Trauma Reflections – June 2020

Thanks to Dr. Andrew Lohoar and Sue Benjamin for leading the discussions this month


 

Major points of interest:

 

A) How are we doing with calling Trauma Codes for qualifying cases?

In the past year, for cases qualifying for trauma team activation, the rate of calling ‘Trauma Codes’ has fallen to 66%.

If a Trauma Code was called, RN trauma note use increased to 85% and time to disposition to an ICE setting was significantly decreased.

 

Please review the attached updated simplified activation criteria – notable changes are:

  • Removal of minor head injuries without signs or symptoms on anticoagulants under “D”
  • Addition of pulseless extremity under “C”


B) ECMO in trauma

MVC victim survived after being submerged x 20 minutes – CPR (with LUCAS) and then managed further with ECMO.

Key to successful outcome will be EARLY recognition of cases that may benefit and early alert/consultation with CV surgery.

Best evidence for ECMO is for re-warming severe hypothermic patients.

 


 C) Significant MOI + spine pain = CT

Obtaining spine x-rays in cases with moderate probability of bony injury inevitably leads to another trip down the long hallway to visit our diagnostic imaging colleagues (and delay to definitive diagnosis).

If your patient needs a CT, order a CT.

See attached consensus guideline.


D) Pelvic binders are not used to ‘treat’ the pelvic fracture

They are used to treat any hemodynamic instability caused by the fracture. If a patient is stable or has a pelvic fracture that is not likely causing significant bleeding, the binder can likely be loosened or removed.

A pelvic binder can exacerbate some fractures, such as lateral compression fractures. Orthopedics should be assisting with this decision.

 


E) That intubated transfer patient just waved at me!

There is a reason trauma transfers should be assessed on arrival.

Consultants are expected to attend to these patients ASAP, but timely review by emergency MD is expected to assess/treat priorities (ventilatory status, analgesia need, sedation etc.)

 


F) The patient is on warfarin…how quaint!

Do you remember when anticoagulants could be reversed? In the event you do meet a trauma patient on warfarin, early correct dosing of vitamin K and PCC may be crucial.

Review of such charts in past 2 years has our dosing all over the map.

Easy dosing regime is:

 

Vitamin K – 10mg IV and PCC – 2000IU if INR unknown,

If INR known: PCC – 3000IU if INR > 5, PCC – 2000IU if INR 3-5, PCC – 1000 if INR < 3.

 


G) Trauma checklist:

“SJRH ED Trauma Process Checklist” is in trauma note package in room 19 and is a very useful prompt (see below).


H/ High MOI Knee injuries are at risk for deterioration in department

Vascular status may change, compartment syndrome may develop.

Consider repeating physical exams, early orthopedic consultation and low threshold for CT with vascular studies.

 


I/ Where is this guy bleeding?

Maybe he isn’t. Failure to respond to resuscitation suggests continued hemorrhage or non-hemorrhagic cause for shock. With neurogenic shock, loss of sympathetic tone may cause hypotension without tachycardia or vasoconstriction.

Consideration should be made to start vasopressors in patients with spinal cord injury with persistent hypotension after attempted resuscitation and no evidence of hemorrhagic shock. Aim for a SBP of 90-100. Avoid overzealous fluid administration.

 


J/ NB Trauma Traumatic Brain Injury Consensus statement – May 2020

See attached

Download (PDF, 1.32MB)

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EM Reflections – June 2020

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Antiviral Toxicity

    • Always adjust dosing in patients with renal impairment
  2. Necrotising Fasciitis

    • Difficult clinical diagnosis
    • Should be on the differential for all soft tissue infections
    • Delayed definitive care always results in poor outcomes
  3. Epidural Abscess

    • Thorough detailed neurological examination required
    • Isolated leg weakness is rare in Stroke
    • Progressive development of symproms and mixed UMN/LMN signs suggests spinal cord compression.

 


Antiviral Toxicity

Case

A 70yr old male presents with a typical zoster rash in the left L1 dermatome. He has a past medical history of chronic renal insufficiency. He is started on Valacyclovir 1000mg TID. He represents 3 days later with hallucinations including a feeling that he was occupying a dead body. What is the differential diagnosis?


 

Varicella Zoster Encephalitis vs Valacyclovir Toxicity

VZV and antiviral toxicity can present with similar symptoms

Two main risk factors increase the risk for VZV

  • age greater than 50 years old
  • immunocompromised due to reduced T cell-mediated immunity

The main risk factor for antiviral toxicity is renal insufficiency

Differentiation

  • Timing
    • Toxicity presents within 1-3 days of starting drug (vs 1-2 weeks)

 

  • Symptoms – both can present with confusion and altered LOC
    • Encephalitis – fever, HA, seizures, more likely with Trigeminal nerve (V1) or disseminated zoster
    • Toxicity – Visual hallucinations, dysphasia, tremor/myoclonus
    • Toxicity – Cotard’s syndrome…

Cotard’s Syndrome

“le délire des négations”

(delirium of negation)

https://en.wikipedia.org/wiki/Cotard_delusion

  • Described in 1880 by neurologist Jules Cotard
    • “patient usually denies their own existence, the existence of a certain body part, or the existence of a portion of their body”
  • Seen in schizophrenia, psychosis and…
  • ….acyclovir toxicity (felt to be due to metabolite CMMB (9-carboxymethoxymethylguanine) crossing BBB)

Further Reading

Varicella Zoster Encephalitis case report and outline

Valacyclovir Toxicity case report and outline

Cotard’s Syndrome

Drug Dosing in Chronic Kidney Disease

 

 

 


Necrotising Soft Tissue Infections (NSTI)

Case

A 28yr old female presents pain, redness and swelling over the right thigh. She has a past medical history of type 2 diabetes. She is managed as an outpatient with intravenous ceftriaxone q24hrs. Her symptoms failed to respond on follow up. What is the concern now? Are there any red flags? What condition needs to be considered in patients with soft tissue infections that fail to respond to antibiotics?


NSTI first described by Hippocrates 5th century BC

“[m]any were attacked by the erysipelas all over the body when the exciting cause was a trivial accident…flesh, sinews, and bones fell away in large quantities…there were many deaths.”

 

Necrotizing fasciitis is characterized by rapid destruction of tissue, systemic toxicity, and, if not treated aggressively, gross morbidity and mortality. Early diagnosis and aggressive surgical treatment reduces risk; however, it is often difficult to diagnose NF, and sometimes patients are treated for simple cellulitis until they rapidly deteriorate.

