Serial ECGs

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I had a fairly interesting patient back in November 2016 when I was at Jewish.  I had picked up a patient with chief complaint of chest pain after an attending handed me the EKG below.  The patient was being rolled back from triage to a room at the attending’s request. 42yo AAM with history of hypertension, hyperlipidemia, diabetes, sleep apnea and CAD status post CABG in 2008.  The patient was complaining of chest pain that initially started when he was sitting at home watching TV about an hour prior to arrival.  He described the pain as sub-sternal and radiating to his left arm. He had associated SOA, palpitations, and diaphoresis along with the pain. He was also nauseated since the onset of pain.

Pretty classic presentation here in a patient with previous heart disease.  His initial EKG recorded in triage is below:

Upon review, you can appreciate that there may be ST elevation in III.  Also, ST depressions are noted in the precordial leads along with ST changes elsewhere. My question to all of you based upon reviewing this EKG: Would you call this is a STEMI and would you activate the cath lab at this time?

The attending that I was working with at the time didn’t feel that we could definitively call this a STEMI based upon the first EKG.  We examined the patient and collected his history after he was brought back.  After labs were collected, the patient received nitro paste.  Despite the paste, he continued to have pain. After approximately 15 minutes of being in the back, the patient reported that his pain was worsening.  The decision at that time was made to get a repeat EKG.  The repeat EKG is below:

 

So now what are your thoughts? There is obvious ST elevation in the inferior leads.  There are also ST depressions in the precordial leads.  This EKG was taken 34 minutes after the first EKG which was performed in triage.  Through these two EKGs, you can appreciate the evolution of a STEMI.  This patient was emergently taken to the cath lab at that time and underwent left heart cath. He underwent an impella-assisted PCI to his SVG-PDA and was started on dual anti-platelet inhibitors. Following his PCI, he also had an episode of wide-complex rhythm which resolved after receiving amiodarone.

So this patient who was found to have a STEMI on his repeat EKG had presented with an initial EKG that was non-diagnostic for his condition. Did this affect his outcome in any measure? What can we learn from this?

According to a 2013 study conducted by Riley et. al, in a national sample of patients diagnosed as having STEMI (41,560 patients), 11.0% had an initial non-diagnostic ECG. Of those patients, 72.4% had a follow-up diagnostic ECG within 90 minutes of their initial ECG. There did not appear to be clinically meaningful differences in guidelines-based treatment or major inhospital outcomes between patients diagnosed as having STEMI on an initial ECG and those diagnosed on a follow-up ECG.

So, did the additional 30 minute delay in activating the cath lab affect this patient? Likely not. However, what this case reinforces is the importance of a repeat EKG as 11% of these patients likely will not have STEMI on their first EKG.

 

References:

Am Heart J. 2013 Jan;165(1):50-6. doi: 10.1016/j.ahj.2012.10.027. Epub 2012 Nov 21. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. Riley RF1, Newby LK, Don CW, Roe MT, Holmes DN, Gandhi SK, Kutcher MA, Herrington DM.

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.

Neonatal Airway

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I’m currently on peds anesthesia and behind on reading Annals, which worked out in my favor.  I was looking through the February 2017 issue and there’s an EM:RAP commentary about the neonatal airway.  So I figured I would give you all the highlights from that article.

  • At birth, an oxygen level of 60% is normal.  There’s a nice chart showing the oxygen saturation and how it increases after birth.
    • 1 minute- 60-65%
    • 2 minutes- 65-70%
    • 3 minutes 70-75%
    • 4 minutes 75-80%
    • 5 minutes 80-85%
    • 10 minutes 85-95%
  • Remember when doing BVM on a neonate, not to press too hard on their face.  Their nose is not stiff and they are obligate nose breathers.  So don’t close off their airway by pressing too hard.
  • Don’t worry about using a paralytic in the neonate.  You can either time passing the tube through the cords or just push it through.
  • Tube size/Blade size
    • Normally in peds we use the formula (age in yrs/4) + 4
    • For neonates, they suggest the 0-1-2-3 rule: Use a 0 straight blade in a 1-2 kg newborn with a 3.0 mm uncuffed tube
    • They also recommend resting your pinky on the cric to provide your own cric pressure since neonatal airways can be very anterior
  • How far to pass the tube
    • 1 kg neonate- 7 cm
    • 2 kg neonate- 8 cm
    • 3 kg neonate- 9 cm

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.

