Haff Time: fish-induced rhabdomyolysis

Buffalo fish

Buffalo fish (Ictiobus cyprinellus)

3 out of 5 stars

Haff Disease: Rhabdomyolysis After Eating Buffalo Fish. Herman LL, Bies C. West J Emerg Med 2014 Sept;15:664-6.


Haff Disease was first described in 1924 after an outbreak of acute muscle rigidity accompanied by dark  urine among patients living near the Königsberger Haff shores along the Baltic Coast.  Similar cases occurred in the following summers along the haff (a shallow lagoon.) Most victims gave a history of recently ingesting various fish — burbot, eel, pike, etc.

Cases of rhabdomyolysis after ingesting fish were not reported in the United States until 1984. Most were associated with eating freshwater buffalo fish. Haff disease is diagnosed when a patient develops rhabdomyolysis without another etiology within 24 hours of eating fish. The toxin causing the condition has not been identified, but appears to be heat-stable since cooking does not prevent illness. Common presenting signs and symptoms include back pain, chest pain, sweating, dyspnea, nausea and vomiting.

This case report, from Resurrection Hospital in Chicago, describes a 34-year-0ld woman who presented with chest pain, back pain and vomiting after consuming cooked buffalo fish. Evaluation revealed markedly elevated myoglobin and creatine kinase levels. Chest CT was unremarkable and troponin levels were normal.

The paper makes the following important points:

  • Because of the presentation, life-threatening conditions such as acute coronary syndrome and aortic dissection must be ruled-out.
  • The causative toxin may be similar to palytoxin, a potent vasoconstrictor found in several marine species.
  • In contrast to cases in Europe, U.S. outbreaks of Haff disease have been associated with ingestion of freshwater fish or shellfish (buffalo fish, crayfish.)
  • Many patients with Haff disease have a moderate leukocytosis
  • The key to treatment is supportive care focused on maintaining adequate urine output.
  • The benefit of alkalinizing the urine in rhabdomyolysis has not been proven.


Additional resources:

Illinois Department of Public Health February 2014 release on Haff disease

MMWR report on Haff disease



Treat and Release vs. Observation After Naloxone for Opioid Overdose

Journal Club Podcast #17: October 2014


Evan Schwarz and I sit down to talk about heroin, naloxone, and personal responsibillity...

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Article 1: Vilke GM, Sloane C, Smith AM, Chan TC. Assessment for deaths in out-of-hospital heroin overdose patients treated with naloxone who refuse transport. Acad Emerg Med. 2003 Aug;10(8):893-6. Answer Key.

Article 2: Wampler DA, Molina DK, McManus J, Laws P, Manifold CA. No deaths associated with patient refusal of transport after naloxone-reversed opioid overdose. Prehosp Emerg Care. 2011 Jul-Sep;15(3):320-4. Answer Key.

Article 3: Watson WA, Steele MT, Muelleman RL, Rush MD. Opioid toxicity recurrence after an initial response to naloxone. J Toxicol Clin Toxicol. 1998;36(1-2):11-7. Answer Key.

Article 4: Rudolph SS, Jehu G, Nielsen SL, Nielsen K, Siersma V, Rasmussen LS. Prehospital treatment of opioid overdose in Copenhagen--is it safe to discharge on-scene? Resuscitation. 2011 Nov;82(11):1414-8. Answer Key.


It's a typical TCC shift when you hear yelling coming from the ambulance bay. You run over to find an apneic patient has just been pushed out of a car that then sped off. As you place him on a gurney and move him into the emergency department (ED), you notice fresh track marks, a recently used syringe on the ground, and drug paraphernalia sticking out of his pockets. You begin to bag him and notice that he has pinpoint pupils and no other signs of trauma. You administer an atomized dose of intranasal naloxone and continue bagging him until he begins to breathe adequately. A few minutes later, the nurse comes to get you to let you know that the patient is now awake and wants to go. You go back to the room and tell him that he needs to stay since you are worried that he will stop breathing once the naloxone wears off. You offer him a turkey sandwich as a compromise to get him to stay and go to see the new patient with respiratory distress.

