Mystery case.

[BruceD]

Actually pretty good for both. That can happen for either field diagnoses.

What I don't like is the A-Fib with ALOC. That tells me CVA until proven otherwise. Which is why I would be hesitant to push Narcan on this kid.

Narcan is contraindicated for resp depression not due to opioid ingestion. Side effects include tachycardia, hypertension, N/V, seizures, even cardiac arrest. Do you really want to cause these side effects on someone who could quite possibly be having a CVA?

I've not endorsed narcan on this patient, I think you are correct about not using it.
Treating this patient with diesel would be ideal, especially when you are 4mins from a hospital.

Effexor has been shown to cause atrial fib along with other arrhythmias -> http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2000637 and has been associated with both NMS and Serotonin Syndrome -> http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)72791-4/fulltext

The SSNRIs have been associated with increased suicidality in patients < 25 yo. Which was directing my thoughts more toward O.D. or drug adverse event.

I leaned away from pontine hemorrhage mostly because it's usually chronic hypertensive in origin (or AVM) and results in hyperventilation (if you go 'by the book'). There's a good quick read on them here: Basic Neurology

Either way...this kid may have a bad outcome.
Heaven knows I've seen enough kids end up as eating(via tube), breathing(via tube), poopin'(via diaper) bed decorations due to attempts at suicide

 

[MSDeltaFlt]

I've not endorsed narcan on this patient, I think you are correct about not using it.
Treating this patient with diesel would be ideal, especially when you are 4mins from a hospital.

Effexor has been shown to cause atrial fib along with other arrhythmias -> http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2000637 and has been associated with both NMS and Serotonin Syndrome -> http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)72791-4/fulltext

The SSNRIs have been associated with increased suicidality in patients < 25 yo. Which was directing my thoughts more toward O.D. or drug adverse event.

I leaned away from pontine hemorrhage mostly because it's usually chronic hypertensive in origin (or AVM) and results in hyperventilation (if you go 'by the book'). There's a good quick read on them here: Basic Neurology

Either way...this kid may have a bad outcome.
Heaven knows I've seen enough kids end up as eating(via tube), breathing(via tube), poopin'(via diaper) bed decorations due to attempts at suicide

Great on the references. I wasn't stuck on Pontine either. Only mentioning it as a possibility with the hot skin and the pinpoint pupils. I was merely trying to get everyone to think about something. With this guy's prehospital presentation, his official diagnosis could have easily gone either way. And pushing Narcan on something that wasn't opioid induced up to and including CVA could have very counterproductive results to an already negative situation. Add to that not getting a definitive airway,regardless of the type, even for a 4 min trip, and you can see how he could end up in a perpetual vegetative state for decades to come.

 

[Melclin]

Well here comes the great and uninteresting reveal. The kid was actually me...BABAH. A few years ago now. I requested the Patient Care Records from Ambulance Victoria.

As far as what it actually was, I'm still pretty sketchy. I spent most of my time drunk in those days, so my memory, she's notta so good. Depression yeah, suicide attempt? Nope.

I'd had about 8 beers earlier that night but was pretty close to sober come 12am when my parents went to bed. After that I can't remember, but I had a habit of purifying codeine out of paracetamol/codeine OTC pain killers (which would explain the paracetamol in my liver). May have tried that and mixed it with some Xanax. Or possibly made opium tea from poppy seeds, that was a common one too. The ICU doctor latter argued with me that it couldn't have been that because poppy seeds are inert...my previous six months of being consistently wasted off them beg to differ. It's also possible that in my general intoxication (experience has show that xanax plus alcohol makes for some decidedly odd decision making) it may have seemed like a good idea to eat a box of panadol. Like I said, I must have aspirated my stomach contents at some stage (they put chemicals in the poppy seeds to make you nauseous if u have to many to discourage stonners like my old self, so that might have something to do with it). Lost about 80% of my lung volume, and got a nasty dose of aspiration pneumonitis. I'm interested to see that the paramedics didn't make any note of being able to hear odd lung sounds. With lungs 80% full of vommit you'd have to hear something.

