Welcome to the “52 in 52” series! This collection of posts features recently published must-know articles. For our first post, Brannon Inman looks at the HALT-IT trial.

Authors: Brannon Inman (Chief Resident, Emergency Medicine Physician, San Antonio, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomized, double-blind, placebo-controlled trial

AKA: The “HALT-IT” Trial

Clinical question:

Does TXA reduce bleeding-related death in patients with GI bleed?

Study design:

• Block randomized placebo-controlled trial

PICO:

Population:

• Included patents in 15 countries:
  • UK, Pakistan, Nigeria, Egypt, Malaysia, Georgia, Romania, Nepal, Sudan, Saudi Arabia, Spain, Ireland, Albania, Papua New Guinea, and Australia
• Included patients above age of adulthood for respective countries (16 or 18 depending on country) with gastrointestinal bleed (upper or lower GI bleed)
• Clinician caring for patient must have been uncertain if TXA would be helpful
• Diagnosis of bleeding needed to be significant, and clinical, defined as “At risk for bleeding to death”. Authors included patients with:
  • Tachycardia
  • Hypotension
  • Shock
  • Expected need for endoscopy/surgery
• Exclusion criteria not stated

Intervention:

• 1g TXA load (in 100 cc 0.9% NS administered over 10 min)
• Following load, 3g TXA infusion administered over 24 hours

Comparator:

• A placebo solution and equal volume of isotonic crystalloid administered over 24 hours

Randomization:

Treatment arms were fairly well balanced.

Outcome:

• Primary outcome included death due to bleeding within 5 days of randomization
• Authors found no significant difference in primary outcome (death due to bleeding at 5 days) (RR 0.99, 95% CI 0.82-1.18)

• Statistically significant risk observed for occurrence of venous thromboembolic events (PE and DVT) and seizures
  • VTE RR 1.85, 95% CI 1.15-2.98, NNH 250
• No increase in arterial thromboembolic events (MI and stroke)

Take away:

• This is a negative trial.
• Included patients with upper and lower GI bleeds as one group, which is not how we typically classify these patients. The majority of patients had variceal bleed, accounting for 75% of deaths. Less than 10% of included patients were on anticoagulants.
• Only 69% of patients required transfusion, and 87% had SBP > 90 mm Hg with 30% having a HR > 107.
• Time from onset to randomization < 3 hours was present in 16% of patients. Most patients received TXA over 8 hours from time of bleeding onset.
• Primary outcome changed from all-cause mortality to GI bleeding related mortality in 5 days. Reportedly this decision was made blind to the accumulating data. Changing a primary outcome from a patient-centered outcome to a disease-centered outcome is odd. Our patients do not care what they die from, nor do their families. With the used primary outcome, patients could have been dying from TXA complications, and this would not have been captured (albeit this is unlikely).
• Very few trials have shown harm associated with TXA. This trial showed a statically significant risk of VTE and seizures.

My take:

• This is a well-constructed, multicenter RCT comparing TXA versus placebo for patients with acute GI bleeding. Based on the results from this RCT, TXA does not reduce death from GI bleeding and may increase risk of VTE and seizure.
• I won’t be using TXA for GI bleed patients in my clinical practice.

Reference:

1. Brenner A, Afolabi A, Ahmad SM, et al. Tranexamic acid for acute gastrointestinal bleeding (the HALT-IT trial): statistical analysis plan for an international, randomised, double-blind, placebo-controlled trial. Trials. 2019;20(1):467. Published 2019 Jul 30. doi:10.1186/s13063-019-3561-7

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Originally published on Ultrasound G.E.L. on 8/31/20 – Visit HERE to listen to accompanying PODCAST! Reposted with permission.

Follow Dr. Michael Prats, MD (@PratsEM) from Ultrasound G.E.L. team!

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Here’s another case from Medical Malpractice Insights – Learning from Lawsuits, a monthly email newsletter for ED physicians. The goal of MMI-LFL is to improve patient safety, educate physicians and reduce the cost and stress of medical malpractice lawsuits. To opt in to the free subscriber list, click here. Stories of med mal lawsuits can save lives. If you have a story to share click here.

Chuck Pilcher, MD, FACEP

Editor, Medical Malpractice Insights

Editor, Med Mal Insights

Death happens

A bad outcome does not necessarily mean negligence

A 36-year-old female presents to a rural ED with a 1 week history of mild dyspnea and dull chest pain, worsening just prior to arrival. She is triaged as a Level 3 and taken immediately to the treatment area.

Timeline:

0:02: VS are normal except for a BP of 169/102. Placed on O2 and cardiac monitor. Physician at bedside. Family history of early heart disease obtained.

0:07: IV is started and labs drawn including a troponin and d-dimer. A quick exam of neck, lungs, heart, abdomen, and extremities is unremarkable. BMI is 39.7.

0:08: EKG is done and ischemia noted.

0:13: CXR is completed and normal.

0:20: Receives prophylactic aspirin for presumptive ACS.

0:32: VS are normal with BP of 138/85.

0:44: Patient reports increasing chest pain.

0:50: Reports extreme SOB.

0:51: Has a grand mal seizure. Monitor shows VF. Labs pending.

0:51-2:07: Resuscitative efforts begin. Labs return about 10 minutes into code (54 minutes after being drawn). The D-dimer is normal but the troponin that was ordered is not resulted anywhere in the record for unknown reasons. CO2 is 19, WBC is 20,330 (48% neutrophils, 44% lymphocytes, no bands). Electrolytes and renal and liver function normal. CPR continues for 1 hour & 16 minutes per ACLS protocols without ROSC.

2:07: Code called.

Post-event: Cause of death is listed as “Ventricular Fibrillation.” No autopsy is performed. An attorney is consulted about her care and the case is reviewed by an ED expert.

Plaintiff Arguments:

• I was only 36 years old. I shouldn’t have died so young.
• You knew I had a positive family history of early heart disease.
• You never gave me a trial of nitroglycerine.
• I had a heart attack. If you had given me tPA in time, I’d still be alive today.

Defense Arguments:

• Your care was timely and reasonable. We treated you the same as we would treat any other chest pain patient.
• Yes, you had unexpected ventricular fibrillation and it was probably due to a heart attack, but without an autopsy that’s a presumption, not a fact. We don’t know what caused your death.
• Yes, we did not give you a trial of NTG. It didn’t matter. 1) If we had given you NTG, your response to NTG is an unknown. 2) If it had helped, it only means that the problem is likely heart related – but not necessarily an MI, given the EKG finding of ischemia only. 3) If it did not help, it could mean that your problem was caused by something else, like a pulmonary embolus or aortic dissection.
• Until the troponin level returned, we had no reason to give you tPA. And you were in VF before the troponin result would have appeared along with the other lab results. We don’t know what happened to the troponin order and we can’t assume what the result would have been.
• Once you went into VF and we began CPR, tPA would not likely have made a difference.
• We are a rural hospital with no cath lab. We transfer patients with an acute MI to a hospital with a cath lab. Once you went into VF, you became too unstable to transfer.
• Finally, if we had known the troponin, given you tPA, been able to transfer you quickly, you can’t assume that you would not have gone into VF during the transfer.
• Your care was timely, appropriate to your presentation and within acceptable local community hospital standards.

Result: Based on the expert’s review, no lawsuit was filed.

Takeaways:

• Young patients can have MI’s. About 8% are < 45 yo.
• Any chest pain patient can crump at any time. Remain diligent.
• Bad things will still happen over which we have no control.
• A rural hospital with no cath lab is held to a different standard than an urban academic hospital.
• Good documentation always helps.
• Was this an MI, a PE, an aortic dissection – or something else? Sometimes we don’t ever learn what we missed.
• Pain relief of nitroglycerin does not modify the likelihood of ACS. This should not be used to rule in or rule out ACS.
• We do not know if the cause of the missing troponin level was ever investigated by the hospital. Clearly it should have been.
• Standard care is defensible. Not every bad outcome results in a lawsuit.

The post Medical Malpractice Insights: Death Happens appeared first on emDOCs.net - Emergency Medicine Education.

• Imaging:
  • Computed tomography (CT) neck with contrast is initial study of choice
    • Allows for imaging of clot and potential abscess formation
    • May demonstrate intraluminal filling defect, peripheral rim enhancement
    • Thrombus can measure 10-20cm and CT allows for evaluation of complete occlusion
    • Can extend to chest to visualize septic pulmonary emboli
  • Ultrasound (US)
    • POCUS allows for rapid identification, though reduced sensitivity for recently formed thrombus as well as deeper infections and areas not amenable to US (e.g., mandibular)
  • Chest plain radiograph may demonstrate septic pulmonary emboli

The post emDOCs Podcast – Episode 56: Lemierre’s Syndrome and Retropharyngeal Abscess appeared first on emDOCs.net - Emergency Medicine Education.

Author: Brit Long, MD (@long_brit) // Reviewed by Alex Koyfman, MD (@EMHighAK)

The American Heart Association/American Stroke Association (AHA/ASA) 2022 Guideline for managing spontaneous intracerebral hemorrhage (ICH) was recently released. This post will focus on the key parts of the guideline that affect ED evaluation and management.

Background

ICH is defined as acute blood extravasation into brain parenchyma. There are approximately 795,000 strokes per year, with 10% of these being an ICH. Unfortunately, ICH disproportionately affects low resource populations worldwide. In the U.S., there is a 1.6-fold higher risk of ICH in Black and Mexican Americans compared to non-Hispanic White people.

Early mortality is severe, approximating 30-40%, and the incidence drastically increases with age. The increasing use of anticoagulants has also resulted in greater numbers of ICH. ICH is often the consequence of several factors, including trauma, cancer, AVMs, aneurysm, venous pathology (cerebral venous thrombosis), hemorrhagic conversion of ischemic stroke, and microvascular disease including arteriolosclerosis and cerebral amyloid angiopathy. Once blood extravasates, it can cause direct pressure effects as well as physiological and cellular damage.

The remainder of this post will provide a brief synopsis of the guidelines, with some editorial thoughts as well.

The Recommendations

All recommendations are designated with a class of recommendation (COR) and level of evidence (LOE).  COR is the strength of the recommendation, while the LOE is the quality of scientific evidence.

