Posted on July 20, 2022 by Mandy Peach

A Case of Abdominal Pain in the Elderly – EM Reflections March 2022

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

An 82 yo male presents to the ED via EMS with 1 day of abdominal pain that started in the late evening. He describes feeling well all day, eating a healthy size dinner and then having sudden onset abdominal pain and distension just before bedtime. He can’t describe or localize the pain but states it is a ‘hard pain’ and has been associated with 2 episodes of nausea/vomiting. He doesn’t think he has had a fever. He is unsure of his last bowel movement and complains of frequent constipation. When asked about urinary changes he describes what sounds like a long-standing history of issues with urinary hesitance. He is unsure if there has been any acute change. He thinks there is no history of abdominal surgeries but “he’s been around a long time”. He is a lifelong non smoker.

PMH: DLP, HTN

Meds: Atorvastatin, Ramipril

Vitals: BP 110/60 HR 102 RR 18 O2 97% RA T – 36.5

On exam he appears in mild discomfort, with his eyes closed. His abdomen is mildly distended. He has generalized tenderness throughout the abdomen, no guarding or peritonitis. The testicles and inguinal region appear normal.

What are some barriers to assessing abdominal pain, or any presentation, in the geriatric patient?^1,2

History may be difficult to intrepret, sometimes with vague symptoms
History may be difficult to obtain due to physical deficits like hearing loss
Vitals are not reliable – most patients are on beta blockers so their heart rate may not be elevated, and ‘normal’ blood pressure may actually be hypotensive for a geriatric patient who will often run much higher at baseline.
Blunted immune response – they may not illicit the typical fever or elevated WBC that we often count on to lead us to infectious/septic processes.
Decreased abdominal wall muscles lead to less guarding or rebound on exam – * peritoneal signs are often absent
Shrinkage of omentum leads to decreased containment of intraabdominal process
Higher rate of perforation and ischemic gut due to chronic issues like atheroscleoris and low flow states

He doesn’t look to be terribly unwell, you plan to treat his pain and nausea and order some labs.

What would be the drug of choice for abdominal pain in the elderly²?

Hydromorphone as it is not renally excreted.

You are ordering your labs – CBC, Cr, electrolytes, LFT’s, bilirubin, lipase and a urinanalysis.

Should you order a VBG and lactate in this man with ‘normal’ vitals and a non-specific abdominal exam²?

If the patient is presenting with pain out of proportion (ie. Ischemia symptoms) these tests are a must. But consider in any patient with risk factors for cardiovascular disease or atrial fibrillation. Our patient has a history of dyslipidemia and hypertension – you order the additional tests and ECG.

Elderly patients have vague abdominal pain all the time – what percentage are actually surgical?

Up to 60% of cases are surgical.

The associated mortality rate of those requiring abdominal surgery is upwards of 7x greater than younger patients with similar presentations.

What are the main causes of surgical abdominal pain the elderly^1,2?

Cholecystitis – consider when working up a septic patient with no obvious source
Appendicitis
Bowel Obstruction – femoral hernia is a commonly missed cause
Hernia

Your patient had already been sent for an abdominal series after they were triaged. Certainly with the history of abdominal pain with n/v obstruction is high on the differential, even in a native abdomen.

What are useful findings on abdominal series^3,4?

You are looking for the following:

Pneumoperitoneum (but really, you should be getting a CT if this is a concern)
Air fluid levels seen in obstruction

Certainly, in a busy department XR is quick, cheap and has minimal radiation. In patients with repeated SBO an XR may be suffice. Findings for SBO on XR include:

Dilated bowel with air fluid levels
Proximal bowel is dilated, but distal bowel is not
Gasless abdomen – where there is a large amount of fluid within the bowel loops, which may underestimate the level of obstruction. There may be a ‘string of pearls’ sign in upright films where small amount of air is seen between valvulae conniventes.

The sensitivity, specificity, and accuracy are 79-83%, 67-83%, and 64-82%, respectively³ – not enough to rely on when the mortality rate is so high in this population. A normal abdominal series does not rule out any serious pathology.

Certainly CT would be the gold standard – it would give the site, severity and etiology of obstruction. Complications such as necrosis, ischemia and perforation would be identified as well as other causes for abdominal pain on your differential. In elderly patients in particular, it has been shown to be more high yield for clinical decision making².

But a CT takes time in an overcapacity and understaffed ED. While you wait for it to be completed you grab for your ultrasound probe – specifically you are looking for signs of SBO as that is top of your differential.

