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Harrison's Podclass - Episode 92- A 24-Year-Old with Weakness
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Harrison's Podclass - Episode 92- A 24-Year-Old with Weakness
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Segment:0 .
[upbeat intro music] [Dr. Handy] Hi, welcome to Harrison's PodClass, where we discuss important concepts in internal medicine. I'm Cathy Handy. [Dr. Wiener] And I'm Charlie Wiener, and we're coming to you from the Johns Hopkins School of Medicine. [Dr. Handy] Welcome to episode 92, a 24-year-old with weakness. [Dr. Wiener] Hey, Cathy. So, today's patient is a 24-year-old woman with a history of developmental delay, who lives in a group home and is brought to the hospital for weakness starting in her head and descending to her legs.
Obtaining a more complete history, you find out that the first symptoms that the staff noticed were lethargy and what the people there thought were an expressionless face. On physical examination, you find that she has symmetric cranial nerve palsies, inability to move, and decreased breathing. Her deep tendon reflexes are normal. Further examination reveals that she's taking only shallow respirations and you note flaccid muscle tone throughout her body.
According to her caretaker, there was no preceding fever, diarrhea, cough, coryza, rash, or new medications. She was recently given amoxicillin / clavulanate for sinusitis. The group home has a diet consisting mostly of foods created with prepared meats. The question's going to ask, which of the following is the most likely cause of her presentation?
And the options are, A. botulinum toxicity; B. Guillain-Barre syndrome; C. hypokalemic periodic paralysis; D. tetanus toxicity; or E. tick paralysis. [Dr. Handy] Okay, this is a bit of a strange presentation, but there're some key findings here that I'll point out. So one is that she had what's described as descending rather than ascending weakness, and a syndrome characterized by flaccid weakness, the symmetric cranial nerve palsies, clearly, she has respiratory muscle involvement, and notably has normal deep tendon reflexes.
[Dr. Wiener] Okay. So what do those findings make you think? [Dr. Handy] So, putting that together, I would say that she has A. botulism. So, botulism is still a real thing. It probably comes up more in Board exams than in real life, but it's a neuroparalytic disease caused by botulinum toxin, one of the most toxic substances known. Her syndrome with bilateral cranial nerve palsies with descending voluntary muscle paralysis is typical.
And it's important to know this constellation of symptoms and signs because it's often not suspected. The ptosis and facial paralysis too does initially manifest as lethargy and expressionless faces. [Dr. Wiener] Okay, well, let's talk about how would one get it and how do you think she got it? [Dr. Handy] While initially thought to be caused only by the ingestion of botulinum toxin in contaminated food or so-called foodborne botulism, three additional forms caused by in-situ toxin production after germination of spores in either a wound or the intestine are now recognized worldwide.
So, that would be wound botulism, infant botulism, and adult intestinal colonization botulism. So in addition to occurring in these recognized natural forms of the disease, botulism symptoms have been reported in patients receiving higher than recommended doses of Botox, which would be considered iatrogenic botulism for therapeutic or cosmetic purposes. [Dr. Wiener] Okay. So now you have my attention about botulism, let's talk a little bit more about it and how common is it?
You mentioned that it's more on Board exams than real life. [Dr. Handy] So it's hard to know the epidemiology exactly because of variable reporting, but in the U. S. there are about 20 sporadic cases per year. There have been a few outbreaks in this country. In 2006, commercially produced and internationally distributed carrot juice was implicated. Inappropriate refrigeration in the setting of a lack of barriers to botulinum toxin production was believed to be the cause.
Then in 2007, botulism developed in about eight people in the United States who had consumed a canned hot dog chili sauce. Significant deficiencies were discovered in that setting. That involved 91 different products and resulted in the recall of 111 million cans of food. [Dr. Wiener] So back to our patient, do you think she has foodborne or do you think she has intestinal colonization botulism?
Because those seem like the likely choices for her. [Dr. Handy] Yeah, I suspect since she seems to be the only person at the group home that's ill that she has intestinal colonization botulism because nobody else was affected, but this form is difficult to confirm because it's poorly understood. So there are no clear criteria available to differentiate cases of adult intestinal colonization botulism from other adult botulism cases.