Snakes and ladders

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Last month I had an interesting Room9 for visual purposes. The story per EMS was jumbled, as it can be from time to time. All we knew was that the patient was a middle aged man who either fell off a roof or jumped off a ladder into a foot and half of water. …agreed. Details were otherwise unavailable. We manage repercussions of injuries, not the causes.

The patent came in intubated, wet, hemodynamically stable. The patient had ketamine en route but was still active with GCS 6T. He required more than your typical sedation to be amenable for the CT scanner. The physical exam showed no motor activity in lower extremities, including to painful stimuli. We noted no step-offs or abrasions. The patient had no signs of trauma other than the motor weakness.He moved his upper extremities and needed restraints due to lack of response to sedation. CT images are below. Most of these images mirror almost exact images from Dr. Ferguson’s lecture on spine fractures, thus I thought it would be good to go over.

As you can see the patient had significant fractures of his cervical spine. Talking with Neurosurgery, the burst fracture is more common in lower thoracic and upper lumbar spine and only is seen in cervical spines to this degree under severe axial load injuries, such as going head first from a significant height (especially when the posterior column has a vertical fracture as seen above).

I’ve always wondered the significance of doing spinal check during the physical exam prior to CT, when they are already getting “manned”. I often feel that if there is real pathology (ie. unstable fractures), won’t palpating (and deep palpation on obese patients) worsen the fracture and theoretically cause neurological issues. I haven’t found much to substantiate that, but it seems to make intuitive sense; I am open to any other opinions / suggestions.

Does anyone want to comment on the type of fractures noted, stable vs unstable (refer to Ferguson’s lecture)?

Are teardrop fractures stable?

Is there any significant retropulsion?

Could you hypothesize flexion vs extension injury?

Answer: Unstable teardrop fracture as well as a burst fracture, and borderline chance fracture (not typical for this cervical spine location).

 

For further spine related information please look at the links below or Dr. Ferguson’s spine lecture. Ferguson’s is a great source covering the importance of stable and unstable fractures, and a great lecture for interns to go over, especially early on in the year.

Here is a good podcast from Scott W. on less traumatic c-spine injuries:

EMCrit 63 – A Pain in the Neck – C-Spine Imaging and Clearance

And some other good sources:

http://www.aafp.org/afp/1999/0115/p331.html

http://www.paems.org/pdfs/online-ce/Evaluation-and-management-of-acute-cervical-spine-trauma.pdf

EMRA 6 minute Lecture Winners

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All,
As we have started to move towards shorter, more concise lectures I thought I would share these brief talks from EMRA. I encourage you to at least watch the first lecture (if not all three).
I want to point out how the first speaker uses essentially no bullet points, slides with minimal words, and images that cue him into what he’s talking about, cue the audience as well, but aren’t insanely distracting so that his audience is listening to him and not reading his slides. He also does a great job at the end of summarizing his talk (again with no bullet points).
I’d like you all to consider this when creating a talk, however big or small and if you have questions/need anything regarding talks fell free to ask me. I may try posting more tips/pages like this in the future if you find it helpful.

Enjoy the videos

Poor Lonely Repeat Troponin – posted by Bertolotti and Huecker

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We have noticed more and more this culture in our ED of obtaining an initial ECG, an initial troponin, and then waiting 2 or 3 or 6 hours to obtain a second troponin only and then discharge if negative.

I dove into the literature and wrote this post to address the SECOND ECG AT TIME OF SECOND TROPONIN as part of a rule out strategy for low risk ED patients.

I will not even address the fact that people are not obtaining a 2nd ECG at time 20-30 minutes from the first. This is on UpToDate, in ACC guidelines, in ACEP guidelines. It is simply standard of care to obtain an early, repeat ECG on anyone you remotely suspect of having ACS. I harp on this in lectures and have posted on it before. I also will not be talking about hs-Troponin (high sensitivity troponin). Many articles and FOAMed commentaries have covered hs-Trop, and we do not have this test at UL. So please do not think you can rule out all comers with 1 troponin, because you need the hs-trop to even consider this.

This post relates to the issue of a repeat ECG at time 2hr or 3hr (I am not a 6 hour guy, I like the 2 or 3 hr depending on symptom time frame). Don and I discussed the 2nd ECG phenomenon and he said it is just our culture at UofL, hence inspring our Room9ER post. Well we need to change the culture.

Now I didn’t want Geralds to cherry-pick an article to try to rebut me on this, so I went down a rabbit hole of ACS rule out, nSTEMI, HEARTS, TIMI and cardiac markers.

If your attention span is reaching its limit here is the bottom line:

All rapid rule out tools and their validation studies involve at least a SECOND ECG with the repeat troponin. HEARTS, ACC/AHS guidelines, TIMI-based rule outs, etc.

