PoCUS & COVID Severity

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Handover from EMS to Trauma Team: an analysis

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A life threatening case of Hiccups

A life threatening case of Hiccups – A Resident Clinical Pearl

Mark McGraw, PGY3 FMEM program,  Dalhousie University Saint John

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Introduction:

Its mid morning on an acute shift in the emergency department and you hear a familiar but somewhat out of place sound coming from around the corner. You look up to see the triage nurse walking in a middle-aged male patient who is hiccuping constantly. The patient looks unwell and is pale, but he is able to walk into the department without assistance. The triage nurse asks the charge doc where she should place the patient. He has had intractable hiccups for over a week and has been unable to sleep or eat anything. His chief complaint is hiccups and weakness. She notes he also has a small infected cyst on his back that is being treated with Keflex from one of the local surgeons and had a subjective fever at home. Vitals on triage were normal but she was concerned because he just didn’t look right. You suggest he take a trauma bed and state you’ll see him now based on his appearance and wonder to yourself how often a trauma bed is taken up with someone who has a chief complaint of hiccups….

A little background:

Hiccups are a bit of a physiologic anomaly and appear to have no protective effect or evolutionary purpose. Hiccups can be found early in life and are can be found as early as the second trimester of pregnancy. The incidence of hiccups in the general pediatric and adult population is unknown but its fair to say the majority of people have experienced them at some point in their lives. To most, hiccups are nothing more than a brief annoyance or embarrassing distraction but in some cases they can herald sinister pathologies.

Hiccups result from inappropriate closure of the glottis through a reflex arc that consists of the phrenic nerve, vagus nerve, and thoracic sympathetic chain. During inspiration our glottis remains patent allowing unimpeded airflow into the lungs. The hiccup reflex triggers glottis closure, typically triggered during the swallowing to prevent aspiration, about 30 milliseconds after the onset of inspiration resulting in a rush of air against a closed glottis.

The majority of problematic hiccup cases arise from stimulation, inflammation, or injury to nerves of the afferent reflex arc. Two of the most common causes of benign hiccups are gastric distension from eating a large amount of food or consuming carbonated beverages and relaxation of the glottis due to alcohol ingestion.

The differential for hiccups is broad. UpToDate lists over 50 items on its differential for persistent/intractable hiccups grouped as CNS disorders, vagus/phrenic irritation, GI disorders, thoracic disorders, CV disorders, toxic/metabolic causes, postoperative, drug induced, and psychogenic.

Hiccups under 48 hours

In patients with hiccups lasting less than 48 hours and without red flag symptoms or other warning signs it is reasonable to try physical maneuvers to stop hiccups. The goal of all these maneuvers is stimulation/irritation of the afferent reflex arc.

• Breath holding or Valsalva maneuvers (increasing hypercapnia),
• Sipping or gargling cold water (nasopharynx irritation)
• Swallowing a spoonful of dry sugar (nasopharynx irritation),
• Pulling a patient’s knees to his/her chest and having them lean forward (decrease diaphragmatic pressure)

Hiccups over 48 hours

There is little quality evidence on the treatment of hiccups. In general, if an etiology is suggested from the history and physical target treatment, i.e. using a PPI in patients with underlying GERD, should be considered.

A 2015 systematic review suggested the use of baclofen and gabapentin as first line agents in treating hiccups with metoclopramide and chlorpromazine used as second line agents. A follow up systematic review in 2017 published in the journal of emergency medicine found that only baclofen and metoclopramide had randomized control trials supporting their efficacy. Baclofen was found to be particularly effective for treatment of intractable hiccups associated with stroke.

Treatment options:

• Baclofen 5 to 10 mg PO TID,
• Gabapentin 100 to 400mg PO TID,
• Metoclopramide 10mg PO TID or QID,
• Chlorpromazine 25mg PO TID,

A recent case report published in the American Journal of Emergency Medicine (Kocak et al., 2020) demonstrated almost immediate termination of hiccups in a patient following a subdermal injection of lidocaine and thiocolchicoside into the sternocleidomastoid muscle and epigastric region.

 

 

Back to our case

Our patient settles into a bed in the trauma bay and his repeat vitals show a declining blood pressure and increasing heart rate. His only complaint at this time continues to be his persistent hiccups. Cardiac, respiratory, abdominal and CNS exams are unremarkable. When you assess the “small lump” on his back you find an area of erythema extending from the superior tip of his scapula to his L1/L2 region inferiorly with a large softball size nodule around the lateral border of his scapula. You initiate empiric therapy with pip/tazo and clindamycin and call for an urgent CT scan and surgical consult.

While prepping for the scan the patient asks about treatment for his hiccups. You decide to try metoclopramide 10mg IV, which does nothing to alleviate his hiccups. His CT scan confirms a massive abscess extending from his deltoid muscle to his obliques with infiltration into the muscle and fascia. He is taken to the OR by a team of 3 surgeons for emergent debridement of his necrotizing fasciitis. After a brief stay in the ICU he is transferred to the surgical floor where you find out his hiccups have resolved.

