A bad trip… to the ICU – A case presentation and general overview of poisonous mushroom ingestion

A bad trip… to the ICU – A Resident Clinical Pearl  on poisonous mushroom ingestion

Scott Fenwick 

PGY-1 Family Medicine, Dalhousie University

Reviewed by: Liam Walsh, Clinical Pharmacist

Copyedited by: Dr. Mandy Peach

Case Presentation:

A 43yo otherwise healthy female presents to the ED with 30 hours of intractable nausea, vomiting, diarrhea, and diffuse crampy abdominal pain. 12 hours prior to the onset of these symptoms, she had foraged six wild mushrooms, fried them with butter, and ate them with her dinner. She had used a wild mushroom reference guide and thought these “pristine white” mushrooms would be a safe steak topping.

In the ED, she was alert and oriented with a GCS of 15 and no apparent encephalopathy. Her vitals were BP 109/68, P 93, T 37, RR 16, O2 97% RA. She was retching and vomiting clear emesis, which settled some with ondansetron 8mg IV. Clinically, she looked dehydrated but otherwise not toxic. Her abdomen was soft and diffusely tender. Cardiorespiratory exams were unremarkable. There were no skin findings.

A 1L bolus of normal saline was administered. Serum laboratory studies, drawn approximately 42 hours post-ingestion returned as follows:

Urinalysis showed trace blood, ketones and protein. ECG showed normal sinus rhythm.

The marked elevation in liver enzymes and abnormal coagulation studies were concerning for hepatocellular injury and fulminant hepatic failure. The local Internal Medicine consultant was contacted, and the patient was transferred to the ICU at the nearest liver transplant center.

In consultation with pharmacy and poison control, it was determined that the most likely offending mushroom was Amanita virosa, more commonly know as a Destroying Angel.

The patient was started on NAC, activated charcoal, penicillin G, cimetidine, vitamin C, and IV silibinin (milk thistle). Consideration was given to percutaneous cholecystostomy, as the toxin can accumulate in the gallbladder, but this was not anatomically feasible at the time.
Laboratory studies peaked at 72 hours post-ingestion as follows

Vitamin K was given to lower the INR. Creatinine continued to climb and was 835 prior to initiation of hemodialysis. Liver studies slowly trended downward with ALT 9774, AST 4586, and INR 1.7 at 96-hours post-ingestion. Ultimately, liver function values returned to normal and enzymes levels continued to trend downward—making liver transplant not necessary.

Overview of Toxic Mushroom Ingestion:

Epidemiology:

According to the 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System, more than half of toxic mushroom ingestions occur in children under the age of 6. Serious toxicity and mortality, however, is more common in foraging adults, as they are more likely to consume larger quantities of a misidentified mushroom. Data for Atlantic Canada was difficult to obtain, but the Ontario Poison Centre received 72 calls related to mushroom exposures in September 2020, generally the peak month for exposures.

Poisoning Syndromes:

Only 20% of the time is the offending mushroom correctly identified, so we often rely on the clinical presentation to identify the likely species and relevant treatment. UpToDate lists 12 different mushroom toxins and 14 unique corresponding syndromes:

  • Acute gastroenteritis (<6hrs) without liver failure
  • Delayed gastroenteritis (6-12hrs) and delayed liver failure
  • Acute gastroenteritis and delayed renal failure
  • Hallucinogenic
  • CNS depression and excitation
  • Disulfiram-like reaction
  • Cholinergic excess
  • Delayed renal failure
  • Delayed rhabdomyolysis
  • Erythromelalgia
  • Delayed encephalopathy
  • Immune-mediate hemolytic anemia
  • Shiitake dermatitis
  • Allergic bronchioalveolitis

The syndrome from this case, bolded above, is delayed liver toxicity and delayed gastroenteritis.

This syndrome follows 3 phases:

  • Phase I: Dysentery – nausea, vomiting, diarrhea (6-24hrs post-ingestion)
  • Phase II: Apparent recovery (24-36hrs post-ingestion)
  • Phase III: Fulminant hepatic and multisystem organ failure (48-96hrs post-ingestion)

Poisonous Mushrooms in New Brunswick:

The New Brunswick Museum has compiled a catalog of the mushroom species discovered in the province. One of the deadliest mushrooms in the province is the Destroying Angel. This nickname refers to a group of mushroom species under the genus Amanita. Amanita virosa is commonly found in New Brunswick and Nova Scotia. They are pristine white and often located in wooded areas or next to trees/shrubs in suburban areas. They are most prevalent in the summer and fall.

In their button stage, Destroying Angels can be confused with white mushrooms that you might buy at the grocery store. Destroying Angels produce an amatoxin—a selective inhibitor of RNA polymerase II, leading to an interruption in protein synthesis and cell death. Amatoxins are especially toxic to the GI tract, liver and kidneys.

Notably, in the NB Museum catalog, there are no reports of Amanita phalloides, aka the Death Cap, in New Brunswick. In Canada, they are more commonly found in British Columbia.

EM Approach:

History:

  1. What did they look like? Ask for photos from the patient’s phone or samples if they have them. Identification assays are available but not always useful in the acute setting.
  2. Were the mushrooms collected in a field or along/underneath trees? Many toxic mushrooms are in wooded areas.
  3. How many types of mushrooms were ingested?
  4. How long after ingestion did symptoms develop? Less than 6hrs is associated with lower risk of—but does not exclude—potentially lethal ingestion.
  5. How much was eaten? Were there multiple times of ingestion?
  6. Did others eat the mushrooms? If so, do they have similar symptoms?

Physical Exam:

  • Assess hydration status
  • Assess for encephalopathy or other signs of fulminant hepatic failure

Laboratory studies:

Treatment:

  • Ondansetron for N/V, do not use anti-diarrheal agents
  • IVF for dehydration and electrolyte abnormalities
  • If a serious ingestion cannot be excluded, patients should be admitted for 24-48hrs for observation and serial bloodwork

Evidence-based recommendations for suspected amatoxin poisoning:
o Multiple dose activated charcoal: 0.5g/kg (max 50g) q4h for 4 days post-ingestion.

o Silibinin: loading dose of 5 mg/kg IV, followed by a continuous infusion at a dose of 20 mg/kg/day for 6 days or until clinical recovery.

If IV silibinin is not available, oral milk thistle capsules (Silymarin) are an effective alternative. The initial dose is 50-100mg/kg q8h, and titrated up to 200mg/kg q8h as tolerated, with a maximum single dose of 2-3g. IV Silibinin is available only through Health Canada’s Special Access Program. Pharmacy should be contacted early to assist with this process if it’s being considered.

o Penicillin G: 300,000 to 1,000,000 units/kg/day given as a continuous IV infusion. A small amount of research shows no benefit to adding this if IV silibinin is available. If penicillin allergy, consider ceftazidime 4.5 g every 2 hours.

o NAC protocol: initial loading dose of 150 mg/kg (max 10g), next a 4-hour infusion at 12.5 mg/kg/hr, then a 16-hour infusion at 6.25 mg/kg/hr. The 16-hour dose may be repeated if significant hepatic dysfunction persists.

o Cimetidine: 300 mg IV every 8 hours until clinical improvement (evidence in animal studies only)

o Vitamin C: 3 g IV daily until clinical improvement (evidence in animal studies only)

o Dextrose for hypoglycemia

o Lactulose for hyperammonemia

o Vitamin K +/- FFP for coagulopathy

o Dialysis for AKI

o Early consultation with liver transplant center

  • Treatments for other mushroom poisoning syndromes can be found in this chart

Bottom Line:

Ask if the patient has photos of the mushrooms on their phone, or if they can describe their appearance. Call local poison control with this information.

