Tag Archives: Neurology

Paraspinous blocks for migraines

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Many of you have probably heard me discuss my love of paraspinous blocks for migraine headaches, and I know several of you have learned how to do them on me when I have a migraine. This seems to be one of those slightly voodoo things that I would have sworn could never work, until I tried it and had almost immediate relief when several traditional abortive therapies failed.

For those who haven’t, this is an incredibly easy procedure that takes a minimal amount of time and can give real relief in migraine patients. There is no complicated anatomy involved, no significant technique or skill level required, and is safe enough that I have talked many novices through the procedure on a patient with supervision.

To do the block, the most important part is selecting the correct patient to increase your chances of success. Technically it won’t hurt anyone to do a block on them, but I’ve quickly learned this has a near zero chance of working in patients who state only an IV cocktail of dilaudid and phenergan works for their migraines. I’ve also found minimal effects on those who are texting while under bright lights and listening to music. I have had the most success on patients that look absolutely miserable: the ones curled up into a fetal position, actively vomiting, crying, with all the lights out and begging you to do ANYTHING to make their headaches go away. These people also tend to be quite enthusiastic about a treatment that you can administer on the spot and will work within 5-10 minutes typically. For all the things we do that sometimes have fairly minimal objective evidence of relief, it makes me very happy to walk back into a room in 20 minutes and see this previously miserable patient looking completely normal, stating their headache has resolved, and being ready to discharge… all without medications from pharmacy or an IV.

I typically use bupivicaine and do not use any subcutaneous lidocaine as the youtube video attached at the end of this post shows. I draw up 3cc, planning to use 1.5cc on each side. Your landmarks will be your C6 or C7 spinous process. I typically go C7 because it is easy to find by asking patients to flex their chin to their chest, and I like to keep things easy. C7 is the most prominent spinous process at the base of the neck. Not sure if you’re at C6, C7, or T1? Even better, for this block it doesn’t really seem to matter because it still works! You’ll be injecting approximately 2cm laterally to the edge of the spinous process, give or take half a centimeter based on body size. Again, don’t get too caught up in the details- it seems to work at 1.5cm to 3cm laterally to the process. After a swipe with an alcohol prep (bonus points- you can hand the patient another alcohol prep pad to inhale for relief of their nausea and vomiting! See last week’s journal club article for more details), you’ll insert the needle (any size, but a 25g hurts less) parallel to the ground in a straight anterior tract. I insert the needle 1.5-2cm. Aspirate to make sure you aren’t in a vessel, then inject 1cc of bupivicaine deep, and the remaining .0.5cc while withdrawing your needle. Repeat on the opposite side, stick a bandaid on, and reasses in about 20 mins. If it’s going to work, most seem to start to get significant relief in about 10 mins. If unchanged in 20ish minutes, I proceed to other therapies.

When I’m in first care, I typically will take a bottle of bupivicaine and a needle/syringe into the room when I walk in for an initial evaluation. If the patient seems to be a good candidate and is agreeable, I go ahead and do the block at that time. By the time I do my charting or see the next patient, I typically have a good idea of if the patient has improved, or rather if I need to start ordering other therapies.

Quick and easy, and I have about a 60-75% success rate on patients. Pretty good considering a standard migraine patient will likely take a couple of hours to receive IVFs, meds and reassess. You can sometimes get these people dispo’d in less than 30 minutes!

I’ve attached a quick video for you visual learners

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.

SIH – Spontaenous Intracranial Hypotension

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Recent EMRAP podcast reminded me of a case from when I was a Medical Officer in the Navy.

One of my Marines, early twenties, with no medical problems presented for follow up in sick call after being seen in the emergency department for a headache.  Since it was the worst headache of his life, an LP was performed.  Both the LP and the CT head were negative. He was given standard headache treatment with “migraine cocktail” from what I remember, however, no significant relief.

He presented to clinic with complaint of ongoing headache that was only better if he laid completely flat with excruciating pain with sitting up.   He refused to do anything other than lay on the gurney in the treatment room.