Summary
The next time you are working in the emergency department and a patient presents with hiccups here are a few helpful points to remember:

• Patients with hiccups lasting less than 48 hours in the absence of red flag / systemic symptoms typically do not require medical workup or treatment.
– Physical maneuvers to terminate hiccups may provide relief for patients in the ED.
• Patients with persistent hiccups over 48 hours warrant a full physical exam and laboratory studies tailored to the patient’s history as hiccups may be the initial manifestation of an underlying neoplasm, infection, or metabolic disorder.
• If no underlying etiology is found there is reasonable evidence to support empiric treatment with metoclopramide 10mg PO TID or baclofen 5 to 10mg PO TID.
• In patients with persistent hiccups secondary to another disease process empiric treatment may be a useful adjunct while the underlying cause is addressed.

 

References

Polito NB, Fellows SE. Pharmacologic Interventions for Intractable and Persistent Hiccups: A Systematic Review. J Emerg Med. 2017 Oct;53(4):540-549. doi: 10.1016/j.jemermed.2017.05.033. PMID: 29079070.
Steger M, Schneemann M, Fox M. Systemic review: the pathogenesis and pharmacological treatment of hiccups. Aliment Pharmacol Ther. 2015 Nov;42(9):1037-50. doi: 10.1111/apt.13374. Epub 2015 Aug 25. PMID: 26307025.
Kocak AO, Akbas I, Betos Kocak M, Akgol Gur ST, Cakir Z. Intradermal injection for hiccup therapy in the Emergency Department. Am J Emerg Med. 2020 Sep;38(9):1935-1937. doi: 10.1016/j.ajem.2020.03.044. Epub 2020 Mar 25. PMID: 32245702.
Chang, F. Y., & Lu, C. L. (2012). Hiccup: mystery, nature and treatment. Journal of neurogastroenterology and motility, 18(2), 123–130. https://doi.org/10.5056/jnm.2012.18.2.123
Image of reflex arc: http://blog.clinicalmonster.com/2017/03/23/so-bored-i-hiccuped/
Marion, DW. Hiccups. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2020.

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Congratulations to Dr. Rob Dunfield – CAEP Resident Research Award Winner!

CAEP 2021 Resident Research Award Winner – Dr. Rob Dunfield

A big congratulations goes out to our very own resident researcher, Dr. Rob Dunfield! Dr. Dunfield is a second year resident in the FMEM Program here in Saint John. He is one of seven residents recognized nationally for their excellent research abstract submissions to the annual CAEP conference. Dr. Dunfield’s research project is a secondary study from the SHOC-ED group and is entitled:  “Does IVC Ultrasound independently predict fluid status in spontaneously breathing, undifferentiated hypotensive patients? SHOC-IVC”.

Congratulations again, Dr. Dunfield!

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EM Reflections February 2021 – Bias & Error in the ED

Big thanks to Dr. Joanna Middleton for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Case

It’s your 7th evening shift in a row and the department is in critical overcapacity. You are at the latter end of your shift. You’re answering multiple charge doc calls when a new acute chart is put up to be seen. You pick it up: it’s a 62 yo male with 1 day of LLQ pain radiating to the flank. You start your history: his pain has been worsening over the day and he describes loose stools earlier in the week. He denies fever/chills and any other infectious symptoms on review of systems. He has a history of diverticulitis in the past and thinks it feels similar. He denies any previous admissions or surgical interventions for his diverticulitis in the past.

Vitals: BP 108/78 HR 102 RR 20 O2 98% RA T 36.3

On exam he has mild tenderness throughout, you feel perhaps focal LLQ tenderness, but no peritoneal signs. He looks in mild discomfort but is otherwise well. His U/A is negative.

“I’d just like some antibiotics doc, so I can get back home”.

You order basic lab work which is within normal limits except for a slightly elevated CRP. You diagnose him with uncomplicated diverticulitis and discharge him with oral antibiotics.

Could there be any bias ongoing with this patient1?

Anchoring bias:  “Prematurely settling on a single diagnosis based on a few important features of the initial presentation and failing to adjust as new information become available”.

In this patient he has a history of diverticulitis and it seems similar. We anchor on the previous diagnosis.

Diagnosis momentum: “Similar to anchoring. Once a diagnostic label has been assigned to a patient by another individual, it is very difficult to remove that label and interpret their symptoms with fresh eyes.”

Again, here we have an easy diagnosis previously established. The symptoms sound the same – so it’s easy to again label the patient with diverticulitis.

Confirmation bias: “Once you have formed an opinion, you have a tendency to only notice the evidence that supports you and ignore contrary evidence.”

From the triage note you strongly suspected diverticulitis, so you subconsciously push aside the fact that he has tenderness throughout, and that it radiates to the flank, not just focally in the LLQ.

Premature Closure: “This is the tendency to stop too early in a diagnostic process, accepting a diagnosis before gathering all the necessary information or exploring all the important alternatives.”

Here the patient feels it’s diverticulitis, there was some loose stools earlier in the week so we close the possibility of other diagnosis.

 

You continue your shift – 2 hours later an EMS patches in.