Physical Examination and Laboratory Assessment

Obtain focused history, exam, and routine laboratory testing to assist with identifying the type of hemorrhage, active medical issues, and risk of unfavorable outcomes. COR 1, LOE C-LD

Neuroimaging

In patients presenting with stroke-like symptoms, rapid neuroimaging with CT or MRI is recommended to confirm the diagnosis of spontaneous ICH. COR 1, LOE B-NR

In patients with spontaneous ICH and/or IVH, serial head CT can be useful within the first 24 hours after symptom onset to evaluate for hemorrhage expansion. COR 2a, LOE B-NR

In patients with spontaneous ICH and/or IVH and with low GCS score or ND, serial head CT can be useful to evaluate for hemorrhage expansion, development of hydrocephalus, brain swelling, or herniation. COR 2a, LOE C-LD

In patients with spontaneous ICH, CT angiography (CTA) within the first few hours of ICH onset may be reasonable to identify patients at risk for subsequent HE. COR 2b, LOE B-NR

In patients with spontaneous ICH, using noncontrast computed tomography (NCCT) markers of HE to identify patients at risk for HE may be reasonable. COR 2b, LOE B-NR

Editorial Comment: The guideline incorporates CTA, which may assist with diagnosis and prognostication. The spot sign may be associated with mortality and poor mRS, score, but the data are heterogenous and have significant limitations.

Diagnostic Assessment for Pathogenesis

In patients with lobar spontaneous ICH and age <70 years, deep/posterior fossa spontaneous ICH and age <45 years, or deep/posterior fossa and age 45 to 70 years without history of hypertension, acute CTA plus consideration of venography is recommended to exclude macrovascular causes or cerebral venous thrombosis. COR 1, LOE B-NR

In patients with spontaneous ICH who undergo CT or MRI at admission, CTA plus consideration of venography or MRA plus consideration of venography performed acutely can be useful to exclude macrovascular causes or cerebral venous thrombosis. COR 2a, LOE C-LD

Editorial Comment: They incorporate venography in a select subset of patients to evaluate for CVT. This is an important consideration, as CVT requires anticoagulation even in the setting of ICH.

Treatment: Acute BP Lowering

In patients with spontaneous ICH requiring acute BP lowering, careful titration to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in SBP, can be beneficial for improving functional outcomes. COR 2a, LOE B-NR

In patients with spontaneous ICH in whom acute BP lowering is considered, initiating treatment within 2 hours of ICH onset and reaching target within 1 hour can be beneficial to reduce the risk of HE and improve functional outcome. COR 2a, LOE C-LD

In patients with spontaneous ICH of mild to moderate severity presenting with SBP between 150 and 220 mm Hg, acute lowering of SBP to a target of 140 mm Hg with the goal of maintaining in the range of 130 to 150 mm Hg is safe and may be reasonable for improving functional outcomes. COR 2b, LOE B-R

HARM: In patients with spontaneous ICH of mild to moderate severity presenting with SBP >150 mm Hg, acute lowering of SBP to <130 mm Hg is potentially harmful. COR 3, LOE B-R

Editorial Comment: The guideline recommends a range between 130-150 for a BP target in those with a presenting BP between 150-220, while avoiding drops less than 130.  For those with higher BPs, decrease that BP by 20% in the first hour. If you drop these patients by too much and too rapidly, end organ injury can occur (ie, renal injury), and cerebral perfusion pressure will also decrease.  The key is a steady, early decrease in BP. Most of the studies included in the guideline included patients where BP treatment was initiated at least 3 hours after onset of the ICH (ATACH-2, INTERACT). Decreasing BP within the first hour can improve patient outcomes. Use a reliable antihypertensive infusion such as nicardipine or clevidipine.  An arterial line can be helpful in these critical patients, but if this is not feasible, make sure the blood pressure cuff is routinely recycled (less than every 10 minutes).

Treatment: Anticoagulant-related hemorrhage

In patients with anticoagulant-associated spontaneous ICH, anticoagulation should be discontinued immediately and rapid reversal of anticoagulation should be performed as soon as possible after diagnosis of spontaneous ICH to improve survival. COR 1, LOE C-LD

VKAs

In patients with VKA-associated spontaneous ICH and INR ≥2.0, 4-factor (4-F) prothrombin complex concentrate (PCC) is recommended in preference to fresh-frozen plasma (FFP) to achieve rapid correction of INR and limit HE. COR 1, LOE B-R

In patients with VKA-associated spontaneous ICH, intravenous vitamin K should be administered directly after coagulation factor replacement (PCC or other) to prevent later increase in INR and subsequent HE. COR 1, LOE C-LD

In patients with VKA-associated spontaneous ICH with INR of 1.3 to 1.9, it may be reasonable to use PCC to achieve rapid correction of INR and limit HE. COR 2b, LOE C-LD

Editorial Comment: Fixed dose 4-F PCC with vitamin K is the optimal reversal in this setting. However, the third recommendation of reversing an INR of 1.3-1.9 is questionable.

DOACs

In patients with direct factor Xa inhibitor–associated spontaneous ICH, andexanet alfa is reasonable to reverse the anticoagulant effect of factor Xa inhibitors. COR 2a, LOE B-NR

In patients with dabigatran-associated spontaneous ICH, idarucizumab is reasonable to reverse the anticoagulant effect of dabigatran. COR 2a, LOE B-NR

In patients with direct factor Xa inhibitor–associated spontaneous ICH, a 4-F PCC or activated PCC (aPCC) may be considered to improve hemostasis. COR 2b, LOE B-NR

In patients with dabigatran- or factor Xa inhibitor–associated spontaneous ICH, when the DOAC agent was taken within the previous few hours, activated charcoal may be reasonable to prevent absorption of the DOAC. COR 2b, LOE C-LD

In patients with dabigatran-associated spontaneous ICH, when idarucizumab is not available, aPCC or PCCs may be considered to improve hemostasis. COR 2b, LOE C-LD

In patients with dabigatran-associated spontaneous ICH, when idarucizumab is not available, renal replacement therapy (RRT) may be considered to reduce dabigatran concentration. COR 2b, LOE C-LD

Editorial Comment: There is limited evidence supporting improved patient-centered outcomes with andexanet alfa. 4-F PCC and aPCC are effective reversal agents, with more literature support compared to anexanet alfa for DOAC reversal. An institutional protocol utilizing aPCC is recommended.

Heparins

In patients with unfractionated heparin (UFH)–associated spontaneous ICH, intravenous protamine is reasonable to reverse the anticoagulant effect of heparin. COR 2a, LOE C-LD

In patients with low-molecular-weight heparin (LMWH)–associated spontaneous ICH, intravenous protamine may be considered to partially reverse the anticoagulant effect of heparin. COR 2b, LOE C-LD

Treatment: Antiplatelet-related hemorrhage

For patients with spontaneous ICH being treated with aspirin and who require emergency neurosurgery, platelet transfusion might be considered to reduce postoperative bleeding and mortality. COR 2b, LOE C-LD

For patients with spontaneous ICH being treated with antiplatelet agents, the effectiveness of desmopressin with or without platelet transfusions to reduce the expansion of the hematoma is uncertain. COR 2b, LOE C-LD

HARM: For patients with spontaneous ICH being treated with aspirin and not scheduled for emergency surgery, platelet transfusions are potentially harmful and should not be administered. LOE B-R

Editorial Comment: Desmopressin 0.3 mcg/kg IV  is promising, especially in patients with renal disease or those on aspirin. Many centers use platelet response testing. This may assist in determining the need for platelet transfusion in those on ASA or clopidogrel. Make sure to speak with neurosurgery as well.

From EMCrit.org

Treatment: General Hemostatic Measures

In patients with spontaneous ICH (with or without the spot sign), the effectiveness of recombinant factor VIIa to improve functional outcome is unclear. COR 2b, LOE B-R.

In patients with spontaneous ICH (with or without the spot sign, black hole sign, or blend sign), the effectiveness of TXA to improve functional outcomes is not well established. COR 2b, LOE B-R

Editorial Comment:  TXA is likely not beneficial in patients with ICH.

General Inpatient Care

In patients with spontaneous ICH, provision of care in a specialized inpatient (eg, stroke) unit with a multidisciplinary team is recommended to improve outcomes and reduce mortality. COR 1, LOE A

In patients with spontaneous ICH and clinical hydrocephalus, transfer to centers with neurosurgical capabilities for definitive hydrocephalus management (eg, EVD placement and monitoring) is recommended to reduce mortality. COR 1, LOE B-NR

In patients with moderate to severe spontaneous ICH, IVH, hydrocephalus, or infratentorial location, provision of care in a neuro-specific ICU compared with a general ICU is reasonable to improve outcomes and reduce mortality. COR 2a, LOE B-NR

In patients with IVH or infratentorial ICH location, transfer to centers with neurosurgical capabilities might be reasonable to improve outcomes. COR 2b, LOE B-NR

Editorial Comment: A dedicated care team and ICU can improve outcomes. Have a low threshold to transfer these patients to centers with a multidisciplinary care team, including neurosurgery and neurocritical care teams.

Thromboprophylaxis

In nonambulatory patients with spontaneous ICH, intermittent pneumatic compression (IPC) starting on the day of diagnosis is recommended for VTE (DVT and pulmonary embolism [PE]) prophylaxis. COR 1, LOE B-R

In nonambulatory patients with spontaneous ICH, low-dose UFH or LMWH can be useful to reduce the risk for PE. COR 2a, LOE C-LD

In nonambulatory patients with spontaneous ICH, initiating low-dose UFH or LMWH prophylaxis at 24 to 48 hours from ICH onset may be reasonable to optimize the benefits of preventing thrombosis relative to the risk of HE. COR 2b, LOE C-LD

Editorial Comment: In most situations, thromboprophylaxis can be left to the intensivist and neurosurgeon.

Glucose

In patients with spontaneous ICH, monitoring serum glucose is recommended to reduce the risk of hyperglycemia and hypoglycemia. COR 1, LOE C-LD

In patients with spontaneous ICH, treating hypoglycemia (<40–60 mg/d, <2.2–3.3 mmol/L) is recommended to reduce mortality. COR 1, LOE C-LD

In patients with spontaneous ICH, treating moderate to severe hyperglycemia (>180– 200 mg/dL, >10.0–11.1 mmol/L) is reasonable to improve outcomes. COR 2a, LOE C-LD

Editorial Comment: Avoid hypo- and hyperglycemia.

Temperature

In patients with spontaneous ICH, pharmacologically treating an elevated temperature may be reasonable to improve functional outcomes. COR 2b, LOE C-LD

In patients with spontaneous ICH, the usefulness of therapeutic hypothermia (<35C/95F) to decrease peri-ICH edema is unclear. COR 2b, LOE C-LD

Editorial Comment: Avoid elevated temperatures, but there is no clear evidence supporting therapeutic hypothermia.

