Apparently, the blood stimulates the vagus nerve. But it doesn’t have to be blood; Drs Doyle and Mark noted in 1990 the well-known phenomenon of bradycardia induced by manipulation of abdominal contents.
My sister and I were talking medical imaging and the fact came up that modern chest plain films expose the patient to a mere 0.02mSv of radiation. She wondered how much older x-ray machines put out. Let’s ask the 1940s!
The early days of radiography were not without danger, not only to patients but also to scientists:
On 12 August 1896, Electrical Review reported that Dr HD Hawks, a graduate of the 1896 class of Columbia College, gave a demonstration with a powerful X-ray unit in the vicinity of New York. After 4 days, he was compelled to stop work. He noticed a drying of the skin, which he ignored. The hand began to swell and gave the appearance of a deep skin burn. After 2 weeks the skin came off the hand, the knuckles become very sore, fingernail growth stopped and the hair on the skin exposed to X-rays fell out. His eyes were bloodshot and his vision became considerably impaired. His chest was also burnt. Mr Hawks’ physician treated this as a case of dermatitis. Hawks tried protecting his hands with petroleum jelly, then gloves and finally by covering it with tin foil. Within 6 weeks Hawks was partially recovered and was making light of his injuries. Electrical Review concluded by asking to hear from any of its readers who had had similar experiences.
I’ve looked around for data to connect these two points—0.02mSv and melt-your-face-off TSv—to no avail.
He had actually been taking propofol nightly since around 1980, not in order to make himself sleep, but to suppress REM sleep. After several months of REM sleep suppression, the user becomes “receptive,” in other words, they enter the same state achieved by prolonged continuous immersion in aerosol LSD.
Is it true? (Not the murder part but the REM part.)
Recovery from Sleep Deprivation Occurs during Propofol Anesthesia
Tung, et al., 2004
Prospective Rats n=32
“… sleep and anesthesia are neurophysiologically related and suggest that anesthesia and sleep may have similar effects on the sleep deprived state.”
Patterns in recovery REM/NREM cycles were essentially the same for the propofol and intralipid group.
Effects of propofol on sleep quality in mechanically ventilated critically ill patients: a physiological study
Kondili, et al., 2012
Prospective Humans n=12
REM was suppressed but not eliminated in propofol group. However, recovery was not studied.
Propofol-induced sleep: Polysomnographic evaluation of patients with obstructive sleep apnea and controls
Rabelo, et al., 2010
Prospective Humans n=15
REM was totally absent in propofol group.
The hypnotic effect of propofol in the medial preoptic area of the rat
Tung, et al., 2001
Prospective Rats n=?
Propofol may enhance sleep.
Changes in subjective sleepiness, subjective fatigue and nocturnal sleep after anaesthesia with propofol
Ozone, et al., 2000
Prospective Humans n=7 Uncontrolled
No changes in REM activity but there was some changes in sleep stage activity the night after the propofol treatment.
Dreaming During Anesthesia and Sedation
REM and dreaming are highly correlated; dreaming occurs under anesthesia. Propofol has a stronger association with dreaming than some other agents.
Propofol-Induced Sleep: Efficacy and Safety in Patients with Refractory Chronic Primary Insomnia
Prospective Randomized Controlled Human n=103
Not only was propofol effective in increasing sleep quality and quantity in insomniacs, but the effects persisted for at least six months.
Looks like Michael Jackson would have been better off with isoflurane or even scopolamine. Furthermore, he would have had to use the early, troubled formulation until 1986 when it was reformulated and introduced to the (New Zealand) market as Diprivan—the US would have to wait for FDA approval (1989).
Physician passengers may suddenly find themselves in a difficult environment, in front of many onlookers, managing conditions they do not normally treat.