“62 yo male previously discharged from ED today with diverticulitis, found down at home by wife. CPR in progress. Asystole on rhythm checks. Down time 30 min. Intubated on scene. ETA 5 minutes”.

 

You prepare your team to receive the code. As EMS rolls in you recognize the man you discharged earlier in the day. You rack your brain, but don’t remember getting a detailed past medical history other than he had diverticulitis. You are unsure if he had any cardiac risk factors.

You begin the resuscitation and ask the resident working with you to look up the patient’s PMH. They find a recent IM consult – the patient has a history of RA and is on immunosuppressants. He also has a history of HTN, DM and a known AAA last checked 3 years ago. It measured 5cm at that time.

You grab your ultrasound probe and scan the aorta:

You see a large AAA and potentially some free fluid anterior to the aorta.

You scan the RUQ:

 

You see a large amount of free fluid.

You suspect a ruptured AAA. You begin Massive Transfusion Protocol and attempt to resuscitate the patient to ROSC. You give the vascular surgeon on call a heads up. Unfortunately the patient has been down 30 min and your resuscitation is unsuccessful. You call the code.

This would be an unfortunate case: the setting in the department is already chaotic, you are mentally fatigued and bias can take over. As ED docs this is a common situation we find ourselves in often. To err is human, but there are ways we can overcome bias.

 

What are the two types of cognitive approaches we often take2?

Type 1: The Intuitive/Reflexive System: automatic decisions based on pattern recognition. Done quickly and with minimal effort. This is the approach we took with our patient.

Type 2: The Analytical/Problem-Solving System: we step back and critically think about the patient presentation, think about pretest probabilities, other diagnoses and question ourselves more. This is not the fast route.

So, Type 2 must be best then2?

Not really – it’s a blend of the two.  “Experts use their experience and past errors/mistakes to reflect on their knowledge and their biases and develop heuristics (cognitive short-cuts) and cognitive forcing strategies that allow them to use their Type 1 system for rapid decision making in EM rather than having to slow down using their Type 2 system.”

So, we gather knowledge as we see more and more patients, but we also need to use our knowledge wisely.

How do we do this2?

Reflection – learn from your mistakes. Easy in theory but will require some work and time on your part to continue reflecting in a useful manner:

  • Follow up on your cases; try and do so within a few days or on your next shift. Check their inpatient chart. Consider touching base with the patient in some cases.
  • Develop your own cognitive short cuts – ones based on experience and previous analytical problem solving so next time you don’t have to evaluate as critically.
  • Consider dictating your chart, or documenting in the EMR your ED uses – when saying it outloud, or typing it out all at once, it can trigger reflection and may lead you to consider other diagnoses.
  • Before you sign off on a chart and put it in the ‘discharged’ pile look at the evidence one last time – does it have internal congruence? Is there evidence against your diagnosis that may support another?

Try and understand your own personal bias, or any that may exist within your thought process.

When you reflect upon your own personal bias, it can help you develop strategies to prevent it from happening.

 

Do you find yourself anchoring on a diagnosis from the triage note before you even see it patient? Force yourself to truly broaden your differential.

Have you ever found yourself subconsciously pushing some data aside while focusing on results that support your leading diagnosis? Maybe write the pertinent results on your chart so you can’t ignore them.

Bottom line – it takes work and time to reflect upon your practice. We all change our practice based on previous mistakes – this is a type of cognitive forcing strategy. The physician in our case will likely scan each aorta in high risk patients with flank pain from now on. This case has forced them to consider AAA in future cases. He/she has created a cognitive heurisitic to consider AAA in abdo pain presentations.

Emergency Medicine is a team -oriented environment. What other ways can we prevent bias2?

Two minds are better than one . During critical situations our brains often focus on one task and can’t process more outside information. Situational awareness can be lost – having a second doc on board if possible can be exceedingly helpful; If you both have your ‘jobs’ you can cognitively unload some of the information.

Practice, practice, practice – evidence shows that mentally rehearsing critical procedures increases chance of success. See Dr. George Kovac’s approach to taking an airway (start at 3 min mark) for a great example.3

 

Prep your team – have a huddle when the EMS dispatch is received. Review the differential and logistically have medications/equipment you anticipate being needed within arms reach. Assign tasks to each person so everyone knows their job. Call any consultants you suspect will be needed.

Talk to your team – no matter how obvious it may (or may not) seem, confirmatory statements can bring everyone on the same page. “This trauma patient is altered and not protecting their airway, we need to take the airway and urgently get a CT head”. Communication on a patient plan doesn’t need to be only in critical resuscitation situations. We are all involved in patient care. When you see a patient talk to the nursing staff, state your suspected diagnosis, how you plan to investigate and any interventions ongoing in the meantime. Paramedic nearby? Discuss the case with them as well, they have firsthand information from the scene that can be incredibly insightful. Plus, they are as much a part of the team as in hospital staff. They will want an update on the patient as well.

Think ahead – when you communicate your confirmatory statement to your team, it’s also a good time to consider what could go wrong and how to prepare. “This patient likely has a significant intracranial injury and could potentially herniate. We need to monitor for signs of herniation, have mannitol at the bedside and be prepared for urgent neurosurgical intervention”.