You have just finished intubating the patient with respiratory distress and are getting ready to place a central line in a patient with severe sepsis when the nurse comes to let you know that your overdose patient is getting belligerent and that you need to do something. Before you even have a chance to calm him down, he tells you that he is leaving now and angrily asks who gave you permission to bring him here, wants to know who is going to give him money to get home, and wants to know why someone filled his pants with ice. You tell him he cannot go yet, and if he doesn't calm down, you will have to call security. After going through this 2 more times, he has now been in the ED for approximately an hour. You offer him chemical dependency information and discharge him. After he leaves, you realize that neither you, the patient, the nursing staff, or the patient sharing a trauma room with him enjoyed this experience and wonder if it was really necessary to go through all that or if you could have just let him go much earlier.

PICO Question:

Population: Patients with acute opioid overdose requiring naloxone administration with return to baseline.

Intervention: Transport to the hospital by EMS or ED observation.

Comparison: Immediate release by paramedics or from the ED

Outcome: Rebound opioid toxicity resulting in death or anoxic brain injury, or requiring additional administration of naloxone.

Search Strategy:

PubMed was searched using the following strategy: “naloxone AND overdose AND (release OR transport OR recurrence)” (http://tinyurl.com/n937tns). The 57 resulting citations were searched for observational or randomized controlled trials evaluating the safety and efficacy of immediate release for patients responding to naloxone after opiate overdose. The following 4 articles were selected for review.

Bottom Line:

Opioid overdose remains an increasing problem in the United States, resulting from the high prevalence of heroin abuse and the increasing abuse of prescription opioids. Death due to opioid overdose has been increasing in recent years, prompting some communities (such as Boston, MA) to institute programs for bystander administration of naloxone to reverse toxicity. Whether administered by a bystander or EMS, naloxone typically results in adequate reversal of toxicity. In most EMS systems, such patients are then transported to an ED for observation, given the theoretically short-lived action of naloxone and concerns for recurrent toxicity. Some have proposed that such observation is unnecessary, and that such patients can be released at the scene as long as they return to their baseline. We sought to evaluate the evidence for such a proposed “treat and release” protocol, and to assess the incidence of recurrent toxicity following naloxone administration.

In those studies involving the treatment and release of patients by EMS, without transport to the hospital, the risk of death from recurrent opioid toxicity was low, ranging from 0% (Vilke 2003, Wampler 2011) to 0.13% (Rudolph 2011). The 3rd of these studies was conducted in Denmark, where a physician is present in the field to assess the patient and make transport decisions. This makes it difficult to extrapolate the study’s results to our EMS system. A strength of this study was Denmark’s centralized database inclusive of all citizens, allowing the authors to easily find anyone that died after being released. In addition, the authors were able to obtain all forensic data surrounding the deaths to determine which were from rebound opioid intoxication and which were from other causes. The former two studies, on the other hand, were conducted in large US cities (San Diego, CA and San Antonio, TX respectively) with more familiar EMS systems, and demonstrated similarly low rates of death due to recurrent toxicity. While no deaths were found in the US studies, it is possible if people died in different counties that they could have been missed, as the US does not have a central database. A fourth study based in Helsinki showed similar results; the authors found no cases of patients dying from recurrent opioid toxicity (Boyd 2006).

A single ED-based study evaluated the risk of toxicity recurrence based on a retrospective chart review (Watson 1998). A Delphi Panel was employed to determine whether rebound occurred following a response to naloxone administration in the ED. In this small study (42 total cases), recurrence of toxicity was identified as either definite or probable in 13 cases (31%, 95% CI 17-45%). Interestingly of the 13 cases, only 2 were noted to have recurrent respiratory depression. The other 11 patients had decreased mental status without any respiratory compromise. The authors later state that neither of the patients with respiratory depression received any specific treatment. As such, it is difficult to determine the significance of their respiratory depression. These results are confounded by differences in baseline patient characteristics from those in our practice as well as the use of a highly subjective outcome. Specifically, nearly 50% of patients in this study presented following suicide attempt, and 81% of cases involved an oral ingestion of opiates. Anecdotally, the large majority of opiate overdoses seen in our setting involve the recreational use of IV heroin, and recurrence rates may therefore be different. Additionally, in those patients receiving naloxone initially, only 27% were noted to have respiratory depression, and thus the indication for naloxone is suspect. Recurrence of toxicity, the primary outcome, was highly subjective and thus determined by a Delphi panel. Only 18 of the 42 cases considered to have had recurrence were deemed “definite,” with the remaining only “probable.” Even in those cases with definite recurrence of toxicity, the exact indication for repeated doses of naloxone remain unclear, and there is no evidence that more serious patient-centered outcomes were prevented in any of these cases.