What is the accuracy of PoCUS for SBO⁵?

Sensitivity 88%, specificity 96%

What is an approach to a SBO scan with PoCUS?

Using your curvilinear probe ‘Mow the lawn’ starting in the RLQ and cover the entire abdomen using graded compression. Take your time⁶.

What are the findings^5,7?

Dilated bowel loops >2.5cm
Thickened bowel wall >3mm
‘To and fro’ peristalsis
Tanga sign – triangular shaped areas of free fluid between bowel loops. Concerning for high grade obstruction

You do confirm all signs of SBO, including tanga sign which is concerning.

By now your patient is over in the scanner when you get some lab results back – although the WBC is at the upper end of normal the lactate is significantly elevated.

While the patient is in CT waiting for a porter to come back you get a call from the radiologist confirming closed loop bowel obstruction with signs of ischemia and necrosis.

Bottom line – have a low threshold to order CT in geriatric abdominal pain. They are high risk patients, with high mortality rates.

References and further reading

Thomas, A (2018). Approach to the Geriatric Patient. CRACKCast E181. CanadiEM. Retrieved July 19, 2022 from https://canadiem.org/crackcast-e181-approach-to-the-geriatric-patient/
Melady, D, Lee, J, Helman, A. Geriatric Emergency Medicine. Emergency Medicine Cases. July, 2013. https://emergencymedicinecases.com/episode-34-geriatric-emergency-medicine/. Accessed July 19, 2022
Bordeianou, L & Yeh, D. (2021) Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults. Uptodate. Accessed July 2019 from https://www.uptodate.com/contents/etiologies-clinical-manifestations-and-diagnosis-of-mechanical-small-bowel-obstruction-in-adults?search=bowel%20obstruction%20adult&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H2918585369
Jones, J., Ramsey, MD, A. Small bowel obstruction. Reference article, Radiopaedia.org. (accessed on 19 Jul 2022) https://doi.org/10.53347/rID-6158
Atkinson P, Bowra J, Lewis D. (2019). Point of Care Ultrasound for Emergency Medicine and Resuscitation.
Tooma, D & Dinh, V. Abdominal Ultrasound Made Easy: Step by Step Guide. Small Bowel Obstruction. POCUS 101. Accessed July 19, 2022 from https://www.pocus101.com/abdominal-ultrasound-made-easy-step-by-step-guide/#Small_Bowel_Obstruction_Ultrasound
Small Bowel Obstruction. PoCUS Atlas. Accessed July 19, 2022 from https://www.thepocusatlas.com/gastrointestinal

A Biopsychosocial Approach to Epigastric Pain

Posted on August 8, 2021 by Mandy Peach

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 GERD¹¹

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

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

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

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

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

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

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

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.

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

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

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

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

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_

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

A case of cholecystitis

Posted on January 7, 2021 by Mandy Peach

Medical Student Clinical Pearl

Alana Jewell

M.D. Candidate, Class of 2022

Memorial University Faculty of Medicine

Reviewed & Edited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

Case Presentation

A 70-year-old gentleman presented with four days of right upper abdominal pain radiating to the LUQ with nausea + vomiting, anorexia, flatulence, and bloating. Patient has PMHx of Crohn’s disease with a history of small bowel obstruction (SBO) and multiple surgeries. He felt these symptoms were like his SBO but he continued to have normal bowel movements. He had a similar episode a few months ago after eating fast food, but did not seek care for.

You suspect cholecystitis.

Differential Diagnosis

Can’t miss diagnoses for atraumatic abdominal pain ⁴:

ruptured AAA

pancreatitis

cholangitis

mesenteric ischemia

obstruction

perforated viscus

complicated diverticulitis

ruptured ectopic pregnancy

Differential for RUQ pain ⁴:

hepatitis

biliary colic

cholecystitis

cholangitis

pancreatitis

pneumonia

pleural effusion

pulmonary embolism

There is no single exam finding or laboratory test that has the ability to rule out acute cholecystitis⁵.

A combination of clinical evaluation, laboratory values, and diagnostic imaging are key to differentiate abdominal pain and make a diagnosis.

Cholecystitis

Cholecystitis is defined as inflammation of the gallbladder, typically caused by persistent stone obstruction in the cystic duct.

Acute cholecystitis (AC): Stone obstruction leads to bile trapping, increased intraluminal pressure, and an acute inflammatory process, typically presenting with RUQ pain, leukocytosis, and fever¹.

