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 elderly1,2?

  • 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 series3,4?

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 findings5,7?

  • 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

  1. 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/
  2. 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
  3. 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
  4. Jones, J., Ramsey, MD, A. Small bowel obstruction. Reference article, Radiopaedia.org. (accessed on 19 Jul 2022) https://doi.org/10.53347/rID-6158
  5. Atkinson P, Bowra J, Lewis D. (2019). Point of Care Ultrasound for Emergency Medicine and Resuscitation.
  6. 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
  7. Small Bowel Obstruction. PoCUS Atlas. Accessed July 19, 2022 from https://www.thepocusatlas.com/gastrointestinal
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Delirium vs. Dementia: Different side on the same coin

Delirium vs. Dementia: Different side on the same coin: A Medical Student Pearl

Khoi Dao, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Todd Way

Copyedited by Dr. Mandy Peach

Case:

Mr. D is an 83yo M today presents to Emergency Department through ambulance after a fall. Paramedics report stated that his wife found him pale and heard his complaints of shortness of breath (SoB), chest pain, and feeling weak. She later heard him called for help on the floor and called ambulance. Furthermore, the report also mentioned that he had a fall a week ago. When having a conversation with Mr. D, he stated that everything is fine, that he had no trouble breathing, or chest pain. The only pain that he felt was from his left arm and leg from the fall. He seems to be confused. He stated that he is from Nova Scotia, currently at an airport, and waiting for his friend to pick him up to go to their cabins at New Brunswick.

His initial vitals taken by paramedics was normal except for O2 Sat in 80’s. At the Emergency Department, he received O2 4L in air cannula and his SatO2 quickly brought up to 95%. He was afebrile, blood pressure at normal range, and heart rate was irregularly irregular. There were bruises at his left facial, left upper flank at axillary region, and left arm. There were no signs of basal skull fractures, nor any lacerations on his head. Cranial nerves exam was normal. Upper extremity motor, sensory, and reflex exams were within normal limits. Lower extremity motor found his dorsal flexion and extension on the left side was weaker compared to right side. Patella reflex exam was within normal limits. Respiratory exam was within normal limit. Cardiac exam reveals irregularly irregular pulse, but normal heart sound, no murmur, no extra heartbeat. Abdomen exam was within normal limits.

Past Medical History: hypertension, dyslipidemia, nephrolithiasis, chronic subdural hematoma, infection secondary to left ankle replacement, and Guillain-Barre syndrome (acute inflammatory demyelinating polyneuropathy)

Past Surgical History: bilateral ankle replacements

Initial Investigations:

With his initial presentation, blood work and imaging were ordered. Mr. D’s CBC showed elevated WBC, CRP, with stable Hgb. His ECG showed a new A-Fib.  Chest X-ray found he has consolidation of his left lower lobe, suggestive of pneumonia. Initial CT scan confirmed of left lower lobe consolidation, with multiple new and old rib fractures.

First, establish between Mild Cognitive Impairment (MCI) and Delirium

Dementia, Mild Cognitive Impairment, and delirium are grouped under the umbrella term of neurocognitive disorders, according to DSM-V. However, each of them has their own definitions, underlying pathology, and maybe etiology.

Dementia, or newly named major neurocognitive disorder in DSM-V, is characterized as cognitive decline involving one or more of neurocognitive domains (learning, memory, attention, executive function, perceptual-motor, and social cognition) that is severe enough to interfere with daily function and independence. These daily functioning includes instrumental ADL (iADL) and ADL (Table 1).

To meet the criteria of diagnosing dementia, one must have an evident decline of one or more cognitive domains, either through a collateral history of someone who is close to the patient, or through standardized neuropsychological testing (MMSE, MOCA, …). The decline of cognitive domains should not occur in the context of delirium and are not better explained by another mental disorder.

 Mild cognitive impairment can be considered somewhere between normal cognition and dementia. While it is considered to have deficit of one or more cognitive domains, it does not interfere with daily function activities. Like dementia, the diagnostic criteria require exclusively not in the context of delirium, and that it is not better explained by another mental disorder.

Delirium, on the other hand, is defined of any disturbance of attention and awareness along with cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception) over a short period of time (hours to days). It can persist from days to month. Delirium is typically caused by medical conditions, substance intoxications, or medication side effect. Thus, for the diagnostic criteria for delirium to be met, there needs to have evidence from history presentation, physical examination, or laboratory findings of physiological changes that consequently may explain the cognitive disturbances.

Cognition decline as a clinical sign can be challenging for a physician since it is overlapped by neurocognitive disorders. However, there are characteristics that are different between them, which can be shown in Table 2.

Mainly, dementia has a gradual onset, whereas delirium has a more abrupt and acute onset. Attention and orientation are usually impaired in delirium, but generally preserved in dementia in earlier stage.

Collateral History:

Initial history taking could be proven to be challenging when patient presents with difficulties with memory or attention. Thus, obtaining a collateral history is pertinent as it is an indicator and a key component to differentiate between dementia and delirium4. Although collateral history is a core clinical skill, it is sometimes overlooked 5. In taking a collateral history, one would need to establish patient’s cognition at their baseline. For instance, questions relate about  a person’s daily activities and whether if they have any difficulties should be explored. Clarification of the onset and progressions of the cognitive changes need to be documented. Furthermore,  other cognitive domains should be also screened, as questions can be seen in Table 2 below 6.