Seizures and Antiseizure Medications

In patients with spontaneous ICH, impaired consciousness, and confirmed electrographic seizures, antiseizure drugs should be administered to reduce morbidity. COR 1, LOE C-LD

In patients with spontaneous ICH and clinical seizures, antiseizure drugs are recommended to improve functional outcomes and prevent brain injury from prolonged recurrent seizures. COR 1, LOE C-EO

In patients with spontaneous ICH and unexplained abnormal or fluctuating mental status or suspicion of seizures, continuous electroencephalography (≥24 hours) is reasonable to diagnose electrographic seizures and epileptiform discharges. COR 2a, LOE C-LD

No Benefit: In patients with spontaneous ICH without evidence of seizures, prophylactic antiseizure medication is not beneficial to improve functional outcomes, long-term seizure control, or mortality. LOE B-NR

Editorial Comment: Treat seizures if they occur, but otherwise, do not provide prophylactic antiseizure medications.

ICP and Cerebral Edema

In patients with spontaneous ICH or IVH and hydrocephalus that is contributing to decreased level of consciousness, ventricular drainage should be performed to reduce mortality. COR 1, LOE B-NR

In patients with moderate to severe spontaneous ICH or IVH with a reduced level of consciousness, ICP monitoring and treatment might be considered to reduce mortality and improve outcomes. COR 2b, LOE B-NR

In patients with spontaneous ICH, the efficacy of early prophylactic hyperosmolar therapy for improving outcomes is not well established. COR 2b, LOE B-NR

In patients with spontaneous ICH, bolus hyperosmolar therapy may be considered for transiently reducing ICP. COR 2b, LOE C-LD

No Benefit:  In patients with spontaneous ICH, corticosteroids should not be administered for treatment of elevated ICP. LOE B-R

Editorial Comment: If concerned about elevated ICP and the patient decompensates, administer a bolus hyperosmolar agent such as hypertonic saline, and a bolus is probably better than a  continuous infusion. Hypertonic saline may be better than mannitol. Steroids are also not recommended.

Surgical Therapies

There are specific patient populations that may improve with surgical interventions, especially those with larger bleeds and depressed GCS. The key is to consult neurosurgery early in the care of these patients.

Outcome Prediction

In patients with spontaneous ICH, administering a baseline measure of overall hemorrhage severity is recommended as part of the initial evaluation to provide an overall measure of clinical severity. COR 1, LOE B-NR

In patients with spontaneous ICH, a baseline severity score might be reasonable to provide a general framework for communication with the patient and their caregivers. COR 2b, LOE B-NR

No Benefit:  In patients with spontaneous ICH, a baseline severity score should not be used as the sole basis for forecasting individual prognosis or limiting life-sustaining treatment. LOE B-NR

Editorial Comment: Be careful using the ICH score to prognosticate. It may be helpful with assessing disease severity. Much of the patient’s prognosis depends on their baseline status prior to the ICH.

Summary:

• ICH is deadly and accounts for 10% of all strokes.
• In the patient with suspected stroke, perform a rapid assessment (such as CPSS, VAN), and obtain a glucose and noncontrast head CT. CTA may be helpful, as can venography in select patients.
• Once ICH is diagnosed on CT, our goals are to stabilize the patient, control blood pressure (rapid control with an IV infusion), prevent further injury (avoid elevated ICP, hypoxia, hypotension, hypoglycemia), and admit to an appropriate facility (ie, transfer may be needed).
• Consult neurosurgery early in the care of these patients.

Reference:

Greenberg SM, Ziai WC, Cordonnier C, et al; American Heart Association/American Stroke Association. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2022 May 17:101161STR0000000000000407. doi: 10.1161/STR.0000000000000407.

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Authors: Elizabeth Adams, MD (EM Resident Physician, UTSW, Dallas, TX); Samuel Parnell, MD (Assistant Professor of EM / APD, UTSW, Dallas, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

Vital signs on arrival to the ED include HR 68, BP 118/72, SpO2 99% on RA, RR 14, Temp 98.8F. On exam, patient is non-toxic appearing, comfortable, without rash. HEENT exam reveals normal external auditory canal and tympanic membrane on the left, but you are unable to visualize the right tympanic membrane due to cerumen impaction. The patient does not experience pain with manipulation of the pinna. There is no erythema or posterior auricular swelling/tenderness present on exam.

What is the most likely cause of this young man’s ear discomfort and hearing loss? What is the next step in management of this patient?

Background:

• Cerumen (also known as ear wax) is produced in the outer portion of the external auditory canal and protects the canal and tympanic membrane from debris, trauma, infection, and water¹.
• Cerumen is made of secretions from sebaceous and ceruminous glands and sloughed epithelial cells².
• As cerumen is produced, it migrates outward and is cleared. Failure of this migration outward due to mechanical obstruction, anatomic variation of the external auditory canal, counterproductive at-home cleaning methods (such as cotton-tipped swabs), or over-production of cerumen can lead to the build-up of cerumen¹.

Pathophysiology:

• Cerumen impaction is defined as blockage of the ear canal by cerumen prohibiting evaluation of the tympanic membrane or leading to symptoms – most frequently, otalgia, itching, ear fullness, hearing loss, vertigo, or even persistent cough¹.

History and Exam:

• Elicit the presence of pain, hearing loss, tinnitus, headache, nausea/vomiting, dizziness/vertigo, fevers, drainage from the ear, and history of frequent ear infections.
• Assess for factors that contribute to disease of the ear including use of in-ear headphones or hearing aids, prior trauma or surgery to the ear, use of home earwax cleaning products, dermatologic conditions (including eczema, psoriasis and seborrheic keratosis), and immunocompromised states or diabetes.
• Examine externally for erythema, swelling, or tenderness to the pinna and posterior auricular area. Evaluate for pain with manipulation of the pinna.
• Inspect inside the ear with an otoscope to evaluate the skin of the external auditory canal (EAC) for rash, vesicles, drainage, presence of cerumen impaction, or foreign body. Inspect the tympanic membrane, if visible.
• Consider the possibility of referred pain from the posterior oropharynx to the ear. Inspect the oropharynx.
• If hearing loss is reported, perform a “Hum Test,” to determine conductive vs sensorineural hearing loss³
  • Have the patient hum and localize which side, if any, sounds louder.
  • If the affected ear is louder, it is likely conductive hearing loss.
  • If the unaffected ear is louder, it is concerning for sensorineural hearing loss. Abrupt hearing loss is abrupt is concerning for sudden sensorineural hearing loss (SSNHL) which can be irreversible if not identified and treated early⁴.

Differential Diagnosis:

• Otitis Externa
• Malignant Otitis Externa
• Otitis Media
• Foreign Body
• Mastoiditis
• Varicella Zoster Virus/Shingles
• Tympanic Membrane Perforation
• Cholesteatoma
• Presbycusis
• Meniere’s Disease
• Labyrinthitis
• Sensorineural Hearing Loss
• Sudden Sensorineural Hearing Loss (SSNHL) – see article below for more information on this time-sensitive otologic emergency⁴

ED Evaluation:

• Perform a thorough exam to determine the presence of foreign body or infection contributing to symptoms.
• When a cerumen impaction is identified, the need to intervene is determined by the presence of symptoms.
• Removal of impacted cerumen is recommended in symptomatic patients, unless there is presence of a non-intact TM.
• Removal of impacted cerumen is recommended in patients who are unable to express symptoms, such as young children or those with cognitive impairment¹.
• Asymptomatic patients should not routinely have cerumen removed^1,2.

Management:

• There are multiple option available for removal of cerumen — including the use of cerumenolytics, irrigation, or manual removal under direct visualization^2,5.
  • Cerumenolytics – variety of options including hydrogen peroxide (diluted in water), normal saline, or pre-mixed cerumenolytics (such as Debrox – combination of hydrogen peroxide and urea); instill solution into the ear canal, place cotton ball in the ear, and position patient in lateral recumbent position to retain solution in EAC for 10-15 minutes, repeating as necessary to soften wax and facilitate removal (possibly combined with irrigation methods)^2,6.
  • Irrigation – use soft catheter tip (for example an 18-gauge angiocath) to flush EAC with warm/room temperature saline solution (or combine with hydrogen peroxide) and continue as patient tolerates until impaction is resolved. Consider pre-treatment with cerumenolytics prior to irrigation⁶.
  • Manual Removal – perform manual removal only under direct visualization with plastic or metal curette in a cooperative patient who can tolerate the procedure without moving.
• Use caution when removing cerumen in patients with diabetes, anticoagulant use, immunocompromised states, ear canal stenosis, perforated tympanic membrane, or prior surgery to the TM (such as tympanostomy tubes).
• Following cerumen removal, inspect for lacerations or abrasions to the EAC and for the presence of trauma to the tympanic membrane.
• If the patient reported hearing loss, assess for subjective improvement in hearing following cerumen removal.
• Referral to an otolaryngologist is recommended for incompletely resolved cerumen impaction, history of recurrent cerumen impaction, TM perforation, or unresolved hearing deficit.

Complications:

• Iatrogenic trauma/bleeding to external auditory canal or tympanic membrane
• Otitis externa from external auditory canal trauma
• Infection or water accumulation behind an untreated cerumen impaction
• Use of cold or hot water during irrigation or removal can lead to nausea, vomiting and vertigo
• Untreated cerumen impaction can contribute to delirium in elderly patients and can affect speech and language development in children if an associated hearing deficit is not addressed

Take-home Points:

• Impacted cerumen can lead to pain, discomfort or hearing deficits and can contribute to delirium in elderly or speech and language delays in children and should be managed appropriately in symptomatic patients.
• Options for management of cerumen impaction include cerumenolytics, irrigation and manual removal. The method of choice depends on availability of equipment and preference of provider.
• Consider the diagnosis of sudden sensorineural hearing loss – an otologic emergency – in patients with sudden onset hearing loss that is not conductive, or not resolved after treatment of cerumen impaction.

A 20-year-old woman presents to the ED with acute onset hearing loss in her right ear. Otoscopy reveals cerumen impaction on the right. The left ear exam is normal. Weber and Rinne tests are performed. What are the expected results of the tests given this information?

