Reanimating the Dead

Posted on June 11, 2018 by James Buchanan

It’s trauma season once again. As room 9 after room 9 roll in the door the rising 2nd and 3rd years will soon be dealing with traumatic arrest patients (if they haven’t already). While the ED resident works to control the airway, the trauma team is placing bilateral chest tubes and a cordis. All of this while the nurses and techs continuously perform compressions and give 1mg of epi every 3-5 minutes, while inadvertently interrupting everything else going on. At the end of the day are all those compressions and all the epi going to change outcomes? We know in medical cardiac arrest it will but is traumatic cardiac arrest different?

Reanimating Patients After Traumatic Cardiac Arrest A Practical Approach Informed by Best Evidence discusses 5 key principles to guide management. The emphasize this is only for isolated traumatic cardiac arrests and that if there is any indication that a medical cardiac arrest occurred prior to a trauma following guidelines such as ACLS should be given priority.

The 5 Key Principles:

Start or Stop
Deprioritrize Chest Compressions
Fix Ventilation
Stop the Bleeding
Fix the Physiology

Start or Stop:

When do you start or stop a traumatic resuscitation? What Factors do you consider? Well there is some food for thought:

Favorable Prognostics Factors:

Penetrating injury, particularly to the Thorax
Vitals Signs at any time
Signs of Life at any time
Short Duration (<10min)
Cardiac Contractility on POC USN

Without 1 of these signs, survival is <1%. Important to keep in mind when EMS is giving a report and you are try to determine how long to attempt a resuscitation.

Spectrum of Output States:

They note for their practice the category of “dead” does NOT receive any further resuscitation. The note this is in part to save the vital limited resource of blood prodcuts. I also found it interesting that they separate PEA from pseudo-PEA from severe hypovolemia. Thats why having the cardiac probe in hand on arrival can save be useful in determining how far you are going to push the resuscitation.

Deprioritize Chest Compressions

Chest compressions may work for medical arrest but the pathology behind traumatic arrest is so vastly different all they do is get in the way of more vital procedures: intubation, chest tubes, central access, cardiac USN. Until all this has been established it would probably be better just to hold compression. Be warned however this will likely be an uncomfortable experience for the nurses/techs.

Fix Ventilation:

Referring back to Table 3 we can clearly see that establishing an airway and decompressing both sides of the chest should be top priority in a traumatic arrest.

Remember that traumatic arrests are a low flow state and while most patients while not require a induction agent or paralytic if you do use a paralytic use TWICE the dose.

Stop the Bleeding:

Simple and straight forward if it’s bleeding make it stop. Direct Pressure, tourniquets, topical hemostatic agents (which as far as I’m aware we don’t have) and pelvic binders are all easily performed in room 9. Thoracotomy is also something to consider discussing with Trauma early on in these resuscitations. Both the Eastern Association for the Surgery of Trauma and the Western Trauma Association recommend thoracotomy and though their conditions vary penetrating trauma to the torso and arrest for less than 15 minutes seems to be a good rule of thumb.

Fix the Physiology:

Pretty straightforward recommendations that we do everyday:

Keep the Patient warm to prevent exacerbating coagulopathies
Establish AccessL Large bore (14-18 gauge) IV access above the diaphragm, IO access of the proximal humerus, 8 or 9-Fr CVC preferably subclavian while avoiding multiple lumen CVCs
Minimize fluids and transfuse blood products 1:1:1 and allow for permissive hypotension

They go into some post-resuscitation recommendations as well when it comes to “fix the physiology” but those are less important to use. I would recommend that everyone should briefly review this article as it has a lot more information and reasoning behind their recommendations.

Push Dose Pressors

Posted on October 17, 2017 by Chelsea Garrison

Are you all tired of hearing about sepsis yet? How about the fact that we apparently suck at sepsis? However, I think we can all recognize when someone comes in with severe septic shock. You know, the sick, hypotensive, altered patient with a source of infection. With a low blood pressure, we just need to keep pushing more fluids right? Just keep pushing them until they are in pulmonary edema.

Well, what could we possibly do to improve outcomes? The longer they are hypotensive, the more end organ damage they are going to sustain, and the worse the outcomes. I know that most of you all listen to EMCrit. If you don’t, you should. So while waiting for that central line to be placed by our intern (and we know that can take a while, j/k interns, I love you) and waiting for the levophed gtt to be started, we can be like Weingart and give some push dose pressors. Not only could they be used for that septic patient needing a boost in BP, but can also be used for the peri- or post-intubation or sedation patient that becomes hypotensive.