Chronic cholecystitis: defined as recurrence of these events and is associated with fibrosis and mucosal atrophy².

Acalculous cholecystitis: consider in chronically debilitated patients, classically elderly patients in ICU on total parental nutrition after sustained trauma or significant burn injury¹¹.

Ascending (or acute) cholangitis: an important complication of cholecystitis – a serious bacterial infection of the common bile duct. It presents with Charcot’s triad of fever, jaundice, and abdominal pain².

Acute cholecystitis is diagnosed and graded on severity by using the Tokyo Guidelines³.

Gallstones (which cause 95% of acute cholecystitis) are common in Western society, with about 10% of people affected, and 80% of those affected being asymptomatic^1,3. The risk of pain or complications is 1-4% per year².

Risk factors for cholesterol gallstones (the most common type) ²:

increased age

female gender

pregnancy

parity

race

high calorie

low fibre diet

low activity

obesity

Clinical Presentation and findings

Clinical presentation varies with severity.

On history, a patient may have anorexia, emesis, fever, nausea, and RUQ pain. On examination, guarding, Murphy’s sign (pain upon deep inspiration while palpating RUQ), rebound tenderness, abdominal rigidity, and RUQ tenderness may be seen². Patients may describe a history of biliary colic, but with the presenting episode being more severe and longer in duration.

Mild-moderate cases have RUQ pain, fever, leukocytosis, and may have a palpable mass in the RUQ². The most severe patients may have jaundice and, if have a secondary bacterial infection, could have signs of sepsis.

Case Continued

Physical Exam

Patient was tender to light palpation over RUQ and epigastric region. No rigidity, rebound tenderness, or guarding was noted.

Bloodwork

Elevated WBC with neutrophilic shift
C reactive protein > 250
Normal lipase, liver enzymes and renal function.

The most common laboratory findings in acute cholecystitis are an increased CRP and leukocytosis².

This patient requires imaging to confirm the suspected diagnosis.

Diagnostic Imaging

Ultrasound

Ultrasound is the first-choice modality for imaging of AC. It is easily available in any emergency department, cost-effective, and minimally invasive³. Ultrasound findings can include^5,6,9, as seen below^6.

GB wall thickening > 3.5 mm

pericholecystic fluid

biliary sludge

gallstones

sonographic Murphy sign

If an ultrasound is positive, there is no need for further testing.

If negative, a CT should be ordered to exclude other diagnoses^2,7.

CT findings for AC may include ^3,6as seen below²:

thickening of GB wall

enlargement of GB

gallstones in GB neck or cystic duct

fluid accumulation around GB

pericholecystic fat stranding

Many gallstones are not radiopaque and may be missed on CT⁷.

Management

Assessment with Tokyo Guideline diagnostic criteria can be used every 6-12 hours until a diagnosis is clear if initially uncertain, and to check severity until surgical management⁸.

In the Emergency Department, a patient is best managed with supportive care.

IV fluids,

NPO

Analgesia (NSAIDs are first-line treatment for AC. If ineffective, opioids are second line². )

Secondary infection can result from bile stasis. Empiric antibiotics may be started against E. coli, Klebsiella, and Enterococcus⁵.

Definitive treatment for AC is cholecystectomy, with the gold standard being done laparoscopically (lap-C)^2,7. Having a lap-C within 24-72 hours of symptom onset is recommended to decrease complication rates. If left unoperated for more than 72 hours chronic inflammation may occur, potentially complicating the surgery¹. If a patient is ineligible for surgery, percutaneous cholecystostomy (gallbladder drainage) may be performed⁷.

Case Conclusion

Formal ultrasound found a hydropic gallbladder with pericholecystic fluid, thickened wall, and stranding. Cholecystitis was diagnosed. The patient was given analgesia and covered with ceftriaxone and metronidazole^10.He went on to have an uncomplicated lap cholecystectomy.