A) Air conduction greater than mastoid conduction on right

B) Lateralizes to the right with forehead conduction

C) No lateralization with forehead conduction

D) Weber test will lateralize to the left

Answer: B

Hearing is a special sensory function of the vestibulocochlear nerve (cranial nerve VIII). There are many causes of hearing impairment or loss, including aging, stroke, blunt or penetrating trauma, cerumen impaction, medications, infection, barotrauma (e.g., loud noises, diving), congenital disorders, electrolyte abnormalities, cholesteatoma, or otoliths within the semicircular canals in the inner ear. Hearing loss is either sensorineural or conductive. Mixed cases are described as well. The Weber and Rinne tests with a vibratory tuning fork can be employed at the bedside to determine the type of hearing loss. The Weber test is performed by placing a vibrating tuning fork on the midline of the forehead. If there is conductive hearing loss, the sound will lateralize to (i.e., be heard louder in) the affected side. If there is sensorineural hearing loss, the sound will lateralize to the unaffected side. The Rinne test is performed by placing the tuning fork on the mastoid process and then, when the sound is no longer heard, placing it in front of the patient’s ear. If the patient is then unable to hear with the tuning fork in this position or the sound is not heard louder in this position, this is considered an abnormal test and conductive hearing loss is present. This suggests that bone conduction (when the tuning fork is in contact with bone) is greater than air conduction (when the tuning fork is in front of the patient’s ear). Cerumen impaction causes conductive hearing loss. Therefore, if the right ear is affected (as in this case), sound lateralizes to the right with forehead conduction (Weber test), and the Rinne test will be abnormal, meaning that sound will be diminished or inaudible when the tuning fork is moved from the right mastoid in front of the right ear.

Air conduction greater than mastoid conduction on the right (A) suggests a normal Rinne test. Cerumen impaction on the right would cause mastoid conduction to be greater than air conduction. No lateralization with forehead conduction (C) indicates a normal Weber test. With right-sided cerumen impaction, the sound will lateralize to the affected (right) side. Therefore, Weber test will lateralize to the left (D) is also incorrect.

Rosh Review Free Qbank Access

Further Reading:

1. Schwartz SR, Magit AE, Rosenfeld RM, et al. “Clinical Practice Guideline (Update): Earwax (Cerumen Impaction) Executive Summary.” Otolaryngology–Head and Neck Surgery. 2017;156(1):14-29. doi:10.1177/0194599816678832
2. Dinces E. “Cerumen.” UpToDate, 17 June 2021.
3. Ahmed OH, Gallant SC, Ruiz R, Wang B, Shapiro WH, Voigt EP. “Validity of the Hum Test, a Simple and Reliable Alternative to the Weber Test.” The Annals of Otology, Rhinology, and Laryngology, U.S. National Library of Medicine, June 2018. 127(6):402-405. doi: 10.1177/0003489418772860
4. Weber P. “Sudden Sensorineural Hearing Loss in Adults Evaluation and Management.” UpToDate, 10 May 2022,
5. Simpson B, and Claire. “Cerumen Removal.” 29 June 2021.
6. Mitka M. “Cerumen Removal Guidelines Wax Practical.” 2008;300(13):1506. doi:10.1001/jama.300.13.1506

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Authors: Laurence Baril, MD (EM Resident Physician, Laval University) // Reviewed by: James Dazhe Cao, MD (@JamesCaoMD, Associate Professor of EM, Medical Toxicology, UT Southwestern Medical Center, Dallas, TX); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Case:

A 30-year-old male without past medical history is brought to you from the airport. The policeman accompanying him tells you that he was caught swallowing packets in the airport hall when he noticed that the police officers were watching him. For now, his only symptoms are a mild agitation and diaphoresis. He denies any illicit drug use or packet ingestion. On exam, the patient looks anxious. He has a blood pressure of 155/89, heart rate of 115, respiratory rate of 14, SpO₂ 98% on room air, and temperature of 37.2°C (99°F). He does not demonstrate any toxidrome on exam and does not have any abdominal tenderness.

Questions:

1. Where do you put this patient in your ED?
2. Do you order investigations?
3. Do you start any treatment up front?

Background and Definitions:

Ingestion of illicit drugs for transportation is not a frequent presentation but can be a challenging one. Those patients have been classified in three groups, according to the mechanism of ingestion:

1. Body packers
2. Body stuffers
3. Body pushers

The first and best known is the body packers. These patients intentionally ingest cautiously prepared drug packets in an important quantity in order to transport them. The packets are resistant and do not tend to break by passing through the digestive tract. However, if they do break, the consequences might be dramatic, due to the impressive quantity of drug now released in the intestines, potentially inducing a fatal overdose.

The second group of patients is the body stuffers. These patients ingest drug packets that are much more artisanal and fragile, in a hurry, in a moment when they feel threatened by law-enforcing officers. The amount of drug ingested is often smaller, but the packets are more prone to break and induce a significant toxicity.

The final group is the body pushers, meaning people who hide drug packets in various orifices (rectum, vagina, nose, ears, etc.). They represent a very heterogenous group, often co-occurring with one of the two previously described modes of ingestion.

When to suspect it?

Drug-transporting patients may present in a variety of ways. They might be reported by police and other law-enforcement officers and not be symptomatic of their ingestion. They might present with gastrointestinal complications (perforation, obstruction, etc.). Finally, they can show signs of toxicity, ranging from mild agitation or sedation to cardiac arrest.

How should we evaluate these patients?

When faced with a history of illicit drug ingestion for transport, the provider should try to understand what drug was ingested and in what type of packaging. The clinician must keep in mind that the patient might have incentives to hide elements and provide an incomplete or changing history. We must keep a high index of suspicion for these reasons.

The first step is to evaluate the patient and look for signs of complications from the ingestion. Leakage of the packets may lead to intoxication by the ingested drug. The most often seen ingestions are cocaine and heroin, but cannabinoids, fentanyl, and other stimulants have been reported.¹ The toxidrome will therefore usually be either opioid or sympathomimetic. Of note, patients are often mildly tachycardic and hypertensive due to their recent detention. It might be useful to observe the patient and see if these signs resolve by themselves and look for other signs of toxidrome (agitation, mydriasis, arrhythmia, diminished peristaltic, diaphoresis, etc.). The other complications to look for clinically are anatomical including obstruction, perforation, and/or bowel ischemia. A thorough physical exam including a good abdominal evaluation is critical for the patient management.^2,3,4,5

What test to order?

The gold standard for identifying body packers is the CT scan without contrast. The sensitivity has been reported up to 100% with a good specificity. This modality enables us to count the number of packets ingested and to look for complications. If anatomical complications are suspected based on the physical exam, a CT with contrast can enhance the sensitivity.^2,3,4

Abdominal X-rays were historically the first exam modalities to identify drug packets. However, most recent studies identified a sensitivity of 60–90% for body packers and much lower for body stuffers or pushers. Some clinical findings on X-rays are the “double condom sign” (a), the “parallelism sign” (b), the “Tic-tac sign” (c) and the “Rosette Sign (d).⁶ However, body packers develop innovative ways such aluminum foil and liquid drugs to make the packets less radio-opaque. Additionally, many false positives have been reported with stools, calcifications, and other intestinal foreign bodies. So, in the end, what to think of the X-ray? It can certainly be a screening tool, but we have to keep in mind that it is neither sensitive nor specific. Some experts advocate for the use of contrast-enhanced or plain abdominal X-ray to confirm the passage of packets if those were proven to be radio-opaque in the first place. In patients for whom we would prefer to limit exposure to radiation (pediatrics and pregnant women), the use of ultrasound has been described, with fairly good results (sensitivity 91%, specificity 70%).⁷

MRI is also an option for pregnant patient, but this is mostly an expert recommendation and case reports rather than strong evidence-based medicine.⁸ (Figure 1)

What about the urine drug screen?

Looking for an indication for the urine drug screen? Unfortunately, it is not the case here. The only situation in which this test would be useful is if it was initially negative, and then turned positive because of leaking packets. However, this condition is quite rare, and patients transporting illicit drugs have often used some in the last hours of days, which ends up in positive tests. Those tests also have their loads of false positives and false negatives and generally are not helpful in guiding management of body packers, stuffers, or pushers.

Your patient has 40 drug packets in his bowel. What to do now?

Three scenarios are possible at this point (Figure 2):

1. First is the asymptomatic patient with no toxidrome or abdominal complication. In this group, most experts recommend whole bowel irrigation with or without activated charcoal an hour before starting the irrigation. Activated charcoal is more clearly recommended for the management of body stuffers, whose packets are at high risk of breaking, but remains controversial in the management of body packers. An in vitro study showed that the use of activated charcoal preceding whole bowel irrigation could decrease to absorption of cocaine more than any of these interventions in isolation.⁹ All asymptomatic patients must be observed at least 6 hours in the emergency department to watch for signs of toxicity or complication.⁷ They can be discharged after if all the packets have been expelled, confirmed by 2 bowel movements without any packets, or a negative radiological testing. The only indication to operate on an asymptomatic patient would be failure to pass all packets or an important number of packets in the stomach that are judged improbable to pass the pylorus. In this case, the recommended approach would be laparotomy, since endoscopic or laparoscopic approach results in a risk of rupturing the packets and releasing the drug.¹⁰
2. The next group of patients is the one with abdominal complications. Those can be obstruction or perforation of the esophagus, stomach, or intestines. The diagnosis is suspected by the physical exam, confirmed by X-ray or CT, and taken care of in the operating room. In these cases, our role in the ED is to provide good supportive care and urgent surgical consultation.
3. The last group of patients is the one showing signs of drug toxicity. This can range from mild symptoms to cardiac arrest. In this group of patients, the symptoms should be addressed with appropriate treatment (naloxone for opioid overdoses and benzodiazepines and cooling for sympathomimetic drugs) and the surgeon rapidly called for an urgent consultation. For any toxicity more severe than mild and reversible symptoms, an operative approach will be the safest treatment.¹⁰

What if my patient is a body stuffer?

If the drug packets are fragile and were rapidly ingested by the patient, the risk of a surgical complication is lower, but the risk of leakage and subsequent toxicity is much higher. Body stuffers therefore differ from packers in the investigations and treatment that is recommended, First, CT imaging is much less useful since both radiographic sensitivity and risk of surgical complications are lower. For the same reason, surgical teams should only be involved if there is a strong suspicion of surgical complications (obstruction, perforation, etc.). These patients should also be observed in the ED and may reasonably receive a dose of activated charcoal if compliant. Since the overall quantity of ingested drugs is lower than packers, this period of observation can be reduced to 6 hours for sympathomimetic xenobiotics.¹¹ Whereas opioid toxicity may be “silent”, overnight monitoring may be reasonable for patients stuffing opioid agonists. Watch for any signs of toxicity and treat accordingly.¹²

And what if my patient had also hidden drugs in his rectum?