His presentation was classic for post LP headache, however, he states that this was the same headache that he presented to the ED for the previous evening and was not changed by the LP.  He was adamant about this timeline and unchanging symptoms after LP. Physical exam was normal to include normal Neuro exam.

I subsequently called the Neurologist on call at Naval Hospital, who stated the likely diagnosis was a “spontaneous CSF leak” and recommended a blood patch.  I was quite confused as I had never heard of such and it seemed like a made up diagnosis to me at the time.   I did, however,  want to help my patient and for him to leave the clinic at some point that day.  I then called anesthesia who was agreeable to the blood patch given recent LP and current exam/symptoms.   The patch lead to resolution of his symptoms and he was able to stand up and walk without a headache.

This is the only case that I have seen, however, the recent EMRAP review leads me to believe that I might see another case while practicing Emergency Medicine.

SIH is caused by a spontaneous tear in the dura in the spine or elsewhere in the meninges and leads to intracranial hypotension from CSF leak.  Symptoms are incredibly similar to post LP headache given the pathophysiology on really differ in that CSF leak in an LP is iatrogenic and SIH is well, spontaneous.  Diagnosis can be by LP, which will demonstrate low opening pressure, or MRI of the Brain W/WO and Spine W/O which will demonstrate the leak.  The symptoms are similar regardless of the level at which the leak occurs so you may have scan the entire meninges to find it.

Treatment initially is caffeine and rest for mild-moderate headaches and lumbar blood patch for moderate-severe headaches.

Uptodate has a lengthy but throughouh algorithm for diagnosis and treatment.   If lumbar patch doesn’t work, a more targeted approach may need to be employed.

  • Take-home point – consider SIH when someone presents with post LP headache symptoms without having had one performed in the recent past.

Baffling Neurology Pathology Strikes Again…

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…forever seeking the unsuspecting emergency medicine intern.

A previously healthy teenage male presented to the emergency department via emergency medical services with the complaint of weakness, sensory changes, and increasing difficulty of breathing.  Family reported the patient went outside to mow the grass approximately 10 hours prior to presentation.  After two passes in the yard with a push mower, the patient had sudden onset occipital headache, fatigue, parasthesias described as tingling in both lower extremities, and generalized weakness.  Patient reported these symptoms to parents and laid down to rest.  After an hour long nap, patient was encouraged to take a shower to see if symptoms improved.  During shower, patient became weaker, had one episode of vomiting and was no longer able to stand on legs.  The patient’s father reports patient was able to make small movements but unable to ambulate or push against resistance.  Emergency medical services were contacted at this point, however, after assessment, the symptoms were deemed related to anxiety and patient was not transported.  Over the course of the day, the patient’s weakness progressed to the complete inability to move legs, followed by inability to move arms, with continued paresthesias in all extremities. After patient demonstrated worsening respiratory distress, EMS was called again.  Parents denied history of asthma, prior wheeze, fevers, recent illness or trauma, recent travel or drug abuse.  Family reports patient went camping one week prior but denies tick exposure.

On exam, the patient had significant respiratory distress with poor air movement and was only able to answer questions with one word responses secondary to respiratory distress.  Neurological exam revealed 0/5 strength in all extremities, areflexic biceps and brachioradialis reflexes, areflexic patellar and Achilles reflexes, and downward going Babinski bilaterally.  Sensation to light touch was intact but diminished in all extremities.  There were no rashes or lesions on skin exam.