Infection typically spreads along the muscle fascia due to its relatively poor blood supply; muscle tissue is initially spared because of its generous blood supply.

Infection requires inoculation of the pathogen into the subcutaneous tissue or via hematogenous spread.

Classification

  • Type 1 – polymicrobial – older/diabetics/EtOH/IC/PVD
  • Type 2 – monomicrobial – usually group A beta-hemolytic strep (often hematogenous) – healthy people of all ages

Early signs and symptoms of NSTI are often identical to those seen with cellulitis or abscesses potentially making the correct diagnosis difficult

‘Classic’ Signs / Symptoms

(1) the presence of bullae
(2) skin ecchymosis that precedes skin necrosis
(3) crepitus
(4) cutaneous anesthesia
(5) pain out of proportion to examination
(6) edema that extends beyond the skin erythema
(7) systemic toxicity
(8) progression of infection despite antibiotic therapy or rapid progression

First 4 are “hard” signs

  • Erythema (without sharp margins; 72 percent)
  • Edema that extends beyond the visible erythema (75 percent)
  • Severe pain (out of proportion to exam findings in some cases; 72 percent)
  • Fever (60 percent)
  • Crepitus (50 percent)
  • Skin bullae, necrosis, or ecchymosis (38 percent)

Streaking lymphangitis favours the diagnosis of cellulitis over necrotizing fasciitis

Diagnosis

  • There is no set of clinical findings, lab test results and even imaging that can definitively rule out necrotizing fasciitis
    • “Surgical exploration is the only way to establish the diagnosis of necrotizing infection”.
    • “Surgical exploration should not be delayed when there is clinical suspicion for a necrotizing infection while awaiting results of radiographic imaging other diagnostic information”
  • But what if you really aren’t sure?  Or if you get pushback?
  • CT is probably the best test – esp Type 1 (gas forming)
    • Findings – gas, fluid collections, tissue enhancement, inflammatory fascial changes
  • Finger test…
    • “After local anesthesia, make a 2-3 cm incision in the skin large enough to insert your index finger down to the deep fascia. Lack of bleeding and/or “dishwater pus” in the wound are very suggestive of NSTI. Gently probe the tissues with your finger down to the deep fascia. If the deep tissues dissect easily with minimal resistance, the finger test is + and NSTI can be ruled in.”  (emergencymedicinecases.com)
  • But what about PoCUS????

PoCUS

Diagnosis of Necrotizing Faciitis with Bedside Ultrasound: the STAFF Exam

Findings – “STAFF”

ST – subcutaneous thickening
A – air
FF – fascial fluid

Ultrasound video demonstrating Subcutaneous Thickening, Air, and Fascial Fluid (STAFF).

 

Soft tissue ultrasound findings are significantly different when compared to normal soft tissue ultrasound

Bottom Line: Limited data, but basically PoCUS is not sufficient to rule-in or rule out, but might be helpful in raising suspicion level for necrotising fasciitis for physicians who routinely scan all soft tissue infections.

 

LRINF Score

The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) Score: A Tool for Distinguishing Necrotizing Fasciitis From Other Soft Tissue Infections

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score.  2004, retrospective – score >6 negative predictive value of 96.0% and a positive predictive value of 92%.

 

A validation study looking only at patients with pathology-confirmed necrotizing fasciitis showed that a LRINEC score cutoff of 6 points for necrotizing fasciitis only had a sensitivity of 59.2% and a specificity of 83.8%, yielding a PPV of 37.9% and NPV of 92.5%. However, the study did show that severe cellulitis had a LRINEC Sscore ≥ 6 points only 16.2% of the time.  Therefore, the available evidence suggests that the LRINEC score should not be used to rule-out NSTI.

Bottom Line: Doesn’t rule-out…… or rule-in

 

Suggested Algorithm – UpToDate

 

EM Cases Review

BCE 69 Necrotizing Fasciitis

 

Further Reading

Necrotizing fasciitis – Can Fam Physician. 2009 Oct; 55(10): 981–987.

 


Epidural Abscess

Case

A 40yr old female presents with left leg weakness. She has a complex recent past medical history including recently diagnosed pneumonia, previous renal colic and type 2 diabetes. Could this be a stroke? What are the other causes of leg weakness? How does the examination differentiate UMN from LMN lesions? When considering a diagnosis of epidural abscess what investigation is required? How soon should it be performed?


Only 4% of Strokes present with isolated or predominant leg weakness. (Brain. 1994 Apr;117 ( Pt 2):347-54.
doi: 10.1093/brain/117.2.347)

Common mechanisms of weakness:

  • Upper motor neuron lesions (Stroke, Tumour, Spinal Cord Compression, etc)
  • Lower motor neuron lesions ( Neuropathy, Disc Prolapse, Spinal Cord Compression, etc)
  • Neuromuscular junction lesions (Myasthenia, etc)
  • Neuropathies (Guillain-Barre, etc)
  • Muscle (Myopathies, etc)

Full review on Muscle Weakness from the Merck Manual here

Weakness that becomes severe within minutes or less is usually caused by severe trauma or stroke; in stroke, weakness is usually unilateral and can be mild or severe. Sudden weakness, numbness, and severe pain localized to a limb are more likely caused by local arterial occlusion and limb ischemia, which can be differentiated by vascular assessment (eg, pulse, color, temperature, capillary refill, differences in Doppler-measured limb BPs). Spinal cord compression can also cause paralysis that evolves over minutes (but usually over hours or days) and is readily distinguished by incontinence and clinical findings of a discrete cord sensory and motor level.

Unilateral upper motor neuron signs (spasticity, hyperreflexia, extensor plantar response) and weakness involving an arm and a leg on the same side of the body: A contralateral hemispheric lesion, most often a stroke

Upper or lower motor neuron signs (or both) plus loss of sensation below a segmental spinal cord level and loss of bowel or bladder control (or both): A spinal cord lesion

 

Epidural Abscess

Spinal epidural abscess (SEA) is a severe pyogenic infection of the epidural space that leads to devastating neurological deficits and may be fatal. SEA is usually located in the thoracic and lumbar parts of the vertebral column and injures the spine by direct compression or local ischemia. Spinal injury may be prevented if surgical and medical interventions are implemented early. The diagnosis is difficult, because clinical symptoms are not specific and can mimic many benign conditions. The classical triad of symptoms includes back pain, fever and neurological deterioration.

