Must-watch: video showing murder of Kim Jong Nam

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Extraordinary security footage from Kuala Lumpur International Airport in Malaysia showing details surrounding the February 13 killing by poison of Kim Jong Nam, the half-brother of North Korea leader Kim Jong Un. The video was posted by Fuji Television and the Wall Street Journal, and can be seen by clicking here.

The video makes it possible to establish a rough time-line. Kim Jong Nam is seen walking through the air terminal.  Although the attack itself takes place in the distance and is difficult to see clearly, it appears that at least one woman comes up behind him, swipes her hands over his face, and walk away with her hands held away from her body. Police later said she had been trained to do that, and to wash her hands immediately afterwards.

Kim can then walks up to security guards to report the incident, apparently telling them that he felt dizzy. They escort him to an airport medical clinic. After arriving, he was described as having a seizure and losing consciousness. He was taken to hospital but could not be resuscitated.

Extrapolating from the video, it looks like the poison was a liquid absorbed through the skin with an onset from exposure to severe toxicity of approximately 10-15 minutes. Discussion on toxicology discussion boards have brought up the following possibilities:

  • Tetramine: Tetramethylenedisulfotetramine (TETS) is a rat poison that has been banned since 1984 but which — according to Wikipedia — is still used in China. It is a white powder that is slightly soluble both in water and DMSO, a solvent that could accelerate dermal absorption. TETS is a neurotoxin that acts as a GABA antagonist causing refractory status epileptics, coma, and death. There is no specific antidote.
  • Aconite: This plant poison is used in several Chinese herbal medicines.Aconite is a sodium channel opener, causing gastrointestinal symptoms, perioral paresthesias, bradycardia, and cardiac arrhythmias. Onset after ingestion is reported to be 10 – 20 minutes. Scientific literature indicates that aconite can be absorbed through the skin.
  • TTX: Tetrodotoxin — a neurotoxin found most famously in pufferfish (fugu) — is a sodium channel blocker. Prominent manifestations of toxicity include perioral paresthesias, paralysis, and respiratory failure — none of which were reported in association with Kim’s death. Also, the time course from exposure to death is longer than 15 minutes, even after ingestion.
  • Cyanide: Considered somewhat unlikely, since the onset of severe toxicity would be expected to occur sooner than is evident in this case.
  • DNP: Dinitrophenol — a mitochondrial poison that uncouples oxidative phosphorylation — has been used as a pesticide as well as a diet aid. It can be absorbed through the skin, but usually presents with severe diaphoresis and GI symptoms, which were not apparent in this case.

Several people have been arrested in this case, and others are being sought. Apparently, the police no longer believe the story offered by two women suspects who claimed they believed they were taking part in a harmless television prank. Recent news reports indicate that there was a break-in attempt at the morgue where Kim’s body is being held.

Do not get a serum acetaminophen level less than 4 hours after an acute ingestion

APAP4 out of 5 stars

Can a serum acetaminophen concentration obtained less than 4 hours post-ingestion determine which patients do not require treatment with acetylcysteine? Yarema MC et al. Clin Toxicol 2017 Feb;55:102-108.


For decades the decision whether or not to treat acute acetaminophen [APAP] toxicity with N-acetylcysteine (NAC) has been guided by a serum APAP level drawn 4 or more hours after ingestion. The thought was that before 4 hours the level might be misleading because absorption of the drug might not be complete.

This paper addresses the question of whether an earlier level can be sufficient to clear a patient and decide that the antidote is not needed. The authors performed a secondary analysis of patients entered into the Canadian Acetaminophen Overdose Study over the years 1980 to 2005. They identified nearly 2500 cases in which a patient had an APAP level obtained less than 4 hours after acute ingestion and a second level obtained between 4 and 20 hours post-ingestion. Acute ingestion was defined as one occurring over a duration of less than 4 hours, and “time of ingestion” was taken at the midpoint of that span. The main outcome was agreement between a < 4 hour APAP level of 100 μg/ml or more (pre-specified) and a subsequent > 4 hour level above the treatment line on the Rumack-Matthew nomogram.