Practice, practice, practice some more – with simulation. Acclimatize yourself to stressful situations so you become more desensitized to your body’s physiologic response when faced with a critically ill patient.

Checklists – you can be a pro at resuscitation and stressful situations, but everyone has an off day. Everyone can suffer from fatigue. Take some of the thinking out of the picture – trauma checklists, airway checklists, etc. These can prevent errors by allowing you to follow the list when giving care and can provide a ‘fail-safe’ approach.

When are we more likely to make errors4?

  • Nightshift – especially around 5AM. The EM witching hour.
  • Handover – especially from nightshift
  • The overconfident physician/learner
  • Extremes of age – very young or very old patients
  • High patient volumes with many interruptions
  • The ‘difficult’ or frustrating patient

One study showed an emergency doctor was interrupted on average 30 times during an 180 min work window, while seeing/responsible for on average 12 patients during this time. 5

What can we do to prevent errors4?

  • Rest well before your nights – sleep deprivation is cumulative. It can lead to tolerance of more risk, increased distractability and poor performance at tasks. This is more likely to happen at the latter end of your shift. Ensure you take breaks to eat and hydrate.
  • Formalize handover – consider handover sheets with pertinent information and plan. Similar to SBAR – “Situation, Background, Assessment, Recommendation”
  • If no formal handover sheet, write a clear plan on the chart as well as verbalize it
  • When handing over a patient you are worried about, consider seeing them together with the doc taking over
  • If possible, try and request a ‘no interruption’ time during physician handover unless crucial. We should extend the same courtesy to our nursing staff.

After errors occur how do we learn from them4?

  • Follow up on cases by reading discharge summaries
  • M&M rounds – not to place blame, but for everyone to learn
  • A system in place to make docs aware of bouncebacks or mortality
  • Schedule ED follow up for patients you are concerned about who have poor follow up or no family doctor

Once an error has occurred, how to we disclose to family/loved ones4?

  • “inform the patient and the family of the mishap at the earliest convenient time in the presence of a 3rd party such as a department chief
  • express your concern, lay out the next steps in the course of care and answer any questions
  • notify CMPA
  • consider writing a ‘late note’ in the chart the next day and write a personal note to yourself outlining all the details for your personal file”

 

Errors will happen. Bias will happen. Do your best to reflect upon your practice and take away skills that will help you overcome these barriers.

 

References & further reading

  1. Justin Morgenstern, “Cognitive errors in medicine: The common errors”, First10EM blog, September 15, 2015. Available at: https://first10em.com/cognitive-errors/.
  2. Helman, A, Himmel, W, Hicks, C, Dushenski, D. Decision Making in EM – Cognitive Debiasing, Situational Awareness & Preferred Error. Emergency Medicine Cases. January, 2016. https://emergencymedicinecases.com/decision-making-in-em/. Accessed March 17, 2021.
  3. EMCrit # 253 – the Kovacs Kata to Optimize a Failing Laryngoscopy Attempt. https://www.youtube.com/watch?v=jCgpRd1R7gY&ab_channel=EMCrit
  4. Sinclair, D, Hicks, C, Helman, A. Cognitive Decision Making and Medical Error. February, 2011. https://emergencymedicinecases.com/episode-11-cognitive-decision-making-medical-error/. Accessed March 17, 2021.
  5. Chisholm, Collison, Nelson & Cordell (2000). Emergency department workplace interruptions: are emergency physicians “interrupt-driven” and “multitasking”? Academic Emergency Medicine Nov;7(11):1239-43. doi: 10.1111/j.1553-2712.2000.tb00469.x.

 

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Carbon Monoxide Poisoning

Carbon Monoxide Poisoning – A Medical Student Clinical Pearl

Mitchell McDonough

DMNB, Class of 2022

Reviewed by Dr. Rachel Goss

Copyedited by Dr. Mandy Peach

Case

A 75 y/o male presented to the Emergency Department one afternoon via EMS with mild confusion and a headache. He recalled a sudden feeling of light-headedness while making breakfast in the morning, lowered himself to the floor, and then has very limited memory of events after this. He did not recall losing consciousness. Given his confusion, he was unable to provide an accurate recount of the events that had initially brought him to the ED and collateral history was required. EMS indicated that he was found by his upstairs neighbour after hearing him yelling. The patient noted that the power went out at his house early during the night, so he turned on his propane stovetop to provide some heat. He admitted to alcohol consumption the night prior but indicated he drinks frequently and that was unlikely to be the culprit of his current state. He had no other complaints at this time and a review of systems was unremarkable apart from a mild headache.

On general assessment the patient appeared well, vital signs were within normal limits. On physical exam he had normal strength in all four extremities. Neurologic, respiratory, cardiac and abdominal exams were unremarkable. The patient was slightly confused but it was difficult to ascertain if this was new or his normal baseline.

