Pediatric Hip Dislocation & Reduction

Pediatric Hip Dislocation & Reduction

Resident Clinical Pearl (RCP) – November 2022

Dr. Nick Byers , R2 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed/Edited by Dr. Brian Ramrattan


Case:
A 10 year old presents to the local emergency department after playing with their sibling. The child was “tackled” from behind. A history and physical exam inform you that the child has been healthy until now with a completely uneventful childhood. They are normal, healthy body habitus and laying on their right side, a pillow between their flexed left knee & hip, and straight right leg. This is the only position of comfort for the child. Neurovascular exam is normal and the child refuses to let you move the leg at all. Foot and ankle move normally. Xrays were obtained promptly. A dislocated hip was readily identified (note the arrow sign below).


Greater than 85% of traumatic pediatric hip dislocations are posterior. Male children are at a greater risk by a 4:1 ratio, and in younger patients, they often occur with minimal force, whereas older children tend to require much greater forces due to the strength of structures surrounding the joint. Fractures can be an associated injury, though it was not in this case. A general triad to consider when evaluating for posterior dislocation is an adducted, shortened, and internally rotated leg as seen below:


Treatment:

A simple dislocation should be treated with closed reduction under sedation, ideally within six hours of injury to reduce the risk of osteonecrosis of the femoral head.


Reduction techniques:

There are many reduction techniques discussed in the literature. Most involve in-line traction of the femur with abduction and external rotation as the leg lengthens, with counter-traction (or downward pressure) placed on the pelvis. This allows for the femoral head to enter the acetabulum gently.

A quick review of technique with attending staff present on shift included the following three options:

  1. The Allis maneuver (https://www.youtube.com/watch?v=zmk3vafjAd4): The physician stands on the stretcher with arms hooked under the flexed knee & hip (both at 90o) on the injured side and an assistant provides downward pressure on the pelvis. Hip extension and external rotation can be applied as the hip reduces.

2.  The Captain Morgan technique (https://www.youtube.com/watch?v=lQMWaFX-MeQ&t=6s): The physician flexes the injured hip and knee to 90o and places their foot on the stretcher at the injured hip of the patient, their knee under the patients. They then grasp the patient’s leg with one hand under the popliteal fossa and one at the ankle. With counter-traction/downward pressure on the pelvis by an assistant, the physician plantar-flexes their foot to put traction on the patient’s femur. External rotation and abduction can be applied with the lower leg as the hip is reduced.

3. The cannon technique: The stretcher is raised and the patient’s knee and hip are flexed to 90o with the popliteal fossa sitting directly over the physician’s shoulder, hands on the patient’s ankle (while facing the patients feet). An assistant stabilizes and provides downward pressure on the pelvis. The physician slowly stands up straight providing in-line traction on the femur until the hip is reduced.


Case Conclusion:

Once x-rays confirmed a posterior hip dislocation, closed reduction under sedation in the emergency department was performed by a resident and staff physician using the cannon technique. Post-reduction films and repeat neurovascular exams were normal and follow-up with orthopedics was in place before discharge home.

Post reduction film:


References:

https://www.merckmanuals.com/professional/injuries-poisoning/dislocations/hip-dislocations

https://www.emnote.org/emnotes/captain-morgan-hip-reduction-technique

CASTED course manual, Arun Sayal

Traumatic hip dislocation during childhood. A case report and review of the literature. American Journal of Orthopedics (Belle Mead, N.J.), 01 Sep 1996, 25(9):645-649

https://usmlepathslides.tumblr.com/post/64398003332/posterior-hip-dislocation-posterior-hip

https://posna.org/Physician-Education/Study-Guide/Hip-Dislocations-Traumatic

https://www.ochsnerjournal.org/content/18/3/242/tab-figures-data

https://coreem.net/core/hip-dislocation/

https://westjem.com/case-report/emergency-physician-reduction-of-pediatric-hip-dislocation.html

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Transfusion Troubles: A review of transfusion reactions and management

Transfusion Troubles: A review of transfusion reactions and management- A Resident Clinical Pearl

Author: Dr. Victoria Landry (iFMEM R2)
Copyedited by Dr. Mark McGraw CCFP EM


Case: A  70 year old female presents to the emergency department via EMS with chest pain and weakness. Her systolic pressure is in the 90s with a MAP of 68. She is placed in a monitored bed. She recently had a STEMI and was successfully thrombolysed but also found to have an LV thrombus. She was discharged on Plavix and warfarin.

Today her bloodwork shows a hemoglobin of 50 and INR 11.6. In the ED she was given 5mg of IV vitamin K. She was typed and crossmatched for three units of blood which were initiated at 85ml/hr. An hour into transfusion she is noted to have temperature of 38.1°C.

