Tag Archives: Toxicology

CO Poisoning

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HPI:      57 yo M w/ PMHx of HTN, HLD presents with concern for carbon monoxide poisoning. Pt reports he was using a gas-powered saw in an enclosed bathroom to cut concrete. After some time, he began to feel hot and dizzy. When he stood up to walk out of the bathroom, he reported being unable to walk straight. He then began to feel lightheaded and developed a headache. He has also developed photophobia since. He reports no other problems. Smokes approximately 1ppd.

 

Exam: Vital Signs WNL

GEN: Alert, with no distress

CV: RRR, S1S2 present, No M/R/G

Pulm: CTAB, Non-labored

Neuro: CN II-XII intact, Strength 5/5 in all extremities, Normal Sensation/Coordination

 

Labs:    CarboxyHb lvl 19.3%

ABG showed normal pH, pCO2, pO2, Bicarb

CBC, CMP, Troponin, EKG, and CXR negative for acute process

 

Dispo:  He was placed on a NRB and symptoms began improving. After discussion with Poison Control and Jewish, pt was transferred to Jewish to receive a hyperbaric O2 treatment. He felt much improved after the treatment and was discharged in good condition.

 

The suspicion for carbon monoxide poisoning is based primarily on history. Most symptoms are non-specific. Mild to moderate CO poisoning presents with headache (most common), nausea, dizziness. Don’t forget to ask about LOC. Severe CO toxicity can produce neurologic symptoms (seizures, syncope, or coma) and/or end organ damage. If CO toxicity is suspected based on history, a careful and detailed neurologic exam should be performed.

 

If sufficient concern after history and physical, the diagnosis is made by an elevated carboxyhemoglobin level measured off an arterial blood gas sample. Nonsmokers should have baseline level of less than 3% carboxyhemoglobin. Smokers may have baseline levels of 10-15%. Once the diagnosis of CO poisoning is confirmed, an EKG should also be performed. CMP should also be considered to evaluate for electrolyte abnormalities and to assess renal function. Troponin should be obtained in patients with EKG abnormalities, cardiac comorbidities, and older patients.

 

CO binds hemoglobin with greater affinity than oxygen. This results in impaired oxygen transport. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae. The half-life of CO can be changed by manipulating O2 delivery to the patient. CO half-life is approximately:

·      250 to 320 minutes on room air

·      90 minutes on high-flow oxygen via a NRB face mask

·      30 minutes with 100 percent hyperbaric oxygen

 

Some evidence suggest that HBO treatment can decrease the chance of delayed neurologic sequelae. Patients can often be discharged soon after HBO treatment is completed.

 

Recommendations for Hyperbaric Oxygen from Rosen’s 9E:

·      Carboxyhemoglobin (COHb) independent of clinical findings

o   >25% with no clinical findings

o   >15% in pregnancy or fetal distress

 

·      Or an elevated COHb with one or more of the following findings:

o   Syncope

o   Coma

o   Seizure

o   Altered mental status (GCS <15) or confusion

o   Abnormal cerebellar function

o   Prolonged CO exposure with minor clinical findings

 

Suggested treatment algorithm from UpToDate:

 

 

 

 

References:

 

Walls, Ron M., et al. “Inhaled Toxins.” Rosen’s Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.

 

Clardy, Peter F, et al. “Carbon Monoxide Poisoning.” UpToDate, 28 Feb. 2017, www.uptodate.com/.

My Lesson on Anchoring

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If I had to pick one case from intern year that truly taught me the importance of keeping a wide differential diagnosis, it would be my final Room 9 of the year. The buzzer went off, and as I made my way to the trauma bays, I was able to get a brief rundown from the attending. “Seizure, 40-sish male, no known history”. OK, this was something I could do. I began running everything I’d need to do through my head as I prepared for the patient. “ABC’s. Vitals. Fingerstick glucose. Ativan… Could be trauma, hypoglycemia, benzo or alcohol withdrawal…” As I was refining my differential, the patient came in. The patient was non-rhythmically jerking, was not responsive to voice or sternal rub. I noticed he was wearing dress pants and a collared shirt. He was breathing spontaneously and maintaining sats in the mid 90’s. Palpable pulses and good heart sounds. Glucose was in the 100’s. EMS said he had been found like this approximately fifteen minutes prior, and his clinical status hadn’t changed since then. No known medical history or medicines.  I called out for the nurse to draw up Ativan, as I said this I noticed the patient had urinated on himself. Everything in my mind pointed towards a seizure. I grabbed the otoscope to perform the secondary survey and pried open his eyes. That’s when I felt the rug come out from under me.