Long story short, the authors found that:

While agreement was very good, the diagnostic accuracy for predicting a subsequent concentration above the treatment line was not perfect, except at extremely low (i.e., below 10 μg/ml or undetectable) or extremely high (above 450 μg/ml) concentrations.

Of course, there is always the question about whether we should seek perfection in this case. Remember that in the United States the Rumack-Matthew nomogram has an FDA-mandated safety margin built in. It is not possible to determine from this data whether the patients missed by the < 4 hour 100 μg/ml cut-off would have gone on to develop clinically significant hepatotoxicity.

There is one very important take-home lesson from this paper. Looking at Figure 2, it is apparent that a large number of patients had an early APAP level > 100 μg/ml but a subsequent 4-hour equivalent level below the treatment line on the nomogram. Thus, in many cases the early level could misleading prompt the clinician to start NAC, risking adverse effects in patients who don’t need the antidote at all. Therefore, since the window for successful treatment with the antidote goes up at least to 8 hours, in acute ingestions it’s probably best to avoid getting a < 4 hour APAP level at all.

At Academic Life in Emergency Medicine, Bryan Hayes has an excellent discussion of these issues.


Related posts:

Early metabolic acidosis and coma in massive acetaminophen overdose

Must-read: consider hemodialysis in cases of massive acetaminophen overdose

High acetaminophen levels protect against adverse reactions due to IV N-acetylcysteine

Review: IV N-acetylcysteine in acetaminophen overdose

Clinical significance of serum lactate levels in acetaminophen toxicity



Amnesia and hippocampal ischemia in 4 opiate abusers: a case series

Hippocampus (

Hippocampus (

3.5 out of 5 stars

Complete, bilateral hippocampal ischemia: a case series. Small JE et al. Neruocase 2016 Oct;22:411-415.


Last week, we reviewed an MMWR investigation into a cluster of 14 cases of acute anterograde amnesia with MRI evidence of bilateral hippocampal ischemia identified in Massachusetts during the years 2012-2016. This constellation of features is distinctly unusual — especially when symmetric and accompanied by scant pathology outside the hippocampus —  but has in the past been associated with cocaine abuse and carbon monoxide poisoning.

The MMWR review contained limited clinical information. This paper, from Lahey Medical Center in Burlington MA, describes the initial 4 cases ins somewhat more detail. Some key features of these cases:

  • Three patients had opiate-positive drug screens (the other had a history of opiate abuse but no drug screen was sent)
  • Two patients were unresponsive when brought to hospital (the other 2 had abrupt-onset amnesia but no history of unconsciousness)
  • Neurological deficits persisted to some extent on long-term follow-up in two patients (one of the others died before repeat test, the fourth did not return to clinic)

The authors propose that “MRI finding of acute pyriform ischemia in the hippocampi should be considered strongly suggestive of a toxic exposure.” While they concede that these 4 cases do not prove a causative link between abuse of any specific drug and this amnesia syndrome, this article serves as a head-up that should alert clinicians to be on the look for additional cases, and report any that are identified.

Related post:

Anterograde amnesia and bilateral hippocampus ischemia: is it caused by substance abuse?

Anterograde amnesia and bilateral hippocampus ischemia: is it caused by substance abuse?

Bilateral hippocampal ischemia on MRI [Source: MMWR]

Diffusion weighted MRI findings in patient with unusual amnestic syndrome — Massachusetts, 2012
[Source: MMWR]

3.5 out of 5 stars

Cluster of an Unusual Amnestic Syndrome — Massachusetts, 2012-2016. Barash JA et al. MMWR Morb Mortal Wkly Rep 2017;66:76-79

Full Text

Late in 2015 a Boston neurologist reported a cluster of 4 cases of anterograde amnesia associated with MRI evidence of bilateral hippocampal ischemia. After a public health alert was issued an additional 10 cases were identified in the years 2012-2016, using the case definition of: “1) new onset amnesia in the absence of evidence to support a readily apparent cause, and 2) changes consistent with acute and complete ischemia of both hippocampi on MRI at initial assessment.”