Spinal Epidural Abscess: Common Symptoms of an Emergency Condition – A Case Report

 

  • 75% are a delayed diagnosis
    • Usually hematogenous spread, usually S. aureus
  • Diagnosis
    • CRP has an sensitivity of 85%, specificity of 50%
    • MRI is gold standard
    • CT with contrast 2nd choice

 

Further Reading

Spinal epidural abscess

Episode 26: Low Back Pain Emergencies

 

 

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EM Reflections – May 2020

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Seizure disorder and safe discharge 

    • Consider risk factors for adverse outcome of discharge for all patients with recurrent seizure disorder
    • Use a checklist
  2. Competency and Capacity

    • Multidisciplinary consultation is paramount in deciding capacity
    • Special circumstances include vulnerable adults and pregnancy
  3. Testicular Torsion

    • Time = Testicle viability
    • Do not delay definitive management

Seizure disorder and safe discharge 

Case

A patient presents with recurrent seizures. They have a past medical history of schizophrenia and mental health delay. Following appropriate ED management with complete resolution of seizures and full recovery of the patient – what is the recommended disposition?


Seizure disorder is a common presentation to the Emergency Department. This EM Cases post provides an excellent summary for the ED approach to resolved seizures:

Ep 132 Emergency Approach to Resolved Seizures

 

ED approach to resolved seizures – Summary pdf


In this study – Ethanol withdrawal or low antiepileptic drug levels were implicated as contributing factors in 177 (49%) of patients. New‐onset seizures were thought to be present in 94 (26%) patients. Status epilepticus occurred in only 21 (6%) patients.

73% of patients were discharged.

 

 

 


Disposition

Most authors recommend admission for patients presenting with FIRST Seizure Episode. Patients with a past medical history of recurrent seizure disorder are more likely to be discharged than admitted.

However – this EBMedicine article cites an incidence of 19% seizure recurrence rate within 24 hours of presentation, which decreased to 9% if patients with alcohol related events or focal lesions on CT were excluded. They suggest, that at present, there is insufficient evidence to guide the decision to admit. They recommend this decision be tailored to the patient, taking into consideration the patient’s access to follow-up care and social risk factors (eg, alcoholism or lack of health insurance). Patients with comorbidities, including age > 60 years, known cardiovascular disease, history of cancer, or history of immunocompromise, should be considered for admission to the hospital.

 

Considerations For Safety On Discharge

Patients and their families should be counseled and instructed on basic safety measures to prevent complications (such as trauma) during seizures. For example, patients should be advised to avoid swimming or cycling following a seizure, at least until they have been reassessed by their neurologist and their antiepileptic therapy optimized, if needed. A particularly important point for seizure patients is education against driving. Although evidence remains controversial on this issue, there is general agreement that uncontrolled epileptic patients who drive are at risk for a motor vehicle crash, with potential injury or death to themselves and others. For this reason, most states do not allow these patients to drive unless they have been seizure-free on medications for 1 year. According to population survey data, 0.01% to 0.1% of all motor vehicle crashes are attributable to seizures


Competency and Capacity

Case

A young female patient with a history of polysubstance drug abuse presents with a psychotic episode. She refuses treatment. What are the competency and capacity implications? She is also pregnant. Does this change the the competency and capacity implications?


This LitFL post provides and excellent outline for Competency and Capacity in the ED:

Capacity and Competence

This article published by the RCPSC provides a useful outline from a Canadian perspective – with the following objectives.

  1. To clarify the role of decisional capacity in informed consent
  2. To discuss problems associated with decisional capacity and addiction

RCPSC – Decisional Capacity

 


 



Capacity in Pregnancy

Recommendations from the American College of Obstetricians and Gynecologists

On the basis of the principles outlined in this Committee Opinion, the American College of Obstetricians and Gynecologists (the College) makes the following recommendations:

  • Pregnancy is not an exception to the principle that a decisionally capable patient has the right to refuse treatment, even treatment needed to maintain life. Therefore, a decisionally capable pregnant woman’s decision to refuse recommended medical or surgical interventions should be respected.
  • The use of coercion is not only ethically impermissible but also medically inadvisable because of the realities of prognostic uncertainty and the limitations of medical knowledge. As such, it is never acceptable for obstetrician–gynecologists to attempt to influence patients toward a clinical decision using coercion. Obstetrician–gynecologists are discouraged in the strongest possible terms from the use of duress, manipulation, coercion, physical force, or threats, including threats to involve the courts or child protective services, to motivate women toward a specific clinical decision.
  • Eliciting the patient’s reasoning, lived experience, and values is critically important when engaging with a pregnant woman who refuses an intervention that the obstetrician–gynecologist judges to be medically indicated for her well-being, her fetus’s well-being, or both. Medical expertise is best applied when the physician strives to understand the context within which the patient is making her decision.
  • When working to reach a resolution with a patient who has refused medically recommended treatment, consideration should be given to the following factors: the reliability and validity of the evidence base, the severity of the prospective outcome, the degree of burden or risk placed on the patient, the extent to which the pregnant woman understands the potential gravity of the situation or the risk involved, and the degree of urgency that the case presents. Ultimately, however, the patient should be reassured that her wishes will be respected when treatment recommendations are refused.
  • Obstetrician–gynecologists are encouraged to resolve differences by using a team approach that recognizes the patient in the context of her life and beliefs and to consider seeking advice from ethics consultants when the clinician or the patient feels that this would help in conflict resolution.
  • The College opposes the use of coerced medical interventions for pregnant women, including the use of the courts to mandate medical interventions for unwilling patients. Principles of medical ethics support obstetrician–gynecologists’ refusal to participate in court-ordered interventions that violate their professional norms or their consciences. However, obstetrician–gynecologists should consider the potential legal or employment-related consequences of their refusal. Although in most cases such court orders give legal permission for but do not require obstetrician–gynecologists’ participation in forced medical interventions, obstetrician–gynecologists who find themselves in this situation should familiarize themselves with the specific circumstances of the case.
  • It is not ethically defensible to evoke conscience as a justification to attempt to coerce a patient into accepting care that she does not desire.
  • The College strongly discourages medical institutions from pursuing court-ordered interventions or taking action against obstetrician–gynecologists who refuse to perform them.
  • Resources and counseling should be made available to patients who experience an adverse outcome after refusing recommended treatment. Resources also should be established to support debriefing and counseling for health care professionals when adverse outcomes occur after a pregnant patient’s refusal of treatment.

