M2E Too! Mellick's Multimedia EduBlog by Larry Mellick, MD

​The M2E Too! blog presents important clinical pearls using multimedia. By its name, M2E Too! acknowledges that it is one of many emergency medicine blogs, but we hope this will serve as a creative commons for emergency physicians.​

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Friday, August 31, 2018

Sometimes when it's time to remove a Foley catheter, the balloon won't deflate. This problem occurs more commonly in patients with long-term Foley catheters. Even though we have all seen nursing home patients present with penile bleeding after pulling out their Foley catheter with the balloon still inflated, that is obviously not an option for emergency physicians. The problem is that the recalcitrant balloon is sitting out of reach, deep in the urinary bladder.

The cause of the balloon malfunction can be anywhere along the catheter, but it's usually found in the balloon inflation port, the balloon drainage channel, or the balloon itself. A commonly reported cause of the problem is using saline to expand the balloon. With time, salt crystals from the saline precipitate in the various locations responsible for deflation failure.

A urologist named Frederic Foley, MD, developed his eponymous catheter in the late 1920s and early 1930s. It was originally an open system, but was turned into a closed system with a bag in the 1950s. I suspect that we are pretty much familiar with the catheter parts, which include the balloon inflation port, the urine drainage port, the inflatable balloon to anchor the catheter in the bladder, and the tip or bladder opening.

Catheters can be made of rubber, plastic, or silicone. The balloon volumes range between 5 mL and 30 mL. There are also straight single-use catheters, the curved or coudé catheter, and a three-way Foley catheter for administering medications or irrigation. Catheters come in multiple diameters, and is measured using the French scale or French gauge system. It is usually abbreviated as Fr, but other variations, including CH or Ch for the system's inventor Joseph-Frédéric-Benoît Charrière can be used. The higher the number, the larger the catheter diameter, and 3 Fr is equal to 1 mm. So a 24 Fr catheter measures 8 mm in external diameter. The range of sizes typically available are as follows: 5 Fr, 6 Fr, 8 Fr, 10 Fr, 12 Fr, 14 Fr, 16 Fr, 18 Fr, 20 Fr, 22 Fr, 24 Fr, and 26 Fr.

Managing the Failure to Deflate

Managing a Foley balloon's failure to deflate includes addressing the potential sites of obstruction in either the balloon inflation port, the balloon drainage channel, or the balloon. Consequently, the techniques used involve drainage port and channel management or balloon destruction. A number of different techniques have been reported in the literature, but I will focus on those most practical for emergency physicians. Having an ultrasound machine available to visualize the balloon would be extremely useful with most of the following techniques.

Consider and Manage Balloon Cuffing

The failure to remove a Foley catheter may not be caused by failure of the balloon to deflate. Instead, it can be caused by balloon cuffing, where the balloon deflates but fails to deflate flush with the catheter. Instead, a circumferential elevated cuff persists at the balloon equator and makes catheter removal nearly impossible. This is remedied by placing 0.5 to 1.0 mL of water into the balloon to smooth out the contour of the balloon, allowing subsequent removal.

Removal of the Balloon Inflation Port

The first step in attempting to deflate a Foley balloon is often cutting off the inflation port with a pair of scissors. The balloon will promptly deflate if the obstruction involves a defective inflation port. The water from the balloon will be observed dripping from the inflation port.

Guidewire Application

Once the inflation port has been removed, the channel is now available for inserting a lubricated guidewire. A guidewire from a central line kit or ureteric guidewire can be used with its floppy end first to try to clear the drainage channel of any debris. If this does not work, the guidewire can be used to puncture the balloon. After instilling 200 mL of water into the bladder, insert the firm end of the guidewire to puncture the balloon. Filling the bladder with water protects it against bladder injury in case the balloon bursts instead of draining slowly.

Balloon Overinflation and Rupture

This technique is generally discouraged because bladder injury can occur and balloon fragments can remain in the bladder requiring removal by cystoscopy. It involves placing an intravenous catheter into the drainage channel of the Foley catheter (after the inflation port removal) and instilling water under pressure. Again, injuries to the bladder have been reported, and unwanted balloon fragments are almost guaranteed.

Direct Puncture of the Balloon

Percutaneous suprapubic puncture of the balloon using ultrasound guidance is another option. The balloon is brought into close contact with the bladder wall, and an ultrasound-guided percutaneous suprapubic puncture is accomplished. Other techniques describe vaginal, transurethral, or transrectal approaches, but these are most likely outside the scope of emergency physicians. Again, any time a balloon puncture technique is accomplished, inspect the balloon after catheter removal to assess for missing fragments. If a portion of the balloon is missing, then a subsequent cystoscopy is recommended.