References

Indar, Adrian A, and Beckingham, Ian J. “Acute Cholecystitis.” BMJ, vol. 325, no. 7365, 2002, pp. 639–643.
Wilkins, Thad, MD, MBA, et al. “Gallbladder Dysfunction: Cholecystitis, Choledocholithiasis, Cholangitis, and Biliary Dyskinesia.” Primary Care, vol. 44, no. 4, 2017, pp. 575–597.
Yokoe, Masamichi, et al. “Tokyo Guidelines 2018: Diagnostic Criteria and Severity Grading of Acute Cholecystitis (with Videos).” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 41–54.
Anjum, Omar, et al. “Ottawa’s Clerkship Guide to Emergency Medicine.” Department of Emergency Medicine, University of Ottawa, Mar. 2018.
Jain, Ashika, et al. “History, Physical Examination, Laboratory Testing, and Emergency Department Ultrasonography for the Diagnosis of Acute Cholecystitis.” Academic Emergency Medicine, vol. 24, no. 3, 2017, pp. 281–297.
Chawla, Ashish, et al. “Imaging of Acute Cholecystitis and Cholecystitis-Associated Complications in the Emergency Setting.” Singapore Medical Journal, vol. 56, no. 8, 2015, pp. 438–444.
Bagla, Prabhava, et al. “Management of Acute Cholecystitis.” Current Opinion in Infectious Diseases, vol. 29, no. 5, 2016, pp. 508–513.
Mayumi, Toshihiko, et al. “Tokyo Guidelines 2018: Management Bundles for Acute Cholangitis and Cholecystitis.” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 96–100.
Flemming, Lewis & Henneberry (2017). PoCUS – Measurements and Quick Reference https://sjrhem.ca/pocus-measurements-quick-reference/
Bugs & Drugs Medical App
Forsythe (2016). Cholecystitis. First Aid for the Emergency Medicine Boards, Third Edition: Abdominal and Gastrointestinal Emergencies. McGraw-Hill Education. China.

Abdominal ACNES: anterior cutaneous nerve entrapment syndrome and trigger point injections in the ED

Posted on April 11, 2019 by David Lewis

Abdominal ACNES: anterior cutaneous nerve entrapment syndrome and trigger point injections in the ED

Resident Clinical Pearl (RCP) March 2019

Devon Webster – PGY1 FMEM Dalhousie University, Saint John NB

Reviewed and edited by Renee Amiro and Dr. David Lewis.

Notice to patients: This article is written for healthcare professionals. We do not offer elective treatment for ACNES in this department.

Case:

A 32 year old woman with a history of chronic abdominal pain has been sitting in RAZ, presenting with, predictably, lower abdominal pain. She has been investigated multiple times over, with comprehensive labs, ultrasounds, pelvic exams and a previous CT, all of which have been normal. She carries with her a myriad of diagnoses; chronic abdominal and pelvic pain, IBS, fibromyalgia, depression and anxiety.

On history she reports near constant, left lower quadrant pain over the past 4 months. It is worse when sitting up and lying on her left side. The pain is sharp and she is able to localize the pain with a single fingertip. On history, you elicit no red flags for an intra-abdominal source of her pain. You ask her to lay down on the examination bed and hold your finger over the area of maximal pain. You feel no mass or abdominal wall defects. You apply light pressure, which triggers the pain, and ask her to lift her legs up. She yelps in pain, noting significant worsening to the site after tensing her abdominal muscles.

While you think of your differential for abdominal wall pain, you are highly suspicious of anterior cutaneous nerve entrapment syndrome (ACNES)…

What is ACNES?

Anterior cutaneous nerve entrapment syndrome (ACNES) is one of the most frequent causes of chronic abdominal wall pain and often goes undiagnosed. It is caused by entrapment of the anterior cutaneous abdominal nerves as they pass through the fibrous abdominal fascia.
This common condition can be treated rapidly and effectively by local trigger point injection of lidocaine and long acting steroid in the emergency department.

Pathophysiology:

The cutaneous branches of the sensory nerves arising from T7-T12 must make two 90* turns, traversing through channels within the abdominal fascia at the linea semilunaris (lateral border of the rectus muscles) in order to innervate the cutaneous surface of the abdomen.
While the neurovascular bundle should be protected from impingement by fat, it is susceptible to entrapment due to the tight passageway through the fibrous channels and sharp angulation.

Risk factors:

There are multiple risk factors for entrapment, and subsequent pain: tight clothing or belts, intra or extra-abdominal pressure, scarring and obesity. Pregnant women and those taking OCPs may also be at higher risk.
4x more common in women, particularly those between ages 30-50 years of age.

Clinical features on history:

Patients may describe chronic abdominal pain with maximal tenderness over a small area of the abdomen, typically <2cm
Pain is typically at the lateral edge of the rectus abdominis muscles and has a predilection for the right side although, the pain may be anywhere over the abdomen and may be in multiple locations.
Pain tends to be sharp in nature, positional and aggravated by activities that tense the abdominal muscles. Pain is generally better supine and worse when sitting or lying on the side.
There should be no red flags associated with the history suggestive of a more nefarious source of pain (e.g. GI bleeding, change in bowel function).