Further Reading:

Ethically Justified Clinically Comprehensive Guidelines for the Management of the Depressed Pregnant Patient

How Do I Determine if My Patient has Decision-Making Capacity?

 


Testicular Torsion

Case

A 12 year old boy presents with scrotal discomfort in the early hours of the morning. The department is very busy and the waiting time to be seen is 4 hours. What triage category is this presenting complaint? If a diagnosis of torsion is considered, how quickly should definitive management be initiated?


Ramachandra et al. demonstrated through multivariate analysis of the factors associated with testicular salvage, that duration of symptoms of less than 6 h was a significant predictor of testicular salvage. They found that the median duration of pain was significantly longer in patients who underwent orchiectomy versus orchidopexy. Similar findings were seen with respect to time to operating room from initial presentation. They concluded that time to presentation is in fact the most important factor in determining salvageability of the testicle in testicular torsion. If surgical exploration is delayed, testicular atrophy will occur by 6 to 8 h, with necrosis ensuing within 8 to 10 h of initial presentation. Salvage rates of over 90% are seen when surgical exploration is performed within 6 h of the onset of symptoms, decreasing to 50% when symptoms last beyond 12 h. The chance of testicular salvage is less than 10%, when symptoms have been present for over 24 h

Factors influencing rate of testicular salvage in acute testicular torsion at a tertiary pediatric center.

Ramachandra P, Palazzi KL, Holmes NM, Marietti S

West J Emerg Med. 2015 Jan; 16(1):190-4.

[PubMed]

 

 

This study (Howe et al). confirmed the relationship between duration of torsion and testicle viability and also found a relationship between the degree of torsion


 

 

AAFP Review of Testicular Torsion: Diagnosis, Evaluation, and Management

 

 

 

 

 

 

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EM Reflections – January 2020

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

 


Discussion Topics

  1. Esophageal Perforation

  2. Neonatal Status Epilepticus


Esophageal Perforation – Boerhaave syndrome

A spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting) otherwise known as Effort Rupture.

Difficult diagnosis in first few hours due to nonspecific early symptoms. But, delayed diagnosis results in significant mortality. Diagnosis and surgery within 24 hours carries a 75% survival rate but drops to approximately 50% after a 24-hour delay and approximately 10% after 48 hours.

25 to 45 percent of patients have no clear history of vomiting, and those that do are often confusing with pain sometimes preceding vomiting due to coexisting pathologies e.g gastroenteritis, gastritis, pancreatitis etc.

Clinical manifestations — The clinical features of Boerhaave syndrome depend upon the location of the perforation (cervical, intrathoracic, or intra-abdominal), the degree of leakage, and the time elapsed since the injury occurred. Patients with Boerhaave syndrome often present with excruciating retrosternal chest pain due to an intrathoracic esophageal perforation. Although a history of severe retching and vomiting preceding the onset of pain has classically been associated with Boerhaave syndrome, approximately 25 to 45 percent of patients have no history of vomiting. Patients may have crepitus on palpation of the chest wall due to subcutaneous emphysema. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation especially if the patient is in the left lateral decubitus position (Hamman’s sign). However, these signs require at least an hour to develop after an esophageal perforation and even then are present in only a small proportion of patients. Within hours of the perforation, patients can develop odynophagia, dyspnea, and sepsis and have fever, tachypnea, tachycardia, cyanosis, and hypotension on physical examination. A pleural effusion may also be detected.

Patients with cervical perforations can present with neck pain, dysphagia or dysphonia.  Patients may have tenderness to palpation of the sternocleidomastoid muscle and crepitation due to the presence of cervical subcutaneous emphysema.

Patients with an intra-abdominal perforation often report epigastric pain that may radiate to the shoulder. Patients may also report back pain and an inability to lie supine or present with an acute (surgical) abdomen. As with intrathoracic perforation, sepsis may rapidly develop within hours of presentation.

Laboratory findings — Laboratory evaluation may reveal a leukocytosis. While not part of the diagnostic workup for an esophageal perforation, pleural fluid collected during thoracentesis may contain undigested food, have a pH less than 6, or have an elevated salivary amylase level.

UptoDate

 

Chest X-ray  showing a pneumomediastinum (closed arrows) and silhouette sign over the right heart border (open arrow).

Case Presentation 1

Case Presentation 2

 

Take Home

  • The diagnosis of Boerhaave syndrome should be suspected in patients with severe chest, neck, or upper abdominal pain after an episode of severe retching and vomiting or other causes of increased intrathoracic pressure and the presence of subcutaneous emphysema (crepitus) on physical exam.
  • While thoracic and cervical radiography can be supportive of the diagnosis, the diagnosis is established by contrast esophagram or computed tomography (CT) scan
  • Delayed diagnosis is associated with high mortality
  • Radiological signs develop over time, repeat imaging is often useful when considering this diagnosis

 

Neonatal Status Epilepticus

When an altered few-day-old baby is brought into the ED, other than requesting immediate pediatric support, opening PediStat on you phone and trying to keep calm – consider the causes of altered LOC in pediatrics – Think VITAMINS:

V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)

I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)

T – Toxins (e.g. environmental, medications, contaminated breast milk)

A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)

M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)

I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)

N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)

S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)

 

Altered Mental Status in Children

 

What elements are highly suggestive of true seizures?

  1. Lateralized tongue biting (high specificity)
  2. Flickering eyelids, deviation of gaze
  3. Dilated pupils with a blank stare
  4. Lip smacking
  5. Increased heart rate and blood pressure, desaturations in pulse oximetry during event

Management of Pediatric Seizures


Newborn Resuscitation

 


Elemental EM: Pediatric Intubation

 

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EM Reflections – December 2019

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

    • Patient with mechanical circulatory support devices have unique clinical signs of cardiac arrest
    • Understanding the function of these devices ids critical to the management of these complex cases
  2. Aortic Dissection

    • Remains a commonly missed or delayed diagnosis
    • Once diagnosed, meeting the therapeutic goals requires a careful and considered approach

Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

Case

A 70yr male presents with cardiac arrest. He has an LVAD. What are the implications for emergency management and cardiopulmonary resuscitation?


Introduction

Cardiac arrest in patients on mechanical support is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure.