I was early to drop the CK and CK-MB on initial and repeat marker testing in favor of solely the troponin, but dropping the ECG is irresponsible. And is not evidence-based.

Below are many quotes and a figure, then a letter to the editor, from various sources. It was actually somewhat difficult to find in the methods exactly when or even if a repeat ECG was done. Much of the time, the ECG done at time of 2nd trop was not even the 2nd ECG, as mentioned above. “Serial ECGs” is the rule. It seemed as though the repeat ECG(s) were implied in the study, and that the research question was simply timing a troponin.

 Dr Huecker composed most of this post because Dr Bertolotti is so excited about and diligently preparing for Research Day. 

Enjoy, and please post comments! 

  

— Patients with probable or possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals (see Section 2.2.8). (Level of Evidence: B)

— The c-statistic of troponin only was 0.70. With addition of the ECG the c-statistic improved significantly to a value 0.78, with a likelihood ration test p-value of <0.001

— Anderson et al. JACC Vol. 50, No. 7, 2007 ACC/AHA UA/NSTEMI Guideline Revision August 14, 2007:e1–157                                                                                                    If the initial ECG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs, initially at 15- to 30-min intervals, should be performed to detect the potential for development of ST-segment elevation or depression. (Level of Evidence: B)

— ACEP (What will be used for or against you in court, as the case may be)

Acute Coronary Syndromes (Non–ST-Segment Elevation – Adult)

Critical Issues in the Evaluation and Management of Adult Patients with Non–ST-Segment Elevation Acute Coronary Syndromes (September 2006)

Complete Clinical Policy on Non–ST-Segment Elevation Acute Coronary Syndromes (PDF)

Scope of Application. This guideline is intended for physicians working in hospital-based emergency departments (EDs) or chest pain evaluation units.

Inclusion Criteria. This guideline is intended for adult patients presenting to the ED with suspected non–ST-segment elevation acute coronary syndromes.

Exclusion Criteria. This guideline is not intended for pediatric patients, patients in cardiogenic shock, or patients with injury on the initial 12-lead electrocardiogram (ECG).

Critical Questions

  1.  Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes?
  • Level A recommendations. None specified.
  • Level B recommendations.Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia. No recommendations can be made in regards to the exact timing of repeat ECGs. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG. 
  • Level C recommendations. None specified.

— Letter: Re: “Troponin-negative chest pain”—a diagnostic evasion?

This brief article is well written and I agree the diagnostic label of ‘troponin negative chest pain’ is unhelpful. However the article repeats some common misconceptions which require correction.

Firstly, the article implies that the majority of patients attending hospital with chest pain have an acute coronary syndrome. This is absolutely not the case – in fact most patients with suspected acute coronary syndrome do not have it. (1) Often patients receive a label of acute coronary syndrome and this is later corrected by the cardiology registrar or consultant on call – although by then it may be too late to change the patient’s perception that they have ‘had a heart attack’.

Secondly, there appears to be a misunderstanding of the value of troponin testing. Troponin assays are positive when there has been myocardial necrosis. They do not give any information about the mechanism of myocardial necrosis – a positive troponin can indicate acute coronary syndrome, but may also occur in heart failure, prolonged arrhythmia, sepsis, pulmonary embolism and many other situations. (2)

Similarly, a negative troponin does not absolutely exclude a cardiac cause for symptoms – nor does it mean the patient is necessarily in a low risk group. (3) Patients with unstable angina, dynamic ECG changes, but negative troponin should be considered as having a similar risk of mortality and morbidity to those with a normal ECG but a positive troponin.

Troponin assays should generally be considered a prognostic, not a diagnostic test, and should be used in conjunction with the patients history and ECG – never alone.

 

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.

Always keep your differential broad

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I had a case in our department that I won’t forget for a while, and it reminded me to keep my differential broad even if the suspected diagnosis seems blatantly obvious.

 

An early 40’s female presented to our ER about 5 days after an MVC in which she was the restrained driver, where the car rolled onto its side going about 40s-50s MPH. + LOC, + airbags. Paramedics arrived on scene after a while when she was up and walking, and she refused to be taken to the ER. Over the following 5 days, she had near constant neck pain as well as a worsening headache and worsening abdominal and “rib” pain on the lower left side.