Obtain a clear history to determine the interval between time of ingestion and time of symptom onset. Acute gastroenteritis onset (<6hrs from ingestion) is associated with favourable outcomes, and delayed gastroenteritis (usually 6-12hrs from ingestion) is more likely to have liver and/or renal failure.

Liver studies may be normal until 24-36 hours and generally peak at 72-96 hours post-ingestion.

Early treatment and consultation/transfer to a liver transplant center is imperative.

 

References:

Cover photo: https://www.deviantart.com/dreadillustrations/art/Poison-Mushrooms-774297817

Gummin, D. D., Mowry, J. B., Beuhler, M. C., Spyker, D. A., Brooks, D. E., Dibert, K. W., Rivers, L. J., Pham, N., & Ryan, M. L. (2020). 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 37th Annual Report. Clinical toxicology (Philadelphia, Pa.)58(12), 1360–1541. https://doi.org/10.1080/15563650.2020.1834219

Nelson, L. S., Howland, M. A., Lewin, N. A., Smith, S. W., Goldfrank, L. R., Hoffman, R. S., & Flomenbaum, N. E. (2019). Goldfrank’s toxicologic emergencies (11th ed.). Mc Graw Hill Education.

Shannon, M. (2007). Haddad and Winchester’s clinical management of poisoning and drug overdose (4th ed.). Saunders.

NB Museum Mushroom Checklist: http://website.nbm-mnb.ca/mycologywebpages/Checklists/NBMushrooms/NBMushroomChecklist.html

Tavassoli, M., Afshari, A., Arsene, A. L., Mégarbane, B., Dumanov, J., Bastos Paoliello, M. M., Tsatsakis, A., Carvalho, F., Hashemzaei, M., Karimi, G., & Rezaee, R. (2019). Toxicological profile of Amanita virosa – A narrative review. Toxicology Reports, 6, 143–150. https://doi.org/10.1016/J.TOXREP.2019.01.002

Amanita virosa photo: https://www.tehrantimes.com/news/423947/Mushroom-poisoning-kills-18-in-Iran

White mushroom photo: https://www.stockfood.com/images/00395464-Several-button-mushrooms

Amanita phalloides photo: http://www.bccdc.ca/about/news-stories/stories/2020/death-cap-mushrooms-make-fall-appearance-in-urban-areas

 

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A Biopsychosocial Approach to Epigastric Pain

A Biopsychosocial Approach to Epigastric Pain – A Medical Student Clinical Pearl

Gabrielle Hibbert, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Jay Hannigan

Copyedited by Dr. Mandy Peach

Case

A 22 year old male presented to the ER with a 6-week history of epigastric pain. The patient described the pain as a burning sensation radiating to his throat and RUQ. The pain was constant, exacerbated post-prandially, and associated with nausea and vomiting. He denied any hemoptysis, hematochezia, melena, dysphagia, odynophagia, symptoms of extra-esophageal reflux, or dyspepsia. He reported having a poor appetite associated with a twenty-pound weight loss. Review of systems was otherwise negative. Pantoprazole recently prescribed by his GP had not improved his symptoms. He denied using NSAIDs. He reported experiencing a lot of anxiety recently due to relationship conflicts with his partner and inability to access counselling services. He was scheduled to have an outpatient ultrasound of his gallbladder.

Past medical history: bipolar disorder, general anxiety disorder, depression, and tonsillectomy

Medications: olanzapine odt, citalopram, lamotrigine, and pantoprazole

Social: The patient worked at American Eagle, and he lived with his partner, his partner’s parents, and their 18-month-old son. He smoked one gram of Marijuana per day, vaped daily, and occasionally consumed alcohol. He was an ex-smoker and had a history of abusing cocaine, LSD, and crystal meth but had not used in three years.

Physical exam: The patient was afebrile, and his other vitals were within normal limits. He looked well and was in no visible distress. He had some mild epigastric tenderness to palpation. Cardiac, respiratory, and abdominal exam were unremarkable.

Investigations

CBC, electrolytes, LFTs, and TSH recently ordered by his GP were within normal limits. Serology testing for celiac disease was negative. CRP was <0.6.

The Biopsychosocial model

The biopsychosocial model illustrated in Figure 1 was introduced in 1977 by the American Psychiatrist George Engel1. He stated that “to provide a basis for understanding the determinants of disease… a medical model must also take into account the patient, the social context in which he lives, and the complementary system devised by society to deal with the disruptive effects of illness”1.

Figure 1. The Biopsychosocial model. Figure modified from 2.

The diathesis-stress model, proposed by Spielman and colleagues in 1987, illustrates how psychological, biological, and social factors contribute to the development and maintenance of disease3. An example of this model is shown in Figure 2.

Figure 2. Summary of potential predisposing, precipitating, and perpetuating factors across biopsychosocial domains3

 

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal reflux occurs when there is inappropriate relaxation of the lower esophageal sphincter (LES) or delayed gastric emptying4. Multiple factors such as hiatal hernias, increased intraabdominal pressure, and certain drugs can contribute to this pathogenesis5. Altered processing of signals from the esophagus leading to hypersensitivity has also been linked to the pathogenesis of reflux6.

As illustrated in Figure 3, the bidirectional communication between the enteric nervous system and central nervous system is termed the “brain–gut axis” 7. Neurotransmitters involved include endogenous opioids, endocannabinoids, and serotonin6. These neurotransmitters are affected by stress and anxiety6. Dysregulation of the brain-gut-axis has been proposed to play a role in physical symptoms commonly reported by individuals with anxiety such as nausea, diarrhea, and abdominal pain7.

Figure 3. The brain gut axis. Figure modified from8.

 

Typical symptoms of gastroesophageal reflux include regurgitation and pyrosis4. Lifestyle modifications listed in Figure 4 and/or a short trial of a medication such as a proton pump inhibitor as illustrated in Figure 5 are reasonable first step in the management of patients with typical symptoms9.

Figure 4. Lifestyle modifications for GERD 11

Figure 5. Pharmacological therapy of GERD10

 

Atypical symptoms of gastroesophageal reflux include chest or epigastric pain, water brash, satiety, burping or hiccups, bloating as well as nausea and/or vomiting4.

Symptoms of extra-esophageal reflux include chronic cough, asthma, sore throat, hoarseness, and sinus or pulmonary problems4.

Alarm symptoms include dysphagia, odynophagia, epigastric mass, unexplained weight loss, as well as hematemesis, anemia, or other signs of upper gastrointestinal bleeding4.

Alarm symptoms, extra-esophageal reflux symptoms, or atypical symptoms raise the possibility of other diseases such as oesophagitis, peptic stricture or ulcer, or cancer and warrant further investigations11.