Almost died, but recovered quite well with anti-biotics, spent a week in ICU (PEEP ventilation majorly sucks when you're awake) and walked out straight into a looney bin where I spent the next week or so, convincing them I didn't try to off myself.

Anyways, I thought it was in interesting case given that none of the practitioners involved could ever really figure out what happened exactly and it had an odd presentation, easily mistakable for a straight up heroin overdose.

PS: Lets not have any "That was stupid thing to do" comments. I realise that. I realised at the time. But in the swing of what I would later know to be my first Bi-polar related depression, I didn't particularly care. I'm quite different now, with the help of a cracking shrink, and planning to enjoy paying back my debt to society while I practice some top notch paramedicine . Oh and not that I expect it, but no sympathy, I just wanted to present an interesting case and hoped to learn a little more about what happened. You've all been extremely helpful so far. Any more stunning insights or thoughts?

 

[boingo]

What did they do to manage your A-fib? Did it spontaneously convert, did they chemically convert you or cardiovert? Did you have a prior hx of A-fib, WPW? Glad to hear you are on the mend, I know I felt pretty damn invincible in my late teens early twenties too. Good luck with your education.

 

[Melclin]

What did they do to manage your A-fib? Did it spontaneously convert, did they chemically convert you or cardiovert? Did you have a prior hx of A-fib, WPW? Glad to hear you are on the mend, I know I felt pretty damn invincible in my late teens early twenties too. Good luck with your education.

No history of A-fib or WPW. I think someone in my family has WPW so there might be something in that but I'm sure they would have noticed that in the ICU some time during the week I was there.

I'm not entirely sure, cos I haven't gotten around to requesting my hospital records yet but they were considering sychronised cardioversion, but I think it spontaneously converted. My parents account of the night has proven to be (understandably) inaccurate. So one of these days I'll fill out the plethora of paper work to get the hospital to send me my records.

Cheers for the encouragement.

 

[BruceD]

Great on the references. I wasn't stuck on Pontine either. Only mentioning it as a possibility with the hot skin and the pinpoint pupils. I was merely trying to get everyone to think about something. With this guy's prehospital presentation, his official diagnosis could have easily gone either way. And pushing Narcan on something that wasn't opioid induced up to and including CVA could have very counterproductive results to an already negative situation. Add to that not getting a definitive airway,regardless of the type, even for a 4 min trip, and you can see how he could end up in a perpetual vegetative state for decades to come.

Absolutely a good point about the Narcan.

Meclin, adding etoh to a bzd opens up a whole new area of bad-ness. Take a few and read up on it, tell us if you think it fits your profile.

tc
-B

 

[triemal04]

You also need to control ICP's as best you can on the prehospital level. EtCO2's in the 60's and 70's is a bit high. High end tidals mean cerebral vasodilation which further increase ICP which take away from CPP which is what is going to drive this poor kid further down the drain. If you have RSI, put him down and get those EtCO2's in the upper 30's.

Be worth considering why the EtCO2 is that high, even after artificial ventilation. Something beyond downtime is causing that increase, which would point more towards med OD than anything in this case.

 

[VGFDEMT34]

Primary thought is an overdose. Secondary is a diabetic emergency. What is the BGL?

If BGL within normal range: push narcan for suspected overdose. Any change in mental status?

If hypoglycemic: D-50 IV push

If hypoglycemic: bolus NaCl

 

[Melclin]

Be worth considering why the EtCO2 is that high, even after artificial ventilation. Something beyond downtime is causing that increase, which would point more towards med OD than anything in this case.

Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.

Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?

 

[Melclin]

Primary thought is an overdose. Secondary is a diabetic emergency. What is the BGL?