Epi-It’s not ideal to give code dose epi to someone with a pulse. Instead take a 10 mL syringe and fill it with 9 mL of NS. Then draw up 1 mL of epi from the cardiac amp. This gives you 10 mcg/mL of epi. Now, give 0.5-2mL (5-20mcg) q1-5 min until improved BP.

Phenylephrine- Draw up 1 mL of phenyl from a vial that is 10 mg/mL and put in a 100 mL bag of NS. This gives you 100mL of phenylephrine at the concentration of 100mcg/mL Now you draw up 10mL into a syringe at push 0.5-2 mL (50-200mcg) q1-5 min.

And for your convenience, here is a link to a PDF from EmCrit with the instructions on how to mix these. Take a pic, keep it on your phone. While doing this, don’t forget patient safety. Make sure you’re labeling your syringes when you mix up push dose pressors. Avoiding medication errors is always plus.

Also, until you are comfortable doing this, make sure you are collaborating with your attending and the pharmacist if they are there at the time.

Finally, read this article on safety considerations in push dose pressors.

And for added fun, read all room9ER posts in Danny DeVito’s voice. It makes everything better.

Cool Name, Not So Cool Results

Posted on August 18, 2017 by Eric Yazel

53yo WM rolls in, wee hours of the am. C/o HA, onset around 4 days ago. Wife says “I think he had a seizure in the middle of the night that night” Def hit his head, has a goose egg middle of the forehead. “Had some labs done at my primary yesterday, they called me and told me to come in” No clue as to what labs those might be when asked. Awesome. Medical hx only significant for HTN and GERD. No chronic meds. Admits to drinking around a case of beer a day. Probably explains the not so full history he provided. Nothing else interesting on physical exam and normal vital signs. So I send labs- CBC, Chem13, Mag, CT his head due to the possible seizure.

Annnnd Na 114, K 2.5, CL 75, Bicarb 32, BUN 12, Cr 1.2, Glucose 111, Ca 8.4. CT normal. ETOH and Tox NL. Serum osmolality 259

So what’s going on here? Hyponatremia and seizure- needs fixed right. Normal saline or even hypertonic saline maybe?

Negative ghost rider

Lets look at this a little deeper.

Start with the algorithm

Image result for hyponatremia algorithm

So we will start with the asymptomatic column. Could argue for the severe side due to the seizure, but he is now 4 days out and asymptomatic. Went the euvolemic side of things. No signs of fluid overload clinically and didn’t look dry. Actually nerded out and ordered urine osmolality. 88. So where does that land us?

Beer Potomania syndrome.

WTH is that? Great name. But too much physiology for my brain.

When patients have poor protein and solute (food, electrolytes) intake, such as in chronic alcoholics, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load includes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake … as long as you are not drinking excessive amounts of water.

Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.

So, we see alcoholics all the time. Why don’t we see this all the time? When you think about it, a pretty low percentage of our EXI all star drinkers are beer drinkers. And most case a day beer drinkers actually have a decent oral food intake. Making this more rare than you originally might think.

So what do we do about it? Classic example of ‘dont just do something stand there!’

Fluid restriction, fluid restriction, fluid restriction.

Back to my case. Admit the patient to my hospitalist, who is half asleep and currently not as excited as I am about hyponatremic management. Orders in for fluid restriction and serial chemistries. A few minutes later, I hear my ER nurse arguing with the floor nurse during calling of report. They are appalled that I am not giving normal saline, and even request hypertonic saline. I politely pick up the phone and discuss the physiology and reason for my treatment plan. We were on the same page by the end of the call.

Fast forward to a couple days later. I come back for another shift, and am checking on my patients from the day before (quick aside, no matter where you are in your career always save the info for 3-4 of your sicker, more interesting patients and look them up on your next shift, by far one of the most high yield learning you can get. And will help you adjust your practice as indicated). I look up the serial sodium results. 114, then 119, 123, then………145. Goooooooo!!!! Assuming I am about to hear from the Kentucky Hammer due to causing central pontine myelinolysis. I talk to the hospitalist- apparently the next shift nurse, after the one I talked to, got her way, and they got an order to blast the guy with normal saline. Hence the huge jump. Patient did have some transient AMS, but was at baseline and neuro intact once levels stabilized. Thank god.

Anyway, interesting case. Beer potomania. cool name, not so cool results. Literature states that central pontine myelinolysis happens in over 20% of these patients due to too rapid correction. So before you pull the trigger on normal saline repletion take a second and scope out the algorithm above. Sometimes the best thing you can do is nothing.

My Lesson on Anchoring

Posted on June 29, 2017 by andrew BINGHAM

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.