You review the differential of transfusion reactions presenting with fever and their features….

  • Acute intravascular hemolytic reaction
    • Cause: recipient antibodies induce hemolysis of donor’s RBCs, usually due to ABO incompatibility (resulting from clerical error) 1
    • Presentation: fever, chills, hemoglobinuria, pain (transfusion site, low back, headache), hypotension, nausea/vomiting, dyspnea, renal failure, DIC, flushing, tachycardia, pulmonary edema, bleeding, bronchospasm1
  • Febrile nonhemolytic transfusion reaction1
    • Cause: recipient antibody vs donor WBCs, release of cytokines produced during storage1
    • Presentation: fever within 4hrs of transfusion, chills, rigors, nausea/vomiting, hypotension, headache, myalgias, dyspnea, tachycardia, chest pain usually mild but can be life threatening if tenuous cardiopulmonary status 1
    • *Consider using leukocyte reduced blood products in the case of recurrent febrile transfusion reactions 1
  • Delayed extravascular hemolytic reaction (FNHTR) 2
    • Cause: in previously sensitized patient, recipient antibodies have delayed reaction to RBC antigens1, may occur with transfusion-transmitted malaria and babesiosis2
    • Presentation: 3 days to 2 weeks2 after transfusion hemolytic anemia occurs with low grade fever or entirely asymptomatic, rarely causes hemodynamic instability1
  • Bacterial sepsis/contamination2
    • Cause: contamination during storage or processing1
    • Presentation: variable based on underlying source, occurs more common in platelets due to storage temperature 20-24°C 2

You consider your next steps….

  • Stop the transfusion1,2
  • Send remaining donor blood and post-transfusion recipient blood specimen for repeat type and cross-match (blood bank will determine if syndrome was due to transfusion reaction)1
  • Send infectious work up:2
    • Bacterial cultures and gram stain of transfusion unit and attached IV solutions
    • Blood culture on patient taken from different IV site
    • Post transfusion urine culture
  • If transfusion-associated sepsis suspected, give broad-spectrum antibiotics immediately1
  • Send hemolytic work up1
    • Direct and indirect coombs test (DAT)
    • CBC, Cr, PT, aPTT
    • Haptoglobin, bilirubin, LDH, plasma free Hgb, urine hemoglobin
  • Treat acute intravascular hemolytic reaction and febrile nonhemolytic transfusion reaction the same as initially can’t distinguish between the two1
    • Maintain renal blood flow and urine output with IV fluids, mannitol, furosemide
    • Cardiorespiratory support (vasopressors) as needed
    • Manage hemorrhage and DIC
    • Acetaminophen, meperidine 25-50mg IV for severe rigors if no contraindications2


Case continued: You re-assess your patient and find her to be asymptomatic aside from having chills and mild rigors.  You stop the transfusion, notify the blood bank and send the remaining blood back to them, send a hemolytic work up, and draw patient blood cultures as well as send a urine culture. You give her acetaminophen. Since she remains otherwise asymptomatic with unchanged stable vitals and negative hemolytic work up, you determine this was a febrile nonhemolytic reaction. You make a note in her chart so that next time she receives blood products she can be pre-medicated with acetaminophen.

 

 


After successfully managing this patient, your review other possible transfusion reactions.

 

If the patient had urticaria, you would consider….

  • Allergic reaction: immune response to transfused plasma proteins1
    • Presentation: urticaria, +/- mild upper respiratory symptoms (cough, wheeze), nausea vomit, cramps, diarrhea2
    • Treatment: stop transfusion, diphenhydramine/antihistamines, notify blood bank, restart transfusion slowly if symptoms resolve/are very mild1
  • Anaphylaxis: 5% of transfusion related fatalities; reaction within 45min to 1hr after start of transfusion2
    • Presentation: urticaria, dyspnea, bronchospasm, hypotension, tachycardia, shock, stridor, wheeze, chest pain, anxiety, nausea, vomiting1
    • Treatment: stop transfusion, epinephrine, steroids, diphenhydramine, H2 blockers, bronchodilators, vasopressors PRN, do NOT restart transfusion1
    • Note: those with IgA deficiency may have severe reactions to IgA in donor products (minimized by washing plasma from RBCs) 1

If the patient had dyspnea, you would consider….