 

Back to our case

 

Impression: 22 year old male with a 6 week history of constant epigastric pain exacerbated post-prandially and associated with pyrosis, nausea, and vomiting. No alarm symptoms are present.  Physical exam and investigations were normal. Patient reported recent stressors exacerbating his GAD.

 

Biological factors:

  • Anxiety and bipolar illness since early teens
  • Substance abuse

Social factors:

  • Relationship conflicts
  • Stressful home environment
  • Responsibility of caring for his son

Psychological factors:

  • Worsening anxiety due to loss of counselling services and relationship conflits.
  • Anxiety/stress due to the Covid 19 pandemic

 

Abdominal pain

Abdominal pain represents 5-10% of emergency department visits13. About 25% of patients discharged from the emergency department receive a diagnosis of unspecified abdominal pain while 35- 41% of patients admitted to hospital receive this diagnosis13. Abdominal pain can be challenging to diagnose because it has a broad differential13.  Patients with recurrent abdominal pain are not exempt from a medical emergency so that must always be ruled out; however, repeating interventions or ‘giving a diagnosis’ of medically unexplained symptoms may perpetuate ongoing distress that ‘something” is being missed12. Addressing any psychological and social factors that may be contributing or exacerbating the pain could help relieve symptoms or increase the efficacy of ongoing treatment13.

Concluding management:

  • Compassionately acknowledged that the pain he is experiencing is distressing
  • Reassured him that there is no evidence of a medical emergency
  • Explained GERD and factors that are likely exacerbating his symptoms
  • Lifestyle modifications as in Figure 4
  • Other avenues for counselling services
  • Pantoprazole twice daily
  • Return to the ER if experiencing alarm symptoms
  • Follow up with GP

 

References

  1. Farre, A., & Rapley, T. (2017). The new old (and old new) medical model: Four decades navigating the biomedical and psychosocial understandings of health and iIllness. Healthcare (Basel, Switzerland)5(4), 88. https://doi.org/3390/healthcare5040088

 

  1. Verril-Schurmanj., & Friesen, Craig, A. (2013, November 6). Inflammation and the Biopsychosocial Model in Pediatric Dyspepsia, Dyspepsia. Advances in Understanding and Management, Eldon Shaffer and Michael Curley, IntechOpen. https://doi.org/ 10.5772/56635. Retrieved July 2, 2021, from https://www.intechopen.com/books/dyspepsia-advances-in-understanding-and-management/inflammation-and-the-biopsychosocial-model-in-pediatric-dyspepsia

 

  1. Wright, C. D., Tiani, A. G., Billingsley, A. L., Steinman, S. A., Larkin, K. T., & McNeil, D. W. (2019). A framework for understanding the role of psychological processes in disease development, maintenance, and treatment: The 3P-Disease Model. Frontiers in Psychology,10, 2498. https://doi.org/10.3389/fpsyg.2019.02498

 

  1. Vakil, N., van Zanten S., V., Kahrilas, P., Dent,J., Jones, R., Vakil,N.,… Zapata, C. (2006). The Montreal definition and classification of gastroesophageal reflux disease: A global evidence-based consensus. American Journal of Gastroenteroly, 101(8),1900-1920. https://doi.org/10.1111/j.1572-0241.2006.00630.x

 

  1. Mikami, D., J, & Murayama K., M. (2015). Physiology and pathogenesis of gastroesophageal reflux disease. Surgical Clinics of North America, 95(3), 515-525. https://doi.org/10.1016/j.suc.2015.02.006

 

  1. Tack, J., & Pandolfino, J. E. (2018). Pathophysiology of Gastroesophageal Reflux Disease. Gastroenterology, 154(2), 277-288. https://doi.org/10.1053/j.gastro.2017.09.047

 

  1. Martin C., R., Osadchiy, V., Kalani, A., & Mayer, E., A. (2018). The Brain-Gut-Microbiome Axis. Cell Mol Gastroenterol Hepatol, 6(2):133-148. Doi: 10.1016/j.jcmgh.2018.04.003.

 

  1. Bajic, J., E., Johnston, I., N., Howarth, G., S., & Hutchinson, M., R. (2018) From the bottom-up: Chemotherapy and gut-brain axis dysregulation. Front. Behav. Neurosci. 12:104. doi: 10.3389/fnbeh.2018.00104

 

  1. Smith, L. (2005). Updated ACG guidelines for diagnosis and treatment of GERD. American Family Physician, 71(12), 2376-2382. Retrieved July 2, 2021, from https//www.aafp.org/afp/2005/0615/p.2376.html

 

  1. Zeid,, Y., & Confer, J. ( 2016). Standards of care for GERD.  S. Pharmacists, 41(12), 24-29. Retrieved July 2, 2021, from https:/www.uspharmacist.com/article/standards-of-care-for-gerd

 

  1. Alberta Health Services. GERD primary care pathway. April 2020. Retrieved July 2, 2021, from https://www.albertahealthservices.ca/assets/about/scn/ahs-scn-dh-pathway-gerd.pdf

 

  1. Kendall, J., L., & Moreira, M. (2020). Evaluation of the adult with abdominal pain in the emergency department. Retrieved July 2, 2021, from https://uptodate.com/contents/evaluation-of-the-adult-with-abdominal-pain-in-the-emergency-department_

 

  1. Daniels, J., Griffiths, M., & Fisher, E. (2020) Assessment and management of recurrent abdominal pain in the emergency department. Emergency Medicine Journal, 37, 515-521. https://doi.org/1136/emermed-2019-209113
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Euglycemia DKA – don’t miss it!

EM Reflections May 2021 – Euglycemia DKA

Big thanks to Dr. Paul Page for leading this month’s discussions.

All cases are imaginary but highlight important learning points.

Authored and Copyedited by: Dr. Mandy Peach

Case

A 65 yo female presents with n/v ongoing for 2 days. She feels fatigued and has not been able to keep down fluids. She denies diarrhea. She has no history of abdominal surgeries. She does describe increasing productive cough that preceded the vomitting. She denies fever, but does complain of shortness of breath.

PMH: DLP, DM, GERD
Medications: Atorvastatin, Empagliflozin, Pantoprazole

Vitals: BP 104/66 HR 110 RR 22 O2 96% RA T 37.8 gluc 7.2

On exam there is obvious dehydration, and she seems fatigued with her eyes closed through most of the exam. She does respond to speech. The abdominal exam is unremarkable for focal tenderness. There are expiratory crackles heard at the R lung base.

You order a portable CXR1 and baseline labs including a VBG and lactate.

You suspect pneumonia with dehydration. You initiate a 1L NaCL bolus and order antibiotics.

You continue seeing other patients when you get a call from the nurse – the VBG is back for the patient.
They appear to have a metabolic acidosis with a pH of 7.10 and an anion gap of 14. The lactate appears surprisingly normal. The patient hasn’t made any urine yet for a sample.

What is the differential for anion gap metabolic acidosis2?

Going through the ‘MUDPILES’ mnemonic and revisiting the history nothing seems to fit. But there is a history of DM.

What red flag should trigger you to consider DKA despite the normal glucose?

The patient is on Empagliflozin. This is a SGLT-2 inhibitor. Patient on these medications are at risk of Euglycemic DKA.