The patient had pinpoint pupils, one millimeter bilaterally. The attending and I immediately had the same thought, and as I opened my mouth I heard him say, “let’s get some narcan for this guy!” The narcan got administered quickly, and soon after the patient woke up agitated, but responsive. His family had driven to the ED soon after he arrived, so questioning him was difficult. We ended up taking him to privacy in an empty x-ray room, where he admitted to using heroin earlier in the day. Sure enough, his toxicology screen was positive for opiates. We counseled him, observed him in the ED to ensure he didn’t need another dose, and then discharged him home.

What struck me about this case was that while I had formulated a differential, I had done so after anchoring to a faulty premise. It taught me a valuable lesson in keeping my differential broad, and it’s a lesson I’ll carry to every patient encounter from here on out.

Reub Strayer – Droperidol and the Dangerous Patient

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Every resident must listen to this podcast (or watch this video) at once. I finally listened to it and was pleased to find it a concise, evidence-based and accurate talk. I avoided watching because I thought he would talk about how much he loves his droperidol and that we should all use it, which would fill me with unbearable envy, since we have not had it in Louisville for years. I have been aware that no US company manufactures it but many EM / FOAMed docs still talk about it. Well Dr Strayer now has no access to the drug and shares his disappointment.

Take home points:

  1. Droperidol is a magical, wonderful drug and we need it back.
  2. The end

No but seriously many great points related to managing the combative patient. From the mildly disorganized schizophrenic, all the way to the truly medico legally dangerous excited delirium, Strayer gives inarguable advice. I love the “shove an O2 mask on the patient who is being restrained by 6 security guards.” He notes that this will often calm the patient, it will protect from spitting, and it will oxygenate the patient. Many other practical pearls here that you WILL USE pretty much every shift at UofL.

Post your favorite tips in the comments.

Don’t Inhale

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Had an interesting case recently while I was working at Jewish Downtown. Approximately 50s male presents in acute respiratory distress. Apparently he rented out some apartments and one of the tenants clogged one of the toilets, I didn’t have a chance to ask how.

Anyway, in an attempt to fix the problem he mixed two plumbing agents: Liquid Fire Drain Opener & some other generic drain-o liquid that he planned to use to clear the pipes. This ended up being a bad idea and a chemical reaction occurred releasing a cloud of chlorine gas. The patient inhaled this and began becoming progressively more short of breath.

While en route, EMS initially had him on a nasal cannula but transitioned him to a non-rebreather as well as a Duo-neb. At the time of his arrival to room 1 the patient was in obvious respiratory distress, diaphoretic, and anxious pulling at the non-rebreather and leads. His O2 sat was from 86%-88% on the non-rebreather with decreased breath sounds diffusely. We elected to intubate the patient with etomidate as our induction agent and rocuronium as our paralytic. After the patient was placed on the ventilator we started the patient on nebulized sodium bicarbonate.

This was something I had never done before – so I wanted to discuss chlorine gas inhalational injuries and the role of nebulized bicarb.

Chlorine gas inhalations typically occur in the setting of chemicals for cleaning an indoor pool. Chlorine gas inhalation rarely progresses to respiratory distress requiring intubation.

In 1994 the Journal of Clinical Toxicology did a two year retrospective review of 86 cases of chlorine gas inhalation and none of the patients progressed to respiratory insufficiency requiring ventilator support.  The most common symptoms are cough, chest pain, and shortness of breath and the chest xray is often unrevealing. In the study all 86 cases received nebulized sodium bicarbonate and none of the patients clinically deteriorated or acutely worsened as a result of the treatment.

While the nebulized bicarb does not reverse or work to eliminate the inhaled chlorine, it helps symptomatically with the cough and SOA. I could not find much information on the MOA or science behind the use of nebulized sodium bicarbonate but it appears to be pretty safe.

The dosing that I found is 4mL of 4% nebulized NaHCO3, and be prepared to explain this to the respiratory therapist because this is not something that they do often. Also this has to come up from pharmacy as code cart sodium bicarb is typically 7.5% so the concentrations are different.

So our patient received his nebulized bicarb once it came up from pharmacy. He was admitted to the ICU and I have not had a chance to follow up on his outcome yet. I just thought this was an interesting case and something that I had not yet encountered and figured I would share for your reading pleasures.