Baffling Neurology Pathology Strikes Again…

Posted on June 13, 2017 by anne hayes

…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.

ED Thoracotomy

Link

#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.

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)

Can you give Vasopressors through a PIV?

Posted on December 8, 2016 by James Buchanan

I looked back and couldn’t find a post about this topic in the last year or so but forgive me if it has already been posted. I have been following R.E.B.E.L. EM for a few months now and I would recommend it to everyone who has the time and wants quick summaries on the latest EM literature. They have short written summaries of papers including pros/cons of the study and what they feel are the most important take away points. It was founded by Salim Rezaie with Rob Rogers, Matt Astin and Anand Swaminatham serving as editors.

Occasionally they will have a “mythbuster” post looking at common myths in the ED and the most uptodate literature available on the topic. (their latest mythbust is on “safe” glucose levels before ED discharge but I digress)

Back in May they reviewed the safety of vasopressors through a PIV. The topic paper was titled “A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters”

What the review found was very interesting: of 318 events, 204 results in local tissue damage, 114 were only extravasation events and 7 events involved the use of a CVC (so clearly not completely safe). Interesting, of the 204 local tissue events 85.3% involved PIV distal to the antecubital fossa and 96.8% involved administration of >4hrs.

REBEL EM’s take away points were:

In critically ill patients, with hemodynamic instability, vasopressor infusion through a proximal PIV (antecubital fossa or external jugular vein), for <4hours of duration is unlikely to result in tissue injury and will reduce the time it takes to achieve hemodynamic stability.

What I feel like this means for us is simple: If you have a crashing, hypotensive patient who needs a pressor without a CVC but good proximal PIVs, start the pressor immediately, stabilize the patient as best you can, then take the time to properly place a CVC.

Continue to monitor the PIV until it can be switch to the CVC and stop the pressor immediately if there is any suspicion for local extravasation. I am sure this will make some people nervous but I think this is better then placing a “crash line” that is less then sterile which will expose an already ill patient to infection or other complications secondary to a hastily placed CVC.

I highly recommend read their review and how they came to this conclusion along with their other posts. I have included the link to this study at the bottom.

http://rebelem.com/mythbuster-administration-of-vasopressors-through-peripheral-intravenous-access/

Headache in a post-neurosurgical patient

Posted on October 10, 2016 by shaun reynolds

Earlier this month while moonlighting I had an approximately 40yM present for a headache (9/10 pain) for 3 days.

I know, this is an everyday occurrence.

But in his case he had a craniotomy with removal of a meningioma 1 month prior. He also noted 2 weeks of swelling on the left side of his head along the surgical scar.
ROS: denied fevers, chills, changes in vision, weakness, numbness, or tingling, etc.

PE: VSS, HEENT: Left side of head extending from his surgical scar and wrapping around to even under his L eyebrow was swollen and firm. NEURO: WNL

So, I know something isn’t right and my guess is that he either had a bleed or infection associated with his surgery. I order a CT head. For his headache I give him a migraine cocktail (IVF, compazine, and benadryl, minus the toradol).

After I see the CT images, I rush to check on the patient as the CT obviously shows quite a bit of midline shift and the patient states his headache is drastically improved (2/10 down from 9/10). Apparently migraine cocktails work on all causes of headache.

I consulted Neurosurgery who promptly admitted the patient to the ICU with plans to go to the OR. Approximately 45 minutes later, after the NES nurse practioner has seen the patient and he is getting packed up to go to the ICU, the radiologist calls to notify me of the CT findings.

This is a reminder to ALWAYS look at CT images yourself, especially if you’re expecting a life threatening finding.

Lactate

Posted on September 10, 2016 by Martin Huecker

Bosse’s favorite molecule (and lab test), lactate has a sordid and confusing history. This article in Emergency Medicine News sheds some light on lactate and its role in disease (or health). The author (Dr Paul Marik) is board certified in internal medicine, critical care, neuro-critical care and nutrition.

It may take a couple reads but this article has a succinct, common sense approach to understanding lactate production and use by the body. You may not be able to apply this knowledge on your next patient encounter, but physiology is fun right?

Chest pain?

Posted on September 5, 2016 by aramsey

Yesterday, 10 minutes before the end of a very busy shift in the middle of nowhere:

Nurse hand’s me an EKG for the mom of one of our best young medics. Ischemic STD in II, III, aVF, V5, V6. No STE. Maybe some LVH. No other EKG on file, she hasn’t been here before. I get up to see her right away.