In Euglycemia DKA there is a “relative carbohydrate deficiency state with normalization of serum glucose and concomitant elevation of counter-regulatory stress hormones. This leads to free fatty acid catabolism and ketone production.” 3

In any patient on a “zin” consider euglycemic DKA.

You order a serum ketone as well as β-hydroxybutyrate.

Clinically how do patients present with euglycemic DKA3?

Nausea/vomiting, malaise, shortness of breath – the differential is huge for this presentation. Again, look at the medication list for any diabetic patient. If you see a ‘zin’ – consider euglycemic DKA.

Alternatively if you order a gas and incidentally find anion gap metabolic acidosis in a diabetic patient consider ordering ketones/ β-hydroxybutyrate.

What about if this patient was an alcoholic? How would these complicate the diagnosis4?

Alcoholics can also present quite similarly with alcoholic ketoacidosis – nausea/vomiting, malaise, and similar lab findings. Other than the history one distinguishing characteristic is that alcoholic ketoacidosis tends to have frankly low blood glucose.

Are the triggers for euglycemic DKA any different3?

No, triggers for DKA are the same. Essentially any physiological stress.

A quick way to remember is the 5 I’s

Infection pneumonia, UTI, skin, abdominal
Infarction MI, CVA, bowel infarction
Infant on board pregnancy
Indiscretion dietary nonadherence
Insulin deficient insulin pump failure or non-adherence

Infection and insulin deficient secondary to non-adherence or inappropriate dosing are the most common causes.

I would also consider adding a 6th I – iatrogenic meaning drugs

What drugs commonly trigger DKA3?
– Glucocorticoids
– Diuretics
– Atypical antipyschotics

Are there any patients at risk of euglycemic DKA other than those taking the ‘zins’3?
Yes!

  • Pregnant patients -due to high placental glucose use they can have a relative euglycemia
  • Chronic pancreatitis
  • Bariatric surgery patients – absorption issues

Your patient was straight cathed for a small amount of urine which shows ketones. The beta-hydroxybuterate is also now back and is positive. You confirm euglycemic DKA.

You grab your nearest DKA algorithm to review with the nurses and begin treatment.

Besides ease of use, what are the clinical reasons for using a standardized DKA order set?
Standardized, evidence based DKA order sets have been shown to decrease time to closure of anion gap, reduce length of hospital admission and minimize complications during treatment3.

You get started with the treatment as per the order set. While treatment is commenced you sit down with your medical student and review the goals of DKA3.

Correct fluid deficits – patients in DKA get a osmotic diuresis from hyperglycemia, or dehydration from underlying illness. You want to restore volume before initiating insulin. This improves organ perfusion, renal function and lowers lactate formation.

What fluid to use? Initially NS or RL, but after initial resuscitation consider switching to RL to avoid hyperchloric acidosis associated with large volume resuscitation.

Normal or high corrected sodium? Switch to 0.45% NaCL

1 bag vs 2 bag? Having 2 bags of half NS (one with D10W) both adjusted to maintain maintenance of 250cc/hr and keep euglycemic has been shown to have better outcomes: less hypoglycemia, faster closure of anion gap and less IV insulin required.

Replacement of potassium – patients in DKA have large total body potassium deficits, however due to volume contraction and acidosis the potassium is often read as normal or high.

Starting the insulin infusion will also shift potassium intracellularly. Therefore potassium should be replaced before starting insulin therapy. See the table below for guidance3.

Closure of the anion gap to stop ketone production – the issue with DKA is not necessarily the hyperglycemia, it is the ketoacidosis from low circulating insulin. After fluid resuscitation and potassium replacement, the goal is to treat the excess of serum ketones by providing insulin. This corrects the metabolic acidosis.

Avoiding hypoglycemia secondary to insulin as you correct the acidosis is pertinent. Goal is 12-14mmol/L. Once glucose drops before 14 add D5 infusion to avoid hypoglycemia as you continue the insulin infusion.

Do not stop the insulin infusion if glucose drops! It is needed to correct the ketoacidosis. If it is stopped ketone production will quickly increase again.

Gluc really low? Decrease the insulin infusion by 50%, give an amp of D50 and switch to D10.

Treat underlying precipitant.

 

It’s been a couple of hours. The medicine team is busy with unwell patients on the floor and you are still managing the DKA patient. You have been reassessing gases and the anion gap is not closing.

What could be going on3?
– Inadequate fluid resuscitation
– Inadequate insulin dose
– Malfunction of insulin infusion
– Underlying diagnosis contributing to anion gap hasn’t been addressed.

You reevaluate fluid status and the patient has not made any additional urine other than the small amount attained on straight cath.
You decide to repeat a 500cc bolus to address dehydration as well as increase the insulin infusion.

Could this patient be at risk of cerebral edema3?
Certainly, over-resuscitating too quickly can put patients at risk of cerebral edema. However, our patient has clinical and laboratory signs that they are still fluid deplete.

When replacing fluids consider isotonic fluids ie. D5 RL to decrease the risk.

Avoid lowering serum osmolality too quickly (ie. No more than 3mmol/kg/hr) or decreasing sodium by > 10mmol/L in 24 hours.

The sodium will often increase initially due to glucose moving intracellularly – this is not actually a measure of serum sodium – do not treat.

Admissions are backed up in the ED and you’re still caring for the patient at the end of your shift. You handover to the senior resident working with the incoming staff.

What are your goals for resolution? 3

Glucose < 11.1 AND 2 of:
– Normalization of anion gap
– Venous pH > 7.3
– Serum bicarbonate ≥15 mEq/L

At this point the patient should be mentally alert and able to eat. At this point, switch to their subcutaneous insulin dose at home. Ensure their basal insulin is also administered.

There should be an overlap of 2-4 hours before stopping the insulin infusion – if insulin infusion is abruptly stopped before administering subcutaneous insulin the patient can quickly return to an acidotic state.

What if this is the first presentation of DM and they are not on any treatment at home5?

“In patients with new-onset type 1 diabetes who have presented with DKA, an initial total daily dose (TDD) of 0.5 to 0.8 units/kg units of insulin per day is reasonable, until an optimal dose is established.

Approximately 40 to 50 percent of the TDD should be given as a basal insulin, either as once- or twice-daily U-100 glargine or detemir, or as twice-daily intermediate-acting insulin (NPH).

The long-acting insulin can be given either at bedtime or in the morning; the NPH is usually given as approximately two-thirds of the dose in the morning and one-third at bedtime. The remainder of the TDD is given as short-acting or rapid-acting insulin, divided before meals.”

The resident astutely asks about respiratory status, and if they were to decompensate what would be suggested management3?
Bottom line – avoid intubation DKA patients if possible

  • These patients hyperventilate to try and correct the acidosis, so the ventilator must also match this large volume and RR. This puts them at risk of ventilator injury and ARDS

  • Because they need to compensate with hyperventilation if there is a prolonged period of apnea from complicated intubation the acidosis can significantly worsen, putting them at high risk for circulatory collapse

But if you have to intubate, some pointers:

  • Like any patient, resuscitate first
  • If you paralyze – bag the patient throughout.
  • Consider anti-emetic
  • If the serum bicarb is < 10, considering giving an amp of bicarb
  • Once tubed the vent settings should have a high tidal volume (8cc/kg) and high respiratory rate (24-28)

How about alternative therapies if the patient is tiring, like Bipap?