Differential for Confusion

Metabolic disorders
• Electrolyte abnormalities
• Endocrine disease
• Hypoglycemia
• Hypoxia

Stroke/CNS structural lesion/Head Injury

Infectious
• Systemic infection
• CNS infection (meningitis, encephalitis)

Intoxication/withdrawal
• Alcohol
• Drugs
• Carbon Monoxide

Investigations

Initial investigations included an ECG, which was normal with no evidence of an ischemic event, a toxicology panel which showed minimal blood alcohol remaining, and a blood gas sample with carboxyhemoglobin. While carbon monoxide poisoning was initially low on our differential, the carboxyhemoglobin level came back severely elevated, at 31%. Interestingly, PO2 from the ABG was within normal limits as the concentration of CO required to cause poisoning is sufficiently low that it does not significantly alter the quantity of oxygen dissolved in the plasma.

Pertinent Arterial Blood Gas Values for our patient:

pH 7.37 [7.35-7.45]
pCO2 36.2mmHg [35-45]
pO2 81.4 mmHg [75-105]
K+ 4.2mmol/L [3.7-4.7]
Na+ 139 mmol/L [136-146]
Ca2+ 1.27 mmol/L [1.15-1.30]
FCOHb 31.4% [0.3-1.8]
ctHb 132g/L [120-150]

 

Carbon Monoxide Poisoning Overview

Carbon monoxide is a gas formed by combustion of hydrocarbons. It is colourless, tasteless and odorless. Carbon monoxide binds to hemoglobin with approximately 200 times greater affinity than oxygen, forming carboxyhemoglobin which results in impaired utilization of oxygen by cells. The mechanism of impaired oxygen usage relates to CO binding cytochrome oxidase in peripheral tissues which prevents cells from using the reduced O2 received.

Potential sources of carbon monoxide include fires, heating systems, stoves, charcoal grills, generators and motor vehicles (1-3).

Figure 1: Oxygen dissociation curve demonstrating the left shift of carbon monoxide (13).

Clinical Presentation

The clinical presentations of carbon monoxide poisoning vary depending on the severity of intoxication and most findings are usually nonspecific (4,5). Patients may describe a general malaise, nausea, dizziness and headaches (6). Depending on the level of intoxication, patients may present with symptoms ranging from confusion to coma, seizures and myocardial ischemia.

Table 2: Symptoms at varying levels of carbon monoxide dissolved in blood. It should be noted that symptoms can vary substantially from individual to individual and that levels of CO do not correlate well with symptoms. For example, a typical cigarette smoker will have up to a 10% level of CO in their blood at baseline. (14).

 

Severe is classified as >30% and the following clinical signs:

  • New neurologic findings
  • Ischaemic ecg
  • Clinically significant metabolic acidosis
  • Requirement for ventilation.

Diagnosis

Diagnosis of carbon monoxide poisoning is based on history, physical exam and elevated carboxyhemoglobin on cooximetry of an arterial or venous blood gas. Due to their similar light absorbancy, standard pulse oximetry is not able to differentiate between carboxyhemoglobin and oxyhemoglobin, and therefore cannot screen for exposure to carbon monoxide (7,8). Because of the similar light absorbancy, SpO2 can also be falsely elevated. It is important to note that even with a normal SpO2 level that the patient is hypoxic.

A non-smoker may have up to 3% carboxyhemoglobin at baseline while a smoker may have 10-15%. Anything above these levels represents carbon monoxide poisoning.

Treatment

Treatment of patients with suspected carbon monoxide poisoning include:

  • removal of the potential source
  • administration of high-flow oxygen by face mask.
  • IV mannitol for any potential cerebral edema.

Indications for treatment with hyperbaric oxygen vary from institution to institution and depend on factors such as symptoms, patient factors, length of exposure to carbon monoxide, as well as COHB levels.

In general, patients that should be considered for hyperbaric oxygen therapy include (4,9-12):

  • carbon monoxide level >25% (>15% in pregnant women)
  • neurosequelae
  • loss of consciousness
  • metabolic acidosis (pH < 7.1)
  • evidence of end-organ ischemia

Case Conclusion

Given their severely elevated carboxyhemoglobin level and prolonged exposure, the patient was given 100% oxygen via a non-rebreather face mask until being transported to a hyperbaric oxygen chamber for further treatment.

This case highlights the importance of carbon monoxide poisoning as a potential diagnosis when a patient presents with a reduced level of consciousness or confusion, especially during the winter months when the risk of exposure is higher.

