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InFocus: Cases Rare and Unusual but Still Relevant to Emergency Medicine

Roberts, James R. MD

doi: 10.1097/01.EEM.0000398219.56415.8e
InFocus
Egress of Urine Halted: A Cause of Agitation in a Cognitively Impaired Patient.

Egress of Urine Halted: A Cause of Agitation in a Cognitively Impaired Patient.

Reviewing prospective randomized placebo-controlled trials, meta-analyses, and review articles helps emergency physicians sharpen their skills and gain clinical perspective. An ED shift is consumed with individual cases, however, and every patient is a little different from how he is portrayed in print.

Because no textbook or article can possibly describe the nuances, peccadilloes, and vagaries of all ED presentations, the medical literature is replete with interesting or unusual individual patient encounters (aka case reports). While journals are unfortunately eschewing this format, case reports are still instructive and a clever way to augment your experience and expertise.

This month's column reviews two case reports relevant to emergency medicine. While they are rare and unusual, they are certainly worth noting. Recognizing either scenario will make you look like a pro.

Images in Clinical Medicine: Agitation Associated with Acute Bladder Obstruction

DeLuca G, Wijdicks EF

New Engl J Med

2010;363(17):1656

When a cognitively impaired 61-year-old man with an exacerbation of a chronic seizure disorder from traumatic brain injury presented to the ED in an agitated and combative state, the authors of this case report rightly assumed that this was just another garden-variety postictal event. Because of multiple seizures, the patient was admitted to the hospital for further therapy.

Appropriately, fosphenytoin was added to the monotherapy, levetiracetam, which was assumed to be inadequate. The agitation and combative behavior increased, requiring mechanical restraints. As the workup progressed, the creatinine was found elevated, and an examination revealed abdominal distention. An abdominal CT identified marked urinary bladder enlargement, secondary to entrapment of a Foley catheter balloon inflated in the penis. The misplaced catheter was causing complete urinary obstruction and the subsequent agitation and combativeness. The errant catheter was replaced, copious urine output followed, and the patient immediately became calm. The creatinine returned to normal, and the patient made a full recovery. This is certainly an unusual urologic cause of acute agitation.

Comment: Agitation and combative behavior following multiple seizures is expected, and is almost always a postictal phenomenon. One would not rush to search for an alternative cause, and increasing the anticonvulsant regimen was an appropriate intervention. Some clinicians may have immediately sedated the patient if the agitation was problematic, and a small dose of a benzodiazepine would certainly be acceptable for postictal agitation. In a cognitively impaired patient, complaints of pain or other symptoms would be absent. I'm not sure I would have even examined the pelvis and genitals for a cause of post-seizure agitation, and the timeline of this case is uncertain. Apparently blood tests were interpreted first, and the report does not state whether a head CT was performed or who ordered the diagnostic scan (perhaps a surgical consult evaluating an abdominal mass?). Of course, a quick bedside ultrasound may have clinched the diagnosis in the ED.

The causes of agitation in patients with chronic brain dysfunction are protean. It is axiomatic that any patient with altered mental status, from the newborn to the nursing home patient, should be checked for hypoglycemia. That's an easy rule-out in the ED. If you have not been flummoxed, embarrassed, or surprised by unanticipated hypoglycemia, you just haven't seen enough patients.

I can appreciate how this case could possibly be further obfuscated if heavy sedation ensued, and I can see being led down an incorrect path by focusing on a potential CNS event. In a busy ED, further intervention for increasing agitation would readily prompt more aggressive sedation, and might include paralysis and mechanical ventilation to expedite a CT scan or to control an obstreperous patient. Had this patient been obese, the bladder distension would be subtle, if not totally clandestine. And when do you do an abdominal CT scan for someone with agitation after a seizure?

I have seen a case similar to this. An agitated, demented, chronic urinary catheter-bearing nursing home patient was sedated to the point of near coma when she became uncontrollable in the ED. The Foley in this case was only partially clogged, allowing for a modicum of urine output. But decreased urine output prompted even additional fluid administration, resulting in additional agitation, followed by even more sedation. When that partially blocked Foley was replaced, voluminous urine flowed and the now near-comatose patient miraculously calmed down. I readily agree that this case was unusual enough and offered important enough concepts to garner case report status in an international journal.

Black tar heroin can be contaminated with botulism spores that germinate and produce botulism toxin in an abscess at an infected soft tissue injection site

Black tar heroin can be contaminated with botulism spores that germinate and produce botulism toxin in an abscess at an infected soft tissue injection site

Images in Clinical Medicine: Wound Botulism

Sam A, Beynon HL

New Engl J Med

2010;363(25):2444

A 42-year-old man with a history of subcutaneous heroin use (aka skin popping) presented with slurred speech, double vision, and trouble swallowing. Most EPs are now thinking this is most likely just another case of narcotic overdose. When the naloxone does not readily reverse the condition, such a presentation also conjures up a cornucopia of neurological problems. Etiologies include CNS dysfunction, such as drug effect and brain abscess, as well as thiamine deficiency, brain empyema, intracranial hemorrhage, stroke, and even sepsis. In this case, multiple skin abscesses were found on the patient's legs, further suggesting a potential infectious etiology.

When the physical exam revealed bilateral ptosis, sluggish papillary responses, and bilateral sixth cranial nerve palsies, the case became even more complex. This patient had rapidly progressing dysphagia, necessitating tracheal intubation to protect the airway. A subsequent electromyography suggested a neuromuscular transmission defect, and the clinical diagnosis of wound botulism was made. The patient was treated empirically with botulism antitoxin and antibiotics, and the abscesses were appropriately debrided. The diagnosis was cemented when botulinum toxin was detected in the serum, and Clostridium botulinum was cultured from the abscesses. As is common with botulism, the patient was extubated after two full weeks on the ventilator, and full neurologic recovery took several months.