Body pushers represent a heterogenous group of patients. Most of them do not hide an important amount of drug using this specific method. Nonetheless, some absorption of the drug has been reported with vaginal packets. Diagnosis is usually clinical. Treatment consists of the removal of the packets with irrigation if possible, and observation in the ED to make sure that no sign of toxicity develops.^11,13

In any of these cases, if the diagnosis is not clear or if the treatment pathway seems ambiguous, local poison centers can be of great help.

Case Followup:

The patient underwent whole-bowel irrigation with PEG-3350. After 3 hours of observation in the ED, the patient developed progressive tachycardia, hypertension, and increased psychomotor agitation. He started to seize and received 4 mg of IV lorazepam. With the diagnosis already made and now signs of severe toxicity, the general surgeon was consulted and brought the patient to the operating room.

Clinical Pearls:

1. Be suspicious. Patients are sometimes reluctant to give complete information due to legal considerations.
2. When suspecting body packing, stuffing, or pushing, look for signs of toxicity and abdominal complications.
3. The best diagnostic tool is abdominal CT. X-ray can be used as a screening tool but is far from diagnostic. Urine drug screens are rarely
4. Asymptomatic body packers should undergo whole bowel irrigation preceded by activated charcoal if they do not have any contraindication. They should be observed at least 24 hours and can be discharged once all their packets have been expelled.
5. Patient presenting with gastrointestinal obstruction or perforation should undergo
6. Imaging is less useful for body stuffers, which can be observed in the ED. The duration of observation depends on what type of drugs they ingested.
7. Patients with signs of drug toxicity are a true emergency. We must provide appropriate treatment for the identified toxidrome, and packets must be removed surgically.
8. Drug toxicity should be treated as for any intoxicated patients: Benzodiazepines and external cooling for sympathomimetic overdose, and naloxone and respiratory support for opioid toxicity.

References:

1. Shahnazi, M., Sanei Taheri, M., & Pourghorban, R. (2011). Body packing and its radiologic manifestations: a review article. Iranian journal of radiology: a quarterly journal published by the Iranian Radiological Society, 8(4), 205–210. https://doi-org.acces.bibl.ulaval.ca/10.5812/iranjradiol.4757
2. Traub, S. J., Hoffman, R. S., & Nelson, L. S. (2003). Body packing–the internal concealment of illicit drugs. The New England journal of medicine, 349(26), 2519–2526. https://doi-org.acces.bibl.ulaval.ca/10.1056/NEJMra022719
3. Booker, R. J., Smith, J. E., & Rodger, M. P. (2009). Packers, pushers and stuffers–managing patients with concealed drugs in UK emergency departments: a clinical and medicolegal review. Emergency medicine journal: EMJ, 26(5), 316–320. https://doi-org.acces.bibl.ulaval.ca/10.1136/emj.2008.057695
4. Heymann-Maier, L., Trueb, L., Schmidt, S., Carron, P. N., Hugli, O., Heymann, E., & Yersin, B. (2017). Emergency department management of body packers and body stuffers. Swiss medical weekly, 147, w14499. https://doi-org.acces.bibl.ulaval.ca/10.4414/smw.2017.14499
5. Mandava, N., Chang, R. S., Wang, J. H., Bertocchi, M., Yrad, J., Allamaneni, S., Aboian, E., Lall, M. H., Mariano, R., & Richards, N. (2011). Establishment of a definitive protocol for the diagnosis and management of body packers (drug mules). Emergency medicine journal: EMJ, 28(2), 98–101. https://doi.org/10.1136/emj.2008.059717
6. Cappelletti, S., Piacentino, D., Sani, G., Bottoni, E., Fiore, P. A., Aromatario, M., & Ciallella, C. (2016). Systematic review of the toxicological and radiological features of body packing. International journal of legal medicine, 130(3), 693–709. https://doi-org.acces.bibl.ulaval.ca/10.1007/s00414-015-1310-3
7. Bulakci, M., & Cengel, F. (2016). The role of radiology in diagnosis and management of drug mules: an update with new challenges and new diagnostic tools. The British journal of radiology, 89(1060), 20150888. https://doi.org/10.1259/bjr.20150888
8. Pinto, A., Reginelli, A., Pinto, F., Sica, G., Scaglione, M., Berger, F. H., Romano, L., & Brunese, L. (2014). Radiological and practical aspects of body packing. The British journal of radiology, 87(1036), 20130500. https://doi.org/10.1259/bjr.20130500
9. Makosiej, F. J., Hoffman, R. S., Howland, M. A., & Goldfrank, L. R. (1993). An in vitro evaluation of cocaine hydrochloride adsorption by activated charcoal and desorption upon addition of polyethylene glycol electrolyte lavage solution. Journal of toxicology. Clinical toxicology, 31(3), 381–395. https://doi-org.acces.bibl.ulaval.ca/10.3109/15563659309000407
10. Das, D., & Ali, B. (2003). Towards evidence-based emergency medicine: best BETs from the Manchester Royal Infirmary. Conservative management [correction of management] of asymptomatic cocaine body packers. Emergency medicine journal: EMJ, 20(2), 172–174. https://doi-org.acces.bibl.ulaval.ca/10.1136/emj.20.2.172
11. Moreira, M., Buchanan, J., & Heard, K. (2011). Validation of a 6-hour observation period for cocaine body stuffers. The American journal of emergency medicine, 29(3), 299–303. https://doi.org/10.1016/j.ajem.2009.11.022
12. Yamamoto, T., Malavasi, E., Archer, J. R., Dargan, P. I., & Wood, D. M. (2016). Management of body stuffers presenting to the emergency department. European journal of emergency medicine: official journal of the European Society for Emergency Medicine, 23(6), 425–429. https://doi-org.acces.bibl.ulaval.ca/10.1097/MEJ.0000000000000277
13. Wankhade, V. K., & Chikhalkar, B. G. (2018). Body packing and intra-vaginal body pushing of cocaine: A case report. Legal medicine (Tokyo, Japan), 31, 10–13. https://doiorg.acces.bibl.ulaval.ca/10.1016/j.legalmed.2017.12.004

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Originally published on Ultrasound G.E.L. on 4/11/22 – Visit HERE to listen to accompanying PODCAST! Reposted with permission.

Follow Dr. Michael Prats, MD (@PratsEM) from Ultrasound G.E.L. team!

Diagnostic Accuracy of Point-of-Care Ultrasound for Intussusception: A Multicenter, Noninferiority Study of Paired Diagnostic Tests

Annals of Emerg Med Nov 2021 – Pub Med Link

Take Home Points

1. The diagnostic accuracy of POCUS for the detection of clinically important intussusception is noninferior to that of RADUS when performed by expert sonologists.
2. Interrater reliability for POCUS studies was high. Agreement between POCUS and RADUS for secondary sonographic findings was high.
3. Further studies are needed to compare expert PEM sonologists with PEM trained physicians in making this diagnosis with POCUS.

Background

‌Intussusception is the most common cause of bowel obstruction in children less than 6 years old. Delayed diagnosis can lead to impaired efficacy of air enema reduction and intestinal ischemia. Ultrasound is the diagnostic test of choice prior to reduction of ileocolic intussusception by radiology or surgery. Recent studies have demonstrated that a small percentage of ileocolic intussusceptions reduce spontaneously, however the vast majority require procedural reduction. In contrast, ileoileal intussusception is often transient and reduces spontaneously without intervention. The current standard of care is radiology-performed diagnostic ultrasound (RADUS), but recently published studies using POCUS demonstrate similar accuracy in diagnosis.

 ‌

This isn’t the first time we have talked about this! Another interesting study on the topic – Intussussception Feb 2018.

Questions

 ‌1. Is the diagnostic accuracy of POCUS performed by ultrasound-trained pediatric emergency medicine sonologists noninferior to that of RADUS for the detection of clinically important intussusception?

2. What is the agreement between POCUS and RADUS for identification of secondary sonographic findings?

Population

Children aged 3 months to 6 years presenting with clinical suspicion for intussusception and RADUS orders were eligible for inclusion. Children with imaging results from referring facilities for whom the sonologist was aware of those results were excluded.

Patients were enrolled when a study sonologist was available to perform the POCUS scan. Children were screened for enrollment by a member of the study team.

Design

Multicenter, prospective, noninferiority study of paired diagnostic tests – RADUS vs. POCUS

17 tertiary care pediatric EDs in North America, Central American, Europe, and Australia

• 12 university-based academic medical centers with affiliated children’s hospitals
• 4 large community children’s hospitals
• 1 large urban academic center with a dedicated pediatric ED
• 12 sites with 24/7 radiology capabilities
• 5 sites with radiology ultrasound services available only during daytime hours with technicians called at night and offsite radiology read

Study conducted between October 2018 – December 2020

If the POCUS study would cause a delay in care, it was performed immediately after RADUS with the study sonologist remaining blinded to RADUS results

If fewer than requested images were obtained, study group used what was obtained for analysis

Deidentified images were shared with the principal investigator

Study sonologists recorded the start and end times of POCUS scanning AND a confidence rating of their POCUS interpretation (positive or negative) as follows: not at all, somewhat, moderately, very, or completely.

POCUS studies were considered positive for intussusception if at least ONE of the following criteria occurred:

1. Presence of a target-shaped mass >/= 2.0 cm in transverse axis diameter
2. Sonologist’s clinical judgment that the intussusception would require intervention (i.e. ileocolic)

If an intussusception was identified, it was classified as/with:

1. Ileoileal or ileocolic
2. Presence of absence of trapped free fluid
3. Presence or absence of color Doppler signal
4. Presence or absence of echogenic foci

The POCUS study was NEGATIVE if:

1. Absence of a target sign in all four quadrants
2. Sonologist judgment that an intussusception was not present

*** 2 cm chosen as a cutoff because this value lies about 1-2 standard deviations above mean for ileoileal intussusceptions and 1-2 standard deviations below the mean for ileocolic intussusceptions

For RADUS studies, the impression of the attending radiologist was the final determination of a positive or negative study

Primary Outcome = whether POCUS and RADUS correctly detected clinically important intussusception (defined as an intussusception that required radiographic or surgical reduction during or within 7 days of the ED visit)

Secondary Outcomes = a) agreement between POCUS and RADUS for identification of secondary sonographic findings (maximal diameter measurement, presence of trapped free fluid, decreased Doppler signal, echogenic foci) b) Frequency of serious complications, defines as peritonitis, bowel perforation, intestinal obstruction, shock, or death

Inter-rater reliability for POCUS image clips was evaluated with Cohen’s kappa => two investigators interpreted a random sample of POCUS studies (20% of goal)

Noninferiority study resources

REBEL EM 

EMCRIT EMNerd

ACEP Now

Biomed Central Article

BMJ Article

Who did the ultrasounds?