References

  1. Thomassen Ø, Brattebø G, Rostrup M. Carbon monoxide poisoning while using a small cooking stove in a tent. Am J Emerg Med 2004; 22:204.
  2. Centers for Disease Control and Prevention (CDC). Carbon monoxide poisoning from hurricane-associated use of portable generators–Florida, 2004. MMWR Morb Mortal Wkly Rep 2005; 54:697.
  3. Hampson NB, Dunn SL. Carbon Monoxide Poisoning from Portable Electrical Generators. J Emerg Med 2015; 49:125.
  4. Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors. Age Ageing 2004; 33:105
  5. Kao LW, Nañagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am 2004; 22:985.
  6. Tomaszewski C. Carbon monoxide poisoning. Early awareness and intervention can save lives. Postgrad Med 1999; 105:39.
  7. Bozeman WP, Myers RA, Barish RA. Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med 1997; 30:608.
  8. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology 1989; 70:98.
  9. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998; 339:1603.
  10. Weaver LK. Carbon monoxide poisoning. Crit Care Clin 1999; 15:297.
  11. Hampson NB, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995; 13:227.
  12. Huang CC, Ho CH, Chen YC, et al. Hyperbaric Oxygen Therapy Is Associated With Lower Short- and Long-Term Mortality in Patients With Carbon Monoxide Poisoning. Chest 2017; 152:943.
  13. https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-medicine/thermal-injury-and-smoke-inhalation/
  14. https://www.cfinotebook.net/notebook/aeromedical-and-human-factors/carbon-monoxide-poisoning

 

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A Case of Posterior Vitreous Detachment

A Case of Posterior Vitreous Detachment – Medical Student Clinical Pearl

Ben McMullin, Clinical Clerk III

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. David Lewis

Copyedited by Dr. Mandy Peach

Case Presentation

A 61 year old female presented to the emergency department complaining of a floater in her right eye, which appeared 3 days prior to presentation. The floater moved with her eye movements. The patient claimed that her vision in the right eye was slightly blurry over the past 3 days but denied any significant decline in visual acuity. She denied any trauma, eye pain, discharge, or redness, but was particularly concerned since she was blind in her left eye since childhood.

On examination, the patients right eye appeared normal, with no discharge or conjunctival injection. Her pupil was roughly 3 mm and reactive to light. Her visual acuity was 20/30 in the right eye, and extraocular eye movements as well as visual field testing were normal. The intraocular pressure in her right eye was 9 mmHg.

Anatomy of the Eye

Figure 1: Normal eye anatomy as seen with ultrasound imaging.1

 

The cornea is the most superficial convex membrane, and immediately posterior to this is the anterior chamber, which is seen as anechoic on sonography. Posterior to the anterior chamber is the iris. Immediately posterior to the lens is the posterior chamber, which is also anechoic on sonography. The outer membrane of the eye from the inner most layer to the outer consists of the retina, choroid, and sclera.2

 

Differential Diagnosis for Non-Traumatic Visual Disturbance
• Posterior vitreous detachment
• Retinal tear
• Vitreous hemorrhage
• Vitreous inflammation
• Ocular lymphoma
• Intraocular foreign body
• Uveitis3

POCUS Ocular Exam

Advantages of POCUS

Ultrasound is a useful tool in the evaluation of some ocular complaints in the ED. Dilated fundoscopic examination is not always easily performed in the ED, but bedside ultrasound is becoming more readily available to physicians.4,5 Ultrasound can be useful in diagnosis of a wide range of ocular complaints, such as retinal detachment, posterior vitreous detachment (PVD), vitreous hemorrhage, and intraocular foreign body.4

Technique

Depending on the clinical history, a bedside ultrasound examination of the eye may be performed with the patient either supine or sitting in a chair.4 A high frequency probe should be used for this exam.1

Liberal amounts of gel should be used when performing a POCUS ocular exam, so as to minimize the amount of pressure placed on the eye.4 The gel does not need to be sterile, however for patient comfort, some physicians place tegaderm over the eye being examined. In order to orient the probe properly, ensure that the indicator on the probe is pointing towards the patients head when performing a longitudinal scan, and to the patients right when performing a transverse scan.1

To ensure that the entire eye is assessed, the eye should be examined in both the longitudinal and transverse planes, and it is important to sweep through in both directions. If the patient is able, it is also helpful to ask them to look to the right and left, as well as up and down with the probe on the eye.1 It is imperative to maximize brightness – if the field is too dark pathology like vitreous detachment can be easily missed.

PVD vs Retinal Detachment on POCUS

Complete retinal detachment will often appear as a V shape on ultrasound, with the apex seen at the optic nerve.5 Partial detachments can be more subtle and can appear differently from case to case.6

PVD is less echogenic than retinal detachment. PVD can often be seen moving with eye movements, more so than with retinal detachment.5 There is often a lag seen between movement of the globe, and movement of the vitreous appendage. In PVD, the detached vitreous is not connected to the optic disc, which contrasts with retinal detatchment.6 PVD can vary widely in size and can be seen with or without vitreous hemorrhage.2

Figure 2: Retinal detachment visualized on point of care ultrasound.6

Figure 3: Retinal detachment on ultrasound. (PoCUS Atlas)

 

Figure 4: Posterior vitreous detachment visualized on point of care ultrasound.2

Figure 5: Vitreous detachment on ultrasound (PoCUS Atlas).

 

Management

In the ED, retinal detachment requires urgent referral to ophthalmology. Retinal detachment can progress to total vision loss and should be seen and treated within 24 hours.3 In contrast, isolated PVD has a much better prognosis. Typically, floaters resolve within 3 to 12 months, but patients should still be referred for follow-up within 3 months to ensure no retinal tear is detected.3

Case Conclusion

Bedside ocular ultrasound showed PVD in the patient’s right eye, with no evidence of vitreous hemorrhage or retinal detachment. The patient was reassured of the prognosis but given that she was completely dependent on her right eye for vision, ophthalmology agreed to assess her the following week.