Initial differential included but was not limited to:

  • Organophosphate toxicity – although patient self-decontaminated earlier in the afternoon and did not have diarrhea, salivation, or lacrimation
  • Guillain Barre – although acute time course without report of recent URI or GI syndromes
  • Tick paralysis – although no known exposure or lesions identified on skin or scalp
  • Transverse Myletitis – although no personal history of recent illness, no family history of multiple sclerosis or other autoimmune disease
  • Spinal Cord Infarct – although patient and family deny trauma, recent surgery, or history of coagulation disorder
  • Conversion Disorder – although no anxiety or other psychiatric history

As concern for bronchospasm, the patient was given IM epinephrine and started on a hour long albuterol while history was being obtained.  Bedside ultrasound demonstrated grossly normal myocardial contractility without effusion, normal lung sliding, and a collapsible IVC.  Chest x-ray was unrevealing. After lack of improvement with initial intervention, second dose of epinephrine and fluid bolus begun.  Intial VBG demonstrated hypercapnea and patient was started on BiPAP.  Within minutes, patient showed improvement in respiratory status and appeared more comfortable.  Initial CMP, CBC, CRP, and ESR were unrevealing.   Lumbar puncture was performed after head CT revealed only an arachnoid cyst.  CSF studies demonstrated mildly elevated segs, mildly elevated glucose, negative gram stain and normal protein.  Foley catheter was placed after patient complained of bladder fullness (confirmed by bladder scan) with inability to void.  Neurology and Neurosurgery were consulted from the emergency department, who requested urgent MRI on admission.  Patient was admitted to PICU with ED diagnoses of acute flaccid paralysis and acute neuromuscular respiratory failure.   After admission, MRI was obtained and demonstrated (drum roll please) ischemia vs. infarct from approximately C2-T5 with predominance in the anterior horns.

The literature review of non-traumatic spinal cord infarction is as rare as the pathology itself in the pediatric population and predominately consists of case studies.  Causes typically include but are not limited to hypotension, vascular injury, thrombus, embolus or compression.  Considering many of these etiologies are already scarce in the pediatric population, finding cause proves to be a difficult task.   Pain in neck, back or legs, weakness, tingling, and numbness are commonly described symptoms in pediatric case studies and were present in the patient that presented to us.   Prognosis studies have been performed on primarily adult patients; one such study demonstrated >40% recovery in ambulation amongst the 37 patients that left the hospital wheelchair bound through aggressive physical therapy and rehabilitation programs.[1]   Poor prognostic factors include female sex, advanced age, severity of symptoms, and lack of improvement within 24 hours after infarction.[2]   It appears as though outcomes are primarily dependent on access to physical therapy and supportive care including psychological treatment.   Workup and treatment recommendations if suspicious of atraumatic spinal cord infarct include obtaining an MRI for definitive diagnosis, followed by autoimmune, hypercoagulable, and infectious evaluations. Treatment in the emergency department is mostly supportive and includes addressing any contributory conditions and the management of respiratory concerns.[3]

On follow up, I found that the patient required intubation after exhibiting respiratory decompensation after the MRI was obtained.  Initial treatment with high-dose steroids and IVIG were discontinued when infectious and immunologic work-ups were unrevealing.  The hospital course was complicated by neurogenic bowel and bladder, neuropathic pain, anxiety, intermittent autonomic instability with hypotension, pneumonia and a urinary tract infection.  The patient required tracheostomy and percutaneous gastric tube placement during his hospital stay.  The patient continued to exhibit flaccid paralysis of all four extremities and ventilator dependence on discharge to acute rehabilitation.

Per my own investigation, I was relieved to find that Frazier has both success managing these cases and many unique resources that may positively impact this patient’s course (if you are curious here is some video evidence https://www.youtube.com/watch?v=8o_w174rI3s).  Needless to say, my differential for motor weakness, particularly in pediatrics, will forever be haunted by this case.

 

[1] Robertson CE, Brown RD Jr, Wijdicks EF, et al. Recovery after spinal cord infarcts: long-term outcome in 115 patients.  Neurology. 2012; 78: 114–121.

[2]Cheshire WP, Santos CC, Massey EW, Howard JF Jr .  Spinal cord infarction: etiology and outcome.  Neurology. 1996;47(2):321.