The bulk of this data supports the “treat and release” strategy adopted by many EMS systems, with the caveat that such a strategy be employed in select patients who have returned to baseline with stable vital signs and are capable of understanding the risks associated with discharge in the field. If patients want to go to the ED, this should still be encouraged as patients could be evaluated for drug related infectious diseases, as well as receive information about addiction treatment and other social services. Transporting the patient against their will, and holding them in the ED, is probably unnecessary and does not seem to be supported by available evidence. However if the patient took a longer-acting opioid such as methadone, it may be prudent to specifically warn them of possible risks associated with these agents as studies did not specifically look at the safety of a “treat and release” strategy in patients exposed to long-acting opioids.

Student Corner: How to Read a Head CT

Head imaging is both a crucial tool in acute medical care, particularly in the setting of trauma, and a very daunting aspect of learning radiology for students. However, as is the case with many clinical skills, a “systematic approach” goes a long way in helping ease the initial challenge of learning how to read and understand head imaging. For this post, we will focus primarily on head CTs because they are more commonly used in emergency departments due to the fact that they are fast, readily available, and highly informative in trauma.

A head CT presents a few unique challenges. The anatomy is subtle and nuanced. The area has numerous pathological possibilities. The pathologies themselves can change over short time periods. There are different types of fluids and soft tissues. In short, the brain is kind of scary.

But, the best way to get over your fears is to face them. And therefore the best way to look at a head CT is to look at it with a plan. The plan in this case is a (surprise!) mnemonic: Blood Can Be Very Bad” and it is detailed below.


Hemorrhage of blood into the cranial vault is one of the easier things to identify on head CT. Acute hemorrhage is hyperdense (bright) and becomes hypodense (dark) as time goes on. Two of the most commonly encountered types are subdural hematoma and epidural hematoma. Subdural hematomas arise from the bridging veins and are seen as crescent shaped anomalies at the periphery of the cranial vault. Epidural hematomas arise from the middle meningeal artery and are lentiform or lens-shaped because their expansion in limited by suture lines (the dura attaches to the cranium at the suture lines).

Other types of hemorrhage include:

Interparenchymal hemorrhage–can either be traumatic or non-traumatic, occur in the brain matter itself

Interventricular hemorrhage–seen as hyperdense fluid in the ventricles, which are usually black because they are filled with hypodense CSF, can be secondary to other types of hemorrhage or trauma

Subarachnoid hemorrhage–most often due to aneurysm rupture and presents with very acute headache (thunderclap headache), seen as fluid in the subarachnoid spaces.  Subarachnoid is also very common in trauma.

The image below is an example of subdural hemorrhage. The left side of the cranial vault is filled with hyperdense fluid, indicating that this process is acute. Also, note the midline shift that occurs, which is shown by the compression of the ventricles more so on the patient’s left than the right and the movement of brain tissue over to the patient’s right. There is also some extracranial soft tissue swelling on the patient’s left, indicating a possible traumatic process. Extracranial soft tissue swelling can help guide your eyes, so to speak, when looking for pathology.

SDH with midline shift 1


Cisterns are spaces between the pia and subarachnoid meningeal layers that can be filled with CSF. There are numerous cisterns that can be identified on a head CT, but the major ones that you should be familiar with are outlined here on Radiopaedia.

These cisterns can be used to identify increased intracranial pressure or subarachnoid hemorrhage (detailed above). In the setting of increased ICP, these spaces become compressed. In subarachnoid hemorrhage, there is hyperdense blood inside them instead of hypodense CSF.


The brain tissue itself is composed primarily of grey matter and white matter. You can see the difference between these two types of tissue because grey matter is more dense and therefore appears more bright on CT. The gyri and sulci can also be visualized and they should be generally symmetric.

The pathologies that can be identified in the brain parenchyma include:

Abscesses–areas of focal infection from bacteria or fungi, often seen as round areas of ring-enhancing hypodensity with associated edema; midline shift is also a possible finding depending on the size of the lesion.

Tumors–areas of abnormal growth whose particular appearance is variable depending on type and location; midline shift is also a possible finding depending on the size of the lesion; particularly well visualized on contrast-enhanced CT because the blood-brain barrier is disrupted during tumor development and growth, which allows the contrast to leak into the tumor and make it bright.

Infarction–when the blood supply is cut off from brain tissue it causes swelling (which can result in midline shift) and the area becomes hypodense and loses grey-white differentiation.