Often these cases are caused by Clostridium baratii type F, but the involvement of both C. botulinum type A and C. butyricum type E have been reported. Botulism following abdominal surgery or antibiotic use has sometimes been considered likely adult intestinal colonization botulism. [Dr. Wiener] I can understand the pathophysiology if someone ingests the toxin, but what about these cases of intestinal colonization?
What's the pathophysiology there? [Dr. Handy] So, like I mentioned before, it's poorly understood, it's believed to have a pathology similar to that of infant botulism but it occurs in adults. Typically, patients have some anatomic or functional bowel abnormality, or have recently used antibiotics that may help toxigenic Clostridium compete more successfully against the normal bowel microbiota.
Despite antitoxin treatment, relapse due to intermittent intraluminal production of toxin may be observed in patients with adult intestinal colonization botulism. [Dr. Wiener] And we noted that this patient had received antibiotics recently, so maybe that was the precipitating cause. You mentioned antitoxin, is that how you treat this? [Dr. Handy] The cornerstones of treatment for botulism are meticulous intensive care and administration of botulinum antitoxin.
Because antitoxin is most beneficial early in the course of clinical illness, it should be administered empirically and before the time consuming workup for other illnesses or laboratory confirmation is complete. Now, persons of all ages in whom botulism is suspected should be hospitalized immediately so that signs of respiratory failure can be detected and managed.
Vital capacity should be monitored frequently, and mechanical ventilation can be provided as needed. The botulinum antitoxin can limit the progression of illness because it neutralizes toxin molecules in the circulation that have not yet bound to nerve endings, but it really doesn't reverse existing paralysis, which can take weeks to improve. Clinical improvement follows sprouting of new nerve terminals, so it can take weeks to months.
[Dr. Wiener] So, yeah, so I assume that the overall recovery for a patient such as this is pretty slow then? [Dr. Handy] Yeah, patients often require outpatient rehabilitation therapy and may experience residual deficits. Death in untreated botulism is usually due to respiratory failure related to airway obstruction, that's from pharyngeal muscle paralysis and inadequate tidal volume, resulting from paralysis of diaphragmatic and accessory respiratory muscles.
Death can also result from hospital-associated infections and other sequela of long-term paralysis, hospitalizations, and mechanical ventilation. [Dr. Wiener] Okay, let's run through the other options in this question. Why was her presentation not likely due to them? [Dr. Handy] All right, so going down the list, Guillain-Barre syndrome is an acute, frequently severe and fulminant polyradiculoneuropathy that's autoimmune in nature, it typically manifests as a rapidly progressive ascending paralysis, often with sensory deficits and absent deep tendon reflexes, and remember, in our case, the reflexes were normal.
It is often, about 70% of the time, associated with an acute respiratory or gastrointestinal infection. [Dr. Wiener] How about the others? [Dr. Handy] Hypokalemic periodic paralysis is a very rare autosomal dominant disease and is characterized by sporadic or episodic acute weakness that's associated with hypokalemia. The history here didn't sound compatible. Tetanus toxicity causes muscle spasms, not paralysis and cranial nerve defects.
And tick paralysis is caused by a tick neurotoxin and may also cause an ascending paralysis that's more similar to Guillain-Barre. In this case, we also don't have any history of a tick bite. [Dr. Wiener] Okay, great. So the teaching points in this case are that botulism presents with a descending paralysis with prominent cranial nerve involvement. While most cases are foodborne, there may be isolated cases of adult intestinal colonization botulism that require awareness, since prompt administration of the antitoxin is imperative.
[Dr. Handy] And you can read more about it, believe it or not, Harrison's has a whole chapter on botulism. [upbeat outro music] [Mr. Shanahan] This is Jim Shanahan, publisher at McGraw Hill. Harrison's PodClass is brought to you by McGraw Hill's AccessMedicine, the online medical resource that delivers the latest trusted content from the best minds in medicine. Go to accessmedicine.com to learn more.