Chemical Deflation of the Balloon

The use of chemicals such as acetone has been reported, but mineral oil is probably the safest. The technique involves instilling 10 mL of mineral oil into the balloon inflation lumen. If balloon rupture does not occur in 15 minutes, the procedure is repeated. Acetone and mineral oil can take several hours to rupture the balloon. These chemicals can be irritating to the bladder, and a new Foley should be placed after the balloon is deflated to irrigate the bladder to remove them. It is recommended that the bladder be filled to capacity with normal saline before chemical deflation is attempted.​

Failure of the Foley balloon to deflate is a relatively rare event, but it can be quite disconcerting when it happens. After watching this month's video and reviewing the options discussed above, you can rest assured that you now have all the tools necessary to successfully resolve this emergency.


Watch a video of Dr. Mellick discussing all the tips and tricks you need to tackle a Foley ballon deflating failure. 

Monday, August 6, 2018

A bursa, a fluid-filled synovial sack, serves in the body as either a pulley or a cushion, and bursitis, of course, is an inflammatory response that can occur to a bursa. The causes of the inflammatory response can be trauma (direct or overuse), infection, or rheumatologic or crystal-induced disease.

Whether a bursa is deep or superficial ultimately determines the most likely pathophysiology and dictates the most appropriate treatment. Superficial bursae are those closest to the skin, and they are most vulnerable to direct trauma and infection—the prepatellar, infrapatellar, and olecranon bursae. Deep bursae include the subacromial, pes anserine, and trochanteric bursae. The superficial bursae generally serve as cushions, while the deep bursae more commonly function as pulleys.

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Watch a video of Dr. Mellick treating a patient with subacromial bursitis.

Deep bursae are less likely to become infected because they are less vulnerable to the direct inoculation of bacteria that can occur with superficial bursae, but they are more vulnerable to diseases surrounding them. Osteoarthritis of the knee commonly causes pes anserine bursitis, for example, and a partial tear of the supraspinatus muscle or acromioclavicular arthritis can cause subacromial or subdeltoid bursitis. Unfortunately, it is almost impossible to differentiate between subacromial bursitis, rotator cuff tear, or rotator cuff tendonitis.

Because the etiologies of the inflammation of deep and superficial bursae are different, the diagnostic modalities and treatments are as well. Superficial bursitis most commonly caused by direct trauma, crystal-induced disease, or infections is treated by needle aspiration and testing the fluid for evidence of crystals or infection. Injecting corticosteroids and anesthetics is not typically performed for superficial bursitis because infections, chronic pain, and changes of the overlying skin can result.

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Watch a video of treatment for a patient with housemaid’s knee.

Instead, NSAIDs, compression dressings, and antibiotics are common interventions used to treat the inflammation of superficial bursae. Staphylococcus aureus is the culprit approximately 80-90 percent of the time when a bursa is infected. Oral antibiotics appropriate for the most common infecting organism and aspiration of the bursa are the mainstays of therapy. Sometimes repeated aspirations of the septic bursa are necessary, and the infected bursa will occasionally need to be surgically drained or have a bursectomy is performed. Surgical interventions, however, are more commonly associated with complications. (Arch Orthop Trauma Surg 2014;134[11]:1517.)

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Watch a video of Dr. Mellick treating a patient with pes anserine bursitis.

The inflammatory responses of deep bursae are most frequently caused by disease of surrounding muscles, tendons, or joints. Infections are much less common, but injections with corticosteroid and anesthetic mixtures are commonly performed to manage these conditions. NSAIDs, physical therapy, and interventions directed at healing the surrounding injured muscles, tendons, and joints are the most common modalities. It is important to remember that one's interventions will be relatively futile when the cause of the bursitis is pathology in the surrounding anatomical structures. The response to subacromial injections of corticosteroids and anesthetics, for instance, will only be transient as long as the rotator cuff partial tear or AC joint arthritis is left untreated.

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Watch a needle aspiration of a patient with olecranon bursitis.​

The videos associated with this blog demonstrate therapeutic interventions for superficial and deep bursae. Needle aspiration of an infrapatellar and olecranon bursae as well as injections of corticosteroids and bupivacaine into an inflamed pes anserine and subacromial bursa are demonstrated.​


Monday, July 2, 2018

The fascial planes in the upper and lower extremities play an important role in function and form, but they also make the extremities vulnerable to compartment syndrome. Emergency physicians are quite comfortable evaluating and diagnosing compartment syndrome: severe unrelenting pain, pain with passive motion of the muscle groups involved, and possibly paresthesias and pallor. The first patient I saw with this condition was at the Tripler Army Medical Center in Hawaii. A sailor dangling his legs over the dock presented after his leg was crushed between the dock and a battleship that suddenly shifted its position. I still remember the patient in the trauma room screaming in severe pain.