1.4% Observed Adverse Reaction Treated With Flumazenil

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Flumazenil (Rx: Romazicon) has recently been described as coming into favor for two unique purposes: (1) hepatic encephalopathy and (2) paradoxical reactions to benzodiazepines.

Regarding the first, flumazenil’s use in hepatic encephalopathy has been well described recently in a Cochrane review of 113 RCTs with a total n = 805, wherein flumazenil had a significant beneficial effect on short term improvement of hepatic encephalopathy.1 This is thought to occur physiologically secondary to reversal of the origin of hepatic encephalopathy—i.e., an accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition1 (principally GABA receptors which are forefront in the stimulation of sedation). Therefore GABA receptor antagonists (such as flumazenil) can be used to directly oppose this mechanism. Effect on full recovery and survival has still not been proven with flumazenil administration.1

Secondly, flumazenil can be used for paradoxical reactions to benzodiazepines2,4 and in a 10 year review of its use, published in the Journal of Emergency Medicine,3 the real safety of this drug has once again come into question, as there were relatively few adverse outcomes even in the highest of seizure provocation risk—which occurred with co administration of pro-convulsant (e.g., TCAs) at a 2.7 % incidence (8/293)—the total incidence including all subjects bore a rate of 1.4% of seizure activity (n = 904).3

I present an example of administration in the second of indications above. I took care of a 26 yo WF with PMH of asthma, a prior severe dental cavity pending root canal and an IV heroin addiction, currently sober and progressing through the the 12 Steps program at the Healing Place. She presented in sepsis, afebrile with qSOFA of 0/3 (Labs: WBC 21.2 with left shift, procal 1.33, ESR 83, CRP 201, lactic acid 0.8 s/p 2 L NS IVFs), and AKI (Cr. 1.6) with dental as well as urinary possible sources. She was eventually discharged on day 3 with Dx of urosepsis, creatinine returned to normal, and had a negative echo for routine endocarditis rule out in the setting of PMH of IVDA.

During her ER stay she was uncomfortable, diaphoretic, pale, GCS of 15, but anxious and in pain, professing severe insomnia for 3 days, stating, “I just want to sleep”. A trial of oral Ativan 2 mg was given, as she did not want any pain medication due to her prior addiction. She noted a small temporary improvement; however 2 hours later this beneficial effect was absent. By now she had received cefepime 2g and vancomycin 25 mg/kg (for potential osteomyelitis coverage), and was requesting more anxiety medications, having already received 50 mg IV Benadryl 30 minutes prior with no improvement noted. Clinically she was GCS 15, pleasant in interaction, increasingly pale, uncomfortable, wide awake at 0445, and subjectively in pain. She was then given 2 mg IV Versed.

Immediately following the administration of midazolam she became altered to GCS 12 (E4, V3, M5), eyes wide, extremities tremulous, pulled out all of her IVs, and was trying to jump off the bed. It was clear she was paradoxically agitated and hyper-aroused. Rather than reversing her (though we doubted history of benzodiazepine use), we opted to watch and see if this reaction would subside without intervention since she responded favorably to the oral Ativan; however the rarely seen but well known paradoxical reaction to Versed was suspected. She was observed 1:1 and thereafter 3:1 for 40 minutes, at which time she appeared to be steadily worsening rather than improving. The decision was made to give an IV push of 0.2 mg of flumazenil (Rx: Romazicon). Within 30 seconds after administration she once again returned to her pleasant self, she was GCS 15, appropriate, and had no recollection of the previous hour, and had no seizure activity noted throughout her stay. She maintained a healthy mental status of GCS 15 and was AAOx4 for the rest of her evaluation and admission.

In 2010, Kreshak et al. reported a similar case and treatment. This paradoxical reaction to Versed in their report is thought to occur at less than 1% incidence, however it is described as commonly as 1.4 %.4 In the reported literature this reaction is described as a patient becoming acutely agitated, restless and aggressive2. Stiffening and jerking of the extremities, and shaking of a part of the body are also noted. When observing a patient with this reaction, after ruling out other etiologies of agitated AMS, Kreshak et al. (2010) opted to administer flumazenil 0.5mg IV, and “…immediately after which the patient became conscious, oriented and calm, the paradoxical reaction was terminated”. The patient had no recollection of the events,2 similar to the patient observed in the ULED.