[3] Spencer, Sandra P. MD; Brock, Timothy D. MD; Matthews, Rebecca R. MD; Stevens, Wendy K. MD.  Three Unique Presentations of Atraumatic Spinal Cord Infarction in the Pediatric Emergency Department Pediatric Emergency Care. 30(5):354-357, May 2014.

Managing Migraine

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As mentioned on R and R in the Fast Lane. This article by Friedman is a welcomed update to evidence-based migraine management. Some people love treating migraine patients, some hate it. But we all have our cocktails we believe in.

I am a fioricet/neurontin/IM compazine, escalating to IV compazine/benadryl/decadron/toradol OR if they want to drive home IV MAG/decadron/toradol … kind of guy.

This article starts with criteria for delineating migraine from other headache forms. Then provides a succinct algorithm for treatment, starting with reglan or compazine +/- benadryl, then another dose plus toradol, then dihydroergotamine, then occipital nerve blocks (very fun), then as a last resort, opioids. I would encourage you to attempt a few other methods before the blocks and especially before the opioids.

Many other medications can be used (keppra, depakote, propofol, etc). But this is a solid overview of the EM approach. Also of note, see the Oct 2016 EM-RAP paper chase of the reglan +/- IV fluids in migraine article which showed no real benefit to the addition of IVF.

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

5 day old with “seizures”

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Recently I had an interesting case at Kosair of a 5 day old male who presented with jerking movements of his arms and legs. He always had “twitches,” which the parents had been assured were normal for a newborn, but the episodes were getting worse. Since the day before, he had had several episodes where both arms would shake and seize up and his legs would curl up under him, lasting about a minute. He is sleepy afterwards, but mom thinks he’s always pretty drowsy. Overall it was unclear if what mom was describing was a seizure. Even her helpful phone videos were not 100% clear, but we proceeded as though they were real seizures. In a 5 day old.

Mom had 3 UTIs during pregnancy, and her labor was likely precipitated by an episode of pyelo. She and baby were briefly tachy during labor but pain meds helped, and the SVD was otherwise uneventful. No STIs, GBS negative.

Baby was afebrile, normal VS. Appeared drowsy until the usual screeching during the cath urine, so overall, well-appearing baby. He did twitch sometimes, but he never had one of the spells while he was in the ER.

Differential diagnosis for neonatal seizures? Bacterial meningitis, viral encephalitis, intraventricular hemorrhage, SAH, SDH, hypoxia, hypoglycemia, hyponatremia, inborn errors of metabolism, etc.

Our patient wasn’t actively seizing and labs were WNL.

Subdural hematoma (from birth) and meningitis were high on our differential. We went ahead and gave antibiotics but got a CT head before proceeding with the LP, and I’m glad we did.  It turned out that he did have a subdural hematoma, likely parturitional. We elected to forego the LP, since he was afebrile and we already had a reasonable explanation for his symptoms. Neurosurgery wanted a repeat CT in 6 hours (surprise!), and neuro wanted an EEG (surprise!). He never had any of the episodes in the ER, so neuro didn’t start any antiepileptic medications.  He was admitted to the PICU.

He never had any seizure activity on EEG, so neuro diagnosed him with neonatal myoclonus. Hypocoagulability workup by hematology was negative. Neurosurgery will follow up in 3 weeks as an outpatient. He was discharged after 4 days.

The other interesting discussion on this patient involved whether or not to involve CPS, since this type of injury could be seen with a shaken baby syndrome. The parents were very appropriate and there was no sign of any other trauma and negative skeletal survey, so CPS was not contacted. The overall assumption was that the SDH was secondary to birth trauma rather than any non-accidental trauma.

Diabetes Insipidus in Intracranial Injury/Trauma

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During a string of nights, I had two separate patients that despite having different injuries presented me with an interesting question. The first was a man in his 50s with a large intracranial hemorrhage, mass effect and the beginning of herniation; the second was a young male that was the victim of a GSW to the head. However, despite the different etiologies of their injuries, they both presented to Room 9 literally yelling for water. One became so combative in his demands for water, he had to be restrained.