Physical exam:

Use a Q-tip to apply pressure as you move along the abdomen and try to locate the area of maximal tenderness. In most ACNES patients, you will find an area of allodynia or hyperalgesia corresponding to the area of nerve entrapment.
Look for a positive Carnett’s sign:
- Ask the patient to either lift the head and shoulders or alternatively, lift their legs off of the bed while lying flat while you apply pressure over the area of pain on the abdomen.
- Tightening of the rectus muscles should protect intra-abdominal pathology and pain will be reduced. In the case of abdominal wall pathology, including ACNES, pain will remain the same or be increased.

Understanding extra vs intra-abdominal pain:
- There are 2 types of pain receptors: A-delta and C fibers.
  - A-delta: These fibers mediate sharp, sudden pain and innervate skin and muscles. Patient’s can localize this pain with a fingertip and this corresponds well with extra-abdominal wall pain, such as in ACNES
  - C fibers: Mediate dull ‘visceral’ pain that is often difficult to localize and results in pain over larger areas of the abdomen. These fibers innervate the viscera and parietal peritoneum.

Approach and Differential Diagnosis for Abdominal Wall Pain:

Look for ‘red flags’ (e.g. GI bleeding, abnormal labs, malnourished appearance) and rule out intra-abdominal sources of pain.
Once this has been ruled out, consider your differential for extra-abdominal wall pain which may include the following…

Diagnosis:

ACNES can be diagnosed on the basis of 3 criteria:

1) Well localized abdominal pain

2) Positive Carnett’s sign

3) Response to trigger point injection of local anesthetic and steroid

Treatment

Trigger point injections:
- Act as both a source of treatment and diagnosis.
- Provides immediate relief of symptoms to 83-91% of patients.
- Injections can be repeated q-monthly.
- Works through immediate anesthetization of the nerve, steroidal thinning of surrounding connective tissue and hydrodissection.
If the pain returns after trigger point injections, after considering other diagnoses, patient’s can be referred for chemical neurolysis (alcohol injections) or in some instances, surgical neurectomy.
Conservative treatment may include activity modification (e.g. avoid stomach crunches) and physical therapy

Technique for trigger point injections:

Mark the site of maximal tenderness
Inject 1-3 mL of 1% lidocaine and 1 mL of a long acting steroid using a 1.5 inch 26 gauge needle. Insert the needle until the tender area is reached (pt will let you know)
Pain should resolve within 5 minutes.

US guidance may be useful for increasing the precision of the injection and can be used to visualize the passage of the nerve through the abdominal fascia.

Video guided review of ACNES:

https://www.youtube.com/watch?v=bDyX3myA0Gw&t=163s

References:

Meyer, G, et al. “Anterior cutaneous nerve entrapment syndrome.” Uptodate. Accessed March 8, 2019. URL: https://www.uptodate.com/contents/anterior-cutaneous-nerve-entrapment-syndrome
Suleiman, S, Johnston, D. “The Abdominal Wall: An Overlooked Source of Pain” American Family Physician. August 2001.
Kanakarajan, S., et al. “Chronic Abdominal Wall Pain and Ultrasound-Guided Abdominal Cutaneous Nerve Infiltration: A Case Series.” Pain Medicine, volume 12, Issue 3, 1 March 2011, Pages 382-386.

EM Reflections – April 2018

Posted on April 15, 2018 by David Lewis

Thanks to Dr. Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis

Top tips from this month’s rounds:

Ondansetron (Zofran) and QTi

Globe Rupture

Ovarian Torsion

Ondansetron (Zofran) and QTi

Ondansetron prolongs QTi in a dose-dependent manner
Patient is most at risk for an arrhythmia when peak serum levels are reached
- Largest difference in QTi was found at 15 minutes (IV), but has seen to persist up to 120 min in heart failure patients.

Arrhythmia after a single dose is EXCEEDINGLY RARE
- No reports of arrhythmia after a single dose of oral ondansetron.
- Consider ECG monitoring (or use another anti-emetic agent) in patients who are receiving IV ondansetron with other arrhythmogenic factors such as QTi prolonging agents or electrolyte abnormalities

Ondansetron and QTc Prolongation: Clinical Significance in the ED

Globe Rupture

When should you suspect?
- Mechanism – severe blunt, penetrating, metal-on-metal
Signs of open globe include:
- penetrating lid injury,
- bullous subconjunctival hemorrhage
- shallow anterior chamber
- blood in the anterior chamber (hyphema),
- peaked pupil
- iris disinsertion (iridodialysis)
- lens dislocation, and
- vitreous hemorrhage. Loss of red reflex can indicate vitreous hemorrhage or retinal detachment.

