Name:
A 56-Year-Old with Frostbite
Description:
A 56-Year-Old with Frostbite
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Duration:
T00H07M18S
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
♪ (music) ♪
CATHY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy.
CHARLIE: And I'm Charlie Wiener,
CHARLIE: and we're coming to you from the Johns Hopkins School of Medicine. ♪ (music) ♪
CATHY: Welcome to Episode 41. Today's episode is about a 56-year-old with frostbite.
CHARLIE: Okay. So, a 56-year-old man is admitted to the surgical service one day ago for care due to exposure injury and frostbite in his distal extremities. He also is being treated for some possible early bacterial infection.
CATHY: Oh, that sounds painful. Sometimes you can also get frostbite to affect other exposed areas, so you'll commonly see it in the ears, nose, and chin, but it's fortunate at least for this person that this is limited to the extremities.
CHARLIE: It is. Complicating his presentation is that he has a long-standing history of alcoholism, drinking about one liter of vodka on a daily basis.
CATHY: Well, that is definitely more than is healthy for him. We know that more than three drinks a day significantly increases the risk of overall mortality, and that's for many reasons, so it's not limited to just liver disease, but also cancer and vascular disease. Overall, it's estimated that chronic, excessive alcohol use disorders decrease the lifespan by about ten years. But since we're in the acute setting, in a hospitalization, you want to know too, if he has any history of alcohol withdrawal, and also when he had his last drink.
CATHY: If he only stopped drinking, for example, on admission, than he could be at risk for acute alcohol withdrawal during the hospitalization.
CHARLIE: Well, let me update you. So, we don't have much past history on this gentleman. Since admission, he's been treated with IV fluids, antibiotics, and he's been medicated since admission for prevention of alcohol withdrawal via a symptom-triggered approach, and he last received lorazepam two milligrams orally, about two hours ago. However, you get called because things are a bit different now than when he first came into the hospital. The nurses tell you that he's expressing a belief that his wounds were the result of burns that were inflicted upon him by torturers in the government, because he knows too much about government surveillance plans.
CHARLIE: The surgical team reports it is difficult to keep the patient in bed, and he seems unsteady on his feet at times. When he was out of bed, he was disoriented, tremulous, and hypertensive. He was actively confused. The delusional thoughts did not respond to treatment with additional lorazepam which was given intravenously in this case.
CATHY: So, it sounds like some of this may have been responsive to lorazepam, but the delusional thoughts persist. What's the rest of his exam now?
CHARLIE: Okay, well you go see the patient-- he's sleeping quietly at this time. His vital signs are: blood pressure 110/82, heart rate of 94, respiratory rate of 16, a temperature of 37° and a room air saturation of 97%. He awakens easily and has minimal resting tremor. On neurologic exam, he exhibits past pointing, difficulty with rapid alternating movements, horizontal nystagmus in both directions, decreased sensation to light touch and pinprick in the lower extremities below the mid tibia.
CHARLIE: You get him up to walk and find that his gait is wide-based and ataxic. He no longer expresses the prior delusional beliefs, but he's disoriented and thinks he is in jail. He states that he was brought to the gulag so that the government could experiment on him. Currently, he has D5 half-normal saline infusing at a 100 milliliters per hour, and he's also receiving nafcillin 2 grams IV every four hours for cellulitis. The question asks: "What do you think is the cause of this patient's altered mental status?" And the options are: A. hypoglycemia; B. hyponatremia; C. niacin deficiency; D. thiamine deficiency; or E. undertreated alcohol withdrawal.
CATHY: Okay. Well, we have a lot of information here. The main points that I took away are that he has normal vital signs, he's disoriented, and he has an abnormal neurologic exam with prominent, mostly cerebellar and sensory findings. When thinking about severe manifestations of alcohol withdrawal, vital sign instability with hypertension and tachycardia are usually seen. But it doesn't sound like he has that now, so we can rule out option E-- undertreated alcohol withdrawal-- as a cause of his current symptoms.
CATHY: The other point that you mentioned that caught my attention, is that he's receiving D5 half-normal saline, and you never mentioned giving thiamine at all during this hospitalization.
CHARLIE: What's notable about that?
CATHY: Well, alcohol interferes with the absorption of vitamins in the small intestine and it decreases their storage in the liver. So, patients can have multiple deficiencies-- usually what we see is folate, pyridoxine, or vitamin B6, thiamine, which is B1, and also nicotinic acid. Glucose infusions can precipitate acute Wernicke syndrome, which is due to the acute precipitation of thiamine deficiency, so thiamine should always be administered before or concurrently to alcoholic patients who require glucose infusions. Acute Wernicke syndrome is on the spectrum of Wernicke-Korsakoff disease which may progress to amnesia and other loss of executive function.
CHARLIE: Why does glucose precipitate the acute thiamine toxicity in the brain?
CATHY: Thiamine is a cofactor for glucose metabolism in the brain. The sudden glucose load that can happen when you give a D5 infusion can cause worsening of the chronic thiamine depletion, thus provoking the neurologic manifestations of acute deficiency or the Wernicke syndrome. In this country, alcoholism is one of the most common causes of thiamine deficiency, and this patient has the classic triad of ophthalmoplegia, ataxia, and confusion.
CHARLIE: Great, so the answer in this case is D -- thiamine deficiency.
CATHY: Yes, that's the right answer.
CHARLIE: Niacin deficiency was option C, and you mentioned niacin is one of the vitamins that may be deficient in chronic alcoholism. Are you concerned that that's contributing to this case?
CATHY: Niacin deficiency causes pellagra which characteristically presents with dermatitis, diarrhea, and dementia. The presentation he presented with here would not be consistent with that, although, later in his course he certainly should be started on vitamin supplementation that includes niacin.
CHARLIE: How would you treat this patient immediately?
CATHY: So first, you want to stop the IV glucose and start him on IV or IM thiamine until there's no further improvement in the acute symptoms. And then long term, oral thiamine should be continued until recovery is complete.
CHARLIE: Are his neurologic abnormalities likely to improve?
CATHY: Stopping the glucose and adequately supplementing thiamine should stop the progression. And hopefully, his acute cognitive deficits will improve during the hospitalization. But the cerebellar changes will require long-term therapy and may not be fully reversible. And the other thing that he'll need is, obviously, alcohol cessation counseling as well, long term.
CHARLIE: Great. So, the teaching point of this case is that chronic alcoholism can result in thiamine deficiency and the Wernicke-Korsakoff syndrome which can be precipitated by glucose administration without prior or concurrent thiamine replacement. The classic symptoms are: ophthalmoplegia, ataxia, and confusion and they can also include long-term memory loss which is not always reversible.
CATHY: To learn more, you can read about this in Harrison's chapter on Cardinal Manifestations of Disease. ♪ (music) ♪