—UpToDate, “Management of inflight medical emergencies on commercial airlines”
Abdominal pain, nausea, vomiting and, less often, diarrhea are commonly reported inflight complaints. Pain, nausea, and vomiting can sometimes be attributed directly to air travel, with the change in barometric pressure, dry air, noise, and vibration of the plane, dehydration, and poor diet.
—UpToDate, “Management of inflight medical emergencies on commercial airlines”
Interestingly, all commercial planes with a flight attendant and weighing than 7500lbs are mandated by the FAA to carry an “Enhanced Medical Kit.” (The basic kit includes bandages, splints, compresses, antiseptic swabs, tape, scissors, and ammonia inhalants.)
Aspirin tablets: 325 mg
Antihistamine (diphenhydramine) tablets: 25 mg
Antihistamine (diphenhydramine), 50 mg injectable single dose
Atropine: 0.5 mg, single 5 mL
Dextrose 50 percents/50 mL injectable
Epinephrine 1:1,000 (for IM injection)
Epinephrine 1:10,000, 2 mL injectable
Inhaled bronchodilator (metered dose or equivalent)
Lidocaine: 5 mL, 20 mg/mL
Nitroglycerine tablets: 0.4 mg
Saline solution, 500 mL
Instructions for medications
Automated external defibrillator
Latex gloves or equivalent
IV administration kit with tubing and connectors
Self-inflating manual resuscitation device (AMBU bag) with masks
Cardiopulmonary resuscitation (CPR) masks
Some United States airlines have enhanced EMKs containing additional acute cardiac life support drugs and equipment.
—UpToDate, “Management of inflight medical emergencies on commercial airlines”
From a description[1. Altman LK. Who Goes First?, The Story of Self-experimentation in Medicine. Univ of California Press; 1987.] of Frederick Prescott’s self-experimentation with curare:
They were now ready for the third stage, a thirty milligram injection…. “That was a real knockout dose. Within two minutes, the muscles of the face, neck, arms and legs were completely paralyzed.”
At this point, Prescott was unable to communicate with his colleagues who were busy watching the graphs being recorded on the revolving drum. They glanced at him every few seconds, but because he did not turn blue, they assumed everything was fine.
Learn more about the remarkable history of curare here.
Jack Barnes dramatically isolates the cause of Irukandji syndrome.
Ahh, the golden age of science! Maybe 150 years from today junkies will be doing quantum theory experiments and building particle accelerators.
This is Anstie:
This is Anstie six months later. Science: not even once.
Here is a portion of an interview of Barry Marshall, of H. pylori fame:
I was aware of famous self-experiments because I read the history of John Hunter’s self-infection with gonorrhea and syphilis (which may have caused his death years later). However, I had been arguing with the skeptics for two years and had no animal model that could prove H pylori was a pathogen. If I was right, then anyone was susceptible to the bug and would develop gastritis and maybe an ulcer years later. So I expected to develop an asymptomatic infection. The experiment was planned with a culture from a patient with dyspepsia and confirmation that it was sensitive to metronidazole. Then I underwent endoscopy in early July 1984 to confirm that I was negative for H pylori. Three weeks later, I drank the ‘brew’ which was a suspension of two culture plates of the organism. If only I knew that people would be so interested, I would have taken a photograph! After five days, I started to have bloating and fullness after the evening meal, and my appetite decreased. My breath was bad and I vomited clear watery liquid, without acid, each morning at approximately 06:00. Then, a follow-up endoscopy showed severe active gastritis with polymorphonuclear infiltrate and epithelial damage. Evidently, H pylori was a pathogen for normal people. The ulcer did not merely set you up for catching the infection. People with asymptomatic H pylori were ‘carriers’ and most people did not have ulcers from the bacterium. Gastritis was explained.
After 14 days, I repeated the endoscopy and then, before the results were known, began taking antibiotics (on my wife’s orders!). However H pylori were not seen on that biopsy so I might have already had a spontaneous cure. Robin Warren believes that the bacteria were still lurking and would have been detected on culture, but by then I was already treated. The paper was published in the third person, but it gradually became known that the ‘male volunteer’ was me.