Per Kreshak et al. (2010), there exist “…different theories concerning the mechanism of paradoxical reactions, involving a central cholinergic effect or the serotonin imbalance”.2 Unfortunately the exact mechanism of paradoxical reactions remains unclear.

Although difficult to locate literature, if seizures develop following flumazenil administration, pharmacology guidelines recommend Valium 20-30 mg IV then immediately switching to barbiturates; some soft EM sources also suggest going straight to propofol.5

Thank you for reading my post.

References

  1. Als-Nielsen, B., Kjaergard, L., & Gluud, C. (2001). Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. The Cochrane Database of Systematic Reviews (Complete Reviews). doi:10.1002/14651858.cd002798
  2. Cabrera, L., Santana, A., Robaina, P., & Palacios, M. (2010). Paradoxical reaction to midazolam reversed with flumazenil. Journal of Emergencies, Trauma, and Shock J Emerg Trauma Shock, 3(3), 307. doi:10.4103/0974-2700.66551
  3. Kreshak, A. A., Cantrell, F. L., Clark, R. F., & Tomaszewski, C. A. (2012). A Poison Center’s Ten-year Experience with Flumazenil Administration to Acutely Poisoned Adults. The Journal of Emergency Medicine, 43(4), 677-682. doi:10.1016/j.jemermed.2012.01.059
  4. Tae, C. H., Kang, K. J., Min, B., Ahn, J. H., Kim, S., Lee, J. H., . . . Kim, J. J. (2014). Paradoxical reaction to midazolam in patients undergoing endoscopy under sedation: Incidence, risk factors and the effect of flumazenil. Digestive and Liver Disease, 46(8), 710-715. doi:10.1016/j.dld.2014.04.007
  5. (n.d.). Retrieved August 23, 2016, from http://www.goodfriendem.com/2013/05/flumazenil-romazicon-is-probably-safer.html

Just another overdose…..right?

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20 yo M with unknown PMH comes in to room 9 with AMS and tachycardia to the 180s. Per EMS, he had been found down in his apartment, with crack cocaine pipes and other drug paraphernalia around him. He was found to be tachy as mentioned, as well as febrile with a temp of 103 axillary.

When he arrived in room 9, his HR was still in the 170s-180s. Blood pressure normal. He was pale, diaphoretic, and looked sick. He was speaking inappropriate words and would localize pain, GCS 12. Pupils dilated and briskly reactive. Rectal temp 104.1. CXR normal. Started IVF bolus and placed ice packs to the groin and axillae. Also gave Ativan as this was likely a stimulant overdose.

First EKG showed SVT at 180 BPM. After 2L of crystalloid and ativan, a repeat EKG showed sinus tachy at 140. The pt’s mental status was unchanged. The iStat showed a lactate of 13.

The plan was to place a rectal probe and monitor his temp, give him more fluids and Ativan prn, and re-assess later. I thought this was 100% an overdose. No problem.

About 2 hours and who knows how many room 9s later, I go to review his labs. I haven’t heard anything from nursing other than him continuously pulling out his rectal thermometer probe, so all must be well…Turns out he has a WBC of 44,000. Lactate has trended down, but he is still febrile to 102. This is when it hits me that maybe the guy who I’ve been treating for stimulant overdose is actually septic? His CXR and UA were normal, but maybe he has meningitis or encephalitis and that’s the reason for his mental status? Maybe I’m now 2 hours late with ABx?

I suppress the awful feeling in my stomach and go re-evaluate the pt. His mental status is unchanged from when I saw him in room 9. At least now his HR is in the low 100s. Given his mental status and tenuous vital signs, I know this patient is going to have to come in to the MICU. He’s going to need a head CT and an LP to rule out meningitis. I gave him antibiotics and called MICU. They evaluated the patient, and they agreed.

I chart checked the patient the next day. His LP was normal. His mental status improved overnight and he was transferred to the floor. Turns out this actually was likely all tox-related, but I thought it was a good learning point nonetheless. Sometimes it’s convenient to go down the path you’re led to by EMS or by nursing. Not only is it easy, but it’s usually the right path anyway. The stroke buzzer goes off and you immediately get your quick assessment over with so the patient can go to CT and stroke can do their thing. EMS tells you they found the patient in a house with drug paraphernalia, so you run with that.

But it’s important to keep the differential wide open when you first see a patient. At least consider less likely and less obvious possibilities. At some point, you’ll catch something that you otherwise would have missed until it was too late.