References

  1. Roque PJ, Hatch N, Barr L, Wu TS. Bedside Ocular Ultrasound. Crit Care Clin 2014; 30(2): 227-241.
  2. Southern, Simon. Ultrasound of the Eye. Australas J Ultrasound Med 2009; 12(1): 32-37.
  3. Arroyo, Jorge G. “Retinal detachment” last modified March 19, 2020, https://www.uptodate.com/contents/retinal-detachment?search=vitreous%20detachment&sectionRank=1&usage_type=default&anchor=H3491968696&source=machineLearning&selectedTitle=1~11&display_rank=1#H1505785278.
  4. Lahham S, Qumber A, Bea MP, Lee C, Fox JC. Role of point of care ultrasound in the diagnosis of retinal detachment in the emergency department. Open Access Emergency Medicine 2019; 11: 265-270. Retrieved from https://search-proquest-com.ezproxy.library.dal.ca/docview/2314891088?accountid=%24%24CLIENTID&pq-origsite=primo.
  5. Botwin A, Engel A, Wasyliw C. The use of ocular ultrasound to diagnose retinal detachment: a case demonstrating sonographic findings. Emerg Radiol 2018; 25: 445-447.
  6. Gandhi K, Shyy W, Knight S, Teismann N. Point of care ultrasound for the evaluation of non traumatic visual disturbances in the emergency department: the VIGMO protocol. Am J Emerg Med 2019; 37 (8): 1547-1553.
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An interesting derm case in the ED: Mycosis Fungoides

Mycosis Fungoides: A Medical Student Clinical Pearl

 

Nicholas Relja, B.Sc.(Hon), M.Sc.
Dalhousie Medicine New Brunswick
M.D. Candidate, Class of 2022

All case histories are illustrative and not based on any individual

Reviewed by Dr. Devon Webster

Copyedited by Dr. Mandy Peach

Case

A 55-year-old male presented to the ED after concerned family brought him in due to ongoing generalized weakness lasting approximately one month. On inspection he had erythematous, scaly, ulcerative lesions covering his entire body with only facial sparing. He mentioned burning-like pain originating from his ulcerative lesions. He had been previously diagnosed with T-cell lymphoma 30 years ago and had gone through multiple rounds of chemo and radiation therapy since that time.

Picture from: Denis D, Beneton N, Laribi K, Maillard H (2019). Management of mycosis fungoides-type cutaneous T-cell lymphoma (MF-CTCL): focus on chlormethine gel. Cancer Management and Research. Vol 11: 2241-2251

Differential for itchy, erythematous rash:

Condition
Atopic dermatitis
Contact dermatitis
Drug eruptions
Erythrodermic psoriasis
Psoriasis
Sezary syndrome
Various lymphomas

 

When reviewing the patient’s past medical history you see they were previously diagnosed with Mycosis Fungoides – a rare cutaneous form of T-cell lymphoma.

Epidemiology

Mycosis fungoides has an incidence of approximately 6 cases per million per year in the United States. It is more common in adults over 50 years of age, with a male to female ratio of 2:1. The disease is also more common amongst the Black population than in Caucasians or Asians.8,9

Etiology

The exact cause of mycosis fungoides is not known; however, there a variety of mechanisms that have been postulated:2

• Genetic and epigenetic abnormalities.3,4
• Environmental and occupational exposure to noxious substances and chemicals.5
• Human T-lymphotropic virus Type 1 – a suspected infection-type etiology.6
• Cytokines such as IL-2 and IL-4 due to their increased presence in patients with mycosis fungoides and Sezary syndrome.7

 

There are three stages of mycosis fungoides and therefore clinical presentation will vary depending on the stage of disease:

Patch stage: Erythematous, or brownish scaly patch, which may show some atrophy. It is possible to have one or multiple lesions develop in areas such as the gluteal region or on the proximal thighs. The likeness of this stage has been compared to “small-plaque” or “large plaque” parapsoriasis; however, the plaques are actually not plaques but patches instead.10

Plaque stage: This is the second stage – lesions will be larger, more numerous and will show infiltration. The lesions appear annular, are raised and have well-defined edges as well as asymmetry in terms of their distribution. Face and scalp involvement can also be seen starting at this stage.11

Tumor stage: The final stage – erythematous-purplish papules or nodules of larger diameter.12

There are other clinical variants of mycosis fungoides, but they are not as common, and some are quite rare.

Sezary syndrome:
In advanced form of the mycosis fungoides, Sezary syndrome may be present. This syndrome involves erythroderma with pruritus, lymphadenopathy and atypical circulating lymphocytes (referred to as Sezary or Lutzner cells).13

Evaluation in the ED

A detailed history and physical exam including checking for lymphadenopathy (most commonly cervical nodes) and organomegaly14,15 in addition to documenting the rash characteristics.