Segment:0 .
[upbeat intro music] [Dr. Handy] Hi, welcome to Harrison's PodClass, where we discuss important concepts in internal medicine. I'm Cathy Handy. [Dr. Wiener] And I'm Charlie Wiener, and we're coming to you from the Johns Hopkins School of Medicine. [Dr. Handy] Welcome to episode 92, a 24-year-old with weakness. [Dr. Wiener] Hey, Cathy. So, today's patient is a 24-year-old woman with a history of developmental delay, who lives in a group home and is brought to the hospital for weakness starting in her head and descending to her legs.
Obtaining a more complete history, you find out that the first symptoms that the staff noticed were lethargy and what the people there thought were an expressionless face. On physical examination, you find that she has symmetric cranial nerve palsies, inability to move, and decreased breathing. Her deep tendon reflexes are normal. Further examination reveals that she's taking only shallow respirations and you note flaccid muscle tone throughout her body.
According to her caretaker, there was no preceding fever, diarrhea, cough, coryza, rash, or new medications. She was recently given amoxicillin / clavulanate for sinusitis. The group home has a diet consisting mostly of foods created with prepared meats. The question's going to ask, which of the following is the most likely cause of her presentation?
And the options are, A. botulinum toxicity; B. Guillain-Barre syndrome; C. hypokalemic periodic paralysis; D. tetanus toxicity; or E. tick paralysis. [Dr. Handy] Okay, this is a bit of a strange presentation, but there're some key findings here that I'll point out. So one is that she had what's described as descending rather than ascending weakness, and a syndrome characterized by flaccid weakness, the symmetric cranial nerve palsies, clearly, she has respiratory muscle involvement, and notably has normal deep tendon reflexes.
[Dr. Wiener] Okay. So what do those findings make you think? [Dr. Handy] So, putting that together, I would say that she has A. botulism. So, botulism is still a real thing. It probably comes up more in Board exams than in real life, but it's a neuroparalytic disease caused by botulinum toxin, one of the most toxic substances known. Her syndrome with bilateral cranial nerve palsies with descending voluntary muscle paralysis is typical.
And it's important to know this constellation of symptoms and signs because it's often not suspected. The ptosis and facial paralysis too does initially manifest as lethargy and expressionless faces. [Dr. Wiener] Okay, well, let's talk about how would one get it and how do you think she got it? [Dr. Handy] While initially thought to be caused only by the ingestion of botulinum toxin in contaminated food or so-called foodborne botulism, three additional forms caused by in-situ toxin production after germination of spores in either a wound or the intestine are now recognized worldwide.
So, that would be wound botulism, infant botulism, and adult intestinal colonization botulism. So in addition to occurring in these recognized natural forms of the disease, botulism symptoms have been reported in patients receiving higher than recommended doses of Botox, which would be considered iatrogenic botulism for therapeutic or cosmetic purposes. [Dr. Wiener] Okay. So now you have my attention about botulism, let's talk a little bit more about it and how common is it?
You mentioned that it's more on Board exams than real life. [Dr. Handy] So it's hard to know the epidemiology exactly because of variable reporting, but in the U. S. there are about 20 sporadic cases per year. There have been a few outbreaks in this country. In 2006, commercially produced and internationally distributed carrot juice was implicated. Inappropriate refrigeration in the setting of a lack of barriers to botulinum toxin production was believed to be the cause.
Then in 2007, botulism developed in about eight people in the United States who had consumed a canned hot dog chili sauce. Significant deficiencies were discovered in that setting. That involved 91 different products and resulted in the recall of 111 million cans of food. [Dr. Wiener] So back to our patient, do you think she has foodborne or do you think she has intestinal colonization botulism?
Because those seem like the likely choices for her. [Dr. Handy] Yeah, I suspect since she seems to be the only person at the group home that's ill that she has intestinal colonization botulism because nobody else was affected, but this form is difficult to confirm because it's poorly understood. So there are no clear criteria available to differentiate cases of adult intestinal colonization botulism from other adult botulism cases.
