
Burlew/WEST guidelines- ’12. The WEST recommendations state a use of the available data and reports on EDT, though specific numbers are referenced only for survival rates in different circumstances. Largely an expert consensus paper and they are clear about this. WEST produces a simples to follow algorithm (Fig 1) with the following components: CPR with no signs of life (SoL) [motor/resp effort, electrical activity, pupillary response] gets divided by injury and time. Penetrating trauma with >15 min CRP is called. Blunt Trauma with >10 min CPR is called. If you’re in the time window, do the EDT. They cite survival rates of 15% for penetrating trauma and for blunt it is 2% if in shock and <1% if no SoL. They DO recommend EMS do CPR, as well as intubate and transport quickly. They go on to state that once in the chest, patients without cardiac injury or tamponade with asystole should be called. If after all resuscitation is preformed the patient cannot maintain a SBP > 70, the patient is deemed nonviable and resuscitation is ended.
Inaba paper- ’15 California. Prospective study of 187 patients undergoing EDT. All got parasternal and subzyphoid views before or during thoracotomy. They found that all survivors (true survivors and organ donors) had cardiac activity on US. Patients’ with pericardial fluid seen on US did not survive. Interestingly, no patients with a cardiac injury survived, which is somewhat contradictory to the physiologic argument for the EDT in the first place. In their conclusions, they state that in patients with no cardiac activity or pericardial fluid on US survival was zero. This somewhat lumps the pericardial fluid finding in with the more clinical significant finding of cardiac activity.
Rhee Paper- ’00. This is the systematic review paper. Rhee and colleagues looked at the prior 25 years of data on EDT and reviewed it. 24 papers of appropriate quality were found and the associated 4,620 patients formed the basis of analysis. Overall survival of EDT was 7.4%. Broken down by mechanism, it was 1.4% for blunt and 8.8% for penetrating, which was further subdivided into 16.8% for stab and 4.3% for GSW. Rhee also looked as SoL (resp effort, electrical activity, pupillary response). They found patients who had SoL in the hospital had an 11.5% survival, versus 2.6% for those without.
Seamon/EAST paper- ’15. A more systematic and scientific look at the literature than the WEST guidelines. This paper did a PICO analysis of specific questions related to EDT and collectively reviewed 72 studies and 10,000+ patients to base their recommendations on. Six questions were formulated based on the following criteria: with/without SoL for penetrating thoracic/penetrating extrathoracic/blunt injuries. They defined SoL as pulse, BP, motor/resp effort, pupillary response and cardiac electrical activity. To simplify the results, I present them in bullet form:
*They do not put a definitive timeframe for this, but mention the 15 minute window discussed in other studies.
+No definitive timeframe outlined.
Rh Alloimmunization- Core Content
When to use Rhogam and at what dose, while seemingly a straightforward subject, can be confusing. In this Core Content we review some brief epidemiology on Rh status, discuss the consequences of Rh alloimmunization, review what Rhogam is, and finally when to use it.
We can remember from medical school that peoples’ red blood cells (RBCs) either have an Rh antigen (also called Rhesus factor or D antigen) or they do not. People without the antigen will therefore recognize the Rh antigen as foreign if it is in their body/blood. The resultant immune response creates antibodies to the Rh antigen, just the same as it would a viral or bacterial antigen.
But how common is this, really? According to the Rhogam website1, the prevalence is variable by race. They give the following table:
Other resources site more general numbers, with Rh negative status being 15% of the population as a whole.2 BMJ best practices actually sites very similar numbers to the Rhogam website, with ~15% for white, ~7% for black, and <1% for Asian and Native American.3
This is the devastating consequence we are trying to avoid. It is VERY important to recognize that the risk does not occur with the first exposure to the Rh antigen. Compare it to an allergy to bee stings, you dont get anaphylaxis with the first sting. Your immune system has to build its antibody army first. It is then with subsequent stings that things start going wrong.