The EyeRounds.org website has some useful tutorials.

Management

Stop Examination
NO PATCH – Use Eyes Shield
Consult Ophthalmology immediately
NPO, Tetanus, IV Antibiotics, analgesia and antiemetics

Download (PDF, 181KB)

Ovarian Torsion

Uptodate: “It is one of the most common gynecologic emergencies and may affect females of all ages”
Most common ages 20-50 years
Acute onset pain with adnexal mass
As size of mass increases, risk of torsion increases
- #1 RF is ovarian mass >5 cm
- benign > malignant
Increased risk during pregnancy, fertility treatments

U/S test of choice, although normal doppler does not rule out torsion
CT not diagnostic, although if you had a CT that didn’t show an ovarian mass of >5cm, unlikely it was torsion…
86-95% of patients with torsion have a mass (exception – pediatric population – more likely to have torsion with normal ovaries)
Pediatric patients – early surgical detorsion more likely to be successful
>36 hours – non-viable

A useful recent review can be viewed here

CoreEM provides another useful summary (as well as a huge amount of other EM Topics)

EM Reflections – September 2017

Posted on September 7, 2017 by David Lewis

Thanks to Dr Paul Page for leading the discussion

Edited by Dr David Lewis

Top tips from this month’s rounds:

Non-specific Abdo pain – Appendicitis is always high on the differential
Intoxicated patients are at high risk for Head Injury
Acute Heart Failure has a higher mortality than acute NSTEMI
Enhancing Morbidity and Mortality Rounds Quality

Non-specific Abdo pain – Appendicitis is always high on the differential

Does a normal white count exclude appendicitis? – No – Clinicians should be wary of reliance on either elevated temperature or total WBC count as an indicator of the presence of appendicitis. The ROC curve suggests there is no value of total WBC count or temperature that has sufficient sensitivity and specificity to be of clinical value in the diagnosis of appendicitis. Acad Emerg Med. 2004 Oct;11(10):1021-7.Clinical value of the total white blood cell count and temperature in the evaluation of patients with suspected appendicitis.

Does a normal CRP exclude appendicitis? – No – Acad Emerg Med. 2015 Sep;22(9):1015-24. doi: 10.1111/acem.12746. Epub 2015 Aug 20. Accuracy of White Blood Cell Count and C-reactive Protein Levels Related to Duration of Symptoms in Patients Suspected of Acute Appendicitis.

A useful review on the diagnosis of appendicitis – JAMA. 2007 Jul 25; 298(4): 438–451. Does This Child Have Appendicitis?

Summary of Accuracy of Symptoms

Download (PDF, 124KB)

Summary of Accuracy of Signs

Download (PDF, 117KB)

Finally – Don’t forget Emergency Physicians can learn how to use Point of Care Ultrasound (PoCUS – ?Appendicitis) which can significantly improve diagnostic accuracy in experienced hands. Experience comes with practice.

J Med Radiat Sci. 2016 Mar; 63(1): 59–66. Published online 2016 Jan 20. doi: 10.1002/jmrs.154
Ultrasound of paediatric appendicitis and its secondary sonographic signs: providing a more meaningful finding

See SJRHEM PoCUS Quick Reference

PoCUS – Measurements and Quick Reference

Intoxicated patients are at high risk for Head Injury

Intoxicated patients with minor head injury are at significant risk for intracranial injury, with 8% of intoxicated patients in our cohort suffering clinically important intracranial injuries. The Canadian CT Head Rule and National Emergency X-Radiography Utilization Study criteria did not have adequate sensitivity for detecting clinically significant intracranial injuries in a cohort of intoxicated patients.

ACADEMIC EMERGENCY MEDICINE 2013; 20:754–760. Traumatic Intracranial Injury in Intoxicated Patients With Minor Head Trauma

Canadian CT Head Rule not applicable to intoxicated patients (GCS<13)

Download (PDF, 76KB)

CMPA provide useful guidance on the duties expected in the management of intoxicated ED patients.

All intoxicated patients, even the so called ‘frequent fliers’ require a full assessment, including history (from 3rd parties if available), full examination (especially neurological), blood glucose level, neurological observations, and this assessment should be carefully documented.

Can we defer CT imaging for intoxicated patients presenting with possible brain injury?