The CT image below shows a few interesting things. The most obvious one is the multiple hyperdensities seen in the brain matter. These lesions are most likely calcified and can represent anything from inflammatory reactions to infections to tumors. The other finding is that the gyri are thin and the space between them is much more evident than normal, which represents atrophy of the brain due to old age, dementia or both.

Multiple calcifications 1


For the sake of brevity, we will not go over the normal anatomy of the ventricular system. The key radiological aspects of the ventricles in the brain are their size and symmetry. They are filled with hypodense CSF and their size can increase due to hydrocephalus, or increased accumulation of CSF. Hydrocephalus is either communicating (obstruction at the arachnoid granulations which function to resorb the CSF) or non-communicating (obstruction at any point in the ventricular system, usually at the foramina which connect the different ventricles.

Symmetry comes into play when there is a mass lesion on one side of the brain, which can cause compression of one of the lateral ventricles with or without midline shift.

One other aspect to keep in mind is that enlargement of the ventricles can be due to atrophy of the brain parenchyma itself, a condition known as “hydrocephalus ex-vacuo”. Therefore if the ventricles do indeed look large, the brain parenchyma should be examined, paying close attention to signs of atrophy. If the ventricles are enlarged and the brain matter looks compressed and the sulci lose their normal wavy pattern (a process called “effacement”), hydrocephalus is more likely.


Skull fractures are a common finding in head trauma and they can be seen on head CT. Fractures are seen as dark lines in the usually bright bones. They must be distinguished from suture lines, which are seen as symmetrical wavy lines across bones. Basilar skull fractures are harder to identify, as the base of the skull has multiple different areas and bones. Radiopaedia has a great example of this here.

One of the things to keep in mind with fractures of the skull is to follow the fracture lines. Fractures often cross into different bones and, especially when looking at the base of the skull, fracture lines can extend much further than you would expect.

The image below shows a painfully obvious frontal sinus fracture, where the the bone fragments actually protrudes back into the brain tissue itself. This view is slightly different from the other images on this post because it is shown in the “bone window”, which is a type of image processing that highlights the hyperdense bones on a CT. It makes fractures much easier to identify (although I’m not quite sure you needed the special window to see this one).

CT head trauma2




All in all, it is also helpful to keep a few other concepts in mind.

Symmetry is key in identifying pathologies, since irregularities in the tissues or fluids are almost never symmetrical.

Utilize the bone window, even if you don’t suspect a fracture.

Soft tissue swelling on the outside of the cranial cavity itself can help you identify the principal point of impact in traumatic injuries and help you find underlying pathologies.

Always use a systematic approach because otherwise it is pretty easy to miss subtle pathology.

Hope this was helpful to you all, but don’t take this as a complete manual of how to read a head CT. Always corroborate your reads with a more experienced physician and always attempt to read the image on your own before looking at any published interpretations. Ask other people about tips and tricks that they might have. And finally, read as many as you can!

Author: Jaymin Patel


University of Virginia tutorialhttp://www.med-ed.virginia.edu/courses/rad/headct/

Elsevier Health, How to Read a CT Scan- http://www.elsevierhealth.com.au/media/us/samplechapters/9781416028727/Chapter%2069.pdf

Agrawal A. How to read a CT scan of a patient with traumatic brain injury?. NMJ. 2013; 2(1): 02-11.

Filed under: CT, Head, Head, How To's, Student Corner, Trauma Tagged: blood can be very bad, bone window, computed tomography, ct, Head, head ct, head trauma, how to, midline shift, student corner

The Central Line 2014-11-24 15:20:45

Annals November podcast is posted for all to hear! Keep the feedback coming, and THANK YOU.

This month look out for:
-LEAN process for reducing ED LOS
-Case law on EMTALA and psych emergencies
-Press Gainey scores and ED analgesics: not what they thought
-Randomized trial of anti-emetics: no better than placebo???

and much much more!

Email any time, annalsaudio@acep.org,


Social Media in Medicine – Useless!

Or, might it be how you use it that matters?

This is a brief report from the journal Circulation, regarding a self-assessment of their social media strategy.  The editors of the journal performed a prospective, block-randomization of published articles to either social media promotion on Facebook and Twitter, or no promotion, and compared 30-day website page views for each article.  121 articles were randomized to social media and 122 to control, and were generally evenly balanced between article types.