The same is true for Rh alloimmunization. The maternal circulation must first see the Rh antigen, recognize it as foreign, and build an immune response to it. This can happen during blood transfusions (not really anymore) and, more commonly, exposure to Rh+ blood during the course of a pregnancy from any number of causes (delivery, miscarriage of any variety, OB procedures, abruption or other trauma, etc).2 How much blood is needed to sensitize is actually not well understood, but some studies show as little as 0.1 mL.2,5 Most sensitization events are thought to be deliveries, where the mother is exposed to the largest amount of fetal blood. Therefore, it is usually not the first born Rh+ kiddo who is the problem but subsequent pregnancies.
Once the fetomaternal hemorrhage occurs, mom’s immune system makes antibodies to the Rh antigen. It is thought that it takes a while for there to be a clinically significant immune response mounted. Again, studies vary from 4 up to 15 weeks.2,5 Once made (or more commonly present in mom ever since the last kid), it is specifically the IgG that crosses the placenta and will start attaching itself to the fetal RBCs.4 This leads to the RBCs destruction in the fetal spleen.
The effects of Rh alloimmunization
The opsonization and destruction of fetal RBCs in their own spleen leads to a profound anemia. The discussion of its recognition and monitoring in utero is beyond the scope of this talk. The significant anemia leads to the fetus having hydrops fetalis, characterized by severe edema and technically consisting of at least two of the following: ascites, pleural effusions, skin edema, and pericardial effusion.5,6 The care and management of a fetus both in utero and post-delivery is complex and mortality rates are high.
Hydrops fetalis is a disease much more easily avoided than treated. To prevent the alloimmunization, science has created Rh-D immune globulins, best known under the trade name Rhogam. This medication is preformed antibodies to the Rh antigen. The physiology behind its functioning is that the Rh-D immune globulins administered to a pregnant patient will find and sequester the Rh antigens that entered maternal circulation during the fetomaternal hemorrhage.
How to use it
The first step to preventing Rh alloimmunization is to think to do so. While our colleagues in Obstetrics and Gynecology are trained to be hyper-vigilant in this regard, consideration of Rhogam is not always high on our priority list. Rh– women are given Rhogam 300 µg at 28 weeks gestation and within 72 hours of delivery by our OB colleagues.7
For our purposes, we need to know when to give the Rhogam and how much to give. The following conditions are considered times in which fetomaternal hemorrhage may occur, and hence, when Rhogam is indicated: Threatened or spontaneous/induced miscarriage, blunt abdominal trauma, ectopic pregnancy, fetal death (2nd or 3rd trimester), antepartum hemorrhage (abruption or previa), and molar pregnancy.7,8 The American Colleague of Obstetrics and Gynecology (ACOG) and UpToDate are in agreement in this list.
In terms of dosing, the “full dose” of Rhogam is 300 µg, and is thought to be effective at suppressing immune response to ~30 mL of fetal blood Rh+ blood. A smaller, 50 µg dose is effective against 5 mL of fetal blood. It is only after 20 weeks gestation that the entire fetal circulation is 30 mL of blood. Therefore, after this timeframe the 300 µg dose may actually be inadequate, depending on how much fetomaternal hemorrhage occurred.8 ACOG makes specific mention of quantifying fetomaternal hemorrhage in cases of placental trauma.7
In the first trimester, there are many who recommend the 50 µg dose, citing that at 12 weeks the fetal circulation contains ~5 mL blood.8 ACOG, however, recommends a 120 µg dose and states its actually ok to give the more readily available 300 µg dose.7
Importantly, using Rhogam in a Rh+ patient is not thought to be harmful, though generally should be avoided.8
ALCOHOL WITHDRAWAL DEEP DIVE SHOW NOTES
Visual Aid created for Benzos in the Healthy Liver vs Cirrhotic.