  • TACO (transfusion-associated circulatory overload): most common cause of death from transfusion2
    • Presentation: dyspnea, hypoxia, pulmonary edema, orthopnea, cyanosis, tachycardia, increased venous pressure, hypertension2
    • To mitigate, transfuse slowly (2-4ml/kg/hr) in those at risk (age >70yrs, infants, Hgb <50, renal impairment, fluid overload, cardiac dysfunction) 2
    • Treatment: stop transfusion, diuretics&O2 PRN, can consider restarting transfusion at reduced rate if clinical status allows1
  • TRALI (transfusion-related acute lung injury):
    • Cause not fully understood; donor anti-leukocyte antibodies produce polymorphonuclear leukocyte degranulation in lung1
    • Definition: acute lung injury (acute onset hypoxemia with bilateral lung infiltrates/pulmonary edema on CXR and no evidence of circulatory overload) within 6hrs of completion of transfusion, and no other risk factors for acute lung injury (ALI) 2 (“possible TRALI” if ALI risk factors present)
    • Presentation: dyspnea, hypoxemia, fever, hypotension, may be followed by acute transient leukopenia2
    • More common with plasma, RBCs, platelets1
    • Treatment: stop transfusion, resolves in 24-72hrs with supportive care1
      • mechanical ventilation required in 72% of cases, death in 5-10%2
      • distinguish from TACO, as aggressive diuresis in TRALI can cause rapid deterioration; steroids not helpful1
      • notify blood bank to perform special donor and recipient testing2

*ALI risk factors: aspiration, pneumonia, toxic inhalation, lung contusion, near drowning, severe sepsis, shock, trauma, burn injury, acute pancreatitis, cardiopulmonary bypass, drug overdose2

If the patient develops hypotension (>30mmHg drop in systolic or diastolic BP; pediatric: >25% drop in systolic BP) 2, you would consider….

  • Acute hemolytic transfusion reaction
  • Bacterial sepsis
  • Severe febrile non-hemolytic transfusion reaction
  • Bradykinin mediated hypotension (ACE breaks down bradykinin, usually pt takes ACEi)
  • TRALI
  • Anaphylaxis

Complications of massive transfusion (>10u of RBCs in 24hrs) 2

  • Independent risk factor for multi-organ failure2
  • Dilutional coagulopathy: monitor with q1h bloodwork, transfuse to keep 2
    • platelets >50 x109/L (>100 in head injury)
    • INR <1.8
    • Fibrinogen >2.0 g/L
    • Give 1g IV TXA bolus then 1g IV over 8 hrs
  • Hypothermia: higher risk with >5 units blood; mortality inversely related to core temperature2
    • low temperature increases blood loss and causes cardiac arrhythmias, platelet dysfunction, reduced citrate clearance, decreased cardiac output, hypotension, decreased coagulation factor activity2
    • Maintain core temp >36°C2
  • Citrate (anticoagulant in blood components) accumulation due to liver metabolism of citrate to bicarbonate being overwhelmed 1
    • Hypocalcemia: citrate binds calcium2
    • Hypomagnesemia: citrate binds magnesium2
    • Hypokalemia: Excess bicarbonate generated by metabolism of citrate, causing alkalemia and driving potassium into cells1
  • Hyperkalemia: Potassium in blood increases during storage (neonates and those with renal insufficiency at most risk) 1
  • Metabolic acidosis (rare; from acid pH of blood products) 2

 

Other complications

  • Cytopenias After Transfusion2
  • Hemolysis not related to RBC alloantibodies2
    • Use of hypotonic IV solutions with RBC transfusions
    • Medical device-related (ex: cell saver or blood warmer malfunction)
    • Overheating of RBCs due to improper storage
    • Freezing of RBCs
    • Transfusion under pressure through small bore needle
    • Outdated RBCs

See – EM Cases – Massive Hemorrhage Protocols


Concluding thoughts….

 

Transfusion pearls1

  • Complications occur in 20% of all transfusions – most are minor, life-threatening reactions are rare
  • Watch for unexpected changes in patient status to identify reactions
  • First steps in all transfusion reactions:
    • Stop transfusion immediately
    • Contact blood bank (the transfusion physician is a valuable resource)
    • Draw new specimen to re-type and cross-match to resume transfusion
  • Do NOT abandon all transfusion! Typically the reaction is due to interaction between individual patient and individual unit – thus is safe if appropriately matched

References

 

  1. Coil C.J., & Santen S.A. (2020). Transfusion therapy. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill. https://accessmedicine-mhmedical-com.ezproxy.library.dal.ca/content.aspx?bookid=2353&sectionid=221179053

 