What I find particularly interesting is that he didn’t just do a bunch of coke and hike for 26 miles. He adhered to Koch’s Postulates.
It’s not what you know, it’s what you use. Clearly, the more you know, the better off you are. Clearly, if you don’t use it, knowledge is a waste. So it’s what you know and what you use. Well, how do you use what you know? Well, you basically have to make a lot of mistakes. So that’s where experience comes in….it’s not experience, it’s experience plus reflection. So you have experience, you make mistakes, you never learn from successes—when you’re successful, you learn nothing. When you make a mistake you may learn something.
Unsolicited show notes for Core EM, ep. 24.0 on hepatic encephalopathy.
Liver failure can result in the buildup of ammonia in the blood.
High levels of ammonia interfere with cognitive function.
Ammonia level is not particularly helpful, especially in the ED. More useful for trending relative to a known baseline. Hepatic encephalopathy is a clinical diagnosis.
Don’t anchor on HE; patients with liver failure are at risk for a slew of other problems too.
Ong, et al. evaluated whether or not there was a correlation between the severity of HE and ammonia level. Although levels of “ammonia increased with the severity of hepatic encephalopathy, “there remains substantial overlap in ammonia levels by grade of hepatic encephalopathy, which may be explained by variability in ammonia levels throughout the day, a possible lag between elevation in ammonia level and hepatic encephalopathy in some patients, or the possibility that compounds other than ammonia are also involved in the pathogenesis of hepatic encephalopathy.”
As the severity of HE increases, the distribution becomes more and more shotgunny. Ong et al. agree with Swami:
Because of the substantial overlap in total ammonia levels and partial pressures between cirrhotic patients with and without hepatic encephalopathy, a single level has little clinical utility in the diagnosis of hepatic encephalopathy. A careful clinical evaluation in patients with cirrhosis presenting with altered mental status remains the “gold standard” for diagnosis.
Ong JP, Aggarwal A, Krieger D, et al. Correlation between ammonia levels and the severity of hepatic encephalopathy. Am J Med. 2003;114(3):188-93.
Pseudoseizures blow my mind. It never ceases to amaze me what happens when the human psyche blows its lid. Rosen’s on pseudoseizures:
…functional events that may be associated with alterations in cognition, abnormal movements and behaviors, and autonomic changes. They are not the result of abnormal CNS electrical activity. Psychogenic seizures may be primarily motor and mimic convulsive generalized seizures, including refractory status epilepticus, or they may be nonconvulsive and mimic either absence or complex partial seizures. Although certain features of convulsive psychogenic seizures may suggest the diagnosis, no clinical criteria are 100% specific; simultaneous video and EEG recordings may be required to confirm the diagnosis.
The automatic reaction of nearly every nurse/doctor/PA/NP is dismissive, that these are malingering people bringing fake problems into the ED and wasting space, time, and resources. Although malingerers can of course fake a seizure for their purposes, patients with pseudoseizures are not faking them. They experience them as events outside of their control.
People with pseudoseizures (or Psychogenic Nonepileptic Seizures) tend to be female and have other somatic disorders such as fibromyalgia, chronic fatigue, and tension headaches (Dixit, et al). Interestingly, certain suggestions can perhaps have a significant effect in testing (Hoepner, et al):
…we investigated the following hypothesis: If patients with PNESs were informed about the possible reduction of seizure threshold caused by hyperventilation and photic stimulation prior to EEG without any other suggestive strategies, PNESs would occur more frequently. In total, 34 inpatients with a diagnosis of PNESs, who had been informed prior to EEG about the increased seizure risk during hyperventilation and photic stimulation (study group), and 80 “noninformed” patients (control group) were enrolled. Psychogenic nonepileptic seizures occurred significantly more often in the study group compared to controls (38% vs. 10.0%, p=0.001). Our results imply that simply providing correct and explicit information about provocation techniques substantially increased the PNES rate.