It is important to understand the difference between blood flow and perfusion when assessing any patient with suspected cardiovascular hemodynamic instability, especially patients with an LVAD, in whom the peripheral arterial pulse is not a reliable indicator. Flow represents the forward movement of blood through the systemic circulation. It can be either adequate or inadequate to provide sufficient oxygen delivery to sustain tissue per- fusion. Assessment of adequate tissue perfusion is the most important factor in determining the need for circu- latory assistance such as chest compressions.

What is a Left Ventricular Assist Device?

With an LVAD, blood enters the device from the LV and is pumped to the central aortic circulation, “assisting” the heart.  The outflow cannula is typically anastomosed to the ascending aorta, just above the aortic valve. RA/RV still working

 

Blue Arrow – Important point as patients often present with iGel in place…

 

Unique Patient Properties

  • Pulses often absent
    • BP measured manually with a Doppler – MAP (50-90)
  • SpO2 may not be measurable
  • Anticoagulated
  • Need power!
  • Very reliant on RV function/preload
  • Leading cause of death – sepsis and stroke

Further Reading

Cardiopulmonary Resuscitation in Adults and Children With Mechanical Circulatory Support. A Scientific Statement From the American Heart Association


Aortic Dissection

Aortic dissection remains difficult to diagnosis with 1 in 6 being missed at the initial ED visit. Why? The diagnosis is rare with and incidence of only 2.9/100,000/year, and the presentation is often atypical mimicking other more common diagnoses such as ACS and stroke.

View The SJRHEM  – Aortic Dissection – Resident Clinical Pearl here:

Aortic Dissection

Diagnosis

The most common initial misdiagnoses are acute coronary syndrome, pulmonary embolism, and stroke. Patients with these suspected diagnoses should also be screened for high-risk features of acute aortic dissection. If none are present, they are unlikely to have an acute aortic dissection. If high-risk features are present, balance your clinical suspicion for an aortic dissection with the likelihood of an alternative diagnosis using an approach such as RAPID

How Do I rule Out Aortic Dissection – Just the Facts – CJEM

PoCUS

Early Screening for Aortic Dissection With Point‐of‐Care Ultrasound by Emergency Physicians

A total of 127 patients were enrolled: 72 in the US group and 55 in the control group. In the US group, compared with CTA, the sensitivity of EP POCUS was 86.4%, and the specificity was 100.0%.

 

 

Treatment Goals

From EMCases.com

 

Further Reading

Episode 92 – Aortic Dissection Live from The EM Cases Course

 

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Trauma Reflections – December 2019

Thanks to Dr. Andrew Lohoar and Sue Benjamin for leading the discussions this month


 

Major points of interest:

 

A) How are we doing with calling Trauma Codes for qualifying cases?

In the past year, for cases qualifying for trauma team activation, Trauma Codes were called 80% of time.

If a Trauma Code was called, trauma note use increased to 90% and time to disposition to an ICE setting was significantly decreased.

Please review the attached updated SIMPLIFIED activation criteria.

 

B) End of year AWARDS –  the “Crashys”

  1. ‘Crashy’ for the Busiest TTL of the Year with 17 cases …

P “I don’t see weak and dizzy patients” P

 

  1. ‘Crashy’ for the Most Trauma Intubations of the Year with 7 …

C “If he’s not move’n, I’m a tube’n” A

 

  1. ‘Crashy’ for the Most Trauma Chest Tubes of the Year with 3 …

T “Fetch me my scalpel” W

 

        Congratulations to all   (Sorry, there is no monetary gift associated with these awards!)     

 

C) Head injury, combative and on methadone – this should be easy..

Not really. Post-intubation sedation and analgesia can be challenging. Key is to avoid starting medications that could potentially drop blood pressure at very high infusion rates, but we need sedation and analgesia promptly. Under-dosing analgesic is often the reason adequate sedation is a struggle. Bolus, then increase infusion. Repeat.

 

D) End-tidal CO2 is an important vital sign

Especially in intubated patients.

 

E) Pediatric head injury transfer for imaging

Reassessing these patients on arrival, prior to CT, may influence management.

If there has been worsening in clinical condition, neurosurgery can be pre-alerted.

If there has been complete resolution of symptoms, CT scan may be deemed unnecessary.

 

F) “Clearing C-spine” can’t be done remotely..

CT C-spine is not 100% sensitive for ruling out injury. If radiologist reports there is no significant abnormality seen, it is a CLINICIAN”S responsibility to examine the neck before removing c-collar. If there is discrepancy (elevated pain, tenderness or neurologic symptoms/signs) or inability to cooperate with exam, leave the collar in place.

Make it known c-spine has not been cleared.

 

G) Pelvic binders are not used to ‘treat’ the pelvic fracture

They are used to treat any hemodynamic instability caused by the fracture. If a patient is stable or has a pelvic fracture that is not likely causing significant bleeding, the binder can likely be loosened or removed.

A pelvic binder can exacerbate some fractures, such as lateral compression fractures. Orthopedics should be assisting with this decision.

 

H) ‘Shock’ dosing of sedatives

Hypotension is not good for damaged neurons.

Shocked patients should have 1/2 dose of induction agents during RSI.

RSI Drugs

ADULT Rapid Sequence Intubation and Post-Intubation Analgesia and Sedation for Major Trauma Patients – NB Trauma

 

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EM Reflections – November 2019

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Popliteal Artery Thrombus

    • Closed loop communication is key to avoid possible poor outcomes with follow up
    • Relying on other specialties to arrange follow up with ED patients can result in error. Direct contact with specialty to arrange urgent follow up is the best approach
    • Also make sure patient is aware of plan
  1. Vertebral Artery Dissection / Thrombus

    • A thorough neurological exam and documentation is essential for vertigo presentation
    • Can’t walk, Can’t go home
  2. Elderly Delirium / Dementia with Sepsis

    • Majority of delirious patients are quiet and withdrawn, not hyperactive
    • For patients with dementia , get baseline functioning from family if possible

Popliteal Artery Thrombus

The full differential diagnosis should be considered in possible cases of DVT including Baker’s cyst, cellulitis, lymphedema, chronic venous insufficiency, superficial thrombophlebitis, popliteal venous or arterial aneurysm, peripheral vascular disease, enlarged lymph nodes compressing the veins, heterotopic ossification, hematoma, and muscle tears.