Notes from Bryan Hayes on material discussed:
Contraindications for outpatient therapy: https://www.ncbi.nlm.nih.gov/pubmed/15706731
ALiEM post on benzos: https://www.aliem.com/2013/all-benzodiazepines-are-metabolized-by-the-liver/
ALiEM post on dexmedetomidine: https://www.aliem.com/2013/dexmedetomidine-precedex-as-adjunct-for/
Handout from SMACC talk on severe EtOH withdrawal: https://pharmertoxguy.files.wordpress.com/2016/07/hayes-2015-smacc-beyond-benzos-for-alcohol-withdrawal-handout.pdf
Phenobarb articles: https://www.ncbi.nlm.nih.gov/pubmed/1986421, https://www.ncbi.nlm.nih.gov/pubmed/22999778, https://www.ncbi.nlm.nih.gov/pubmed/17255852
Maryland EtOH withdrawal protocol:
Updated and Reviewed: March 2009, December 2013.
Reviewed By Siu Yan Amy Yeung, Pharm.D.; Christopher Welsh, MD; Carl Shanholtz, MD; Mangla Gulati, MD
Core Content Show Notes
Alcohol withdrawal is an issue faced in nearly every Emergency Department. What we are going to review here is the physiology of withdrawal, who is most at risk for severe symptoms, and how to manage the withdrawing patient on all levels of the spectrum from the shakes to florid DTs.
Alcohol (EtOH) withdrawal is obviously incredibly common, and it is estimated that ~1/2 million people in the US get pharmacotherapy for symptoms of withdrawal each year.2 To understand this, first let’s talk about what EtOH does to the brain.
Alcohol causes a one-two punch on important neurotransmitters in the brain- GABA and glutamate. Think of GABA as the breaks (inhibitory neurotransmitter) and Glutamate as the gas (excitatory neurotransmitter). EtOh is a neuro suppressant because it enhances GABA (slams on the break) and inhibits glutamate (takes the foot off the gas).
Because the body doesn’t want your life to pass by in a coma, when alcohol is chronically present in the blood, it will up regulate glutamate and down regulate GABA to allow the chronic alcoholic to be alive and walky talky with higher and higher blood alcohol levels.
So now the stage is set for abrupt withdrawal. The severity of withdrawal depends on the chronicity of their alcohol abuse, how much they drink per day/sitting (ie average blood alcohol level), and if they ever have periods of abstinence. Genetics is also thought to possibly play a role.3
Before we delve into symptoms and spectrum, let’s briefly discuss concurrent conditions and get that out of the way. The withdrawing alcoholic has the potential for many concurrent disease processes that can confound and need treatment. Quickly, here they are:
Dehydration- EtOH has a diuretic effect and will often replace water as the PO liquid of choice. If the patient is vomiting that can increase this volume depletion.
Hypoglycemia- poor nutrition and low glycogen stores can lead to this.
Low thiamine- this is the classic definiency, thought to be nutritional, that precipitates a Wernike’s encephalopathy.
Hypomagnesaemia- etiology to this is likely similar to above (diuresis, nutritional deficiency), but some Canadian research has shown the most common cause behind hypomagnesemia was severe chronic alcoholism.4 Others, however, have questioned the validity of this.7
“Minor” withdrawal symptoms: Autonomic instability is the name of the game in EtOH withdrawal. The question is how bad. In the minor withdrawal patient, they will have the first signs of this, which include:
Anxiety, epigastric discomfort, tremulousness, diaphoresis, tachycardia and hypertension.4
These patients have a normal mental status. Timing for these symptoms is usually within 6 hours of EtOH cessation.
“Moderate” withdrawal symptoms:
These include further/more severe autonomic instability- significant tachycardia/hypertension, tremor affecting motor function, etc. Really, the next ‘step” if you will in severity of alcohol withdrawal is progression to seizures and hallucinations. Let’s talk about each individually:
Hallucinations- Despite their association with and inclusion in the definition of DTs (see below), hallucinations in and of themselves do not signify DTs. The distinction between withdrawal hallucinations and DTs is made by two aspects of presentation: timing and mentation. Withdrawal hallucinations with an otherwise normal sensorium occur early in the course, usually at 12-24 hours. Hallucinations of DTs is later in the game, typically 2-3 days out, and the patient is confused.