She presented to our ER in a hallway bed, where her initial HR was in the mid 80s, but BP was 80s/40s on multiple checks. O2 sat and temperature were normal. Mental status was normal, and there were no physical signs of trauma on her body. She had tenderness to the L lower and lateral ribs, as well as LUQ/LMQ abdominal tenderness, and lower midline C-spine tenderness. I quickly had her placed in a cervical collar, and brought the ultrasound to bedside a performed a FAST, which was negative (to my surprise).

I ordered fluid boluses, trauma labs, type and crossmatch, and planned to send her for a man scan, but her kidney function showed an AKI and therefore had to wait for one fluid bolus before going to the scanner. BP slowly started to trend upwards, not reaching over mid 90s systolic before she went to the scanner. Of note, she did have a slightly elevated white count in the mid-to-upper teens.

My differential? Trauma, trauma, trauma. She has to be bleeding somewhere, she may have a fractured C-spine, intracranial injury, intraabdominal injury, likely splenic laceration. My FAST just must not have picked it up. Given the history and clinical circumstance, I don’t think I was completely wrong for not having anything else on my differential for this hypotensive patient with concerning physical exam findings 5 days out from a serious car accident.

Once her man scan was done, I looked though the scans and noticed her right kidney was heterogenous with contrast enhancement with stranding around it. No fluid in her pelvis, and the rest of the man scan was entirely negative. Radiology soon called and said she had the “worst case of pyelonephritis I think I’ve ever seen”. A urine sample was finally collected after the scan resulted, which was, no longer to my surprise, infected. Upon talking to the patient, she denied any dysuria or frequency, but said her urine was “green” this morning. She never had any suprapubic pain.

That is the story of how I admitted a patient to medicine for pyelonephritis after getting a man scan and diagnosing it on CT. I don’t think I’ll be changing the top item on my differential, but I think I will keep other causes of hypotension and shock on my differential until they are ruled out in cases of delayed trauma presentation, such as this one.

ED Thoracotomy

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ED THORACOTOMY
Hey guys! Here’s the latest overview of ED thoracotomies from LITFL.com posted on March 11, 2016.  I’ve only seen 3 of these during my medical career, two of them were last week. One was my patient and the other was Jenny’s. While both didn’t survive their hospital course, my patient did regain a pulse and make it through several hours of surgery. If you haven’t encountered this scenario yet, I’m sure you aren’t alone. Still, it’s important to know not only how to perform it, but when.
Interesting articles to review:

  • #1 To be blunt: are we wasting our time? Emergency department thoracotomy following blunt trauma: a systematic review and meta-analysis.

    Slessor D1, Hunter S2.

    Author information

    Abstract

    STUDY OBJECTIVE:

    The role of emergency department (ED) thoracotomy after blunt trauma is controversial. The objective of this review is to determine whether patients treated with an ED thoracotomy after blunt trauma survive and whether survivors have a good neurologic outcome.

    METHODS:

    A structured search was performed with MEDLINE, EMBASE, CINAHL, and PubMed. Inclusion criteria were ED thoracotomy or out-of-hospital thoracotomy, cardiac arrest or periarrest, and blunt trauma. Outcomes assessed were mortality and neurologic result. The articles were appraised with the system designed by the Institute of Health Economics of Canada. A fixed-effects model was used to meta-analyze the data. Heterogeneity was assessed with the I(2) statistic.

    RESULTS:

    Twenty-seven articles were included in the review. All were case series. Of 1,369 patients who underwent an ED thoracotomy, 21 (1.5%) survived with a good neurologic outcome. All 21 patients had vital signs present on scene or in the ED and a maximum duration of cardiopulmonary resuscitation of 11 to 15 minutes. Thirteen studies were included in the meta-analysis. If there were either vital signs or signs of life present in the ED, the probability of a poor outcome was 99.2% (95% confidence interval 96.4% to 99.7%).

    CONCLUSION:

    There may be a role for ED thoracotomy after blunt trauma, but only in a limited group of patients. Good outcomes have been achieved for patients who had vital signs on admission and for patients who received an ED thoracotomy within 15 minutes of cardiac arrest. The proposed guideline should be used to determine which patients should be considered for an ED thoracotomy, according to level 4 evidence.