35 sonologists, PEM physicians

• All had completed either a) an ultrasound fellowship, b) Registered Diagnostic Medical Sonographer designation (RDSM), or c) had previously completed at least 20 abdominal POCUS exams with at least 1 positive intussusception study
• All study sonologists required to watch a standardized training video that covered study procedures and scanning protocol (technique, image acquisition/storage, measurements, secondary findings)

The Scan

Long Linear

PROTOCOL

• Patient supine
• Move transducer superiorly from the RLQ to the hepatic flexure, right to left to the splenic flexure, and then inferiorly to the left lower quadrant
• At least 2 still images or video clips were obtained in transverse and longitudinal planes in each quadrant (total of 8 images/clips)
• If an intussusception was identified, the sonologist captured at least 1 still image in the short axis plane of the intussusception (with caliper measurement of the maximal intussusception diameter), 1 still image in longitudinal plane, and 1 still image with color Doppler over the intussusception

Learn bowel ultrasound from 5 Minute Sono!

Check out Intuss Pathology at The POCUS Atlas!

Results

262 patients enrolled, n = 256 in primary analysis

• Median age = 21.1 months
• Most presented with concerns for abdominal pain (82.8%) or fussiness (80.5%)
• POCUS occurred prior to RADUS in 248 children (96.9%)

58 (22.7%) children had cases of clinically important intussusception

• 55 (21.5%) treated with radiographic reductions
• 16 (6.3%) required surgical reduction

POCUS identified 60 (23.4%) cases as positive => 4 false positives, 2 false negatives

Primary Outcome

Diagnostic accuracy of POCUS 97.7% (95% CI 94.9% to 99%) vs. RADUS 99.3% (95% CI 96.8% to 99.9%)

• Excluding the site with high rate of positive scans, as well as higher proportion of transfers and bloody stools: diagnostic accuracy of POCUS 97.5%, sensitivity 92.9%, specificity 97.9%

Secondary Outcomes

96.9% agreement between POCUS and RADUS with respect to clinically important intussusception (Cohen’s kappa 0.911 [95% CI 0.852 to 0.972])

Median POCUS scanning time was 6 minutes vs. median time to RADUS results was 65 minutes

Agreement between POCUS and RADUS for:

1. Presence of trapped free fluid – 83.3% (95% CI 70.4% to 91.3%; n = 40/48)
2. Decreased color Doppler signal – 95.7% (95% CI 78.1% to 99.9%; n = 22/23)
3. Presence of echogenic foci – 80% (95% CI 44.4% to 97.5%; n = 8/10)

Telephone follow up data was available for 190 children (74.2%)

• 14 children (7.4%) had an ED return visit within 7 days of discharge
• 5 children (2.0%) had serious complications, but all were correctly identified by POCUS at the index visit

Interrater reliability was high between the two study sonologists (Cohen’s kappa of 0.835 [95% CI 0.615 to 1.000] for binary interpretation of findings)

Strengths

• Multicenter and international
• Largest prospective study to date
• Appropriate reference standard
• Had follow up on patients
• High agreement between POCUS and RADUS for most secondary sonographic findings
• Probably best evidence on POCUS accuracy for intussusception

Limitations

• Convenience sampling based on availability of sonologists
• Sample size below target so study slightly underpowered
• Differences between sites – some sites with much higher positivity rate, referrals, use of RADUS
• Sonologists may have completed the POCUS scan after taking the history and performing a physical exam which may have influenced how diligently they evaluated for intussusception (but not sure this is really a limitation…)
• Using expert sonologists is ideal for testing the accuracy for POCUS, but is not as generalizable to different sites as most PEMs do not have this level of POCUS training

 ‌

Discussion

This was the largest prospective study to date comparing POCUS to RADUS for diagnosing intussusception which is awesome. Accuracy of POCUS was impressive with 96% accuracy for clinically important intussusception, and only 4 false positive and 2 false negative cases. There have been multiple prior studies looking at the test characteristics of POCUS in intussusception, most were retrospective but with decent accuracy in diagnosis. Prospective studies were limited by small case numbers. Additionally, essentially all prior studies included scanners reflecting all levels of POCUS skill, as opposed to only experts as seen in this study. The authors chose to focus on expert sonologists so as to prove POCUS non-inferiority as compared to RADUS, and more accurately represent how POCUS is used in the PEM world.

One interesting thing these authors did was investigate accuracy by PEM sonologists in identifying secondary signs of clinically important intussusception. As I like to tell my PEM fellows, secondary signs are often primary signs when it comes to abdominal POCUS… such findings are known to aid diagnosis by sonologists and radiologists alike. There was good agreement (>80%) between POCUS and RADUS, with the exception of significantly smaller measurements of the intussusception by POCUS.

At many tertiary PEDs, there is access to radiology ultrasound 24/7. But what about general EDs or satellite/rural PEDs where there are no pediatric sonographers available overnight? POCUS users who can accurately risk stratify clinically important intussusception will in theory speed up a necessary transfer of patient, or prevent an unnecessary one. Additionally, as PEM providers across the board improve their POCUS skills, we can in theory expect even higher accuracy in delineating ileoileal vs. ileocolic pathology. Lastly, as those who do this type of research know… clinical research on pediatric POCUS is difficult to pull off for various reasons (low incidence, convenience sampling, not enough skilled sonologists at site) so congrats to Bergmann et al. on your excellent study.

Summary

In this 18-center prospective observation study of 256 children being evaluated for intussusception, the accuracy of POCUS was not inferior to radiology ultrasound. POCUS had a sensitivity of 96.6% (95% CI 87.2 to 99.1) and specificity of 98% (95% CI 94.7 to 99.2) for intussusception requiring reduction ‌

Take Home Points

1. The diagnostic accuracy of POCUS for the detection of clinically important intussusception is noninferior to that of RADUS when performed by expert sonologists.
2. Interrater reliability for POCUS studies was high. Agreement between POCUS and RADUS for secondary sonographic findings was high.
3. Further studies are needed to compare expert PEM sonologists with PEM trained physicians in making this diagnosis with POCUS.

More Great FOAMed on This Topic

Ultrasound GEL – Intussusception Feb 2018

Brown EM – A Bowel Inside a Bowel

ALiEM PEM POCUS Series: Intussusception

Our Score

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Welcome back to Small Talk.  Every first Wednesday of the month we will release high yield PEM content written by PEM talent from around the country.  We hope you enjoy these reviews. Comments, questions, accolades or concerns: feel free to reach out to Joe Ravera, MD (pemgemspod@gmail.com).

Authors: Drew Weinstein, MD, MS (EM Resident physician, UC San Diego Health) and Kristy Schwartz, MD, MPH, FACEP (Assistant Health Sciences Clinical Professor, UC San Diego Health/Rady Children’s Hospital San Diego)

Reviewed by: Joe Ravera MD (@pemuvm1, Director of Pediatric Emergency Medicine, Assistant Professor of Surgery, Division of Emergency Medicine, University of Vermont Medical Center); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

The Emergency Department (ED) is a chaotic, loud, and busy environment. Patients in the ED often face long wait times and a substantial amount of stimulation, which can be especially problematic for people with autism spectrum disorder (ASD). Individuals with ASD require health care or hospitalization at a higher rate when compared to their peers.^1,2People with ASD may have trouble coping with new and uncertain environments, such as the ED, have difficulty communicating, and suffer from hyperacusis, making it more complex to provide adequate patient-centered care to these individuals. Therefore, it is critical to understand the challenging concerns of a patient with ASD in the chaotic ED environment, and the effects on clinician interaction and care. This review discusses a case study of a patient with ASD who presented to the ED and strategies for clinicians to make their patients with ASD more comfortable, thereby providing the best care.

Case

A 13-year-old male with a past medical history of autism spectrum disorder and juvenile myoclonic epilepsy presented to the emergency department via emergency medical services (EMS) from daycare for evaluation of abdominal pain. The patient’s mother had yet to arrive. Per EMS, the patient had not been acting himself for the prior two days, had been grabbing his abdomen, crying inconsolably, and was witnessed to be hitting himself more frequently. Starting that morning, he had multiple episodes of non-bloody, non-bilious emesis.

His vital signs on arrival included heart rate 137, respiratory rate 29, oxygen 96% on room air, temperature 38.9^oC. Blood pressure was unable to be obtained because the patient flailed his arm when attempts were made.

The patient was dressed in clean clothes, strapped down to an EMS gurney, yelling out, and trying to break free from the safety belts. He appeared flushed and had dried nasal mucus along his cheek. He was tachypneic. An attempt to listen to his lungs was unsuccessful due to the patient’s vocalizations and thrashing. His capillary refill was slightly delayed at 3-4 seconds.

Definition/Prevalence

Autism spectrum disorder can be diagnosed at any age, though most often the diagnosis occurs after age 2 years as the characteristic symptoms become more apparent. Symptoms include deficits in social communication and interaction with others, limited interests, and repetitive behaviors that cause significant impairment in functioning.^3,4,5 While early diagnosis is recommended given opportunities for intervention, many children do not receive a final diagnosis until later, most commonly by 4 years of age.⁶ The prevalence of ASD in the United States is about 1 in 44 children and ASD is 4.2 times more prevalent in boys than girls.⁷ Individuals with autism may present with a wide variety of symptoms of varying severity, as defined by the DSM-5 diagnostic criteria.³

Autism Spectrum Disorder is frequently associated with a variety of comorbidities. Medical comorbidities include but are not limited to: obesity, gastrointestinal conditions, seizure disorders, and sleep disorders. Psychiatric/behavioral comorbidities include: anxiety disorders, attention deficit-hyperactivity disorder, and depression.^8,9 These comorbidities may put people with ASD at greater risk for requiring ED care. It is imperative that physicians in the ED be prepared to properly treat a patient with ASD, with consideration to care of commonly associated conditions and ASD symptoms, which the patient may find challenging to communicate.