Seizures- these are usually isolated, or short spurts of tonic-clonic seizures from the ol’ GABA-glutamate imbalance. These seizures kinda have a rule of 6 to them: they occue 6-48 hrs after cessation, they must be 6 or fewer seizures, and they must be grouped within 6 hrs of the first seizure.5 Interestingly, these seizures are not uncommon and do not portend a rapid progression to DTs. If untreated though, 1/3 of patients will eventually go on to DTs.6 If the patient is in status or won’t stop going into and out of seizures, then think outside EtOH withdrawal seizures to the other badness that can accompany alcoholics (subdural, hypoglycemia, etc).
“Severe” withdrawal symptoms/Delirium Tremens (DTs) aka Alcohol Withdrawal Delirium
Lets be real. When we’re talkin’ severe withdrawal from alcohol, we’re talkin’ DTs. The better term for this is alcohol withdrawal delirium (AWD).
AWD is defined simply by two components: 1) alcohol withdrawal 2) delirium.
The DSM-V defined AWD this way: EtOH withdrawal as cessation/reduction of heavy/prolonged EtOH use and 2 of 8 symptoms (autonomic instability, hand tremor, insomnia, Nausea/vomiting, transient hallucinations, psychomotor agitation, anxiety, seizures).7 Delirium: disturbance in memory, awareness, attention that is a change from normal level for patient and fluctuates over course of day.7
Timing is also vitally important here as many of the symptoms involved in the diagnosis are also present earlier in the evolution of disease (ie hallucination and seizures). Delirium Tremens does not manifest until 2 to 3 days after alcohol cessation.8
We will skip the treatment of concurrent diseases as that was outlined above.
The treatment of the patient withdrawing from alcohol is going to depend on a few things: time from last drink, history of prior withdrawals and severity of symptoms.
The first two elements of this can be gathered from history. The severity of symptoms can be assessed generally, but calculation tools also exist. The most common is the CIWA score. This system scores from 0-67. While CIWA assists in determining severity of symptoms, many other factors come into play when deciding the modality and location of treatment. One must also consider: severity and chronicity of alcohol abuse, time since cessation, any concurrent use of other sedative-hyponotics, age, concurrent diseases, and history of prior withdrawals. All of the above have been show to increase the chance a patient goes into DTs.9
Low Risk History/Mild Symptoms (CIWA 0-8)
It is important to point out that many patients may not require active treatment. Patients without a heavy alcohol use history, who don’t have the red flags noted above, and have minimal symptoms (categorized quantitatively as a CIWA < 8) often require no medications.
Moderate Risk History/ Moderate Symptoms (CIWA 8-15)
This is the ambulatory treatment patient, if all the boxes are checked. Patients with moderate symptomatology and fall in the CIWA range of 8-15 can be considered for outpatient management if they: -Can take oral medications. -Have a reasonable level of self-care (aren’t psychotic, suicidal, cognitively impaired). -Have good social support for the withdrawal and treatment process. The ideal agent for treating withdrawal would be one that allows the GABA/glutamate imbalance in the brain to gradually return to normal without the hyper excitation. Comparisons of benzodiazepines to neuroleptic agents have shown neuroleptics to be inferior, with a RR of death at ~6.6 with these agents.8 The ideal benzo to use is a topic of debate. Unfortunately, attempted metanalyses on the topic have not shown one drug to rise to the top.8,10,11 Essentially, two schools of thought arise: 1) Use a long acting agent like Diazepam or Chlordiazepoxide which has a smooth, nature taper given its half life. Down side of these is they are metabolized by the liver 2) Use a short acting but “cleaner” agent like Lorazepam or Oxazepam, which do not have hepatic metabolism. Many opinions exist on this.12 How much to give is the next question. An approach I have liked and adopted is to tally the total ED dose required to cause symptomatic improvement/relief and create a taper in the following manner: 1) Day 1: Total ED dose of medication divided out four times a day. 2) Day 2: ¾ ED dose divided out four times a day 3) Day 3: ½ ED dose divided four times a day 4) Day 4: ¼ ED dose divided four times a day 5) Day 5: transition off While 4 days of therapy may not be a long enough treatment timeframe, by this period the patient should be in contact with an outpatient provider or detoxification center.4
Severe Risk History/ Severe Symptoms (CIWA >15)
This material could be its own podcast in and of itself. Luckily, alcohol withdrawal delirium (AWD, aka DTs) is relatively rare. It is estimated to be seen in ~5% of patients admitted for management of withdrawal.7 Mortality rates for AWD used to be as high as 15%, but with current treatment regimens numbers are closer to 1%.8
For treatment, benzos again are the agent of choice. Patients with AWD require aggressive and frequent dosing of a benzo, which leads to the recommendation of IV administration by most. The dose is unique to the individual and their tolerance, but the overall goal is the same— light sedation.