    #2 Inaba K et al. FAST Ultrasound Examination as a Predictor of outcomes After Resuscitative Thoracotomy: A Resuscitative Thoracotomy. Ann Surg 2015; 262 (3): 512 – 8. (Inaba et al. 2015)*

    • Background #1: In patients who suffer a traumatic cardiac arrest, a final salvage maneuver that is performed in the Emergency Department (ED) is a resuscitative thoracotomy (RT). There are two lines of thought about RT that are on opposite sides of the spectrum. The first line of thought is that if RT is not performed the patient is going to die anyways, so why not try it as a last ditch effort. The second line of thought is that due to the low yield in survival with RT, why expend resources and create a potential risk of harm to providers. The Focused Assessment Using Sonography for Trauma (FAST) has a high sensitivity and specificity for identifying hemopericardium and cardiac activity in a matter of seconds. Since there is really no good way to discriminate between which patients with traumatic cardiac arrest would benefit from RT, maybe adding a bedside FAST could help make this distinction.
    • This was a prospective, observational trial in 1 Trauma center in California
      • Patients undergoing RT in the ED
        • All penetrating trauma patients with absent vital signs
        • All blunt trauma patients with loss of vital signs en route or in the resuscitation bay
      • FAST performed just before or concurrently with RT
    • Bottom Line #1: ALL survivors and organ donors had visible cardiac motion on FAST. If no cardiac motion or pericardial effusion was seen on FAST, then survival was zero.

These are useful especially when you’re looking at who to perform this on. End goal is for the patient to survive the hospital course or in the case of possible organ donation.

Due to the large regional and facility variation in practice of who/when to perform this procedure, it will be very important for you to know what your facility’s policy is or your trauma team’s stance is as well.

Quick ED thoracotomy video. ..no instructional audio, so go over the steps prior to watching this. Otherwise, you may be lost. ..

Below is LITFL’s most recent post from 03/11/16:
ED Thoracotomy

Resuscitative Thoracotomy

OVERVIEW

  • resuscitative thoracotomy is a thoracotomy performed prehospital, in the emergency department or elsewhere that is an integral part of the initial resuscitation of a patient
  • an alternate term is emergency thoractomy
  • survival 4-33%
  • determinants of survival include mechanism of injury, the location of injury and the presence or absence of vital signs
  • best outcomes in:

-> penetrating chest
-> those exsaunginating from chest tube
-> isolated chest trauma
-> cardiac injuries
-> abdominal trauma that benefits from aortic clamping
-> time since loss of vitals

REQUIREMENTS

  • ETT
  • shock or arrest with a suspected correctable intrathoracic lesion
  • specific diagnosis (cardiac tamponade, penetrating cardiac lesion or aortic injury)
  • evidence of ongoing thoracic haemorrhage

INDICATIONS

Accepted

  • penetrating injury + arrest + previous signs of life
  • blunt injury + arrest + previous signs of life

Relative

  • penetrating injury + no signs of life and CPR < 15min – blunt injury + signs of life in field or during transport -> arrest 15 min
  • blunt injury + no signs of life
  • multiple blunt trauma
  • severe head injury

RESUSCITATION IN TRAUMATIC ARREST

  • 1. Intubate (reverses hypoxia)
  • 2. Insert bilateral chest drains (or thoracostomies)
  • 3. Resuscitative Thoracotomy
  • 4. Limit fluid as this worsens outcome in penetrating thoracic trauma unless haemorrhage controlled
  • 5. Limit inotropes and pressors until circulation restored (will need once defect repaired)

TECHNIQUE

Goals

  • relieve cardiac tamponade
  • perform open cardiac massage
  • occlude aorta to increase blood flow to heart and brain
  • control life threatening thoracic bleeding
  • control bronchovenous air embolism

1. Full aseptic technique*** –> This was recently an issue where the Trauma attending cited both his team and ours in Rm9 for lack of full prep –> masks, surgical gloves, gowns, etc. should be worn when performing this procedure.
2. Scalpel through skin and intercostal muscles to mid axillary line.
3. Insert heavy duty scissors into thoracostomy incisions.
4. Cut through sternum.
5. Lift up (clam shell)

-> relieve tamponade (longitudinal incision through pericardium)
-> repair cardiac wounds (non-absorbable sutures, 3.0)
-> stop massive lung or hilar bleeding with finger (partial or intermittent occlusion may be performed to avoid right heart failure)
-> identify aortic injuries (repair with 3.0 non-absorbable sutures or use finger)
-> consider aortic cross clamping at level of diaphragm (limits spinal cord ischemia)

The Awful Facet of Compare and Contrast Essay Subjects

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Trach Management Algorithms/Videos

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As a follow up to Dr. Dennison’s presentation yesterday: see this link if you’d like to watch a couple videos on replacement/troubleshooting. They go through passing a new Trach over an airway exchange catheter as well as a Bougie.

http://www.tracheostomy.org.uk/Templates/Videos.html

This link is the algorithms for both Tracheostomy and Laryngectomy: http://www.tracheostomy.org.uk/Templates/Algorithms.html