Treating BB/CCB overdose

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Systemic review article on treating BB/CCB overdose

CCB poisoning A systematic review

Key points:

1) High dose insulin 1u/kg bolus and then 0.2-0.3u/kg/h in conjunction w a vasopressor improves survival.

2) No mortality benefits with glucagon or atropine

3) In animal studies , lipids, levophed and dopamine improves survival

4)Consider ECMO for pts in cardiac arrest or refractory shock.

 

 

 

Urine Drug Screen

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So while on my ICU months this year, I had upper levels that were very insistent that we needed to get a urine drug screen on everyone.  I would try to make the point that it most likely was not going to change our management of the patient at all.  My point was often ignored and after countless urine drug screens obtained during those months, most if not all proved to be of no utility.

Interestingly, Foamcast just put out a podcast about false positives and false negatives on the UDS.  What I found most interesting was that ibuprofen can cause a false positive for just about anything under the sun including cocaine, PCP, THC, and barbiturates.  Also, the benzos tested on this really only test for oxazepam which is a metabolite of diazepam.  So Ativan, Klonopin, and Xanax won’t show up.

Here is the link if you want to read the whole thing.   https://foamcast.org/2016/04/26/episode-48-urine-drug-screen-cocaine-and-pcp/

Spice/Heroin Reactions

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So I’ve had to encounter my two sickest patients in the holding area within the past 2 weeks or so. One was a reminder from intern year while looking through spice charts, while the other was an actual patient that I had 3 days ago.

We always tend to take the “Tank” patients lightly and overlook them sometimes. I just want to use this as a warning (especially to the interns) that sick patients can also use heroin/ETOH/Spice, so pick up on the small interactions that don’t go right. I’ll try to present these starting with how their chief complaint lead to the final diagnosis.

Patient 1 (intern year)

  • middle aged male
  • CC: Spice OD, Nausea/Vomiting
  • Final Diagnosis: Subarachnoid Hemorrhage
  • Time to Diagnosis: 7 hours

So this guy presented as a spice reaction. This was before spice became as widely spread as it is now, and no one knew what to expect symptomatically (not that there is ANYTHING that is characteristic to spice anyways).

General story from talking with this guy is that he used spice for the first time that night. No significant past medical history. He was on a first date where everything had been going well. He had borrowed some spice from his friend where he used back at his place after dinner. Soon after he started having nausea and projectile vomiting and was acting ‘goofy.’ At that his date called EMS and the date ended.

Exam:

  • Gen: Fully A&O, slightly odd in that he seems incredibly happy to be here
  • CV: RRR
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

This man was like most of our intoxicated patients–a sober re-evaluation. At approximately 2 hours he was still vomiting in the ED, so the medical workup was initiated. Due to his odd behavior with vomiting, we got a CMP/CBC/Tox & CT Head. The night continued busy and I almost forgot about him as I waited for results. Ultimately he never got his CT Head due to being uncooperative but I wasn’t told until hours later. He ended up getting Geodon/Ativan in the ED but instead of calming him down he became more agitated and was no longer oriented. Ultimately getting rolled into room9 to be intubated prior to CT and the final diagnosis was made.

Certain forms of spice that lead to agitation also lead to spikes in blood pressure, and there are a few case reports of significant hypertension occurring after spice use. This guy had the unfortunate case of rupturing an aneurysm after using spice likely from a BP spike. I’m honestly not sure if the outcome would have been any different had I reached the diagnosis sooner — he got repetitive Head CTs and ultimately an EVD on hospital day 3. I didn’t really take him seriously even after I ordered a lab workup. This really changed my perspective on patients being held for intoxication. He spent 1.5 months in the hospital (1 month intubated) before being discharged to rehab.

Patient 2 

  • Middle aged white female
  • CC: Heroin OD got Narcan
  • Final Diagnosis: Cardiogenic Shock
  • Time to Diagnosis: 3.5 hours

This case I handled a bit better (I’d hope after 2 years). Story I could get is that this man had a syncopal episode. Received Narcan PTA by EMS and woke up. In the ED the patient adamantly denies heroin use–states he simply passed out. Luckily I got to him before EMS left, and EMS confirmed reports of bystanders stating opiate use.