If BGL within normal range: push narcan for suspected overdose. Any change in mental status?

If hypoglycemic: D-50 IV push

If hypoglycemic: bolus NaCl

A Random Blood Glucose test showed it to be 15.3 mmol/L. That's a little more than twice what it should be if you're not familiar with that format. But its not even close to enough to have caused all this.

 

[BruceD]

Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.

Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?

The original high CO2 is probably due to respiratory acidosis (pt isn't blowing off CO2 'cause his resps are 6).

Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?), inadequate amount of time/volume of artificial ventilation, or an ongoing metabolic process producing acid (organic acids such as EtOH, lactic acidosis, or Rhabdo), but I think Vent would be the best person to answer this question as this is beyond my realm o' knowledge.

 

[bonedog]

What was the QT interval, QRS? Effexor could be causing the arrythmia.

Methamphetamine binge followed by a dose of GHB. End up with the electrolyte imbalance and the patient that goes from GCS of 3 to ripping out the ET tube and back to a 3.

 

[VentMedic]

The original high CO2 is probably due to respiratory acidosis (pt isn't blowing off CO2 'cause his resps are 6).

Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?), inadequate amount of time/volume of artificial ventilation, or an ongoing metabolic process producing acid (organic acids such as EtOH, lactic acidosis, or Rhabdo), but I think Vent would be the best person to answer this question as this is beyond my realm o' knowledge.

You're doing a decent job explaining it.

Originally Posted by Melclin
Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.

Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?

Oxygenation and ventilation are two very different concepts. You can not tell much about ventilation from an SpO2. In this case you may not even be able to tell much about oxygenation either since the oxyhemoglobin dissociation curve will shift in the face of acidosis. In fact, if the shortness of breath was severe to start with the SpO2 may not be an adequate indication of oxygenation if the A-a is unknown. If you are giving an FiO2 of 1.0 but only getting a PaO2 of 85 mmHg, you have a significant A-a gradient which indicates a serious problem. Normal A-a gradient increases 5-7 mmHG for every 10% increase in FiO2 due to the overcoming of hypoxic vasoconstriction opening blood flow to poorly ventilated lung areas. There is also the relationship between pulmonary vasoconstriction if it is released with an FiO2 of 1.0 and an increase in CO2 with deadspace and V/Q mismatching. For some patients, this is now a more accepted theory to hypercarbia (hypercapnia) than the "hypoxic drive".

 

[fma08]

the oxyhemoglobin dissociation curve will shift in the face of acidosis.

Yet another thing I learned in college A&P and not the "A&P" we got in medic school... <_<

 

[Melclin]

Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?),

Lungs full of aspirated stomach contents would fit the bill here right? Cos I sure had that. Should the persistant ^ etCO2 have been an indicator, given the setting, that aspiration was a possibility? How relevant is identifying a significant stomach contents aspiration to the initial pre-hospital treatment?

What was the QT interval, QRS? Effexor could be causing the arrythmia.

Methamphetamine binge followed by a dose of GHB. End up with the electrolyte imbalance and the patient that goes from GCS of 3 to ripping out the ET tube and back to a 3.

Don't have the details on the ECG just that it was A-Fib.
And I'd know if I'd been into the methamphetamines, and I would have mentioned it here already ^_^ but I assume you were throwing out ideas from a theoretical point of view, so cheers.

oxyhemoglobin dissociation curve will shift in the face of acidosis.

Ahh yeah, I forgot my old A&P. Didn't see the direct relevance of that particular until bit of info at the time. Now I know better.

Thanks guys, very illuminating. Keep it coming. Honestly, sometimes I reckon I learn more off this forum that I do off my lecturers.

 

[Amack]

Narcan is contraindicated for resp depression not due to opioid ingestion. Side effects include tachycardia, hypertension, N/V, seizures, even cardiac arrest. Do you really want to cause these side effects on someone who could quite possibly be having a CVA?