  1. Callum, J. L., Ontario Regional Blood Coordinating Network Staff, Pinkerton, P. H., Lima, A., Lin, Y., Karbouti, K., Lieberman, L., Pendergrast, J. M., Robitaille, N., & Tinmouth, A. T. (2016). Bloody Easy 4: Blood Transfusions, Blood Alternatives and Transfusion Reactions. Ontario Regional Blood Coordinating Network. https://books.google.ca/books?id=6G1ZDQEACAAJ

 

  1. Helman, A. EM Cases Episode 152: The 7 Ts of Massive Hemorrhage Protocols. February 9, 2021. https://emergencymedicinecases.com/7-ts-massive-hemorrhage-protocols/

 

 


 

 

Figure 2: Red Blood Cell Pre-Transfusion Checklist (Bloody Easy 4) 2

EM Cases – Massive Hemorrhage Protocols

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Positive Blood Cultures – convincing or contaminant? EM Reflections April 2022

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

All cases are imaginary but highlight important learning points.

Authored & Copyedited by Dr. Mandy Peach

You are working an evening shift and a nurse hands you a printout of positive blood culture results for a patient seen previously in the department. You don’t recognize the name and ask for the chart to be pulled.

The results state:

Anaerobic vial: Gram positive bacilli suggestive of the genus Bacillus/Clostridium seen after 0.64 days incubation

What is your approach?

It’s concerning that there is growth so soon in a vial, but you don’t know the patient or story yet. Although your immediate thought is to bring the patient back in, the question is – how likely is this to be a contaminant?

North York General Blood Culture Algorithm provides a step by step approach to dealing with positive blood cultures. You review your case

  1. Are there two cultures showing growth of the same organism?
    1. No – so far just one vial
  2. Is it gram negative bacilli or yeast?
    1. No – it is Gram Positive
  3. Is it gram positive cocci in pairs or chains?
    1. No – it is bacilli

So far, these are more reassuring factors for potential contamination. At this point, patient risk factors come into consideration. You get the patient chart and review:

Patient risk factors associated with poor outcome include:

  • Immunocompromised (HIV, active chemo, active immunosuppresants, uncontrolled DM)
  • Internal hardware (artificial heart valves, pacemakers, joints)
  • Suspicion/history of endocarditis
  • Central line
  • MSK pain concerning for osteomyelitis/discitis
  • Age < 3 months

The chart describes a 70 yo male who presented with a likely syncopal episode NYD. On scene with EMS there was documented hypotension that improved with fluid resuscitation. Blood cultures were drawn as sepsis was on the differential for hypotension. The past medical history includes DLP, HTN and a L TKA for OA.

The TKA counts as internal hardware, therefore the patient has a risk factor for poor outcome. This patient is called back to the ED for repeat cultures and search for an alternative source.

What if this was a healthy 20 yo non-pregnant female with the same presentation who has no risk factors for poor outcome?

You can further risk stratify the bacteria.

Bacteria that are considered high or intermediate risk must be called back for reassessment and repeat cultures.

Blood cultures should include:

  • 2 sets from 2 peripheral sites collected at least 30 min apart
  • If considering endocarditis or fever of unknown origin consider taking an additional set.

High risk bacteria is unlikely to be contaminant

Intermediate risk bacterial could possibly be contaminant.

Regardless, once cultures are redrawn and the patient reassessed in the ED, discuss the case with IM or ID for management.

If the patient is healthy, unlikely to have true bacteremia based on organism isolated and reports feeling well on verbal reassessment over the phone – give good discharge advice on when to return to the ED and follow up on speciation results.

Feeling unwell? Return to ED for reassessment and repeat cultures, looking for an alternate source.

What features are concerning for true bacteremia?

If 2 vials are growing the same organism, or the organism is reported as gram negative or yeast it is most likely true bacteremia – call the patient back to the ED, redraw blood cultures, start appropriate antimicrobials or anti-fungal agents and admit to hospital.

If the patient grows gram positive cocci in pairs or chains this is also unlikely to be a contaminant with a 82% chance that it is true bacteremia – call the patient back to the ED, redraw blood cultures and start IV antibiotics: Vancomycin to cover MRSA and Ceftriaxone; admit to hospital.

Pen allergy? Cover with vancomycin alone.

We see S. epidermidis reported all the time – is this always a contaminant?

Although a common contaminant, in the setting of any hardware (even remote orthopedic procedures) this can be pathological. If it grows in 2 vials with a history of hardware, treat as true bacteremia. If growing in 2 vials and no hardware, still reassess the patient and obtain repeat cultures.