Exam:

  • Vitals: HR 120, RR 16, O2 96%, BP 80/45, T 98.0
  • Gen: Fully A&O, drowsy
  • CV: tachycardia
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

My initial thought was that he may need some more narcan or that he received a longer acting opiate. The tachycardia was a wild card and didn’t make much sense with the picture. He remained afebrile and temp recheck, so I wasn’t thinking sepsis much at that time. At this point due to the tachycardia not making sense I ordered labs (and a tox for co-ingestants) and thought his BP/HR would improve with fluids.

I reassessed him after bolus #1 and #2 and neither HR or BP improved. Labs returned with an elevated WBC at 19.6. Opiates positive on top but otherwise were unremarkable. EKG sinus tachycardia. CXR and urine unremarkable. At this point even though I had no fever or source I felt compelled to initiate a septic workup and Lactate returned at 7.9.

I was starting to get lost as why this guy was so unresponsive to fluids and O’Brien and I threw the USN to bedside at this point. Turns out he was in acute systolic failure with an ejection fraction of 11%. No history of CHF and also no signs of volume overload on exam except very mild pulm edema. Troponin peaked at 0.5.

He was admitted by cardiology while they trended his status. He went to the cath lab on hospital day 3 with clean coronary arteries. Ejection fraction improved to 60% by time of discharge. Talking with the team today they are still uncertain of the cause.

These are two cases of sick patients being in the holding area. Hopefully, it serves to remind everyone that any patient can be sick.

Interesting case from the weekend – thoughts?

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Hey guys, I was hoping to get your input on an interesting case I had at Kosair over the weekend.

16 yo F (6 ft, 150 lb…so basically an adult) with a PMH of depression, self injury, and prior suicide attempt presents after ingesting citalopram 40 mg x 90 pills (her prescription, just filled 2 days ago) and concerta 10 mg x 8-9 pills (her brother’s). Patient had been at a party the night before, admitted to EtOH.  Parents found out about the party the morning of admission and they had a big fight, took away car keys, etc. Patient decides to retaliate by swallowing pills, doesn’t tell anyone. Parents find her altered about 10:30, at Kosair at 11:40. Best guess is ingestion occurred sometime around 9-9:30am.  Had one seizure at home per family, and one en route per EMS. Generalized, tonic-clonic, brief.

Initial exam shows a drowsy but arousable patient. Answers orientation questions x3. Initial vitals show HR 147, BP 135/70, RR 25, 93% on some oxygen (can’t remember if NC or nonrebreather). Patient denies CP, palpitations, SOB, abd pain, N/V, weakness/numbness.  4mm, PERRL. MAE equally. Old self injury scars noted on wrists bilaterally. Exam otherwise unremarkable.

We start IVs, get her on a non-rebreather, get IV fluids going. Agree that charcoal seems like a bad idea with her mental status and seizures. Mom has shown up, and as we’re getting some additional history from her, respiratory is placing EKG leads. I’ve talked to poison control. Then, about 20 minutes into her stay, she seizes again. We bag her through the seizure, again generalized tonic-clonic, and just as we’re pushing 2 mg of IV Ativan she comes out of it. She appears post-ictal, but is maintaining her airway. We load her with Keppra, and as I glance at the monitor behind the attending’s head, I notice that her rhythm has changed and she looks like she’s got a wide QRS. We confirm she still has good pulses, still out of it mentally, and since she’s already connected to the EKG leads we grab one (time stamp 12:04):

EKG 1

By the time we get this printed off (!!!!) she appears to have spontaneously converted back to sinus on the monitor. But woah, holy wide QRS/long QT batman! As the attending and I are pouring over the first EKG we get another one immediately (time stamp 12:08):

EKG 2

Thankfully, the QRS appears to have normalized, but we’ve still got a loooong QT, one of the things poison control definitely told us to look out for. Having seen a few similar ingestions at University, I suggest it’s time for bicarb. The attending wants to confirm and we quickly call poison control back, they agree and suggest starting a bicarb gtt, with pH goal of 7.45-7.55.  Now we look back at the monitor and she’s throwing a ton of PVCs, captured here on EKG #3 (time stamp 12:12):

EKG 3

At this point, we opt to push an amp of bicarb while we’re waiting for pharmacy to tube up the bicarb gtt. I have to say, we see it start to work pretty darn quickly. The PVCs slow down, and her rate really starts to head back towards normal. We get an iStat (shot me down when I suggested one earlier), and a few minutes after we’ve pushed the bicarb we get an initial pH of 7.15, pCO2 of 51.5, HCO3 of 18, BE -11, and AG of 21. Electrolytes were WNL. By this time we also know her pregnancy is negative, and her serum tox is negative, no acetaminophen/salicylates on board.  At this point, we talk about intubation as the patient’s mental status is still waxing/waning and she’s breathing shallowly with brief periods of apnea, almost like an opiate overdose. Attending wants to hold off, so I go off to call the PICU resident…and end up having to hang up the conversation halfway through when he changes his mind.