DKA patients often have gastroparesis so are high risk of aspiration and emesis. Ideally, BiPap should be avoided.
If there are oxygenation issues consider high-flow nasal cannula.

The patient has resolution of their DKA within the ED and is finally admitted for treatment of the underlying cause – community acquired pneumonia.

 

References and further reading

  1. https://radiopaedia.org/cases/right-lower-lobe-consolidation-pneumonia
  2. https://www.picmonic.com/pathways/physician-assistant/courses/standard/pathology-10894/acid-base-disorders-39738/normal-gap-metabolic-acidosis_259
  3. Helman, A. Baimel, M. Sommer, L. Tillmann, B. Episode 146 – DKA Recognition and ED Management. Emergency Medicine Cases. September, 2020. https://emergencymedicinecases.com/dka-recognition-ed-management. Accessed [July 16, 2021
  4. Helman, A. Himmel W. Best Case Ever 58 Euglycemic DKA. Emergency Medicine Cases. June 2017. https://emergencymedicinecases.com/euglycemic-dka/. Assessed July 19, 2021.
  5. Hirsch I, Emmett M. 2020. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment?search=dka&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H23160691
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Cannabis Hyperemesis Syndrome – a hot topic!

Cannabis Hyperemesis Syndrome – A Medical Student Clinical Pearl

Alyssa Dickinson, Med II
Dalhousie Medicine New Brunswick, Class of 2023

Reviewed by Dr. Erin Slaunwhite

Copedited by Dr. Mandy Peach

Case presentation:

A 24yo male, Mr. X, presents to the emergency department with a 12-hour history of sudden onset vomiting. The vomiting came on without warning and was associated with epigastric abdominal pain and sweating. Mr. X took one Gravol at home but was unable to keep it down. He explains that taking a hot shower will briefly relieve his symptoms, and he has already taken four showers today. He is otherwise well, and denies recent fever/chills, chest pain, shortness of breath, or changes in bowel/bladder patterns.

Mr. X has no relevant past medical history and is not currently taking any medications. He denies drinking alcohol but states that he smokes three joints of cannabis daily, and has done so for the past 3 years. He does not use any other recreational drugs.

On physical exam, Mr. X appeared pale and was actively vomiting. All vitals were within normal limits. Cardio, resp, abdo, and neuro exams were all normal.

Cannabis Hyperemesis Syndrome:

Cannabis is the most commonly used recreational drug in the world, with the highest prevalence among those ages 18-25 years old.1,2 Although sometimes used as an anti-emetic, chronic cannabis use has been associated with paradoxical hyperemesis, which has been described as cannabis hyperemesis syndrome (CHS).3 CHS is a chronic functional gastrointestinal disorder that presents with episodic hyperemesis following prolonged cannabis use.4 Most cases of CHS present within 1-5 years of regular weekly cannabis use, although the pathophysiology remains unclear.1 Unfortunately, CHS is underrecognized and underreported, and as a result many patients experience a delay in diagnosis up to 9 years.1,2,5

The clinical course of CHS can be divided into three phases:

  • prodromal,
  • hyperemetic, and
  • recovery phase.2,5

Although similar in presentation, CHS is different then cyclic vomiting syndrome (CVS), as categorized by the Rome IV classification for functional disorders.4

Features that may help distinguish CHS from CVS include the following:
– All patients with CHS will have a history of regular weekly cannabis use, while those with CVS may or may not use cannabis products.

  • CVS may be a manifestation of migraine diathesis, and therefore is associated with a high prevalence of migraines or family history of migraines. CHS is not associated with headaches and will not respond to migraine-abortive medications.6

  • CVS patients are more likely to have psychological comorbidities including depression and anxiety.2

  • Gastric emptying rates in CVS are often accelerated, while in CHS they are more likely to be delayed.2

  • Relief with hot showers is present in 91% of patients with CHS, and only 50% of patients with CVS.1,4

With increasing prevalence of cannabis use, the incidence of CHS is likely to rise.7 It is therefore important to ask all patients with otherwise unexplained cyclic vomiting about cannabis use and compulsive bathing.5

Initial Assessment:

The differential diagnosis for CHS is broad, so it is therefore important to collect a comprehensive history and perform screening tests to rule out other potential causes.

Investigations:

Screening tests include routine blood work with a pregnancy test, if applicable. Further investigations vary based on each individual presentation.

Red flag symptoms that warrant further investigations to rule out alternate diagnoses include hematemesis, neurologic findings on exam, and abdominal tenderness.2

 

Diagnosis:

In most cases of CHS, all laboratory, radiographic, and endoscopic results will be negative.1 Diagnosis therefore is based on the following clinical criteria, retrieved from Simonetto et al (2012):

Note: CHS is a diagnosis of exclusion – all other pathologies must be ruled out.

 

Management:

The mainstay of treatment for CHS includes supportive therapy, with or without hospitalization. If volume depletion is present, immediate IV fluid resuscitation is warranted.2 The patient’s condition is expected to resolve within 12-24 hours of fluid replacement therapy.3

 

The following is the Emergency Medicine Saint John algorithm for CHS:

Notes on Symptom Management:

  • The most effective treatment for CHS symptoms is a warm bath or shower.2 This has been shown to quickly settle nausea, vomiting, and abdominal pain, although these effects do not persist. Symptom relief is temperature dependent, with hotter water producing a greater effect.3
  • Ruberto et al (2020) demonstrated superiority of IV haloperidol (one time dose of 0.05mg/kg) over ondansetron in improving symptoms of nausea, vomiting, and abdominal pain. Patients who received haloperidol also had a shorter discharge time from the ED and had fewer return visits to the ED for ongoing symptoms.
  • Traditional anti-emetic therapy such as 5-HT3 receptor antagonists or H1 receptor antagonists may used in addition to haloperidol, although most patients will have little to no response.2

 

Prevention of Recurrence:

  • Cannabis cessation is the only proven treatment for CHS.
  • Patients should be counselled on cannabis cessation, ideally from a specialized addiction team member.9 They may also benefit from outpatient treatment options including cognitive behavioural therapy and/or motivational enhancement therapy.2

 

Case Conclusion:

Mr. X was started on IV fluids to restore volume. He was also given capsaicin 0.075% topical cream and haloperidol (0.05mg/kg) for symptom management. His symptoms resolved within 4 hours and he was discharged home with a plan for outpatient follow-up to support cannabis cessation.