Again, there is no one benzo proven better than the others. Given that AWD often requires rapidly escalating dosing or drips, consideration of duration of action and active metabolites comes into play.
The agents with good pharmologic profiles include: Diazepam (Valium), Lorazepam (Ativan), Midazolam (Versed), and chlordiazepoxide (Librium, not IV!!). Generally, many prefer diazepam or other long acting agents with active metabolites because of the smoother transition and tapering. One should consider shorter acting agents and ones without hepatic metabolism (lorazepam) in patients with severe agitation or hemodynamic compromise requiring rapid escalation of dosing or in patients with cirrhosis. This helps prevent over-sedation down the road.
When do you know you’ve given enough? The answer isn’t in milligrams but in examination. Quietly sedated but rousable is the goal.8 To put this in a quantitative measurement, you want a RASS of -1.
Adjunctive agents may be needed to achieve this. The ones with the greatest amount of literate to support their use include phenobarb and propofol.1,5,7,8 Dosing of such agents will clearly be dependent on your amount of benzo given and patient dynamics. With dual sedative-hypnotic agents, preparation for airway control is a must.
1) What are the two neurotransmitters most disregulated in chronic alcoholics? What are they’re roles and how do they present in the withdrawal state?
2) Name 4 concurrent diseases to look for in the withdrawing alcoholic.
3) Do hallucinations and seizures mean DTs/AWD? Explain why or why not with a focus on timing.
4) What is the mainstay pharmacotherapy class for treating AWD? What scoring system can aid you in determining severity of withdrawal?
5) How do you prepare an outpatient medication regimen for the withdrawing patient? Who is fit for this treatment plan?
6) Outline your approach to the patient with AWD, when do you know you have reached your treatment goals? What is the patient’s disposition?
2) Management of drug and alcohol withdrawal. Kosten TR, O’Connor PG Engl J Med. 2003;348(18):1786.
3) Med Clin North Am. 1997 Jul;81(4):881-907. Pharmacotherapies for alcohol abuse. Withdrawal and treatment. Saitz R1, O’Malley SS.
4) Etherington JM. Emergency management of acute alcohol problems. Part 1: Uncomplicated withdrawal. Can Fam Physician. 1996 Nov;42:2186-90.
5) Etherington JM Emergency management of acute alcohol problems. Part 2: Alcohol-related seizures, delirium tremens, and toxic alcohol ingestion. Can Fam Physician. 1996 Dec;42:2423-31.
6) Victor M, Brausch C. The role of abstinence in the genesis of alcoholic epilepsy. Epilepsia. 1967;8(1):1.
7) Schuckit MA. Recognition and management of withdrawal delirium (delirium tremens). N Engl J Med. 2014 Nov 27;371(22):2109-13.
8) Mayo-Smith MF, Beecher LH, Fischer TL, Gorelick DA, Guillaume JL, Hill A, Jara G, Kasser C, Melbourne J; Working Group on the Management of Alcohol Withdrawal Delirium, Practice Guidelines Committee, American Society of Addiction Medicine. Management of alcohol withdrawal delirium. An evidence-based practice guideline. Arch Intern Med. 2004 Jul 12;164(13):1405-12.