This study suggests that deferring CT imaging while monitoring improving clinical status in alcohol-intoxicated patients with AMS and possible ICH is a safe ED practice. This practice follows the individual emergency physician’s comfort in waiting and will vary from one physician to another.

http://www.sciencedirect.com/science/article/pii/S0735675716306805

Download (PDF, 172KB)

Acute Heart Failure has a higher mortality than acute NSTEMI

Cardiac markers are routinely used to exclude NSTEMI in patient presenting with chest pain. However the diagnosis of acute heart failure (AHF) is mainly clinical, including CXR, ECG, PoCUS.

Ultrasound B Lines and Heart Failure

There is good evidence that BNP can be helpful in ruling out AHF – BMJ 2015;350:h910

Recommended Link – Emergency Medicine Cardiac Research and Education Group

Download (PDF, 1.32MB)

Emergency Treatment of Acute Congestive Heart Failure

Most recent recommendations from Canadian Cardiovascular Society (2012)

1 – We recommend supplemental oxygen be considered for patients who are hypoxemic; titrated to an oxygen saturation > 90% (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places relatively higher value on the physiologic studies demonstrating potential harm with the use of excess oxygen in normoxic patients and less value on long-term clinical usage of supplemental oxygen without supportive data.

2 – We recommend CPAP or BIPAP not be used routinely (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places high weight on RCT data with a demonstrated lack of efficacy and with safety concerns in routine use. Treatment with BIPAP/CPAP might be appropriate for patients with persistent hypoxia and pulmonary edema.

3 – We recommend intravenous diuretics be given as first-line therapy for patients with congestion (Strong Recommendation, Moderate-Quality Evidence).

4 – We recommend for patients requiring intravenous diuretic therapy, furosemide may be dosed intermittently (eg, twice daily) or as a continuous infusion (Strong Recommendation, Moderate-Quality Evidence).

5 – We recommend the following intravenous vasodilators, titrated to systolic BP (SBP) > 100 mm Hg, for relief of dyspnea in hemodynamically stable patients (SBP > 100 mm Hg):

i
Nitroglycerin (Strong Recommendation, Moderate-Quality Evidence);

ii
Nesiritide (Weak Recommendation, High-Quality Evidence);

iii
Nitroprusside (Weak Recommendation, Low-Quality Evidence).

Values and preferences. This recommendation places a high value on the relief of the symptom of dyspnea and less value on the lack of efficacy of vasodilators or diuretics to reduce hospitalization or mortality.

6 – We recommend hemodynamically stable patients do not routinely receive inotropes like dobutamine, dopamine, or milrinone (Strong Recommendation, High-Quality Evidence).

Values and preferences. This recommendation for inotropes place high value on the potential harm demonstrated when systematically studied in clinical trials and less value on potential short term hemodynamic effects of inotropes.

7 – We recommend continuation of chronic β-blocker therapy with AHF, unless the patient is symptomatic from hypotension or bradycardia (Strong Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places higher value on the RCT evidence of efficacy and safety to continue β-blockers, the ability of clinicians to use clinical judgement and lesser value on observational evidence for patients with AHF.

8 – We recommend tolvaptan be considered for patients with symptomatic or severe hyponatremia (< 130 mmol/L) and persistent congestion despite standard therapy, to correct hyponatremia and the related symptoms (Weak Recommendation, Moderate-Quality Evidence).

Values and preferences. This recommendation places higher value on the correction of symptoms and complications related to hyponatremia and lesser value on the lack of efficacy of vasopressin antagonists to reduce HF-related hospitalizations or mortality.

Emergency Medicine Cases – Episode 4: Acute Congestive Heart Failure

In Summary

AHF is a serious life-threatening condition in its own right, excluding NSTEMI does not change that. Appropriate management and disposition (almost always admission) is required.
Oxygen and intravenous Diuretics are the first-line treatment
Nitrates are recommended in the relief of dyspnea in hemodynamically stable patients (SBP > 100 mm Hg)

Enhancing Morbidity and Mortality Rounds Quality

The Ottawa M&M Model

CalderMM-Rounds-Guide-2012

EM Reflections – May 2017

Posted on May 8, 2017 by David Lewis

Thanks to Dr Paul Page for his summary

Edited by Dr David Lewis

Top tips from this month’s rounds:

DVT – Anticoagulation Bridging… when is it needed?
Anticoagulated elderly patient with minor trauma. Can we rely on a recent INR?
Abdominal pain in an elderly patient. Does a nonspecific exam and normal vitals exclude serious illness?