And, the answer – unfortunately, for their 3-person associate editor team – is: no difference.  Articles posted to social media received an average of 409 pageviews within 30-days, compared with 392 to those with no promotion.  Thus, the journal of Circulation declares social media dead – and ultimately generalizes their failures to all cardiovascular journals via their Conclusions section.

So, we should all stop blogging and tweeting?  Or, is journal self-promotion futile?  And, are page views the best measure of the effectiveness of knowledge translation?  Or, is there more nuance and heterogeneity between online strategies, rendering this Circulation data of only passing curiosity?  I tend to believe the latter – but, certainly, it’s an interesting publication I hope inspires other journals to perform their own, similarly rigorous studies.

[Note: if my blog entries receive as many (or more!) pageviews as Circulation articles, does this mean my impact factor is higher than Circulation’s 14.98?]

“A Randomized Trial of Social Media from Circulation”

A Response to the “How a SHPOS is Born” article in The National Post

You may have read the article “How a SHPOS is born: What doctors call their very worst patients”, which was written by Anne Skomorowsky and published in The National Post (originally appearing on the Slate Magazine website) on November 10, 2014. Many people in the social media universe had very strong emotional responses to the article. If you haven’t read it, I encourage you to do so. I collaborated with several other individuals (Eve Purdy @eve_purdy, Teresa Chan @tchanMD, Swapnil Hiremath @hswapnil, Heather Murray @heatherm211, Ross Morton @signindoc) to produce a letter to the editor, which was submitted but was not published by The National Post. Thus, we decided to publish our letter on three FOAM websites (TheChartReview.org, manuetcorde.org, BoringEM.org) to share our response with the medical community online. Read below. Feel free to share your thoughts on the comments or on Twitter.

Dear Editor,

We read with horror the recent article “How a SHPOS is born: What doctors call their very worst patients” by Anne Skomorowsky dated November 10, 2014.

We were appalled that the author conveyed the impression that this offensive term, SHPOS, is common and used by the general medical community. The opening line “A medical acronym, SHPOS, helps a doctor summarize a patient’s history in just five letters” implies that the term “a doctor” would include a large number of practicing physicians.

This is false.

This article has sparked discussions over several social media platforms and in the hallways of our hospitals. The consensus from our investigation is that the majority have never used, nor heard of this disgraceful and offensive term. Physicians and learners spanning many generations (medical students to experienced physicians of greater than 20 years) and specialties (emergency medicine, internist, surgeons) agree that that the SHPOS term is completely foreign. The term is as uncomfortable to us as it is the intended readership. On digging a bit deeper (as a result of this article), it seems this term may have been used in the past, in the early 80s or before but given the unfamiliarity of currently practicing physicians, it is unlikely that it is used with any frequency today (1,2). Thus, to taint all current doctors with this archaic and unused term is a reckless overreach at best and slanderous at worst. In fact, the journalistic ethics of reintroducing such a horrible term back into the current lexicon is both irresponsible and dangerous. Language evolves over time, and most of the time with good cause, because terms like SHPOS are eliminated because of their inherent problems.

As a community we do recognize that the language physicians choose is important and appreciate that in many instances we might do better. We have explored issues around language in medicine through an international and open-access case study that can be accessed at one of the world’s pre-eminent medical education blogs (3). We would encourage readers interested in the use of slang by medical professionals to read this much more up to date, balanced and thoughtful exploration of the important topic. This document incorporated patient, allied health, and physician voices all together to generate a very robust discussion and handout for young physicians to read and better understand the importance of words in clinical practice.

Sadly, the information in this article was likely not verified among the health care professionals to whom it refers. Unfortunately, the message conveyed to the readership of the National Post and general public is that terms like “SHPOS” are commonplace and accepted among the medical community, and this supposition is largely unverified in Canada too – especially since it is merely a repurposing of a previously featured article from an American magazine. Acknowledging that slang and language are contextual, and cultural, the National Post might have been better served to do their own, contextually relevant, investigation into this issue, rather than simply feature the article of an American author.

We do not use the term SHPOS. The thesis of the article is simply untrue. This article potentially biases and inflicts pre-arrival damage to future doctor-patient encounters, creating barriers and potentially interferes with the relationship developed by current health care staff and the people they wish to help.

We urge your newspaper to consider the ramifications of posting such inaccurate and potentially damaging materials in the future.

Elisha Targonsky, MD CCFP-EM
Eve Purdy BHSc MD Candidate
Teresa Chan MD FRCPC
Swapnil Hiremath, MD MPH
Heather Murray MD MSc FRCPC


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