So we intubate her (finally got a peds tube…in an adult), the bicarb gtt comes up from pharmacy, they’re cleaning the PICU bed her, the last EKG looks 1000x better, and all’s well that ends well (time stamp 13:08):

EKG 6

So I’m curious to see what your all’s suggestions/thoughts are on this case.  Looking back at that first EKG, how would you classify it? We’ve got a wide complex, monomorphic tachycardia that to me looks like sustained V tach (with a pulse).  The long QT doesn’t surprise me, but this rhythm does as you’d typically you’d worry about it devolving into Torsades, but that’s not what this is.

Looking back, things I would have done differently:  get a temperature sooner/order a total CK (serotonin syndrome could have been a factor and we don’t have a recorded temp until she’d almost 2 hours into her stay, no one ever ordered a CK), intubate sooner, loading her with keppra when she hit the door after 2 witnessed seizures, maybe could have prevented the 3rd?

Also, if you’re curious, I found this “Toxicology Conundrum” on LITFL that specifically discusses citalopram overdose. Has some good info, citalopram is definitely one of the more potent SSRIs, and QT prolongation is dose dependent and can be seen after ingesting >600 mg (this chick took 3.6 GRAMS). Seizures are also fairly rare, only seen in 2-3% of cases.

Snakebite

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Recently saw at case at ULH (Not mine but posted with permission from resident involved) of a young female (18-20yo) flown from OSH for copperhead bite to L foot. Pt had been hiking in the woods with her boyfriend when she felt a stabbing sensation on her foot, looked down and there was a snake. Pt took a picture of it – sure enough it was a copperhead. Labs at OSH wnl, sent to ULH for concern for possible need for antivenin. I realized – being an urban trauma center – we don’t see a lot of snake bites. If you’re from the area, you may not be familiar with our venomous critters.
There are four species of venomous snakes in KY, all pit vipers (triangular heads, heavy bodies, cat-like pupils) – fw.ky.gov
1. Copperhead – extremely common throughout the state, most common envenomation, mildest venom of the four. (As an acquaintance of mine, Jim Harrison of East KY Venom Extraction lab used to say – no recorded history of death from copperhead envenomation in KY history
2. Timber Rattlesnake – found throughout state, potent venom, relatively docile. Dark coloration, have a rattle (obviously)
3. Pygmy Rattlesnake – found in extreme Western KY. Also have a rattle, potent venom
4. Cottonmouth – found in Western KY, potent venom, can be aggressive. Can be mistaken for Eastern Water Snake (common, non-venomous, aggressive water-dwelling snake found throughout KY)
Best identification – hopefully someone took a picture – otherwise, one to two small puncture wounds with increasing swelling and pain are good signs of envenomation. However, approximately 25% of viper envenomations can be dry bites – where snake gives a warning bite, injects no venom.

Signs and Symptoms of snake bite:
Venomous snakes in KY typically have venoms containing cytotoxins and hemotoxins – they break down tissue and can act on coagulations factors
-puncture wounds (usually paired, can be one)
-erythema and swelling
-intense pain at site and increasing proximally
-systemic symptoms can include nausea, vomiting, abdominal pain, vertigo. Altered mental status and hypotension can present as well

First Aid if bitten:
-Walk slowly – increased activity increases circulation of venom
-Elevate affected part: most bites are on distal extremities: feet, hands. More serious complications are associated with bites involving trunk, neck, face
-Wash with soap and water
DO NOT:
-Apply a tourniquet
-Attempt to suck venom from wound
-Apply ice to wound

Medical Work-up for known or suspected envenomation
-ABCs (always the first step)
-Good H&P – observe amount of swelling, movement of affected area. Mark swelling and erythema with marker to observe for progression
-CBC
-Comp
-Coags
-Total CK
-Fibrinogen
-U/A – to look for myoglobinuria
-Consider ABG and lactic acid if signs of systemic toxicity
-Xray to r/o retained teeth