DVT – Anticoagulation Bridging… when is it needed?

Consider the type of anticoagulation best suited for your patient. Remember warfarin needs bridging until therapeutic INR is achieved. Ensure that patients discharged after hours have a robust plan for follow up and enough supply until follow up occurs.

Outpatient Management of Anticoagulation Therapy – American Family Physician 2013

For Warfarin therapy in DVT, Thrombosis Canada recommends:

Full-dose low molecular weight heparin (LMWH) overlapping with warfarin for at least 5 days and until the INR is at least 2.0 for at least 2 days.

Bridging is not required when prescribing a Direct Oral Anticoagulant (DOAC) e.g Apixaban or Rivaroxaban.

Thrombosis Canada tool to support decision making for Anticoagulation therapy in DVT

Management of DVT:

General measures:
Unless compression ultrasound (CUS) is rapidly available, patients with moderate-to-high suspicion of DVT (except those with a high risk of bleeding) should start anticoagulant therapy before the diagnosis is confirmed. Imaging confirmation should be obtained as soon as possible.
Outpatient management is preferred over hospital-based treatment unless there is an additional indication for hospitalization.
Initial treatment should have an immediate anticoagulant effect. Therefore, warfarin monotherapy is not appropriate initially.

Treatment Regimens:

Depending on the clinical presentation, one of following regimens should be used for the initial 3 months:

Full-dose low molecular weight heparin (LMWH) overlapping with warfarin for at least 5 days and until the INR is at least 2.0 for at least 2 days.

Full-dose IV heparin overlapping with warfarin for at least 5 days and until the INR is at least 2.0 for at least 2 days.

Apixaban 10 mg PO BID for 1 week before reducing dose to 5 mg PO BID.

Rivaroxaban 15 mg PO BID for 3 weeks before reducing dose to 20 mg PO once daily.

Full-dose SC LMWH or IV heparin for at least 5-10 days before switching to dabigatran 150 mg PO BID or to edoxaban 60 mg PO once daily.

Full-dose LMWH alone without switching to an oral anticoagulant.

Full-dose LMWH for the 1st month or so before switching to a DOAC or warfarin.

Anticoagulated elderly patient with minor trauma. Can we rely on a recent INR?

Elderly patients on warfarin presenting with minor trauma are commonly seen in the ED. Many will have been on warfarin for a prolonged period and will have stable INRs. However we can not rely on a previous INR level when assessing the current presentation. Consider the following rational:

Why did the patient fall?
Do they have a concomitant illness?
Are they compliant with their medication?
Have they been prescribed or are you considering prescribing new medication that may interact with warfarin?

Clinically Significant Drug Interactions

Anticoagulated patients frequently re-attend the ED with complications of bleeding after discharge following minor injury e.g enlarging hematoma, blood soaked dressings, missed internal bleeding, mobility failure. Consider whether admission for observation may be more appropriate than discharge in this group of patients. For those discharge ensure that they have close support and clear advice on when to return.

Practical tips for warfarin dosing and monitoring – Cleveland Clinic Journal

See this recent Medical Student Pearl on Reversal of Anticoagulation in the ED

Reversal of Anticoagulation in the Emergency Department

Abdominal pain in an elderly patient. Does a nonspecific exam and normal vitals exclude serious illness?

Elderly patients presenting to the ED with acute abdominal pain should be considered extremely high risk. Published series have reported mortality rates approaching 10% (https://www.ncbi.nlm.nih.gov/pubmed/7091511)

Presentations can be delayed, physical exam can be innocuous, lab results can be misleading. The risk of serious pathology is much greater and the outcome of delayed diagnosis can be significant.

Abdominal emergencies in the geriatric patient – Int J Emerg Med. 2014; 7: 43.

An excellent post from ALIEM – 10 Tips for Approaching Abdominal Pain in the Elderly

After seeing your fifth young patient of the day with chronic pelvic pain, constipation, and irritable bowel syndrome, it is easy to be lulled into the mindset that abdominal pain is nothing to worry about. Not so with the elderly. These 10 tips will help focus your approach to atraumatic abdominal pain in older adults and explain why presentations are frequently subtle and diagnoses challenging.

Erect CXR – Abdominal Series – Free air under diaphragm in perforated bowel

Bottom Line –

Elderly patients with abdominal pain are at a much greater risk of serious pathology and require an extremely thorough assessment before (if ever) discharging with a rule-out diagnosis e.g constipation, gastro, abdo pain NYD etc.