 

Ultrasound for Lower Extremity Deep Venous Thrombosis
Multidisciplinary Recommendations From the Society of Radiologists in Ultrasound Consensus Conference

It’s Not All Deep Vein Thrombosis: Sonography of the Painful Lower Extremity With Multimodality Correlation

 

Consultations and Referals

One of the most common ways for doctors to collaborate is through referral and consultation. Poor communication between referring physicians and consultants can lead to disruptions in care, delayed diagnoses, unnecessary testing, iatrogenic complications, and frustrated physicians and patients. Improving the referral-consultation process is one of the most effective ways of providing safer care and reducing the risk of medical-legal difficulties.

  • What is the question I want answered?
  • Who has the specialized knowledge and skill to answer it?
  • How urgent is the clinical situation?
  • Do I need advice from the consultant or would a transfer of care to the consultant be more appropriate in the specific circumstances?
  • Have all the appropriate steps been taken to this point?
  • Has the patient consented to the referral?

CMPA Guidance on Referrals

 

 


Vertebral Artery Dissection / Thrombus

See these SJRHEM Reflections post on the same subject:

EM Reflections – March 2017

EM Reflections – May 2019

 

and this post on the HINTS exam:

HINTS exam in Acute Vestibular Syndrome

 

 

 

 


Elderly Delirium / Dementia with Sepsis

The fluctuating presentation of delirium makes it difficult to recognize but we should be attentive to certain hallmarks, including alterations in attention and awareness and acute changes in cognition.  These can be associated with hallucinations or other perceptual disturbances.  Collateral information and family input can be critical in detecting changes from baseline function and cognition.  The more acute temporal course of delirium is important to distinguish from underlying dementia, which is itself one of the most important risk factors for delirium.  The most common presentation, the hypoactive form, is a quiet, subdued, withdrawn state.

The Seriousness of Deliriousness: Delirium in the ED

 

See this SJRHEM Rounds

ED Rounds – Delirium in the ED

 

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EM Reflections – October 2019

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Subarachnoid Hemorrhage

    • Misdiagnosis of SAH is not infrequent and usually results from common errors
      • Failure to appreciate the spectrum of clinical presentations associated with SAH
      • Failure to obtain a head CT or to understand its limitations in the diagnosis of SAH
  2. Spontaneous Bacterial Peritonitis

    • Like peritonitis but different…
    • Early iv albumin in selected case reduces mortality

Subarachnoid Hemorrhage

Headache is one of the most common reasons for presentation to the emergency department (ED), seen in up to 2% of patients. Most are benign, but it is imperative to understand and discern the life-threatening causes of headache when they present. Headache caused by a subarachnoid hemorrhage (SAH) from a ruptured aneurysm is one of the most deadly, with a median case-fatality of 27–44%. Fortunately, it is also rare, comprising only 1% of all headaches presenting to the ED

Approach to the Diagnosis and Management of Subarachnoid Hemorrhage

 

Missed Diagnosis

Missed Diagnosis of Subarachnoid Hemorrhage in the Emergency Department

Over 3 years there were 1603 patients hospitalized with a diagnosis of nontraumatic SAH; 1507 (94.0%) of these were admitted through the ED. Of the 176 EDs in the province, 147 (83.5%) admitted at least 1 patient with SAH, ranging from 1 to 49 per ED. Of these, 38 (25.9%) were in small hospitals, 93 (63.3%) in community hospitals, and 16 (10.9%) in teaching hospitals. With the exception of age, triage level, and hospital type, persons with missed SAH did not differ from those initially diagnosed with SAH.

A total of 150 (10.0%; 95% CI, 8.5 to 11.6) patients had an ED visit in the 14 days preceding their SAH admission. SAH was missed on a prior ED visit in 81 (5.4%; 95% CI, 4.3 to 6.6) cases.

The majority of missed cases were diagnosed with “migraine” or “headache” at the prior related visit

 


Spontaneous Bacterial Peritonitis

…spontaneous bacterial peritonitish

similar but more subtle

The signs and symptoms of SBP are subtle compared with those seen in patients with bacterial peritonitis in the absence of ascites – By separating the visceral from the parietal peritoneal surfaces, ascites prevents the development of a rigid abdomen

 

Fever = >37.8

Who to test?

In addition, patients with ascites admitted to the hospital for other reasons should also undergo paracentesis to look for evidence of SBP. A low clinical suspicion for SBP does not obviate the need for testing

E.coli ~50%

 

Intravenous Albumin?

It is estimated that 12-25% of patients with ascites in the ED will have spontaneous bacterial peritonitis (SBP) but the classic triad of fever, abdominal pain, and worsening ascites is often absent (Borzio 2001)(Runyon 1988). With a mortality rate approaching 40%, rapid diagnosis and evidence-based treatment is critical in the management of patients presenting with SBP (Salerno 2013).

The 2012 AASLD Guidelines, based largely on the trial by Sort, et al., recommend that patients with ascitic fluid PMN counts greater than or equal to 250 cells/mm3 and clinical suspicion of SBP, who also have a serum creatinine >1 mg/dL, blood urea nitrogen >30 mg/dL, or total bilirubin >4 mg/dL should receive IV albumin (1.5 g/kg) within 6 hours of detection and 1.0 g/kg on day 3. (Class IIa, Level B)

Should You Give Albumin in Spontaneous Bacterial Peritonitis (SBP)?

 

 

Further Reading

Spontaneous Bacterial Peritonitis

 

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EM Reflections – September 2019

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

 


Discussion Topics

  1. Refractory Hypotension / Sepsis – ‘ringing the changes

  2. Hypertensive Urgency / Emergency – “I was sent to the ER by the pharmacy checkout assistant

  3. Investigation Reports / Systems / Adverse Events


Refractory Hypotension / Sepsis

 

This interesting historical perspective from NPR makes an interesting read on the origins of Normal Saline

As it turns out, normal saline isn’t very normal at all. The average sodium level in a healthy patient is about 140 (as measured in something called milliequivalents per liter). For chloride, it’s about 100. But the concentration of both sodium and chloride in normal saline is 154. That’s pretty abnormal—especially the chloride.

Sidney Ringer (click for biography)

 

 “Among critically ill adults, the use of balanced crystalloids for intravenous fluid administration resulted in a lower rate of the composite outcome of death from any cause, new renal-replacement therapy, or persistent renal dysfunction than the use of saline.” Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adultsN Engl J Med. 2018;378:829-839.