 

Want a deeper dive into CHS? Visit this medical student clinical pearl

References:

  1. Simonetto, D. A., Oxentenko, A. S., Herman, M. L., & Szostek, J. H. (2012, February). Cannabinoid hyperemesis: a case series of 98 patients. In Mayo Clinic Proceedings(Vol. 87, No. 2, pp. 114-119). Elsevier.
  2. Galli JA, Sawaya RA, Friedenberg FK. Cannabinoid hyperemesis syndrome. Curr Drug Abuse Rev. 2011;4(4):241-249. doi:10.2174/1874473711104040241
  3. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut. 2004;53(11):1566-1570. doi:10.1136/gut.2003.036350
  4. Venkatesan T, Levinthal DJ, Li BUK, et al. Role of chronic cannabis use: Cyclic vomiting syndrome vs cannabinoid hyperemesis syndrome. Neurogastroenterology & Motility. 2019;31(S2):e13606. doi:https://doi.org/10.1111/nmo.13606
  5. Soriano-Co M, Batke M, Cappell MS. The cannabis hyperemesis syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: a report of eight cases in the United States. Dig Dis Sci. 2010;55:3113–9.
  6. Batke, M., & Cappell, M. S. (2010). The cannabis hyperemesis syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: a report of eight cases in the United States. Digestive diseases and sciences55(11), 3113-3119.
  7. Ruberto, A. J., Sivilotti, M. L., Forrester, S., Hall, A. K., Crawford, F. M., & Day, A. G. (2020). Intravenous Haloperidol Versus Ondansetron for Cannabis Hyperemesis Syndrome (HaVOC): A Randomized, Controlled Trial. Annals of Emergency Medicine.
  8. Dezieck L, Hafez Z, Conicella A, et al. Resolution of cannabis hyperemesis syndrome with topical capsaicin in the emergency department: a case series. Clinical Toxicology. 2017;55(8):908-913. doi:10.1080/15563650.2017.1324166
  9. Pélissier F, Claudet I, Gandia-Mailly P, Benyamina A, Franchitto N. Cannabis Hyperemesis Syndrome in the Emergency Department: How Can a Specialized Addiction Team Be Useful? A Pilot Study. The Journal of Emergency Medicine. 2016;51(5):544-551. doi:10.1016/j.jemermed.2016.06.009
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Dr. David Lewis – Professor of Emergency Medicine

Dr. David Lewis – Professor

 

A huge congratulations goes out to Dr. David Lewis on his recent promotion to the rank of Professor of Emergency Medicine within Dalhousie University!

This is no small feat – candidates are examined by both internal and external reviewers in the areas of academics, teaching, collegiality and personal integrity. Those reaching the title of Professor must have demonstrated significant career development and contribution to the university in their chosen field.

It comes as no surprise that Dr. Lewis was successful – he is a foundational member of our local department and a forward-thinking leader, he is actively involved in supervision and review of national research in emergency medicine, he is revolutionizing how medical students learn ultrasound – and he does all this while maintaining a love for the field and a positive energy.

Congratulations Dr. Lewis!

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Elbow Injuries

EM Reflections April 2021 – Elbow Injuries

 

 

Thanks to Dr. Joanna Middleton for leading this month’s discussions.

All cases are imaginary but highlight important learning points.

Authored and copyedited by Dr. Mandy Peach

A 25 yo male presents to the ED with his R arm in a makeshift sling. He’s complaining of elbow pain post fall while trail running in a local park. He describes slipping downhill on some loose terrain and landing with his arm hyperextended behind him as he tried to grab a branch. He is otherwise healthy and takes no medications. His vital signs are within normal limits with the except of a HR of 102, which you attribute to pain. The nurse has placed an IV.

You begin your examination of the R elbow. You see significant swelling of the joint and some superficial abrasions. The joint does not feel warm to the touch. There is no overt bleeding.

Other than palpation for focal tenderness and assessing range of motion, what are some important tips for a focused elbow exam1?

Eliminating gravity when testing flexion/extension so pain is less likely to hinder your exam findings. To do this have the patient point their elbow at you, while the forearm is parallel to the floor and have them flex/extend in this plane2.

Remember to test for supination and pronation – this is also a key part of the elbow exam and assessing both with patient’s arms tucked into their sides can help reveal more subtle injuries. Asking the patient to point their thumbs up can make assessing ROM compared to the ‘normal’ side easier to see.

You examine your patient and they cannot fully extend the elbow, even after pain control. What is the significance of this3?

Your patient needs imaging. The ‘elbow extension test’ can help predict the likelihood of fracture. In both adult and pediatric patients presenting within 72 hours of injury, those who could not fully extend the joint had a 48% chance of fracture, while that percentage decreased to 2% if the patient could fully extend the joint.

How can supination and pronation be helpful in picking up on injury1?

Subtle injuries can be found such as radial head or neck fracture. This ROM brings the radial head out during examination.

An Essex-Lopresti fracture-dislocation is another potential injury: a fracture-dislocation injury involving the radial head (fracture) and DRUJ – distal radioulnar joint (dislocation)4. These are important to identify as they require immobilization with the patient’s limb in supination.

The patient has difficulty with supination and pronation secondary to pain. You are concerned for a radial head injury. On exam he has diffuse tenderness of the joint and you have difficulty identifying landmarks as they are lost – you are concerned about an elbow dislocation as well.

What are potential neurovascular injuries involved with such a significant elbow injury5?

Important neurovascular structures associated with the elbow joint are the brachial artery, radial artery, ulnar artery, median, radial, and ulnar nerve.

The most common injury to the elbow is radial head fractures. The mechanism is usually FOOSH or direct trauma5.

You proceed with a neurovascular exam. Radial and ulnar pulse are palpable, capillary refill is 2 seconds.

What is an easy way to remember the nerve testing for elbow injury1?

You complete your neurovascular exam and send the patient for XR’s. You suspect there will be significant injury.

You quickly review normal elbow anatomy on lateral XR with your learner on shift7.

You point out two important lines in the lateral view of the XR

  1. Anterior humeral line: A vertical running drawn on the anterior surface of humerus. This must run down to intersect middle 1/3rd of CAPITELLUM
  2. Radiocapitellar line : it runs through the central radius and passes the central capitellum on a normal image. Important: this rule applies to EACH image, so not only a purely lateral image

You also point out that that in the AP view the radiocapitellar line should also be drawn and should intersect the central capitellum.

By now your patient’s XR is up for review8.

First you notice the elbow luxation – neither your anterior humeral line or radiocapitellar line intersects the capitellum.
You also can see a radius head fracture.

What other injury should you be concerned about1?

After any proven or suspected radial head injury always look for the second injury. Here you have obvious luxation, but you should also examine the coranoid process and anterior ulna for any subtle irregularity indicating fracture. Coranoid fractures tend to be associated with elbow luxation and often indicate an unstable joint.

On history the mechanism of injury is FOOSH or hyperextension of the elbow.

The mechanism fits and your patient does have both radial head fracture and luxation. You examine the coranoid and notice that the trochlear is not completely smooth. You diagnose a coranoid fracture as well.

What is the significance of these injuries1?

This patient has the ‘terrible triad’ of the elbow.

  • Radial head/neck injury
  • Luxation of the elbow
  • Coranoid fracture

This requires orthopedic consultation immediately – it is an unstable joint. You reexamine neurovascular status again and confirm the limb is still perfused and intact before immobilization. You place the patient in a posterior long arm splint with the forearm in supination and discuss with orthopedics on call.

 

 

You pick up the next chart and there is another elbow pain. It looks like the patient was already sent for XR in triage and is now back and in the orthopedic room. This is a 16 yo female who was participating in an orienteering competition. She tripped while running on a tree root and sustained a FOOSH injury. She describes the grade being on a downward slope and felt her entire weight fall forward onto her wrist. She is otherwise healthy. Her vitals are within normal limits.