Emotional stress or intensity has been associated with PNESs (Tintinalli’s, ch. 165). Seongtaek, et al PET scanned both people with PNES and controls; they found a couple of interesting things: white matter abnormalities in an increase in activity in areas of the brain associated with emotion and motor activity.
Convulsive, Tonic-Clonic Seizure
Long inspiratory & expiratory phases, hyperpnea
Short inspiratory & expiratory phases, hyperpnea
Postictal Confusion, Lethargy
Yes / Hard to Tell
Note the glossolalia-like utterances.
Note the persistence of consciousness.
Epileptic general tonic-clonic seizures
If unsure if it is pseudo or not, you can try this (at 1:00):
Here is a discussion of pseudoseizures/PNES from Stanford.
Bergen DC. Diagnosing pseudoseizures: don't hold your breath. Epilepsy Curr. 2008;8(6):154-5.
Dixit R, Popescu A, Bagić A, Ghearing G, Hendrickson R. Medical comorbidities in patients with psychogenic nonepileptic spells (PNES) referred for video-EEG monitoring. Epilepsy Behav. 2013;28(2):137-40.
Hoepner R, Labudda K, Schoendienst M, May TW, Bien CG, Brandt C. Informing patients about the impact of provocation methods increases the rate of psychogenic nonepileptic seizures during EEG recording. Epilepsy Behav. 2013;28(3):457-9.
Lee S, Allendorfer JB, Gaston TE, et al. White matter diffusion abnormalities in patients with psychogenic non-epileptic seizures. Brain Res. 2015;1620:169-76.
Marie gillig P. Psychogenic nonepileptic seizures. Innov Clin Neurosci. 2013;10(11-12):15-8.
Marx JA, Hockberger R, Walls RM. Rosen's Emergency Medicine, Concepts and Clinical Practice. Saunders; 2013.
Sussman NM, Jackel RA, Kaplan LR, Harner RN. Bicycling movements as a manifestation of complex partial seizures of temporal lobe origin. Epilepsia. 1989;30(5):527-31.
Tintinalli J, Stapczynski J, Ma OJ et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Seventh Edition (Book and DVD). Mcgraw-hill; 2010.
I am torn between the hierarchical and the team model of emergency medicine. I recognize the superior level of physicians but I also think that we do a better job working together than alone. The 2014-11-21 episode of ALiEM’s book club reveals a way for physicians to teach trainees. It also offers a way for docs to interact with nurses in the team model. It helps when a physician teaches me something I don’t know so that I can be a better part of the team. Humble Inquiry recognizes that we all have something to offer.
haptoglobin (hăp ”tō-glō ’bĭn) A mucoprotein to which hemoglobin released from lysed red cells into plasma is bound. It is increased in certain inflammatory conditions and decreased in hemolytic disorders.1
The haptoglobin then transports the free hemoglobin to be phagocytosed by monocytes/macrophages. The heme ends up in the liver and is turned into bilirubin. Quimby, et al propose an interesting idea for the chronic hemolysis of sickle cell disease:
In SCD, the Hb-binding capacity is overwhelmed by chronic hemolysis; our previous research shows serum Hp as the depleted component. This deficiency could result in the harmful consequences of circulating fHb going unbridled.
The hypothesis we explore here is that Hp infusions, in excess of fHb concentration, will allow the [haptoglobin scavenging system] to remain functional, and thereby achieve improved clinical outcomes, tracking albuminuria as a sentinel. Albuminuria was selected because of its high prevalence in SCD and its relative ease of diagnosis and monitoring.4
Apparently, haptoglobin is “virtually absent” in patients with mechanical valves (especially aortic valves).3,5 It is not found in about 1% of whites and 4-10% of blacks and newborns have no haptoglobin until four months old.6 Lactic dehydrogenase levels increase as haptoglobin levels decrease.2