In the room is a 50 yo lady in severe distress. BP 250/140. Describes “tearing” L sided CP radiating to her upper back. I ask her if she has a family hx of sudden death or aneurysms, her son says yes. No SOA. No N/V. Lungs are clear. Can’t palpate pulses in her feet. Slightly obese. She is sweating. There isn’t a CT surgeon in this county; I am sweating, too.

The nurse gets CT ready and I start the ball rolling for big IVs, blood, helicopter, etc. She gets dilaudid 1 mg then 0.5 then 0.5 again for pain and hopefully BP control. I tell everyone she’s now the ED’s top priority. The family of another patient grabs me twice in the hallway and asks why their mom, who fell, hasn’t gotten her home dose of lisinopril yet.

~30 minutes from door to imaging – CTAs = no dissection. Great, I have some time. Pain is well controlled now and BP 150s/80s. Repeat EKG w ischemia resolved completely, normal. Hypertensive emergency? She has a bit of a headache so I scan her head because we’re in CT, but it’s not useful due to the residual contrast. Trops, CBC, CMP, urine, tox, etc. all negative. Now looks great and feeling much better. Wants to go home.

Her son, her nurse, and I spend a long time convincing her she needs to stay overnight. She doesn’t want to be admitted, as she’s starting a new job Tuesday and can’t miss it. Eventually, she agrees to stay. Then we have to convince her to be transferred, since ED MD is the only MD in house overnight and she had me straight terrified. Reluctantly, she agrees to the transfer as long as her son will bring her home Monday night, no matter what. Hospitalist at the local mothership accepts readily. At that hospital, she’d had a negative stress 8 months ago and NES had placed her shunt (pseudotumor, she has a lot of headaches); hospitalist will consult cards and NES when she gets in.

I arrive back to work this morning to find out she’d made it upstate only to be transferred again overnight. She’d been flown to a bigger center after repeat CT head demonstrated SAH. She had 2 aneurysms, 1 was bleeding, both were definitively addressed. 24 hours after walking in the door, at the time of this writing, she is extubated and thriving.

Found this article from 1988 with a similar presentation, but I can’t say I’d ever heard of it before. Something else for your differential. Really consider that admission for observation when something seems wrong, even if you don’t know what it is.

Going to change my drawers now.

Emergency Escharotomy

Posted on August 21, 2016 by tiffany campbell

Case: 57 yo M who presents via EMS found with circumferential burns on bilateral lower extremities, left upper extremity, lower pelvis, and left side of chest after being trapped in a burning tent. Unknown time of incident.

VS: HR: 128, RR: 24, BP: 112/64, SpO2 96% on 4L O2

Alert, oriented x 2. SEVERELY DISTRESSED. Singed nares bilaterally. Bilateral wheezes, tachypneic. Tachycardic, RR. Abd S/NT/ND. Once again, 3rd degree burns circumferential burns from lower pelvis, extending to groin, and down to bilateral lower extremities. The 3rd degree burn covered the left side of his chest and his RUE. No pulses were palpated in his LUE or BLE. Though burned, BLE and RUE appeared blanched with poor cap refill and cool to touch. 72% estimated burn coverage total. Pt stated he was unable to feel or move bilateral lower extremities.

During the process of IV, O2, monitor, and moving the pt over. I called for pain medication, intubation meds, and got the equipment ready for intubation.

Trauma, Plastics, Urology – paged. Don’t wait to get consults on board in a case where you are preparing to do this procedure.

On physical exam, remember Wallace rule of nines (see total body surface area): 9% for each arm, 18% for each leg, 18% for the front of the torso, 18% for the back of the torso, and 9% for the head and 1% for the perineum. At the same time, think Lactated Ringers at 4 mL x kg x percentage burn = total fluids needed for replacement in initial 24hrs. First half of amount in first 8 hours with the second half over 16hrs{{Parkland}}.

But, first, intubate to secure the airway, provide pain control, and facilitate further exam. Needless to say, burns are extremely painful.. . so are escharotomies.

Trauma wedge took the RLE, and I had the LLE. In the race to get pulses back, I succeeded and was rewarded with getting to do the LUE as well.

How did I perform the procedure you ask? Well, it was with the Trauma fellow standing at the foot of the bed giving instructions and guidance . .. I had never seen anything like this except for textbook cases of a circumferential burn to the chest/trunk. This procedure is not on our sign off list, required list, or on anything that I had seen in cadaver lab.

While these procedures are as rare as a Trauma fellow eager to teach at 2 am, you may be faced with the same in a rural ED or with a wedge stuck in the OR, etc.

Advice: Be nice to your colleagues. And, more importantly, prepare.