 

 

 

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Peritonsillar Abscess Considerations and Treatment

Flimsy on Quinsy: Considerations and procedures to help diagnose and treat peritonsillar abscess  

Author: Iain McPhee- PGY1

Case study:

A 30 y.o. female presented to the emergency department with a 2-3 day history of sore throat, a unilateral, right sided oral pain that was worsening, and mild right ear ache. Although she was able to swallow food and liquid with discomfort, she reported an increased pooling of saliva in her mouth. She became more concerned when she noticed voice changes and decided to come to the hospital. 

On exam, she looked well and her vitals were within normal limits. On examination of the oral cavity there was a noted mild deviation of the uvula to the left. There was clearly demarcated erythema of both the hard palate and soft palate on the right side. Her right tonsil was only mildly enlarged and the presence of tonsillar stones were appreciated bilaterally. There was very mild fluctuance when palpating the junction between the hard and soft palate. There was an obvious dysphonia (Hot potato voice).

Background:

Peritonsillar abscess (PTA) (Quinsy) and peritonsillar cellulitis (PTC) are often indistinguishable, sharing similar clinical signs and symptoms (1). As management differs depending on the condition, several aspects warrant consideration in the differentiating process

Considerations

  1. Assess for severe upper airway obstruction
    • Look for signs of trismus, suprasternal retractions and anxious appearance. If present consider airway management.
  2. Computed tomography of the neck
    • Consider if you suspect signs of deep neck infection like a retro or parapharyngeal abscess. The CT scan should be obtained with contrast to help identify an abscess (4)
  3. Ultrasound guided exam 
    • Intraoral ultrasound has been shown to be a superior method to both diagnose and assist in the execution peritonsillar abscess drainage when compared to classic landmark-based needle aspiration (2,3). 
  4. Time
    • In the absence of a significant/apparent fluctuating mass in the mouth, consideration of the amount of time the symptoms have been present can help distinguish between the two conditions. Peritonsillar cellulitis is considered a transition phase of peritonsillar inflammatory process which leads to abscess formation (1). Look for 1-2 day history of symptoms as peritonsillar cellulitis, Abscesses are more likely to form between 2-8 days.

Algorithm: Approach to diagnosis and treatment of peritonsillar abscess in the emergency department

https://www.uptodate.com/contents/image?csi=59e98f58-4a45-4ff2-b021-31528346c088&source=contentShare&imageKey=EM%2F112062

Intraoral Ultrasound approach to drainage (as described on emdocs)

http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/

  1. Use intracavitary probe with cover (Fig 1).
    • Examine affected area and locate abscess 
    • Also locate depth of carotid artery and any potential vascular anatomy anomalies (Fig 2).

      Figure 1: Intracavitary Probe with cover

      Figure 2: Anechoic abscess and carotid artery highlighted in red

       

  2. Analgesia/anesthesia
    • Consider IV analgesia, anxiolytics
    • Anesthetize oral cavity using topical spray like cetacaine or nebulized lidocaine
    • Inject lidocaine with epinephrine into the area of abscess with 18g needle with cut sheath (Fig 3).

      Figure 3 : Scalpel with taped guard and

  3. Optimize Abscess visualization 
    • Insert laryngoscope blade to a depth that is comfortable for the patient. Ask patient to hold laryngoscope (Fig 4)

      Figure 4: Laryngoscope blade optimizing view

  4. Drainage
    • Once adequate visualization is achieved, approach superior pole of abscess with sheathed spinal needle and continuously aspirate when advancing until pus is reached (Fig 5).
    • Consider incision with scalpel with protective guard and used 
    • Insert curved hemostat into abscess space to break up remaining loculations

      Figure 5: Anatomical picture showing superior pole

 

References

  1. Mohamad I, Yaroko A. Peritonsillar swelling is not always quinsy. Malays Fam Physician. 2013 Aug 31;8(2):53-5. PMID: 25606284; PMCID: PMC4170468.
  2. Costantino TG, Satz WA, Dehnkamp W, Goett H. Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess. Acad Emerg Med. 2012 Jun;19(6):626-31. doi: 10.1111/j.1553-2712.2012.01380.x. PMID: 22687177.
  3. Froehlich MH, Huang Z, Reilly BK. Utilization of ultrasound for diagnostic evaluation and management of peritonsillar abscesses. Curr Opin Otolaryngol Head Neck Surg. 2017 Apr;25(2):163-168. doi: 10.1097/MOO.0000000000000338. PMID: 28169864.
  4. Galioto NJ. Peritonsillar abscess. Am Fam Physician. 2008 Jan 15;77(2):199-202. PMID: 18246890.

Procedures and Algorithms

  1. http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/
  2. https://www.uptodate.com/contents/image?imageKey=EM%2F112062&topicKey=EM%2F6079&search=peritonsillar%20cellulitis&rank=1~19&source=see_link

 

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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.
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