This got me thinking; in the setting of very serious injuries, why is the only thing that concerns these men oral hydration?

The most concise information I found comes from Life in the Fast Lane. While it is referring to TBIs, the pathology relates to both of my patients as well. Thirst is controlled mostly by ADH released by the hypothalamus and transported to the posterior pituitary. Any disruption in this production chain can decrease ADH, leading to central diabetes insipidus.

In the setting of trauma, this can be caused by direct damage to the hypothalamus or posterior pituitary, disruption in their vascular supply or increased intracranial pressure/herniation that can compress these structures. Whether by a large hemorrhage or direct trauma like a GSW, intracranial injury can damage the ADH supply, leading to diabetes insipidus and the extreme thirst felt by these patients. Endocrinopathies have been associated with 30-50% of TBIs with the most common disorder being diabetes insipidus.

 

Head injury patients with delayed presentation to ED

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Another pearl from EM Lit of Note. Bottom line: Retro review of CT head obtained for trauma divided into <24 hours and >24 hours time of presentation. The delayed presenters had a HIGHER percentage of positive CT and had a similar amount of patients requiring NES intervention.

We discussed this the other day. First Care obtained a head CT on a patient several days after a minor head injury. We presumed it was not indicated. Then I read this paper.

Unfortunately I cannot find in the paper a description of time to presentation. It is grouped into less than 24 hours and greater than. I wonder if the likelihood of positive CT scan decreases as time from injury to presentation increases.

In any event, this poses difficult questions. Should we obtain more CTs on the delayed presenters? They are as likely to have positive findings. In addition, the NICE guideline is 70% sensitive, versus its comforting 98% in the less than 24 hour group.

Would be a good article to discuss for journal club. Would love to see some comments.

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.

April Journal Club

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Hey, all,

There is multimedia for this month’s journal club, so I wanted to post it all in one place. The theme will be impossible decisions in the department (eg ED thoracotomy without surgery backup, but we’ve talked about that issue ad nauseum). In my mind, it’s best to think about how you’ll approach impossible decisions now, before they show up overnight on single coverage in the middle of nowhere. Other ideas for discussion are welcome.

Closing the emergency department: EP Monthly, Diversion 1, Diversion 2

Crashing VP shunt patient: Tapping a shunt article, Tapping a shunt video

Epidural hematoma: Burr hole for epidural hematoma article, Burr hole presentation, Video of a burr hole

 

Just some thoughts on stroke management in the acute setting…

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A couple months ago (during lecture), we had a discussion regarding tPA and acute onset of stroke. As you would expect, we discussed the indications, contraindications, etc of treating stroke with tPA. We also touched on the subject of our role in pushing tPA here at UofL.

Obviously as a stroke center, our stroke team is working around the clock- and as such, generally takes the ball on this one. However, when we are practicing outside of UofL, a stroke team is not always going to be available and ultimately the management will fall on us. Hence the discussion and considerations for us making the call or at least working towards that possibility in the future.

Coincidentally, at precisely the same time as this conversation, a small journal, based out of New England, with a primary focus on medicine, published three fine articles on a similar topic. These articles were focused on the treatment of stroke in  the acute setting.

As pertinent to this post, they explored the use of thrombolysis as well as mechanical removal of thrombus when said thrombus is located in a proximal vessel. Now I won’t pretend I can read, but for those of you who can- below, are links to two “previews” and one complete view of the above mentioned articles. Additionally, an audio file is embedded, containing a break down of the articles by Dr. Dave Newman, of the Mt. Sinai School of Medicine in the Department of Emergency Medicine, to be featured on a future episode of EM:Rap.

Ultimately, I guess the questions I have regarding this as a post on Room9er are as follows:

1. I believe the Stroke team has embraced these articles and to my knowledge (as of February) may have moved towards mechanical retrieval of thrombus in proximal vessels in appropriate candidates. If we are trying to move towards a more ED involved decision tree, what will we need to know and where will our policies stem from? At least as a concept. At this time, I have only heard us discuss tPA, but if we as a hospital are moving towards multiple modalities for treatment of acute stroke, should we not be discussing these as well?