After taking initial history, you thought that Mr. D is confused and could not give a good history of presenting illness, so you decide to call his substitute decision maker (SDM), who happens to be his wife. His wife recalled that he looked pale at lunch, complained of SoB, and when he walked she thought he looked weaker than usual. Then, she heard a called for help and found him on the floor, conscious. He couldn’t get up by himself and so she decided to call an ambulance. His wife mentioned that Mr. D has had some memory loss over half a year, where there were multiple episodes of Mr. D forgetting things. However, a week ago he had a fall walking outside, and she reported that his memory has been progressively worse since the fall. There were several nights when he woke up and asked her what the dates or where he is at. He also appeared to be weak, and, the day before his emergency admission, he complained of chest pain. When asked whether he has any difficulty of performing activity of daily living (ADL), his wife mentioned he had hard time getting dressed. His wife reported he had not seen a specialist for memory decline. She was concerned, however, that his memory was acutely declining over a week compared to the last few months. When asked about EtOH use, he had history of excessively drinking in the past, but currently only one serving per day.

As Mr. D was suspected of delirious that is overlapping of MCI, more investigations were added to investigate the cause of his delirium.

Risk and Precipitating factors of delirium:

Most identified risk factors are involving with underlying brain pathologies (e.g dementia, stroke, or Parkinson)7. With respect to precipitating factors, common examples include, but not limited to, polypharmacy, infection, dehydration, immobility, malnutrition, and the use of bladder catheters (predisposes patient to urinary tract infections)

Differential Diagnoses:

Besides major neurocognitive disorders (e.g. dementia) and mild cognitive impairment that were discussed above, other differential diagnoses should also be considered such as2:

Sundowning – behaviour deterioration seen in evening hours that might be due to impaired circadian regulation or nocturnal factors in the environment

Focal syndromes – includes temporal-parietal, occipital, and frontal dysfunctions

Nonconvulsive status epilepticus – patients often showed non-classical ictal features, but with the following features such as: prominent bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, spontaneous hippus, prolonged “postictal state”, automatism, and acute aphasia without structural lesion

Psychiatric illnesses – includes bipolar and depressive disorders with psychotic features

Acute stress disorder – associated with fear, anxiety, and dissociative symptoms, such as depersonalization

Approach to the source of delirium:

As Mr. D was suspected to be delirious, the potential causes can be reflected through laboratory results as well as imaging studies. Sources of cognitive decline can be from systemic illness, isolated organ system dysfunction, drug adverse reactions, intoxications or withdrawal, psychiatric illness, trauma, or neurologic disease2,3. A concise and comprehensive acronym that could be used to establish the source of change in delirium can be used like DIMES8:

Drugs – anticholinergic, anti-emetics, anti-parkinsonian, beta-blockers

Infections – pneumonia, urinary, skin/soft tissue, CNS-related

Metabolics – altered pH, hypo/hyper Na+ or Ca+, acute organ failure, hypoglycemia

Enviromentals – heavy metals,

Structurals – brain injury, CNS pathology, malignancy

Treatment for delirium usually is to manage the underlying cause of the delirium.

Case continues:

                Although Mr. D’s initial imaging investigations found lower lobe consolidation that suggestive of pneumonia, he has a past medical history of chronic subdural hematoma in 2010. A CT head scan was ordered to rule out if there any new bleeding. When the CT head was negative it was most likely his newfound delirium and A-fib were secondary to pneumonia . Blood culture was done, and 2g IV Ceftriaxone was given empirically for his pneumonia. He was transferred to Hospitalist Unit for monitoring for improvement and referred to Geriatric Unit at St. Joseph’s Hospital for further investigation to his MCI.

Key points:

  1. Delirium is characterized as disturbance in attention and in cognition domain over a short period of time that could not be explained by other neurocognitive disorder.
  2. Delirium shared many cognitive declines feature with dementia and MCI. However, features such as acute onset, inattention, and evidence of physiological changes can be used to differentiate
  3. Collateral history is an important clinical tool to identify between delirium and other neurocognitive disorders.
  4. Mnemonics in approaching for delirium can be remembered as DIMES

References:

  1. American Psychiatric Association. (2013). Neurocognitive Disorders. In American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. https://doi-org.ezproxy.library.dal.ca/10.1176/appi.books.9780890425596.dsm17
  2. Francis J., Young, G.B. (2021). Diagnosis of delirium and confusional states. Retrieved from https://www.uptodate.com/contents/diagnosis-of-delirium-and-confusional-states?search=delirium&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  3. Larson, E.B. (2021). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved from https://www.uptodate.com/contents/evaluation-of-cognitive-impairment-and-dementia?search=delirium%20and%20dementia&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4
  4. Dyer, A. H., Foley, T., O’Shea, B., & Kennelly, S. P. (2018). Cognitive assessment of older adults in general practice: the collateral history. Irish Journal of Medical Science (1971-), 187(3), 683-687
  5. Fitzpatrick, D., Doyle, K., Finn, G., & Gallagher, P. (2020). The collateral history: an overlooked core clinical skill. European Geriatric Medicine, 11(6), 1003-1007.
  6. Mahdy, R., Amer, M. S., Adly, N. N., & Rasheedy, D. (2021). The Value of Collateral History in Screening for Mild Cognitive Impairment in Elderly with Diabetes Mellitus in Outpatient Clinics. The Egyptian Journal of Geriatrics and Gerontology, 8(1), 21-28.
  7. Fick, D. M., Agostini, J. V., & Inouye, S. K. (2002). Delirium superimposed on dementia: a systematic review. Journal of the American Geriatrics Society, 50(10), 1723-1732.
  8. Melady, D. (2013). Cause of delirium. In Geri-EM. Retrieved from https://geri-em.com/cognitive-impairment/causes-of-delirium/
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