The authors comment that botulinum toxin inhibits acetylcholine release at the peripheral cholinergic synapses, inhibiting neuromuscular transmission. This is permanent, and requires sprouting of new presynaptic nerve terminals to reverse the neurotransmitter deficit. Heroin contaminated with spores of C. botulinum brews toxin in the abscess cavities, culminating in the release and systemic absorption of the botulinum toxin.

Comment: This is a strange case, indeed, one that most physicians may not see in an entire career. It is, however, reported in this country, usually in California, when Mexican black tar heroin likely contaminated with soil containing botulinum spores reaches the street. Most would not make this diagnosis in the ED. Botulism is an unusual event in itself, and one that requires great diagnostic skills and in-depth cerebration. The ptosis might prompt one to administer tensilon, searching for myasthenia gravis, or naloxone, suspecting a narcotic overdose. The sixth cranial nerve palsy would be a fortuitous pickup in a busy ED while one is focusing on the rather impressive multiple abscesses. Of course, an EMG is not available in the ED, and confirmation of the botulism toxin is a test that requires a few days. For the reader's edification, one can call the Centers for Disease Control and Prevention to query the individual who carries the botulism pager for clinical insight and prompt delivery of antitoxin.

Droopy Eyelids and Multiple Abscesses in an Injection Drug User: Consider Wound Botulism.

Droopy Eyelids and Multiple Abscesses in an Injection Drug User: Consider Wound Botulism.

Most clinicians will not see a single case of botulism in their careers, and even index cases of foodborne botulism are frequently missed because of the nonspecific early symptoms. Dry mouth, slightly blurred vision, and vague neurological complaints of weakness can easily prompt misdiagnosis in the ED. Likewise, a floppy tired infant who is constipated, if such a complaint is even considered by the doctor, is just another case of a worried mom unless one has previously seen infant botulism. These cases progress rapidly, and the ultimate cause of death is respiratory paralysis. This is considered bad form if it occurs in the radiology suite or in an unattended back room of the ED. Whether one can intervene with anything other than an endotracheal tube is questionable.

Botulism by any means (foodborne, wound, infant ingestion of spores) produces a descending symmetrical paralysis. Lyme disease can produce bilateral 7th nerve palsy, and a variety of exotic toxins or a bevy of neurological problems, as well as embolic strokes, could further confuse the picture. This disease cannot be diagnosed with a CT or MRI scan, and I can see physicians trying to argue for an MRI in the middle of the night on this neurologically challenged patient, performing an urgent lumbar puncture, and considering heavy metal poisoning at the same time. This is clearly a difficult diagnosis in the ED, one that likely would not have been made by even the most erudite clinician without the help of a neurology colleague and a bevy of fancy, albeit non-ED, testing.

The first case of drug injection botulism surfaced in the literature in 1982. (Ann Intern Med 1985;102[5]:616.) Wound botulism from black tar heroin in California has been well known since the late 1990s. (JAMA 1998;279[11]:859.) Physicians know of wound botulism developing in traumatized, crushed, or devitalized tissue, with anaerobic environments similar to that of an abscess. The botulism organism is introduced from the environment, thrives in the soft tissue, and produces toxin. Another particularly devastating sequela of injection drug abuse is necrotizing fasciitis. Tetanus also has been reported. Both of these conditions are rare but rapidly fatal despite even early diagnosis and intensive treatment.

The CDC recently labeled wound botulism from black tar heroin an epidemic. Wound botulism is increasing much more rapidly than either foodborne or infant botulism, and the majority of cases in this country have the black tar-California-wound botulism moniker. Even a prior episode of wound botulism has not deterred subsequent injection drug abuse, and a recurrent case of wound botulism in the same patient is a great testimony to the power of drug addiction. (Clin Infect Dis 2011 Feb 11 [Epub ahead of print]). Apparently, near-death experiences do not change behavior among these injection drug users.

If one is prescient or sagacious enough or has the mental prowess to suspect any form of botulism in the ED, the administration of antitoxin may decrease the duration of ventilator use, but this does not guarantee that long-term ventilation will be negated. The mortality rate of botulism is about five percent, and recovery takes weeks to months. Many patients who survive have fatigue and shortness of breath for many years, and are never back to normal.

All cases of botulism are supposed to be reported to the CDC. In 2008, only 153 cases were documented. Of these, 11 were foodborne, 111 were infant botulism, and 23 cases were wound botulism. Note the incidence of infant botulism, the leading etiology so far. In some cases, no cause or risk factors are found; go figure. There is only a miniscule chance that an EP will encounter any type of botulism. But if you happen to live in Alaska, you may be familiar with botulism from my favorite and always delicious delicacies: fermented fish heads, seal flippers, or beaver tails. Burying food in the ground to allow it to ferment facilitates toxin production, perhaps more likely if you are high tech and use Tupperware instead of a traditional grass-lined pit. (http://www2.cdc.gov/phtn/botulism/who/who.asp.)

Perhaps some EMN aficionado has had experience with wound botulism, particularly our colleagues in California where black tar heroin is readily available, but even as a toxicologist, I have never seen such a case. I suggest you buy your heroin in Philadelphia. We peddle only the good stuff. Intravenous drug use would not produce this syndrome, nor would smoking heroin, but perhaps snorting contaminated heroin would. How the emergency physician is expected to diagnose this one is beyond me, hence my consciousness-raising efforts.

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Dr. Roberts

Dr. Roberts

© 2011 Lippincott Williams & Wilkins, Inc.