You initially examine the patient and see the following, what are the clues that this is a posterior elbow dislocation1,9?

When standing behind the patient you can see the olecranon sitting posteriorly behind the humerus.

You are palpating the elbow for tenderness – in the normal elbow the medial condyle, lateral condyle and olecranon should form a symmetrical triangle. Here they do not – this is suggestive of subluxation/dislocation of the elbow.

You assess neurovascular status and find no abnormalities.

What are the other types of dislocations? Which is most common10?

Posterior is the most common. 50% have associated fractures.

You look at the XR11:

This is a frank posterior dislocation – but, what are clues of subtle subluxations1?

“A smooth, symmetric clear space around the trochlea, similar to assessing the clear space of the ankle mortise.”

What about if your patient described a “popping sensation” during the injury and the XR appears normal1?

Sometimes patients can dislocate and  relocate before presentation to the ED. Although there is no bony injury the mechanism is associated with significant ligamentous injury and should be immobilized.

You prepare for sedation and elbow reduction. You consent the patient and the parent, perform an airway assessment and gather the team.

What are methods to reduce an elbow dislocation?

Before deciding to reduce ensure there are no vascular or neurological deficits and no open fracture/dislocation – this would require immediate orthopedic consultation10.

Your patient is neurovascularly intact and it is a closed dislocation.

Traction-Countertraction1

  1. The patient is seated sitting up
  2. Place the forearm in supination – this allows the trochlea to pass more easily over the coronoid process of the olecranon
  3. Elbow is flexed 30 degrees with an assistant immobilizing it and applying counter traction at the middle or distal end of the humerus
  4. Apply downward traction to the distal forearm

Doesn’t work? Try applying downward pressure at the mid-forearm and the olecranon posteriorly while maintaining in-line traction12

Still no luck1?

While standing at the posterior aspect of the humerus hook the fingers of both hands anterior to the condyles and put both thumbs on the olecranon at the junction with the triceps. Try and push the olecranon up over the trochlear.

Modified Simson12

  1. The patient is in a prone position with the affected arm handing over the side of the bed
  2. Slow downward force is applied on the wrist while the opposite hand attempts to guide the olecranon back into place.
  3. If a second provider is available they can manipulate the olecranon.

 

Which method works best?

I don’t think there is much evidence that one is better than the other! Traction-countertraction is the most commonly described method in the literature.

Working single coverage in a rural area with only one nurse who is doing cardiorespiratory monitoring and administering meds? The Modified Simson can be single provider. If the patient is compliant and not sedated then they can provide counter traction while holding the flexed elbow over the chest12.

 

Another option when you’re flying solo is the Leverage Technique12
1. Gently supinate the patients forearm
2. Interlock your fingers with the patients
3. Place your elbow against the distal potion of the patient’s biceps
4. Slowly draw the patient’s wrist into flexion while using your own elbow as a fulcrum.
5. Use your other hand to apply lateral or medial force as needed

One small study found this technique to be superior to traction-countertraction.

At the end of the day, elbow reductions can be tricky. Having more than one technique in your back pocket can be helpful.

 

You and your learner choose the traction-countertraction method and “clunk” – so satisfying.

How do you immobilize now1?

Immobilize at 90 degress of flexion with a padded backslab.

You arrange for ortho follow up – as this was a simple dislocation with no fracture you ensure the appointment is within 3 weeks as this is the maximal period the joint should be immobilized.

For complicated dislocations associated with fracture – ortho should see within 72 hours as they require ORIF.

The patient has recovered from sedation and is asking what to expect in terms of prognosis for this dislocation1.

In simple dislocations that are reduced and immobilized you advise the patient that they will be unable to extend beyond 30 degrees for 6 weeks, and that it may take up to 3 months before full extension is regained. Given that this is an athletic patient you advise her not to return to weight bearing exercises before 4 months unless directed safe by ortho in follow up.

 

 

You grab one last chart with your learner – surprise! It’s a 50 yo male with an elbow injury. He tripped while doing sprints as part of a work out and fell with arm fully extended in front of him. He is otherwise healthy and his vital signs are within normal limits.

On initial examination there is no obviously deformity. The limb is neurovascularly intact.

You palpate the elbow and there is tenderness over the radial head.

You ask the learner to palpate the radial head, they are unsure where. How do you help guide them1?

You describe the triangle between:
– The lateral aspect of the olecranon
– The lateral condyle (anterior to olecranon)
– Radial head

You also suggest examination in supination and pronation as this can bring out the radial head.

You remember your previous case of the terrible triad and go on to examine the coronoid – there is no concern of injury and the elbow doesn’t grossly appear dislocated.

You order XRs – what are some findings associated with radial head injury1?

  • Disruption of the surface of the radial head
  • Anterior sail sign
  • Posterior fat pad
  • Disruption of the radiocapitellar line

Your patient’s lateral XR13

You see both anterior sail sign and a posterior fat pad, so although no obvious fracture is seen of the radial head you diagnose a radial head fracture.

How long does this patient need to be immobilized for1?

Most fractures are not surgical. They are treated with a sling. Do not immobilize for more than 3 weeks or chronic elbow stiffness can ensue.

What if there was a visible fracture through the radius? How do you know which fractures will require ORIF and more urgent ortho evaluation1?

The 30-3-33 rule

30 degrees angulation
3 mm displacement of the fracture fragment
33% surface area of the radial head involved

References for further reading:

  1. Helman, A. Sayal, A. Dantzer, D. Ten Pitfalls in the Diagnosis and Management of Elbow Injuries. Emergency Medicine Cases. March, 2019. https://emergencymedicinecases.com/elbow-injuries. Accessed [date]
  2. https://www.hep2go.com/exercise_editor.php?exId=36147&userRef=gciaake
  3. Appelboam A, Reuben A D, Benger J R, Beech F, Dutson J, Haig S et al. Elbow extension test to rule out elbow fracture: multicentre, prospective validation and observational study of diagnostic accuracy in adults and children BMJ 2008; 337 :a2428 doi:10.1136/bmj.a2428
  4. https://www.startradiology.com/internships/orthopedics/elbow/x-elbow/index.html
  5. (2) Tintinalli, JE, Stapczynski JS, Ma OJ, Yealy D, Meckler GD, Cline DM. 9th ed. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill.
  6. Cornelis, A (2017). Elb-‘ow’! Does my patient with an elbow injury require an x-ray? Resident Clinical Pearl. Emergency Medicine, Saint John. https://sjrhem.ca/rcp-elb-ow-patient-elbow-injury-require-x-ray/
  7. https://www.startradiology.com/internships/orthopedics/elbow/x-elbow/index.html
  8. https://www.orthobullets.com/trauma/1021/terrible-triad-injury-of-elbow
  9. https://litfl.com/elbow-dislocation/
  10. Paris (2016). Elbow Dislocation. Core EM. https://coreem.net/core/elbow-dislocation/
  11. Oppenheim, Osborn (2016). Posterior Elbow Dislocation. Journal of Education & Teaching of Emergency Medicine. DOI: https://doi.org/10.21980/J8X593
  12. Michael Gottlieb, Jessen Schiebout (2018). Elbow Dislocations in the Emergency Department: A Review of Reduction Techniques. The Journal of Emergency Medicine. Volume 54, Issue 6; Pages 849-854. ISSN 0736-4679 https://doi.org/10.1016/j.jemermed.2018.02.011.
  13. https://radiopaedia.org/articles/sail-sign-elbow-1