During my two years as an FBI doctor in the training academy at Quantico, I became quite familiar with chronic and acute exertional compartment syndrome. Agents-in-training and older police officers in physical fitness training would often present with this condition. Severe pain would typically develop in the anterior compartment while they were running and could usually be relieved with rest. Some had this condition chronically, and worked around and through it. Surgical release of the compartment was eventually the outcome for most of these cases.​

Compartment syndrome of the hand is another rare condition that can have devastating consequences. Several decades ago, a colleague of mine in Columbus, OH, accidentally impaled her hand with a recently used large central line needle. The wound became infected, and she ended up receiving emergent fasciotomies of her hand. More recently, I saw a patient who presented late after a fall from a ladder that crushed his hand under his body. This patient presented with unrelenting pain despite the fasciotomies of the hand done a week or two earlier. He had run out of his pain medications several days prior to his presentation. Only healthy doses of parenteral opiates and intermittent infusions of low-dose ketamine seemed to bring him relief.


Watch a video showing a patient with late-presentation compartment syndrome. His hand was crushed after a fall from a ladder.​

A rarer presentation of lower extremity compartment syndrome, the spontaneous compartment syndrome, presented on at least two occasions recently. One patient was an older colleague. He colleague and the other patient shown in the video had spontaneous onset of severe pain in the distribution of the anterior leg compartment. Shortly following the onset of this pain, both developed a foot drop of the involved extremity. The inciting event for the compartment syndrome almost assuredly had to be a vascular event, but other cases of spontaneous compartment syndrome have been associated with diabetes mellitus, ruptured peroneus muscles, and exertional activity. These two cases of spontaneous anterior compartment syndrome did not require fasciotomy, and were followed up by the appropriate services.

Compartmental pressure measurements with the Stryker instrument has been the recommendation until recently. Remember the Stryker? Yes, that tool that always seemed to be missing when you or your consultant needed it. Now we have a much better and more disposable tool: the Compass device by Centurion. This disposable pressure gauge efficiently and effectively measures compartment pressure. A training video showing emergency medicine residents learning to use this device by measuring artificially elevated compartmental pressures of oranges demonstrates how easy this tool is to use. (Below.)

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Watch a video showing how to use the Compass device for compartment syndrome and how to practice using it on an orange.​

Compartment syndrome has classic causes and clinical presentations. Crush injuries, infections within the fascial space, and muscle damage during extreme overexertion can cause compartment syndrome. Intermittent exercise-induced compartment syndrome and spontaneous compartment syndrome of the lower extremity are less common presentations that are at risk of misdiagnosis.


Watch this video showing a man with compartment syndrome in his foot.​


Friday, June 1, 2018

Alcoholism has been treated with disulfiram (Antabuse) ever since the drug received FDA approval in 1951. Disulfiram is one of a number of medications that produces unwanted side effects caused by the accumulation of acetaldehyde when taken with alcohol.

The story behind the discovery of disulfiram is typical of serendipitous observations. A physician noted in 1937 that workers in the rubber industry exposed to disulfiram developed a reaction after drinking alcohol. Several decades later, two Danish researchers evaluating disulfiram as an antihelminthic developed symptoms after attending a cocktail party. (Medscape, Jan. 6, 2016; http://bit.ly/2HsHfnu.)

These observations led to the clinical application of disulfiram in treating alcoholism. Cyanamide (carbimide), certain anti-infectives such as cephalosporins, nitroimidazoles (e.g., metronidazole), furazolidone, and dermatological medications such as tacrolimus and pimecrolimus are also associated with this effect. The toxic effects of acetaldehyde accumulation associated with disulfiram are actually the aversive effect desired to discourage further alcohol intake. Facial flushing, nausea, vomiting, tachycardia, and hypotension are toxic side effects seen with acetaldehyde accumulation.

Early on there were hard-learned lessons when high doses were used, and severe or fatal reactions occurred. Subsequently, lower and safer doses were used, and a marked reduction in life-threatening side effects were noted. Disulfiram is currently used less often as a first-line agent, but patients still present to the ED occasionally with a severe disulfiram reaction.

The video demonstrates such a patient who presented with severe hypotension, nausea, vomiting, and flushing. Reactions may occur several days after treatment has ended, as this patient showed. She had stopped taking disulfiram several days before her alcohol consumption occurred. The most prominent associated findings in our patient were hypotension and flushing. The hypotension was treated with and responded to intravenous fluids and pulse dose boluses of epinephrine. We also review the preparation and application of pulse doses of intravenous epinephrine in this video.