9) Ferguson JA, Suelzer CJ, Eckert GJ, Zhou XH, Dittus RS. Risk factors for delirium tremens development. J Gen Intern Med. 1996;11(7):410.
10) Michael F. Mayo-Smith, MD, MPH. Pharmacological Management of Alcohol Withdrawal: A Meta-analysis and Evidence-Based Practice Guideline. JAMA. 1997;278(2):144-151.
11) Holbrook, Anne M., et al. “Meta-analysis of benzodiazepine use in the treatment of acute alcohol withdrawal.” Canadian Medical Association Journal 160.5 (1999): 649-655.
12) Bird RD, Makela EH. Alcohol withdrawal: what is the benzodiazepine of choice? Ann Pharmacother. 1994 Jan;28(1):67-71.
Core Content Show Notes & Questions
In this podcast we review a case of Ludwig’s Angina.
The objectives are as follows:
1) Introduce the physical findings of this often thought of but rarely seen diagnosis
2) Outline the associated anatomy
3) Create a treatment approach for the Ludwig’s patient
In order to diagnose this bad boy, you have to know the definition of the disease, which involves maxillofacial anatomy.
Ludwig’s has three important components:
1) Infection of the submandibular space (composed of the submylohyoid and sublingual spaces)
2) The infection is bilateral
3) The infection is aggressive and rapidly spreading
Don’t get lost in the terminology and all the potential spaces of the mouth. Remember K.I.S.S. (kept it simple, stupid)- Ludwig’s is a fast and mean floor of the mouth infection.
Mechanisms and Spread– “Its your stanky tooth”
Ludwig’s is most often from them chompers the patient hasn’t flossed, brushed, or noticed were rotting out of their face for years. Over 2/3 the time the infection is odontogenic, usually from the mandibular teeth. As a general principle, maxillary tooth infections tend to spread up and/or out, involving the infraorbital region or buccal area, whereas mandibular teeth will create infectious spread out or down.1
With all the fascial planes and potential spaces of the mouth, things can get confusing—We care about two spaces in Ludwigs: Sublingual and Submylohyoid. The scrawny little mylohyoid muscle separates these two potential spaces which actually communicate in the back of the mouth. The cellulitis of Ludwig’s tears right through this area, involving both spaces bilaterally.2
Once in the submandibular region, the cellulitis takes the potential space and fills it with infection. The tongue is displaced by this and can head out up or back—all of which are bad. Further communication can occur with the paraphyarngeal and then the retropharyngeal spaces. Epiglottitis, retropharngeal infections and even mediastinitis have been described.3-4 These complications are a talk for another day.
Manifestations– “Your double chin looks reeeeal angry”
It’s a gnarly infection- fevers, chills, and mouth pain are kind of a given. As the cellulitis takes potential spaces and makes them real, certain things have to get displaced:
Floor of the mouth– the submandibular face is swollen, exquisitely tender and has a classic “woody” feel to it, meaning it is taught and hard.2 If the patient didn’t have a double chin before, they will now.
Tongue– This is part of the life-threat and why we are scared of this disease. The tongue gets elevated and can occlude the airway. A slow suffocation from airway occlusion is the end outcome. In the pre-antibiotic era, this led to Ludwig’s having a near 50% mortality rate.5 Today numbers are cited in the single digits.3,6
Other clinical features of the disease basically stem from the above anatomic changes:
Muffled voice– Talking with your tongue pressed firmly against the roof of your mouth is no easy task
Drooling– Swallowing, too, can be a tall order with tongue mechanics so disrupted
Sniffing position- Just like our epiglottitis kids, when we want to maximize airway diameter as our throat starts to close, we may take a sniffing position.
Stridor– A step past the sniffing position (though not always a progression of symptoms), if you patient has stridor you better be prepping your ETT… and your scalpel.