 

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A Case of Herpes Simplex Virus Keratitis in The Emergency Department

A Case of Herpes Simplex Virus Keratitis in The Emergency Department – A Medical Student Clinical Pearl

Patrick Gallagher, MED III

MUN Class of 2022

Reviewed by Dr. Robin Clouston

Copyedited by Dr. Mandy Peach

Case

A 53-year-old female presents to the emergency department with a two-day history of left-eye pain, which she describes as “something being stuck in her eye.” The patient endorses left eye tearing, pruritis, and photophobia. She notes that her eye has been “blurry” since she awoke this morning. The patient denies any infectious symptoms at present but states that a cold sore erupted on her upper lip seven days ago. She does not use contact lenses.

Past medical history: T2DM and hypothyroidism.

Past surgical history: None.

Medications: Metformin 500 mg OD and Synthroid 125 mcg OD.

Physical exam:

Upon inspection, the patient has conjunctival injection and tearing in the left eye. Mild periorbital edema and erythema is noted. The patient’s pupils are equal and reactive to light, and visual acuity is 20/20 in the left eye and 20/40 on the left eye. Extraocular eye movements and visual fields are normal. The patient has decreased corneal sensation.

On slit lamp examination using fluorescein-based dye, a small branching dendritic ulcer was seen (Figure 1).

Figure 1: Dendritic ulcer noted on slit-lamp exam with fluorescein-based dye.

 

What is the differential diagnosis of dendrites?

• Herpes simplex keratitis
• Acanthamoeba keratitis
• Other keratitis caused by Varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein–Barr virus (EBV), or adenovirus.
• Dendritiform keratopathy
• Ramous epithelial changes
• Limbal stem cell deficiency
• Drug induced corneal changes (epinephrine, antivirals, beta-blockers) 1,2

Herpes simplex virus keratitis :

Herpes simplex is a DNA virus that can cause a wide variety of infections, most commonly involving the mouth, genitalia, and eyes3. While HSV-1 and HSV-2 can involve the eye, HSV-1 is the most common cause of keratitis1. Herpes simplex keratitis (HSK) is characterized by recurrent infections of the corneal epithelium and stroma2. HSK can be classified as primary or recurrent and further divided into three subtypes: epithelial, stromal, and endothelial3. Epithelial keratitis is the most commons subtype of ocular herpes (50% to 80%)2.

Herpes simplex virus (HSV) infections are the leading cause of infectious corneal blindness in developed countries3. It is estimated that 1.5 million people worldwide experience HSV keratitis every year2.

Pathophysiology:

Primary HSV eye infections occur when the virus enters mucous membranes by direct contact. This initial infection is usually subclinical, but it can cause unilateral blepharitis, follicular conjunctivitis, and occasional epithelial keratitis (Figure 2)4. The initial infection is typically asymptomatic, and it occurs in children less than five years old5.

Figure 2: Pictorial representation of blepharitis (inflammation of the eyelid), keratitis (inflammation of cornea), conjunctivitis (inflammation of conjunctiva), and ocular anatomy. Diagram retrieved from 7

After the initial infection, the virus can remain latent in the ophthalmic division of the trigeminal ganglion for the lifetime of the host. HSV reactivation in the latently infected ganglia can lead to corneal scarring, thinning, stromal opacity, and neovascularization5. The cumulative effect of numerous infections results in vision loss and eventually blindness if left untreated.

History and physical:

Diagnosis of HSK is primarily diagnosed by clinical presentation on slit lamp exam using fluorescein and either rose bengal or lissamine green3. However, it is crucial to complete a thorough history and physical exam to narrow the differential diagnosis (Table 1).

Table 1: Key points on history and physical

Figure 3: Slit-lamp corneal findings for patient’s diagnosed with HSV epithelial keratitis. A: Classic dendritic lesion with terminal bulbs. B: More advanced dendritic lesion presenting as geographic ulcer. Figure modified from 6.

Investigations:

The diagnosis of HSVK is based off of clinical findings and does not require additional investigations; however, for atypical lesions, polymerase chain reaction has been used to confirm HSVK. Enzyme-linked immunosorbent assay and viral cultures are also effective in the diagnosis of the HSVK subgroups3.

Treatment/management of HSVK in the emergency department:

In the emergency department, typical findings on the slit lamp exam is diagnostic for epithelial HSVK.

Care providers should initiate treatment immediately to reduce the risk of complications; however, the patient must be referred to ophthalmology within the next few days for follow-up.

Topical and oral antiviral treatments effectively treat epithelial HSVK, although no topical ophthalmic antivirals are currently available in Canada7. It is crucial to adjust the dose of oral antivirals according to the patient’s renal function. See Table 2 for available oral antiviral treatments. For symptomatic management, artificial tears or eye lubricants can ease eye discomfort and over-the-counter analgesics can help relieve pain7.

Table 2: Oral antiviral treatment for epithelial HSVK in adults. Modified from 7

Back to the case:

Given our patient’s classic symptoms of epithelial HSVK (conjunctival injection, tearing, vision changes, foreign body sensation, photophobia, hx of HSV infection) and finding of dendritic ulcers on slit lamp examination, we treated this case as epithelial HSVK until proven otherwise. Therefore, we prescribed the patient valacyclovir 1000mg PO TID and arranged an urgent ophthalmology consult for the following day.

References:

  1. Roozbahani, M., & Hammersmith, K. M. (2018). Management of herpes simplex virus epithelial keratitis. Current opinion in ophthalmology, 29(4): 360-364.

  2. Wilhelmus, K. R. (2015). Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database of Systematic Reviews, 1.

  3. Azher, T. N., Yin, X. T., Tajfirouz, D., Huang, A. J., & Stuart, P. M. (2017). Herpes simplex keratitis: challenges in diagnosis and clinical management. Clinical Ophthalmology, 11:185–191.

  4. Sibley, D., & Larkin, D. F. (2020). Update on Herpes simplex keratitis management. Eye, 34: 2219–2226.

  5. Toma, H. S., Murina, A.T., Areaux, R.G., Neumann, D.M., & Bhattacharjee, P.S. (2008). Ocular HSV-1 Latency, Reactivation and Recurrent Disease. Seminars in Ophthalmology, 23(4), 249–273.
  6. Leon, S., & Pizzimenti, J. (2017). Be a Hero to Your HSVK Patients. Review of Optometry-Leadership in clinical care. Retrieved from https://www.reviewofoptometry.com/article/ro0717-be-a-hero-to-your-hsvk-patients2
  7. Institut national d’excellence en santé et en services sociaux. (2018). Herpes Simplex Eye Disease. INESSS Guides. Retrieved from https://www.inesss.qc.ca/fileadmin/doc/INESSS/Outils/GUO/Herpes/Guide_HerpesSimplex_web_EN_VF.pdf

 

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