The Visit

Individuals with ASD typically react better in structured environments with set expectations. In the ED, patients with ASD often face unfamiliarity and unpredictability, which may exacerbate their symptoms and put a strain on the patient-clinician relationship. Individuals with ASD have unique sensory, behavioral, and communication needs that are often difficult to assess or address when in an emergent situation. It is important that clinicians be prepared for such patients so that treating them and addressing their unique needs becomes second nature.¹

One thing that remains true throughout treating all patients with ASD, beyond the patient, is that parents/guardians, caregivers, and family are the experts. Never delay consulting them. Include them in the care early and often.¹

​​Preparation is critical to caring for patients with ASD in the ED. It begins with team members who are trained in appropriate, effective communication and providing a safe, comfortable environment for patients with ASD and their caregivers. The Center for Disease Control (CDC) and the American Academy of Pediatrics (AAP) provide training resources on ASD and offer evidence-based practices.¹⁰ Preparation and ongoing professional development can build the team’s confidence and effectiveness when treating patients with ASD in the ED, therefore improving overall patient care.

When a patient with ASD arrives at the ED, strive to identify them early. If possible, offer a separate waiting area with less stimulation, or allow the patient to wait outside or in their car if a separate space is not available.⁹ Additionally, placing these patients in rooms earlier and providing them with developmentally appropriate toys may also be beneficial.¹

An instrument to identify patient-specific information may help, such as a short questionnaire to assist the team with knowing and understanding the patient. Offer this questionnaire at triage to collect details on stressors, triggers, and communication styles. Here is an example of an ASD questionnaire used at Rady Children’s Hospital San Diego.¹¹

Child Life Specialists are excellent allies in treating patients with ASD. They provide the team with helpful tools and offer calming techniques to create an environment suitable for the patient.

Placing patients with ASD in a private room modified to best suit the patient’s needs should be a priority.¹ Often, caregivers will come prepared with adequate interventions such as headphones or electronic devices for the patient. On the occasion that caregivers did not bring these items or the patient arrived alone, utilizing the ED’s devices (or, if willing, the team’s personal devices) to play videos or providing noise-canceling headphones may be helpful.

Clinicians may have difficulty taking a medical history and performing a physical exam on patients with ASD. It is important to build rapport and talk with the patient at their level of understanding. Clinicians should not force themselves into the patient’s personal space. When describing what will happen or eliciting information from the patient, utilize visual charts or drawings, as people with ASD often respond better to visual rather than verbal information. It may be helpful to use a “First-Then” board to illustrate the plan and identify a reward once completed. The Autism Speaks Treatment Network has an example of a “First-Then” board.¹² Additionally, roughly 30% of people with ASD are nonverbal, so give caregivers an opportunity to provide the medical history and help the team interpret the patient’s nonverbal cues.^8,9

This table adapted from the AAP may be useful in interpreting behaviors suggestive of  abdominal pain or discomfort in patients with ASD (Table 1).⁸

Individuals with ASD benefit from consistency and predictability. Therefore, try to maintain a consistent care team with as few staff members as possible who interact with the patient. New faces may cause undue stress on the patient and impede quality patient care. Limit the number of people in the room, ensuring that each team member introduces themselves and clearly explains their role. Team members and, if helpful, caregivers should talk outside the room and only the necessary individuals should enter the room to interact with the patient. The goal remains the same: cultivate a safe, calm environment for the patient.¹

Communicating with patients with ASD may be different than with other patients. Do not be surprised if the patient with ASD avoids eye contact.^3,4,5 They are listening to everything you say and will take things quite literally. Use a calm and gentle voice, give simple commands, and avoid idioms or sarcasm. People with ASD may have a slower processing speed, so pause to give them time to respond to questions or requests.¹³ Since patients with ASD benefit from predictability and touching can be stressful, explain or demonstrate what will happen before touching them. Reassure them that nothing will happen without you telling them what to expect first, then be consistent with this practice.^1,13

If a procedure is indicated for a patient with ASD, a considerable amount of time should be taken to prepare for it. Procedures can be the most stressful part of the experience for these patients; therefore, take time to discuss the procedure in advance with the patient and their caregiver. When discussing the procedure with the patient, use visual aids to help them understand.¹ For example, allow the patient to see and touch a tourniquet or catheter (with the needle removed, of course) before placing an intravenous (IV) line.¹³ Clinicians and team members should review the patient’s coping mechanisms and ensure that their environment is still suitable for them. Patience is key. The team should plan for a longer procedure time than the average patient, ensuring that steps are carefully explained and performed without rushing.¹

Pearls and Pitfalls

• People with ASD are four times more likely to be seen in the ED when compared to their peers.² 
• People with ASD peasant atypically and have barriers to communication which can obfuscate the diagnosis. Caregivers are a vital resource. They are knowledgeable of the patient’s nonverbal cues, can help obtain a history and exam, and can help the team provide a smooth visit for the patient.
• Preparation is key: have tools such as a triage survey to identify triggers and coping mechanisms, noise-canceling headphones, developmentally appropriate toys, visual aids, and separate waiting areas and staff training on how to interact with patients with ASD is extremely important
• Making the patient feel comfortable is critical. Modify the environment to make it more suitable for the patientby providing a private room, lowering the lights, and decreasing the number of staff interactions.
• Communication is important: be calm and patient, use literal phrases, and explain everything. Look for nonverbal cues, give the patient time to process, and be patient if procedures take more time.

Case conclusion

The 13-year-old boy was well-known in the hospital system. When he arrived, a private room was identified for him, as his caregiver had not yet arrived. The team used a preference questionnaire previously recorded in the electronic healthcare record to identify patient preferences and subsequently created a comfortable environment for him. His nurse provided the patient with a stress ball and used her phone to play animal videos, which the patient identified as one of his preferences. The patient’s mother, who was en route, was contacted and placed on speakerphone to help soothe the patient and to provide further information for the staff. When a new team member entered the patient’s room, they introduced themselves and explained in detail what they were going to do. Antipyretics were administered to the patient in his preferred manner and visual aids were utilized by the clinician to perform an adequate physical examination. Upon examination, the patient was found to have McBurney’s point tenderness. With the help of a Child Life Specialist, an IV was placed, labs were collected, and antiemetics were given. The patient underwent an ultrasound, which showed findings suggestive of appendicitis. Surgery was immediately notified and the patient underwent emergent appendectomy later that evening. The patient spent two days in the hospital recovering and was discharged in stable condition.

References

1. Straus J, Coburn S, Maskell S, Pappagianopoulos J, Cantrell K. Medical Encounters for Youth With Autism Spectrum Disorder: A Comprehensive Review of Environmental Considerations and Interventions. Clin Med Insights Pediatr. 2019;13:1179556519842816. Published 2019 Apr 29. doi:10.1177/1179556519842816.
2. Liu G, Pearl AM, Kong L, Leslie DL, Murray MJ. A Profile on Emergency Department Utilization in Adolescents and Young Adults with Autism Spectrum Disorders [published correction appears in J Autism Dev Disord. 2017 Mar 23;:]. J Autism Dev Disord. 2017;47(2):347-358. doi:10.1007/s10803-016-2953-8.
3. Diagnostic criteria. Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/autism/hcp-dsm.html. Published June 29, 2020. Accessed April 18, 2022.
4. National Institute of Mental Health. Autism spectrum disorder. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/autism-spectrum-disorders-asd. Accessed April 18, 2022.
5. Hyman SL, Levy SE, Myers SM, et al. Identification, evaluation, and management of children with autism spectrum disorder. Pediatrics. 2020;145(1). doi:10.1542/peds.2019-3447.
6. Spotlight on: Delay between first concern to accessing services. Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/autism/addm-community-report/delay-to-accessing-services.html#:~:text=Of%20the%20children%20who%20received,limiting%20the%20services%20they%20receive. Published August 27, 2019. Accessed April 18, 2022.
7. National Institute of Mental Health. Autism spectrum disorder (ASD). National Institute of Mental Health. https://www.nimh.nih.gov/health/statistics/autism-spectrum-disorder-asd. Published January 2020. Accessed April 18, 2022.
8. American Academy of Pediatrics. AAP – Welcome to Identifying and Caring for Children with Autism Spectrum Disorder: A Course for Pediatric Clinicians. Identifying and Caring for Children with Autism Spectrum Disorder. http://asd.pedialink.courses.aap.org/script/unit-4-management-of-co-occurring-conditions/unit-4-recording?req=202205051414312495. Accessed April 18, 2022.
9. Al Sharif S, Ratnapalan S. Managing Children With Autism Spectrum Disorders in Emergency Departments. Pediatr Emerg Care. 2016;32(2):101-103. doi:10.1097/PEC.0000000000000705.
10. Autism case training landing page. Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/actearly/act.html. Published October 6, 2020. Accessed April 18, 2022.
11. Rady Children’s Hospital San Diego. Autism-Friendly Healthy System Initiative. 2022.
12. Visual Supports and Autism. Autism Speaks. https://www.autismspeaks.org/sites/default/files/2018-08/School%2520Community%2520Tool%2520Kit.pdf. Published March 2011. Accessed May 3, 2022.
13. Watson LR, Fraser M, Ballas P. Interacting with a child who has autism spectrum disorder. University of Rochester Medical Center-Health Encyclopedia. https://www.urmc.rochester.edu/encyclopedia/content.aspx?contenttypeid=160&contentid=46. Accessed May 3, 2022.

The post Pediatric Small Talk – Caring for Patients with Autism Spectrum Disorder in the ED, a Success Story appeared first on emDOCs.net - Emergency Medicine Education.

Today on the emDOCs cast with Brit Long, MD (@long_brit) and Skyler Lentz, MD (@SkylerLentz), we cover a challenging condition: adrenal insufficiency.

Adrenal Insufficiency

Background:

• The adrenal glands release cortisol, a glucocorticoid.
• Glucocorticoid receptors are present throughout the body, and glucocorticoids affect energy production, electrolyte and volume regulation, vasomotor tone, cardiac activity.
• Deficiency can lead to profound hypoglycemia, hypotension, and general hemodynamic instability.
• The endocrine pathway involving the hypothalamus in response to stress releases corticotropin releasing hormone to the anterior pituitary. The pituitary releases ACTH stimulating the adrenal gland to produce cortisol.
• Adrenal insufficiency can be result of a problem anywhere on this pathway.
  • Primary adrenal insufficiency is when the adrenal gland itself fails.
  • Secondary or central adrenal insufficiency occurs with failure of the hypothalamic-pituitary axis to stimulate the adrenal gland.
  • Adrenal insufficiency can be acute or chronic.
  • Acute is often more challenging to diagnose.