Diagnosis– “Your mouth is being eaten, which is ironic”
The diagnosis of Ludwig’s is via the constellation of symptoms. While CT is the imaging modality of choice, never send a tenuous airway to CAT scan. As mentioned above, there are a few definitions that need to be met for it to be Ludwig’s:
a. Submandibular (submylohyoid + sublingual) infection
c. Aggressive and mean
Abscesses are typically not present in Ludwig’s given the rapidity of spread and early presentation of patients. However, in patients presenting later in the course (typically greater than 24-48 hours), abscesses can be present and do not preclude the diagnosis.6
As noted above, concurrent infection of the surrounding structures (epiglottis, parapharngyeal areas, etc) can occur.
Treatment– “A is for Asphyxia”
Airway Control– Its back them good ol’ ABCs. And with Ludwig’s it’s a hard stop at A. From an EM perspective, the cornerstone of treatment is airway protection. As noted, this is a hard livin’ fast movin’ infection, and any signs of airway compromise is a four alarm fire. Preparation for securing a difficult airway should commence. While prior recommendations were for awake surgical airway, advanced techniques including fiberoptic awake intubations have put this practice into anquity.7,10
Fight the Bugs– Antibiotics are the corner stone of management once the above is managed (ideally concurrently). It’s a mouth infection, so you are dealing with aerobes and anaerboes. This is not a time to skimp on antibiotic coverage. Activity against Bet-lactamase producing bacteria, MRSA, aerobes and anaerobes should be present.8 Combo penicillins like ampicillin-sulbactam or piperacillin-tazobactam are a great starting point.6,8 Clinda in your pen-allergic patients. Obviously, vanco or linezolid need to be added if MRSA is suspected and honestly, when is it not these days.
Source Control– Given most Ludwig’s stems from mandibular odontogenic infections, source teeth often have to be extracted.9 Abscesses, though uncommon and late in presentation, require I&D. While surgical flaying of the submandibular space to decompress the region was a common practice, it has fallen out of favor.11
Core Content Review Questions:
1) Define Ludwig’s angina.
2) Where does it usually originate from?
3) List the manifestations of Ludwig’s angina and those which are of concern.
4) How is this disease process diagnosed?
5) What is the treatment for ludwigs? Is there a role for surgery?
1) Fehrenbach MJ, Herring SW. Spread of Dental Infections. Practical Hygeine. 1997: 13-19
2) Srirompotong S, Art-Smart T. Ludwig’s angina: a clinical review. Eur Arch Otorhinolaryngol, 260 (2003), pp. 401–403
3) Furst IM, Ersil P, Caminiti M. A rare complication of tooth abscess–Ludwig’s angina and mediastinitis. J Can Dent Assoc 2001; 67:324.
4) Spread of Dental Infections. Fehrenbach MJ, Herring SW. Practical Hygeine. 1997: 13-19
5) Williams AC, Guralnick WC. The diagnosis and treatment of Ludwig’s angina: a report of twenty cases. N Engl J Med 1943;228:443–50
6) Reynolds SC, Chow AW. Life-threatening infections of the peripharyngeal and deep fascial spaces of the head and neck. Infect Dis Clin North Am 2007; 21:557.
7) Wolfe M, Davis J, Parks S. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4
8) Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am 2007; 21:355.
9) Emerg Med Clin North Am. 1985 Feb;3(1):161-78. Odontogenic infections. Rothwell BR.
10) Ovassapian, Andranik MD*; Tuncbilek, Meltem MD†; Weitzel, Erik K. MD‡; Joshi, Chandrashekhar W. MD† Airway Management in Adult Patients with Deep Neck Infections: A Case Series and Review of the Literature. Anesthesia & Analgesia: February 2005 – Volume 100 – Issue 2 – pp 585-589
11) Bross-Soriano D, Arrieta_Gómez JR, Prado-Calleros H, Schimelmitz-ldi J, Jorba-Basave S. Management of Ludwig’s angina with small neck incisions: 18 years experience. Otolaryngol Head Neck Surg 2004;130:712-7