CONTRAINDICATIONS — Hypersensitivity to naloxone or any component of the formulation

WARNINGS / PRECAUTIONS
Concerns related to adverse effects:

Acute opioid withdrawal: May precipitate symptoms of acute withdrawal in opioid-dependent patients, including pain, hypertension, sweating, agitation, irritability; in neonates: shrill cry, failure to feed. Carefully titrate dose to reverse hypoventilation; do not fully awaken patient or reverse analgesic effect (postoperative patient).
Disease-related concerns:

Cardiovascular disease: Use with caution in patients with cardiovascular disease or in patients receiving medications with potential adverse cardiovascular effects (eg, hypotension, pulmonary edema or arrhythmias); pulmonary edema and cardiovascular instability, including ventricular fibrillation, have been reported in association with abrupt reversal when using narcotic antagonists. Administration of naloxone causes the release of catecholamines; may precipitate acute withdrawal or unmask pain in those who regularly take opioids.
Seizures: Use caution in patients with history of seizures; avoid use in treatment of meperidine-induced seizures.
Other warnings/precautions:

Opioid overdose: Recurrence of respiratory depression is possible if the opioid involved is long-acting; observe patients until there is no reasonable risk of recurrent respiratory depression.
Postoperative reversal: Appropriate use: Excessive dosages should be avoided after use of opiates in surgery. Abrupt postoperative reversal may result in nausea, vomiting, sweating, tachycardia, hypertension, seizures, and other cardiovascular events (including pulmonary edema and arrhythmias).