Usually the blood pressure drop associated with the disulfiram-alcohol reaction is only moderate, but severe life-threatening arterial hypotension and shock can occur. (Am J Med Sci 2007;333[1]:53; J Pharmacovigilance 2014;2:145; http://bit.ly/2JqzniX.) Myocardial infarctions and acute strokes have also been reported. (J Pharmacovigilance 2014;2:145; http://bit.ly/2JqzniX; Folia Med (Plovdiv) 2010;52[3]:70.) Epinephrine or norepinephrine are the pressor agents of choice for hypotension, but fomepizole, an alcohol dehydrogenase inhibitor, may also be an effective treatment. (J Pharmacovigilance 2014;2:145; http://bit.ly/2JqzniX.)

Despite its known limitations, disulfiram treatment is still considered a valuable option for treating alcohol dependence, and more recently, has shown potential benefit in treating other presentations. These include treating those with co-morbid alcohol dependence and post-traumatic stress disorder, those with co-morbid cocaine and alcohol dependence, and those with cocaine dependence alone. (CNS Neurol Disord Drug Targets 2010;9[1]:5.)

Be on the lookout for patients who may present with serious side effects such as refractory hypotension and its associated ischemic complications.​

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Watch a video showing the treatment of a patient with a disulfiram (Antabuse) reaction.​

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Monday, April 30, 2018

The hair or thread tourniquet syndrome is a relatively rare condition that has evaded me in the emergency department for several decades, until past year when three cases showed up over six months. This condition has been around for as long as there has been hair or thread and body appendages. In fact, this condition may have first been described in the 1600s. (J Pediatr Adolesc Gynecol 2005;18[3]:155.)

The etiology of this condition seems almost unbelievable. How in the world does a hair get wrapped repeatedly and tightly around an appendage of the body? Some authors expressed the need to consider nonaccidental etiologies more frequently. Stranger things, however, have happened in emergency medicine (e.g., the urinary catheter tying itself in a knot in the bladder of a patient). (APSP J Case Rep 2011;2[3]:21; J Clin Ultrasound 2009;37[6]:360.)

The risks of strangulation and autoamputation of the involved appendage are very real. This condition does not respect age, gender, or appendage. Hair tourniquets of the penis, clitoris, labia minora, teeth, uvula, fingers, toes, and even the larger extremities have been reported in the young and the elderly. They are, however, much more common in infants and young children than they are in adolescents or adults. In fact, a fascinating temporal association has been made between hair tourniquets and the mother's postnatal telogen effluvium, which causes significant maternal hair loss months after the infant's delivery. Consequently, we include hair tourniquets in that long checklist of potential issues afflicting the inconsolable infant. Corneal abrasions and colic may be much more common, but it makes perfect sense to examine all of the infant's appendages for a hair tourniquet.

I have been shocked by how rapidly these hair tourniquets burrow into the chubby subcutaneous tissues, making examination and quick removal nearly impossible. Hair has significant tensile strength, stretches when it's wet, and can be inadvertently tightened when an unsuspecting parent starts tugging on the exposed end of the hair. Furthermore, it can act like a garrote and cut through the soft skin of the infant while becoming increasingly inaccessible. When the health care provider begins to tease out the hair with a needle or forceps, bleeding quickly begins, making visualization even more difficult. Timely removal of the tourniquets is critical to preventing complications. The removal technique can be manual, chemical, or surgical.

Manual removal entails simply finding the free end of the hair or thread and unwinding it. This is often easier said than done. It can also involve using a blunt object such as forceps or an ear wax speculum, pushing it underneath the constricting material, lifting the tourniquet, and then cutting it and removing it. Chemical removal involves the use of depilatory agents that chemically break down hair protein. I have never used this technique, and some have reported that it can be a slow process. The failure rate will be high if the hair is already deeply buried. Most emergency departments don't plan ahead for hair tourniquets by stockpiling depilatory agents.

Surgical removal is sometimes necessary when presentation is late or the hair has rapidly burrowed deep into the subcutaneous tissue, preventing easy access for manual removal or lessening the potential effectiveness of depilatory agents. The surgical technique often requires anesthesia of the appendage, followed by a limited but relatively deep incision to ensure that the hair or thread has been released. In fact, the phrase "cut to the bone" is used on fingers and toes. A no. 11 scalpel blade is inserted at locations that avoid neurovascular bundles, and one goes all the way to the bone before withdrawing the blade. The incision on the penis or clitoris is made to the underlying fascia while being careful not to lacerate the three penile corpora bodies, the urethra, or the dorsal penile nerves. Incisions at the four and eight o'clock positions are recommended.​

Potential complications of the procedure can be trauma to the skin, bleeding, and infection, as well as injury of underlying neurovascular bundles. Contact dermatitis or skin irritation may occur if a depilatory cream is used. Assessment of tetanus immunization status is also recommended. Finally, close follow-up the next day is recommended to assess for continued improvement and absence of ischemia signs or infection.

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This child had a hair tourniquet deeply embedded in his pinkie.mellick photo 2 with video.JPG

Watch the removal of a hair tourniquet from a child's toe.