2. With consideration of a 6 hour time frame to thrombus retrieval, what is our (UofL) policy on timelines regarding retrieval. (This is not reflecting any current policies, merely one parameter from one study.)

3. How much time is required from page to cath? This is undoubtedly a big question. What does it take to have a vascular team, NES team, etc ready do go. How will this influence our time of onset to treatment guidelines.

4. Outside of UofL, taking into consideration transit time, etc. how will this influence the management of stroke? Based on CTA availability, transit time, local resources, etc.

ESCAPE

EXTEND_IA

MR CLEAN

 

The Trauma-Stroke Eval

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Middle age male brought into Room 9 s/p crush injury. The patient was reportedly crushed against a box truck and a wall for a short period, but no prolonged extrication.

He complains of LUQ chest pain, pleuritic in nature, and denies abdominal pain. He was ambulatory after the event. PMH only significant for HTN, otherwise no PSH, no allergies, and takes lisinopril and hydrochlorothiazide.

He is AOx3, moving all extremities, well appearing in Room 9, and acting appropriate. He goes for man scan as he did strike his head and although can give me all the details of the accident he reports LOC.

Upon return from the CT scanner his VS are stable, and is placed in a regular ED bed.  Image review revealed multiple rib fractures, and suspicious appearing spleen.  Radiologist confirms grade 1 spleen laceration, but no active extravasation, as well as bilateral rib fractures.

While evaluating another Room 9 patient, the nurse came to update me that the patient was now unresponsive and foaming at the mouth.  I told her to give Narcan, thinking it could be iatrogenic analgesia toxicity, and I would be right there.

I arrive in the room, and he does NOT look right. He is foaming at the mouth, the narcan certainly changed his pupil size when she gave it, but did nothing to his mental status. Sternal rub, nipple pinch, and ammonia capsule all failed to appropriately arouse him.  The trauma resident is now at the bedside as well and just as perplexed as this isn’t what I described on the phone. I call radiology ask them to re-check his CT head but they said no, they see nothing. I again re evaluate him and now he will move only his L side, and follow commands on the L side of his body.

Well…..crap, this is dysarthria R sided hemiplegia. Stroke paged, obtained stat CTA head and neck, and then straight to Room 9 to intubate him. See the CTA imaging below:

CTA

Carotid artery dissection…

He obviously is not a tPA candidate, but he did go for an intervention procedure with the stroke service.  He did have a clot retrieved, but I have visited him on the floor a few days later and he had no improvement.

He went on to develop cerebral edema as well and had a large hemicraniectomy. He also had an ex-lap for an increase in abdominal distension, and found to have pancreatic ascites (3L removed from the abdomen). The spleen did fine.

Looking back, his mechanism did not support a reason for him to dissect a carotid. He had no external signs of injury, he had no neck pain, my guess is he did have a whiplash type injury but again, not something I expected. In addition, this man had a normal neuro exam upon presentation, full strength, no numbness/tingling with the exception of reporting headache, which I thought was from him striking his head.

After a lit review, there are a few teaching points I want to highlight from this case.

Traumatic Dissection (carotid, vertebral, spinal arteries)

– consider it with hangings, significant head/neck trauma, hyper-extension injuries, lateral rotation injuries of the head, base of the skull fx, c-spine fractures(especially those with displacement or involvement of the transverse foramen,vertebral body), lefort fractures (types II and III), or seat-belt sign over the neck
– Sign/Symptoms vary greatly. Stroke like symptoms are concerning but can be as generalized as headache/migraine, neck pain, neck hematoma, blindness, aphasia, weakness/sensory loss, Horner’s syndrome, tinnitus, CN deficits, diplopia, locked in syndrome, ataxia, vertigo, dizziness