Often these cases are caused by Clostridium baratii type F, but the involvement of both C. botulinum type A and C. butyricum type E have been reported. Botulism following abdominal surgery or antibiotic use has sometimes been considered likely adult intestinal colonization botulism. [Dr. Wiener] I can understand the pathophysiology if someone ingests the toxin, but what about these cases of intestinal colonization?
What's the pathophysiology there? [Dr. Handy] So, like I mentioned before, it's poorly understood, it's believed to have a pathology similar to that of infant botulism but it occurs in adults. Typically, patients have some anatomic or functional bowel abnormality, or have recently used antibiotics that may help toxigenic Clostridium compete more successfully against the normal bowel microbiota.
Despite antitoxin treatment, relapse due to intermittent intraluminal production of toxin may be observed in patients with adult intestinal colonization botulism. [Dr. Wiener] And we noted that this patient had received antibiotics recently, so maybe that was the precipitating cause. You mentioned antitoxin, is that how you treat this? [Dr. Handy] The cornerstones of treatment for botulism are meticulous intensive care and administration of botulinum antitoxin.
Because antitoxin is most beneficial early in the course of clinical illness, it should be administered empirically and before the time consuming workup for other illnesses or laboratory confirmation is complete. Now, persons of all ages in whom botulism is suspected should be hospitalized immediately so that signs of respiratory failure can be detected and managed.
Vital capacity should be monitored frequently, and mechanical ventilation can be provided as needed. The botulinum antitoxin can limit the progression of illness because it neutralizes toxin molecules in the circulation that have not yet bound to nerve endings, but it really doesn't reverse existing paralysis, which can take weeks to improve. Clinical improvement follows sprouting of new nerve terminals, so it can take weeks to months.
[Dr. Wiener] So, yeah, so I assume that the overall recovery for a patient such as this is pretty slow then? [Dr. Handy] Yeah, patients often require outpatient rehabilitation therapy and may experience residual deficits. Death in untreated botulism is usually due to respiratory failure related to airway obstruction, that's from pharyngeal muscle paralysis and inadequate tidal volume, resulting from paralysis of diaphragmatic and accessory respiratory muscles.
Death can also result from hospital-associated infections and other sequela of long-term paralysis, hospitalizations, and mechanical ventilation. [Dr. Wiener] Okay, let's run through the other options in this question. Why was her presentation not likely due to them? [Dr. Handy] All right, so going down the list, Guillain-Barre syndrome is an acute, frequently severe and fulminant polyradiculoneuropathy that's autoimmune in nature, it typically manifests as a rapidly progressive ascending paralysis, often with sensory deficits and absent deep tendon reflexes, and remember, in our case, the reflexes were normal.
It is often, about 70% of the time, associated with an acute respiratory or gastrointestinal infection. [Dr. Wiener] How about the others? [Dr. Handy] Hypokalemic periodic paralysis is a very rare autosomal dominant disease and is characterized by sporadic or episodic acute weakness that's associated with hypokalemia. The history here didn't sound compatible. Tetanus toxicity causes muscle spasms, not paralysis and cranial nerve defects.
And tick paralysis is caused by a tick neurotoxin and may also cause an ascending paralysis that's more similar to Guillain-Barre. In this case, we also don't have any history of a tick bite. [Dr. Wiener] Okay, great. So the teaching points in this case are that botulism presents with a descending paralysis with prominent cranial nerve involvement. While most cases are foodborne, there may be isolated cases of adult intestinal colonization botulism that require awareness, since prompt administration of the antitoxin is imperative.
[Dr. Handy] And you can read more about it, believe it or not, Harrison's has a whole chapter on botulism. [upbeat outro music] [Mr. Shanahan] This is Jim Shanahan, publisher at McGraw Hill. Harrison's PodClass is brought to you by McGraw Hill's AccessMedicine, the online medical resource that delivers the latest trusted content from the best minds in medicine. Go to accessmedicine.com to learn more.
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