Labs: CBC, liver function tests, LDH

Radiological tests: depends on extent of lymphadenopathy and organomegaly. Can do a CXR in the ED for lung involvement, but otherwise advanced imaging can be decided upon by specialist consultant and may include CT, US, PET or MRI.

Biopsy: lymph nodes and rash – by consultants

Treatment and Management – refer to your friendly neighborhood dermatologist.

Early stage:

Treatment options include topical therapies such as corticosteroids and other agents, UV therapy, local radiation and systemic immunosuppressants 15,16,17.

Advanced Stage:

Treatment for the advanced stages of mycosis fungoides are directed at disease control and symptom relief. Localized radiation, targeted immunotherapy or chemotherapy. 15, 18

Prognosis

The prognosis of mycosis fungoides is variable but in general as the stage gets more advanced and with patients over the age of 60, the prognosis becomes poorer. Other poor prognostic factors include increased LDH, tumor distribution and organ involvement.2

Case Conclusion

The patient seen in hospital by the dermatologist on call and was deemed to be in the plaque stage. He was admitted due to the advancing course and and inability to manage his symptoms from home. Further care will involve palliation and a focus on quality of life.

 

References:

  1. Olisova, O. Y. et al. [Current possibilities of the differential diagnosis of plaque parapsoriasis and the early stages of mycosis fungoides]. Arkh. Patol. 81, 9–17 (2019).
  2. Lim, H. L. J. et al. Epidemiology and prognostic factors for mycosis fungoides and Sézary syndrome in a multi-ethnic Asian cohort: a 12-year review. J. Eur. Acad. Dermatol. Venereol. JEADV 33, 1513–1521 (2019).
  3. Bergallo, M. et al. DNA from Human Polyomaviruses, MWPyV, HPyV6, HPyV7, HPyV9 and HPyV12 in Cutaneous T-cell Lymphomas. Anticancer Res. 38, 4111–4114 (2018).
  4. Väisänen, E. et al. Cutavirus DNA in Malignant and Nonmalignant Skin of Cutaneous T-Cell Lymphoma and Organ Transplant Patients but Not of Healthy Adults. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 68, 1904–1910 (2019).
  5. Slodownik, D., Moshe, S., Sprecher, E. & Goldberg, I. Occupational mycosis fungoides – a case series. Int. J. Dermatol. 56, 733–737 (2017).
  6. Blaizot, R., Ouattara, E., Fauconneau, A., Beylot-Barry, M. & Pham-Ledard, A. Infectious events and associated risk factors in mycosis fungoides/Sézary syndrome: a retrospective cohort study. Br. J. Dermatol. 179, 1322–1328 (2018).
  7. Fujii, K. New Therapies and Immunological Findings in Cutaneous T-Cell Lymphoma. Front. Oncol. 8, 198 (2018).
  8. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Clinical and epidemiological profile of patients with early stage mycosis fungoides. An. Bras. Dermatol. 93, 546–552 (2018).
  9. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Hypopigmented mycosis fungoides: a 20-case retrospective series. Int. J. Dermatol. 57, 306–312 (2018).
  10. Pimpinelli, N. et al. Defining early mycosis fungoides. J. Am. Acad. Dermatol. 53, 1053–1063 (2005).
  11. Burg, G., Dummer, R., Nestle, F. O., Doebbeling, U. & Haeffner, A. Cutaneous lymphomas consist of a spectrum of nosologically different entities including mycosis fungoides and small plaque parapsoriasis. Arch. Dermatol. 132, 567–572 (1996).
  12. Keehn, C. A., Belongie, I. P., Shistik, G., Fenske, N. A. & Glass, L. F. The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control J. Moffitt Cancer Cent. 14, 102–111 (2007).
  13. Lopez, A. T., Bates, S. & Geskin, L. Current Status of HDAC Inhibitors in Cutaneous T-cell Lymphoma. Am. J. Clin. Dermatol. 19, 805–819 (2018).
  14. Prince, H. M. & Querfeld, C. Integrating novel systemic therapies for the treatment of mycosis fungoides and Sézary syndrome. Best Pract. Res. Clin. Haematol. 31, 322–335 (2018).
  15. Wain, T., Venning, V. L., Consuegra, G., Fernandez-Peñas, P. & Wells, J. Management of cutaneous T-cell lymphomas: Established and emergent therapies. Australas. J. Dermatol. 60, 200–208 (2019).
  16. Dairi, M., Dadban, A., Arnault, J.-P., Lok, C. & Chaby, G. Localized mycosis fungoides treated with laser-assisted photodynamic therapy: a case series. Clin. Exp. Dermatol. 44, 930–932 (2019).
  17. Photiou, L., van der Weyden, C., McCormack, C. & Miles Prince, H. Systemic Treatment Options for Advanced-Stage Mycosis Fungoides and Sézary Syndrome. Curr. Oncol. Rep. 20, 32 (2018).
  18. Alpdogan, O., Kartan, S., Johnson, W., Sokol, K. & Porcu, P. Systemic therapy of cutaneous T-cell lymphoma (CTCL). Chin. Clin. Oncol. 8, 10 (2019).

 

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