Data Suggests Lactated Ringer’s Is Better than Normal Saline – ACEP Now

PulmCrit- Get SMART: Nine reasons to quit using normal saline for resuscitation

Take Home

  • Re-consider cause of hypotension in patients not responding to IV fluid resuscitation.
  • High mortality for elderly patients presenting to ED with hypotension.
  • Early switch to Ringers Lactate for IV fluids if needed for large volume resuscitation in sepsis.
  • If a British doc asks for Hartman’s, use Ringer’s… it’s the same.

 


 

Hypertensive Urgency / Emergency

Although elevated blood pressures can be alarming to the patient, hypertensive urgency usually develops over days to weeks. In this setting, it is not necessary to lower blood pressure acutely. A rapid decrease in blood pressure can actually cause symptomatic hypotension, resulting in hypoperfusion to the brain

RxFiles.ca summary pdf

How should I manage patients who present with a hypertensive urgency — i.e. BP > 180/120 mm Hg without impending or progressive end-organ damage (e.g. patient with headache, shortness or breath or epistaxis)?

  • For patients with hypertensive urgencies
    • Optimize (or restart) their current treatment regimens
    • Consider oral short-acting agents (e.g. captopril, labetalol, clonidine)
    • Do not treat aggressively with intravenous drugs or oral loading
    • Ensure that the patient has a follow-up appointment within a few days

How should I manage patients who present with a hypertensive emergency — i.e. BP > 180/120 mm Hg and impending or progressive end-organ damage (e.g. neurologic, cardiovascular, eclampsia)?

  • Reduce BP immediately with intravenous drugs, and monitor BP continuously in an intensive care setting.
  • Consider using the following drugs:
    • Vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, nitroglycerin, enalaprilat, hydralazine
    • Adrenergic blockers: labetalol, esmolol, phentolamine
  • Do not use short-acting nifedipine (lowers BP fast enough to provoke ischemia).
  • Aim for 25% reduction of the mean arterial blood pressure within minutes to 1 hour o Then if the patient is stable, reduce BP to 160/100-110 mm Hg over 2-6 hours and normalize within 24-48 hours.
  • Exceptions include stroke (unless BP is lowered to allow thrombolytic agents to be used) and dissecting aortic aneurysm (target systolic BP is < 100 mm Hg if possible).

from GAC Guidelines

Episode 40: Asymptomatic Hypertension

 

Take Home

  • Most patients with elevated BP (greater than 180/110) that are asymptomatic can safely follow up with Family Doctor.
  • True hypertensive emergencies are infrequent.
  • If mild symptoms consider starting antihypertensives in ED if unsure about follow up.
  • No good evidence that starting in antihypertensives ED for patients that can access their Family Doctor within next few days improves outcomes.

 


 

Radiology Reports / Systems / Adverse Events

 

Failure to follow up on radiology studies has become a frequent claim against both EPs and radiologists, according to Darien Cohen, MD, JD, an attending physician at Presence Resurrection Medical Center and clinical assistant professor in the Department of Emergency Medicine at University of Illinois, both in Chicago.

  • ED policies should ensure that all radiology alerts are available in a single location, and it must be clear who is responsible for follow-up.
  • Follow-up must be clearly documented in the medical record.
  • Any incidental finding mentioned on the radiology report should be communicated to the patient, and this communication must be clearly documented in the medical record.

 

Adverse Events Related to Emergency Department Care: A Systematic Review

A greater proportion of AE were preventable among the discharged population (71.4%; n = 15) than among the admitted population (40.9%; n = 9). Among discharged patients, management issues (47.6%; n = 10), diagnostic issues (33.3%; n = 7), and unsafe dispositions decisions (19%; n = 4) were the most common causes of AE

 

Safeguards in the system of care are like slices of cheese with holes representing possible failure points. See the Swiss Cheese Model at CMPA.ca

 

WTBS 9 – EM Quality Assurance Part One: Improving Follow up from the ED

 

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ADULT Rapid Sequence Intubation and Post-Intubation Analgesia and Sedation for Major Trauma Patients – NB Trauma

Consensus Statement:

ADULT Rapid Sequence Intubation and Post-Intubation

Analgesia and Sedation for Major Trauma Patients

NB Trauma Program – July 2018

Background:

  • Major trauma patients frequently require advanced airway control.
  • Endotracheal intubation is the preferred advanced airway intervention in major trauma patients.
  • Intubated trauma patients also need significant post-intubation pharmacological support.
  • Specifically, these patients require analgesia and sedation. This is particularly true when transfer to another facility is required, during which ICU level support is not available unless transfer occurs via Air Ambulance.
  • In New Brunswick, there is significant variation in the approach to both advanced airway control and post-intubation analgesia and sedation practices for major trauma patients.
  • Physicians in smaller centres in particular have asked for standardized, evidence-based guidance for both Rapid Sequence Intubation (RSI) and post-intubation pharmacological support in preparation for (and during) ground-based interfacility transfer.
  • Rapid Sequence Intubation (RSI) is a method to achieve airway control that involves rapid administration of sedative and paralytic agents, followed by endotracheal intubation.
  • The purpose of RSI is to affect a state of unconsciousness and neuromuscular blockade, allowing for increased first pass success of endotracheal intubation.
  • Post-intubation analgesia and sedation is a method of controlling pain, agitation and medically induced amnesia for major trauma patients.

 

Consensus Statements:

 

  • A provincially standardized, evidence-based guideline for Rapid Sequence Intubation should be available in all NB Trauma Centres (Appendix A).
  • Similarly, a provincially standardized, evidence-based guideline for Post-Intubation Analgesia and Sedation should be available in the Emergency Department of all NB Trauma Centres (Appendix B).
  • In addition to standardized, evidence-based guidelines, a provincially standardized equipment layout is recommended to optimize the preparation for RSI (Appendix C).
  • Ambulance New Brunswick should ensure consistency with the provincially standardized guidelines for RSI and Post-Intubation Sedation and Analgesia in procedures for Ambulance New Brunswick’s Air Medical Crew.
  • RSI should not be considered or applied for trauma patients who are in cardiac arrest or who are apneic.
  • RSI should not be considered in patients with a predicted difficult airway.
  • RSI should be considered for all trauma patients meeting the following:
    • GCS < 8, quickly deteriorating GCS or loss of airway protection
    • Facial trauma with poor airway control
    • Burns with suspected inhalation injury
    • Respiratory failure
    • Hypoxia
    • Persistent or uncompensated shock (reduction of respiratory efforts)
    • Agitation with possible injury to self or others
    • Potential for eventual respiratory compromise
    • Possible respiratory and/or neurological deterioration during prolonged transport
    • Transport in a confined space with limited resources
  • In addition to the above, RSI Guidelines should include
    • Assessment of the possibility of a difficult intubation
    • Troubleshooting
    • Immediate reference to post-intubation analgesia and sedation
  • In addition to standardized, evidence-based guidelines, a provincially standardized pre-induction checklist is recommended to optimize the preparation for RSI (Appendix D)