(Taken from the following references

REFERENCES


American Academy of Pediatrics Committee on, Drugs. Naloxone Dosage and Route of Administration for Infants and Children: Addendum to Emergency Drug Doses for Infants and Children. Pediatrics 1990; 86:484.
American Heart Association Emergency Cardiovascular Care, Committee. 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC), Part 10.2: Toxicology in ECC. Circulation 2005; 112(24 Suppl):IV126.
American Heart Association Emergency Cardiovascular Care, Committee. 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC), Part 12: Pediatric Advanced Life Support. Circulation 2005; 112(24 Suppl):IV167.
Bergasa, NY, Alling, DW, Talbot, TL, et al. Effects of Naloxone Infusions in Patients With the Pruritus of Cholestasis. A Double-Blind, Randomized, Controlled Trial. Ann Intern Med 1995; 123:161.
Boeuf, B, Gauvin, F, Guerguerian, AM, et al. Therapy of Shock With Naloxone: A Meta-Analysis. Crit Care Med 1998; 26:1910.
Chamberlain, JM, Klein, BL. A Comprehensive Review of Naloxone for the Emergency Physician. Am J Emerg Med 1994; 12:650.
Drugs for Pediatric Emergencies. Pediatrics 1998; 101:E13.
Goldfrank, L, Weisman, RS, Errick, JK, et al. A Dosing Nomogram for Continuous Infusion Intravenous Naloxone. Ann Emerg Med 1986; 15:566.
Hantson, P, Evenepoel, E, Ziade, D, et al. Adverse Cardiac Manifestations Following Dextropropoxyphene Overdose: Can Naloxone Be Helpful. Ann Emerg Med 1995; 25:263.
Hoffman, RS, Goldfrank, LR. The Poisoned Patient With Altered Consciousness. Controversies in the Use of a'Coma Cocktail'. JAMA 1995; 274:562.
Johnson, C, Mayer, P, Grosz, D. Pulmonary Edema Following Naloxone Administration in a Healthy Orthopedic Patient. J Clin Anesth 1995; 7:356.
Kaplan, JL, Marx, JA, Calabro, JJ, et al. Double-Blind, Randomized Study of Nalmefene and Naloxone in Emergency Department Patients With Suspected Narcotic Overdose. Ann Emerg Med 1999; 34:42.
Kendrick, WD, Woods, AM, Daly, MY, et al. Naloxone Versus Nalbuphine Infusion for Prophylaxis of Epidural Morphine-Induced Pruritus. Anesth Analg 1996; 82:641.
Kjellberg, F, Tramer, MR. Pharmacological Control of Opioid-Induced Pruritus: A Quantitative Systematic Review of Randomized Trials. Eur J Anaesthesiol 2001; 18:346.
Merigian, KS. Cocaine-Induced Ventricular Arrhythmias and Rapid Atrial Fibrillation Temporally Related to Naloxone Administration. Am J Emerg Med 1993; 11:96.
Mokhlesi, B, Leikin, JB, Murray, P, et al. Adult Toxicology in Critical Care: Part II: Specific Poisonings. Chest 2003; 123:897.
National Comprehensive Cancer Network, (NCCN). Clinical Practice Guidelines in Oncology ™ : Adult Cancer Pain. Version 1 2008. Available at http://www.nccn.org/professionals/physician_gls/PDF/pain.pdf;
O'Connor, PG, Kosten, TR. Rapid and Ultrarapid Opioid Detoxification Techniques. JAMA 1998; 279:229.
Olsen, KS. Naloxone Administration and Laryngospasm Followed by Pulmonary Edema. Intensive Care Med 1990; 16:340.
O'Malley-Dafner, L, Davies, P. Naloxone-Induced Pulmonary Edema. Am J Nurs 2000; 100:24AA.
Pasero, C, McCaffery, M. Reversing Respiratory Depression With Naloxone. Am J Nurs 2000; 100:26.
Salvucci AA, Jr, Eckstein, M, Iscovich, AL. Submental Injection of Naloxone. Ann Emerg Med 1995; 25:719.
Storrow, AB, Wians FH, Jr, Mikkelsen, SL, et al. Does Naloxone Cause a Positive Urine Opiate Screen. Ann Emerg Med 1994; 24:1151.
Tandberg, D, Abercrombie, D. Treatment of Heroin Overdose With Endotracheal Naloxone. Ann Emerg Med 1982; 11:443.
Trujillo, MH, Guerrero, J, Fragachan, C, et al. Pharmacologic Antidotes in Critical Care Medicine: A Practical Guide for Drug Administration. Crit Care Med 1998; 26:377.
Waters, C. Cognitive Enhancing Agents: Current Status in the Treatment of Alzheimer's Disease. Can J Neurol Sci 1988; 15:249.


I didn't see anywhere about withholding naloxone dude to respiratory depression not caused by opioids...and furthermore, without proper laboratory screening, you wouldn't be able to tell if was or wasn't due to opiods unless naloxone is a administered and a + effect is noted or not.


Also, the side effects you mentioned are probably (as explained above) sympotomatic of acute withdrawal sx from the naloxone, and not from naloxone itself

 

[triemal04]

Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.

Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?

Pretty much. Someone else already pointed out that with full lungs the gas-exchange is inhibited which could also have contributed to the problem. I was leaning more towards it being a metabolic acidosis more than anything; many many drugs (including normal over the counter drugs like aspirin, tylenol and ibuprofen) will cause acidosis, sometimes due to respiratory depression and lactate build up, but often not.

And I can't humor you if you insist on using the British way of spelling.

 

[Melclin]

Pretty much. Someone else already pointed out that with full lungs the gas-exchange is inhibited which could also have contributed to the problem. I was leaning more towards it being a metabolic acidosis more than anything; many many drugs (including normal over the counter drugs like aspirin, tylenol and ibuprofen) will cause acidosis, sometimes due to respiratory depression and lactate build up, but often not.

And I can't humor you if you insist on using the British way of spelling.

Ah interesting. Its all kind of coming together. I'm ganna have to do some more reading about gas exchange I think. Seems an interesting business.

Damn yanks and your sensible spelling. Whoever heard of spelling a word in a way that would make phonetic sense? That's just not sporting. The queen would not approve.