Of the 14 identified patients, all had a history consistent with substance abuse or drug screening consistent with such abuse. In 13 of the patients, this history involved opioids. Additional neurological findings in these cases included deficits in attention orientation, and executive functioning. Some of these deficits resolved over time, but several patients had residual impairment at 1-year follow-up.

Authors note that previously reported causes of amnestic syndrome with bilateral complete hippocampal ischemia include cocaine, carbon monoxide, and influenza. They admit that hypoxia-induced hippocampal ischemia is a possibility. Others have speculated that changes in glutamate balance may be responsible.

The authors’ conclusion:

MRI of the head,toxicology screen, and neurologic consultation should be considered in all adults age > 18 years with sudden-onset amnesia, particularly in patients with altered consciousness. Advanced laboratory testing, including testing for synthetic opioids (e.g., fentanyl) and their analogies, as well as extraneous substances not assessed in these reported cases, might further clarify an association with substance use.

The initial 4 cases have been reported previously in the medical literature.










Is commercial kratom being spiked with a naturally occurring potent opioid


3.5 out of 5 stars

Suspected Adulteration of Commercial Kratom Products with 7-Hydroxymitragynine. Lydecker AG et al. J Med Toxicol 2016;12:341-349.


This well done paper provides — among other things — a helpful short review kratom, a psychoactive product  derived from the Mitragyna speciosa plant.

M speciosa contains more than 40 distinct alkaloids. The primary alkaloid — mitragynine — is an opioid agonist at the mu and delta receptors. Mitragynine has about 33% the opioid potency of morphine.

A minor component of M speciosa —  7-hydroxymitragynine — is a much more potent  opioid agonist with about 17 times the mu-receptor activity of morphine. However, it is normally present in only small amounts in the plant (approximately 2% of content.) This alkaloid produces much of the analgesic effect attributed to kratom. In animal models it has been shown to produce dependence, tolerance, and cross-tolerance to morphine.

The effects of kratom are often described as dose-dependent, with low doses producing stimulation while higher doses produce opioid-like manifestations. This phenomenon may be related to the relative amounts of mitragynine and 7-hydroxymitragynine in the plant.

This authors purchased several commercially-available kratom preparations and quantitatively analyzed the amounts of the 2 alkaloids present. They found amounts of 7-hydroxymitragynine in most of those products. They conclude:

We have found multiple packaged commercial Kratom products to contain artificially elevated concentrations of7-hydroxymitragynine, the alkaloid responsible for M speciosa‘s concerning mechanistic and side effect profile. The amount of 7-hydroxymitragynine exceeded that found in naturally occurring material by up to 500%.

The authors argue that this observation can not be explained by natural chemical conversion or variation in alkaloid content among different specimens of the plant. They suggest that the most convincing explanation is that some products had been spiked with added 7-hydroxymitragynine, and that these products should be regulated more closely by the FDA.

Although it is not remarked upon in the body of the paper. I note from Table 2 that all the products with elevated 7-hydroxymitragynbine levels came from the same manufacturer.

The legal situation regarding kratom is somewhat murky. Although it is legally available in most states, the FDA has seized shipments into the country. Last year, the DEA announced their intention to classify the active alkaloids in kratom as Schedule I drugs. There were strong protests against this move by people who use kratom for pain control or to alleviate withdrawal symptoms, as well as inquiries from members of congress. As a result, the DEA ended up delaying the rescheduling.

The long recent feature on kratom from PBS Newshour at the head of this post is excellent and balanced and well worth watching.

Related posts:

Kratom, it’s a stimulant AND it’s an opioid

Kratom: a unique leaf with stimulant and opiate-like effects

Hepatotoxicity from abuse of kratom: first reported case