Here are some very informative links that would’ve been great to have seen or reviewed prior.

Step 1: Read the Overview

Video 1: Robot voice explanation: Best display of lines for incision, but more from a surgical perspective

Video 2: Australian Escharotomy How-to

FYI:

Suprapubic catheter was also placed in the ED prior to the pt going to the OR. Another rare procedure, not required, but useful to know.

Hypertonic Saline vs Mannitol

Posted on July 21, 2016 by Martin Huecker

Research and Reviews in the Fast Lane (which is a must for anyone consuming FOAM) just covered a SR and meta-analysis on hypertonic saline. Relevant after our discussion in conference this morning.

Berger-Pelleiter E, et al. Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials. CJEM 2016. PMID: 26988719

Hypertonic saline seems to be recommended more and more often for intracranial hypertension. What is the evidence in traumatic brain injury?
This is a systematic review and meta-analysis that identified 11 RCTs covering 1820 adult patients with traumatic brain injury comparing hypertonic saline to either mannitol (½ the studies) or another solution (often normal saline, or even hypotonic saline.) Hypertonic saline did not decrease mortality (RR 0.96, 95%CI 0.83-1.11). It didn’t lower intracranial pressure (weighted mean difference -0.39, 95%CI -3.78 – 2.99). And it didn’t improve functional outcomes (RR 1.12, 95% CI 0.92-1.36). Maybe we shouldn’t be rushing to adopt hypertonic saline in the management of traumatic brain injury.

Recommended by Justin Morgenstern

Just another overdose…..right?

Posted on June 27, 2016 by Scott McClain

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

Posted on June 13, 2016 by samuel aya

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.

Sick PEs

Posted on June 10, 2016 by Martin Huecker

We had a very ill patient recently. She was found down upstairs visiting her family member. She was calmly altered, not agitated but was in mild distress. Consciousness fluctuated. Tachycardic and hypertensive initially, then had more labile BP and some hypotension.

We had to intubate her due to poor MS and clinical condition. She coded in CT, we placed a central line on the CT table between her noncontrast head CT and her CT chest. We pushed an amp of Epi and ran out of the room for the CT chest. We were worried about dissection and PE in equal amounts. We could not get good cardiac windows on bedside Echo in room 9 prior to the CT.

She continued to intermittently lose her pulse and drop her BP. We confirmed bilat PEs on the CT when we saw NO contrast left her right ventricle. The CT tech noticed first and became worried the patient had no cardiac output (ie pulseless).

We rushed the patient back to room 9 and gave a tPA bolus (50mg) followed by infusion of 40mg. She was on pressors and heparin and improving. Dr Smith accepted her to Jewish for possible EKOS or even ECMO if needed. On arrival to Jewish a few hours later she coded and died.

I was surprised when I found out she had died. Her O2 sat was improving, HR was decreasing, blood pressure was stable (though dependent on pressors). She received a large amount of crystalloid IV which according to some data might not have been optimal management. She also had the following ECG:

I think she was infarcting her myocardium. She likely had pulmonary infarction considering her poor oxygenation. She had coded a few times. She had a lot of strikes against her. Her BEST SHOT was going to a place with catheter assisted treatment for PE and ECMO if needed.

I am posting the case to let everyone know:

How to manage sick PE patients (see post below)
To use tPA in massive and in many cases of submassive PE
TRANSFER sick PE patients to Jewish for EKOS/ECMO
The decision to diagnose PE with RV strain on BEDSIDE Echo with no formal Radiologic testing will depend on your attending

This post from EmCrit / PulmCrit is a beautiful summary with potential dogmalysis related to PE management (see take home points below but do read the post).

In addition, here is a nice review article on catheter-based reperfusion treatment for PE with nice references for further reading.

Take home points from the Emcrit post:

The only evidence-based intervention that seems to improve mortality in massive PE is thrombolysis. The primary goal of therapy should be administration of thrombolysis as soon as possible to patients without contraindication.

Consider early stabilization of blood pressure using a norepinephrine infusion, administered peripherally if necessary.

Volume administration may facilitate dilation of the right ventricle and hemodynamic deterioration.

Intubation is very hazardous and should be avoided if possible. Patients die from cardiovascular collapse, and intubation may worsen this.

For a coding PE patient consider 50mg alteplase bolus as well as an infusion of epinephrine. Patients can do well despite requiring CPR and high dose vasopressor infusions.

Room9er ["Room Niner"]:

The sickest patients, who receive world-class care in the trauma/critical care bay of University of Louisville Department of Emergency Medicine

Tag Archives: Critical Care