Severe complications
-Rhabdomyolysis – from muscle breakdown from venom
-Compartment syndrome – cannot be diagnosed on clinical exam alone. Venom can cause tingling and paresthesias. If concerned, consult your surgeon
-Thrombocytopenia and coagulopathy – caused by thrombin-like molecules in venom. Treated with antivenom
-Systemic toxicity – can be life-threatening

Treatment:
-Update Tdap if indicated
-Pain control, elevation
-Antivenom if indicated

Antivenin: Always contact your toxicologist prior to giving
-Recommended for moderate to severe envenomations
(http://www.uptodate.com.echo.louisville.edu/contents/image?imageKey=EM%2F53948&topicKey=EM%2F6595&rank=2%7E39&source=see_link&search=snake+bite&utdPopup=true)
-Dosing: Moderate envenomation – 4 to 6 vials (1g each) over 60 min with repeat dose as needed
Severe envenomation – 6 to 9 vials over 60min with repeat dose prn
-Contraindications: papaya allergy (contains enzyme papain)
-Stop if signs of anaphylaxis

Disposition
-Requires antivenom – admission. Complications can include compartment syndrome, delayed coagulopathy (up to 48hrs). May need redosing of antivenom
-Mild envenomation or no symptoms – can be discharged home if pain controlled and no signs of toxicity at 8-12hrs s/p bite. If bitten by rattlesnake or cottonmouth, recommend CBC, PT, fibrinogen at 2-3d and 5-6d after initial bite

Everything including the lipid sink

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80+ yo gentleman with PMH of COPD, CHF, CAD, CKD, initially hospitalized for urosepsis and NSTEMI with a worsening AKI, and baseline CKD. Tuned him up and sent him to the floor where he accidentally received an overdose of his carvedilol. Got the call that the patient was hypotensive to 70s systolic, bradycardic to 30s.

Immediately pacer pads were placed to ward off evil spirits
-Started with 1L crystalloid bolus –> no response and with risk factors and pmhx, didn’t want to fluid overload
-Tried atropine (3-4 doses) –> no response
-Tried glucagon 50mcg/kg loading dose followed by 3mg/hr infusion –> still no luck and exhausted all the glucagon in the pharmacy
Running out of options here. I remember reading an article in Annals about using lipid infusions in beta blocker overdoses and figured it was worth a shot.

Started 20% Intralipid bolus through central line at 1.5ml/kg followed by 0.25ml/kg/min for 30min. Maybe it was the lipid infusion or just the combined effects of everything but by 6am, pt’s BP and HR had improved to normal limits and he began talking again.
It was a nice result but one I couldn’t celebrate that much – within a week, patient decided to go to palliative care and that was the last I heard of him.

The Kitchen Sink

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Fairly early into an overnight shift the radio goes off.  EMS is approximately 6min out with mid 30s male undergoing CPR. Per bystanders, the patient was going running from door to door, banging on doors and yelling for help. Shortly after being taken into police custody he was found to be pulseless. Had been undergoing CPR approx 10 min. King airway in place. No improvement with dextrose and naloxone.

The intern on and myself go to Room 9 to get set up. When EMS arrives about 10 minutes later, CPR is still ongoing and rhythm has been asytole/PEA throughout. The story remains consistent with him going from door to door yelling for help but now there is some variation as to whether he was cuffed and then lost his pulse, was found without a pulse, or if he got into a physical altercation with the neighbor and then lost pulse shortly after arrest. There are no signs of trauma and we elected to not invite additional chaos by calling a Level 1.

CPR is continued. King airway switched out for ETT. Accucheck 250’s. Central venous access and bilateral chest tubes placed with no rush of air or blood. Sats persist at 85% on vent, etco2 is in 60’s. He gets epi q3m. A dose of vasopressin and steroids. Istat has K 5.5. Lactate >20. Received 2-3 amps of bicarb. Received calcium. Upon rhythm checks he was primarily asystole except for 2-3 checks with a narrow pea that would not persist. Each time the ultrasound was placed on his heart there was no cardiac activity. My thought process at this time was that he was either excited delirium that I’m not going to be able to do much about or some kind of ingestion/overdose. We called pharmacy and asked for lipid emulsion. His ETCO2 had remained between 40-60 and we were about 40 minutes out from reported time of arrest. I decided if the lipids were unsuccessful that would be when we would call it.

They arrived about 15 minutes later and were infused. By now his etco2 had drifted down to 10 on the most recent pulse check. No changes occurred and TOD was called.