 


 

Download (PDF, 885KB)

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EM Reflections – June 2019 – Part 2

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

Edited by Dr David Lewis 


Discussion Topics

  1. When is a pregnancy not a pregnancy? (see part 1)
  2. Caustic Ingestions (see part 1)
  3. Transient Ischemic Attack – ED Questions

 

Transient Ischemic Attack – ED Questions

 

Transient Ischemic Attack (TIA): A brief episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, with clinical symptoms and without imaging evidence of acute infarction. Transient ischemic attack and minor stroke are the mildest form of acute ischemic stroke in a continuum that cannot be differentiated by symptom duration alone, but the former typically resolves within one hour.

https://www.strokebestpractices.ca/

 

Dual Anti-Platelet Therapy (DAPT)?

Patients who present within 48 hours of a suspected transient ischemic attack are at the highest risk for recurrent stroke

Uptodate – DAPT for high-risk TIA, defined as an ABCD2 score of ≥4

For CVA – ASA only unless already on ASA, then DAPT.  For minor CVA/TIA – DAPT


Hold Birth Control?


 

Admission?

Of all ischemic strokes during the 30 days after a first TIA, 42 percent occurred within the first 24 hours.

 


Stroke Assessment Pocket Cards

Saskatchewan TIA Referral Pathway

Saskatchewan TIA Patient Information Leaflet

 

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EM Reflections – June 2019 – Part 1

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

Edited by Dr David Lewis 


Discussion Topics

  1. When is a pregnancy not a pregnancy?
  2. Caustic Ingestions
  3. Transient Ischemic Attack – Emergency Medicine (see part 2)

When is a pregnancy not a pregnancy?

Molar Pregnancy

Hydatidiform mole (molar pregnancy) is a relatively rare complication of fertilization with an incidence in the United States of 0.63 to 1.1 per 1000 pregnancies, although rates vary geographically. It is included in the spectrum of gestational trophoblastic diseases and is comprised of both complete molar pregnancies (CM) and partial molar pregnancies (PM).

The most well characterized risk factor for CM is extreme of maternal age. Maternal ages less than 20 or greater than 40 years have been associated with relative risks for CM as high as 10- and 11-fold greater respectively. Other potential risk factors include oral contraceptive use, maternal type A or AB blood groups, maternal smoking, and maternal alcohol abuse.

Molar pregnancy typically presents in the first trimester and may be associated with a wide array of findings, including vaginal bleeding (most common), uterine size larger than expected according to pregnancy date (CM), uterine size smaller than expected according to pregnancy date (PM), excessive beta-human chorionic gonadotropin (β-hcg) levels, anemia, hyperemesis gravidum, theca lutein cysts, pre-eclampsia, and respiratory distress.Studies comparing modern clinical presentations of CM with historical presentations have demonstrated a significant reduction in many of the classic presenting signs and symptoms such as vaginal bleeding and excessive uterine size. This reduction is attributed to early detection by transvaginal ultrasound and increasingly sensitive β-hcg assays. Numerous studies evaluating the efficacy of ultrasound in detecting molar pregnancy demonstrate a 57–95 percent sensitivity for the detection of CM compared to only 18–49 percent sensitivity for PM.

More here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791738/

PoCUS – Normal Early Pregnancy

Arrow = Yolk sac (YS) within Gestational sac (GS), note the hyperechoic decidual reaction surrounding GS, Arrow head = Fetal Pole

PoCUS – Molar Pregnancy

 

PoCUS SIgns:

  • enlarged uterus
  • may be seen as an intrauterine mass with cystic spaces without any associated fetal parts
    • the multiple cystic structures classically give a “snow storm” or “bunch of grapes” type appearance.
  • may be difficult to diagnose in the first trimester 6
    • may appear similar to a normal pregnancy or as an empty gestational sac
    • <50% are diagnosed in the first trimester
  • More on Radiopedia.org

Useful post from County EM blog- click here

 


Caustic Ingestions

 

 

Hydrochloric Acid – pH 1-2

Dangerous if pH <2 or >11.5-12

For alkaline – higher percent, shorter time to burn – 10%NaOH – 1 min of contact to produce deep burn, 30% within seconds

 

Acid – painful to swallow so usually less volume, bad taste so more gagging/laryngeal injury, more aqueous so less esophageal injury, pylorospasm prevents entry into duodenum producing stagnation and prominent antrum injury.  Food is protective.  Acid ingestion typically produces a superficial coagulation necrosis that thromboses the underlying mucosal blood vessels and consolidates the connective tissue, thereby forming a protective eschar.  In enough amount – perforation.

Alkali – burns esophagus more, neutralized in stomach.  Liquefaction necrosis.

Management

Decontamination: Activated charcoal / GI decontamination / neutralisation procedures are contraindicated

Obtaining meaningful info from endoscopy after treatment with charcoal is very difficult

If asymptomatic – observe, trial of oral intake at 4 hours after exposure, earlier if low suspicion or likely benign ingestion after discussion with Poisons Centre

Symptomatic patients or those with a significant ingestion

(high-concentration acid or alkali or high volume [>200 ml] of a low-concentration acid or alkali)

Upper GI endoscopy should be performed early (3 to 48 hrs) and preferably during the first 24 hrs after ingestion to evaluate extent of esophageal and gastric damage and guide management.  Endoscopy is contraindicated in patients who have evidence of GI perforation. (Ingestion of >60 mL of concentrated HCl leads to severe injury to the GI tract with necrosis and perforation, rapid onset of MODS and is usually fatal – endoscopy within 24 hours (unless asymptomatic at 4 hours)

Complications – 1/3 develop strictures – directly related to depth/severity of injury, years later

 


 

TAKE HOME POINTS

  1. PV Bleed, Hyperemesis, PoCUS = bunch Grapes or Snowstorm – consider Molar Pregnancy
  2. Don’t use Activated Charcoal for Caustic Ingestions
  3. Discuss Caustic Ingestions with Poisons Centre
  4. Consider early endoscopy
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