Epidemiology:

• Autoimmune adrenal insufficiency in modern countries most often appears between 30-50 years old.
• 60% of cases requiring two or more clinician evaluations before diagnosis.
• Adrenal crisis carries a mortality rate of 6-15%.

Risks and Etiologies:

• Risk Factors
  • Primary: autoimmune, infectious, malignancy, genetic, vascular, medications
  • Central: pituitary problems, hypothalamic problems, exogenous steroids
• Primary in modern countries is mostly due to auto-antibodies destroying adrenal gland. Other auto-immune diseases or a family history of auto-immune disease is a risk factor.
• Infiltration by tuberculosis is a common worldwide cause. Other causes of primary include adrenal hemorrhage, infiltration by malignancy, surgical removal, and medications affecting cortisol metabolism.
• Common secondary causes include failure of the pituitary to release ACTH by tumors particularly after resection, brain radiation, brain trauma, pituitary gland ischemia.
• Steroid use should be ascertained. The rate of adrenal insufficiency in those on long term inhaled glucocorticoids for asthma is about 5%.
• Variety of triggers (anything requiring a stress response): gastroenteritis (most common), fever and infection, pregnancy, MI, hypoglycemia, surgery or trauma, recent discontinuation of steroids, emotional stress.

Presentation:

• Non-specific signs and symptoms are common and can develop over weeks to months as the adrenal gland slowly fails.
• Fatigue, malaise, and general weakness are the most common symptoms occurring in nearly all cases of adrenal insufficiency; loss of appetite (53-67%), weight loss (66-76%), gastrointestinal symptoms (nausea, vomiting, and abdominal pain in 49-62%).
• The patient may have salt craving, and postural hypotension and syncope are also common symptoms. Fever, delirium may be present.
• Skin hyperpigmentation in primary by ACTH stimulating melanin.
• Key: Consider it in patients with recurrent ED visits for unexplained fatigue, GI symptoms and postural syncope.

Adrenal Crisis Definition:

• Severe signs and symptoms of glucocorticoid and/or mineralocorticoid deficiency with at least two of the following: systolic BP < 100 mm Hg; nausea or vomiting; severe fatigue; hyponatremia (≤ 132 mmol/l), hypoglycemia or hyperkalemia; fever; somnolence or altered mental status; and clinical improvement with parenteral glucocorticoid administration
• Hypotension and/or hypovolemic shock present in most adrenal crisis cases. Shock is often refractory to fluids and vasopressors.

Evaluation:

• Hypoglycemia is often refractory; hyponatremia present in most cases.
• Hyperkalemia and non-anion gap metabolic acidosis occur in primary adrenal insufficiency, but not in secondary Hyperkalemia is not present because aldosterone is regulated by renin and serum potassium not ACTH from the pituitary.
• Hypercalcemia and eosinophilia may be present, but are not reliable for diagnosis.
• Blood cultures, urinalysis, urine culture based on concern for infection.
• Obtain imaging based on patient assessment (i.e., abdominal pain, obtain CT).
• Cosyntropin test:
  • Standard test is to administer 250 mcg cosyntropin. A functioning adrenal gland should respond by producing a peak cortisol of > 18-20 μg/dL (500-550 nmol/L) when measured at 30 and 60 minutes after cosyntropin administration.
  • A random cortisol > 18-20 mcg/dL suggests against adrenal insufficiency.
  • DO NOT withhold therapy in the ED for the cosyntropin test. You can always add on a random cortisol and ACTH to the pretreatment labs. A low cortisol and high ACTH suggest primary adrenal insufficiency.

Management:

• Key components are hydrocortisone, resuscitate, and treat underlying trigger. Patients are toxic and require resuscitation. Antibiotics are necessary, as these patients will look like septic shock, and infection is also a trigger.
• For those in crisis give 100 mg IV of hydrocortisone. This can be followed by 200-300 mg/ day of hydrocortisone such as 50 mg every 6 hours or a continuous infusion.
• Resuscitate with fluids–these patients are often hypovolemic. Normal saline is a good option for the initial fluid because of losses. If hypoglycemic, add dextrose to fluids and replete electrolytes as needed.
• Search for a trigger and treat suspected causes–since it can look like sepsis, antibiotics and cultures are warranted.

Disposition:

• Admit patients with adrenal crisis to ICU.
• Patients with chronic adrenal insufficiency are themselves the experts at treating their illnesses. They may present with a GI illness. Administer fluids, check and correct electrolytes, give an initial IV dose of 100 mg hydrocortisone if vomiting. The patient may have already administered IM/SubQ dosing of steroid.
• If they can tolerate oral fluids and medication, they may be able to go home, with a double or triple dose of their home doses of hydrocortisone while ill and endocrinology follow-up.
• They need to increase home steroid dosing for stressors such as fever, UTI, surgery, or trauma.
• Consult and coordinate with their endocrinologist.

Summary:

1. Adrenal insufficiency is a life-threatening emergency and mimic of sepsis; we must recognize early and treat aggressively.
2. The hallmark is hypotension refractory to IV fuid/vasopressors and refractory hypoglycemia.
3. Suspect in patients with unexplained hypotension and risk factors (prior steroid use, history of autoimmune disease, hyperpigmentation etc.).
4. Treat empirically with hydrocortisone 100mg IV and search for and treat precipitating cause; provide IV fluids and glucose.

The post emDOCs Podcast – Episode 55: Adrenal Insufficiency appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Ashley Weisman, MD (EM Attending Physician, University of Vermont Medical Center) and Catherine Platt, PharmD (EM Clinical Pharmacist, University of Vermont Medical Center) // Edited by: Kayvan Moussavi, PharmD, BCCCP (Faculty, Clinical Education, Providence St. Joseph Hospital Orange; Assistant Professor, Department of Pharmacy Practice / College of Pharmacy, Marshall B. Ketchum University); Alex Koyfman, MD (@EMHighAK); Brit Long, MD

Case

You are working in a rural, critical access hospital two hours from the nearest tertiary center.  The 6 bed ED is covered by a solo physician and one RN. It’s 2AM, and a 79-year-old male presents with fever and dyspnea. You place the patient on the monitor and see a wide complex tachycardia and a blood pressure of 81/42 mmHg. You administer 50 mcg of fentanyl IV and attempt cardioversion; however, this tachycardia is refractory to three attempts at 200 joules. You ask your nurse teammate to prepare a norepinephrine drip and an amiodarone bolus and infusion. You fear for the worst, so you ask him to prepare a vasopressin drip and push dose epinephrine boluses as well. Your nurse colleague kindly reminds you that you are not in the big city anymore. This is a rural ED, there is no ED pharmacist, and we need to mix all our own medications. How do you prepare them? Can you mix them in normal saline (0.9% sodium chloride) or dextrose 5% in water (D5W)? Are they all Y site compatible if you have only one peripheral IV? What resources can you use to find this information?

Introduction

Rural EDs operate with many limited resources including limited or no onsite pharmacy support and single provider and nurse coverage, especially at night. Rural EDs often stock fewer premixed critical medications, since they tend to be more expensive, expire more quickly, and are less frequently used than in tertiary centers (1-4). Thus, single nurse and physician teams in rural EDs often find themselves mixing and administering numerous essential medications to provide care for critically ill patients.  If you are unfamiliar with medication preparation, there may be significant delays in initiating life-saving therapies.  Therefore, it is important for all ED providers to be comfortable with preparation, dosing, and administration of IV medications. Fortunately, the list of medications that you need (and have) to care for critically ill patients in rural hospitals is quite small. Mastering the preparation, dosing, and administration of this small but mighty subset of critical medications dramatically improves your efficiency and reduces your cognitive load when caring for sick patients.

Case Resolution

I came across this very patient in a rural ED a few years ago with no pharmacy coverage and no idea how to mix the medications we needed. Our two-woman MD/RN team spent the night running around like crazy, rifling through our pharmacy’s old paper ‘cookbook’, supplementing with Lexicomp and Google, mixing a med, cross checking dosing and Y site compatibility on Micromedex, and hoping it matched the concentrations listed in our IV infusion pump library. When it did not, we sighed, and triple checked our arithmetic as we manually entered the medication and calculated the infusion rate. The patient made it to tertiary care and had a good outcome, but it wasn’t pretty.

ED/Critical Care Pharmacy Recipe Cards

Following this case, I conferred with physician, nurse, prehospital, and pharmacist colleagues working in rural and tertiary EDs. We generated a short list of important critical care medications and created a set of critical care pharmacy “recipe cards” These cards summarize preparation, dosing, and compatibility, and can be tailored to your hospital formulary and infusion pump library. We have used these many times in our small EDs and found them very helpful. We hope others will find them useful.

General Approach to Preparing and Administering IV medications

Begin with hand hygiene and aseptic technique, including wiping the tops of vials with alcohol swabs before drawing up medications. Gather your supplies – medication vials, solvent (NS or D5W) in an appropriately sized bag, syringes to draw up medications and remove solvent, IV tubing, IV infusion pump. Label all mixed medications with name, concentration, date, and time prepared. Prime your IV tubing. If you are using a medication concentration that matches your pump library, you will be able to input the medication and concentration, select your dose, and the pump will do the math and ensure the correct infusion rate. If the concentration you mix does not match your library, be prepared to do the math yourself.  For example, you prepare norepinephrine at 4mg/250mL, but your pump library only has the 8mg/250mL concentration, and the infusion rate must be entered in mL/hr. If you want to run this 4mg/250mL norepi at 10mcg/min, you will need to manually convert mcg/min to mL/hr and enter an infusion rate of 37mL/hr (recommend this calculator – https://www.manuelsweb.com/McgPerMin.htm).

When mixing medications, it is also helpful to be aware of how to account for overfill and drug volume. Commercially available parental solutions are labeled with a given volume – 100, 250, 500, 1000 mL – but are slightly overfilled to account for evaporative water losses over time. Thus, the actual volume is a little larger than listed and concentrations will vary slightly based on the age and storage conditions of the bag. When mixing a medication infusion, you can do one of three things: 1) just add the medication to the solvent, 2) withdraw some solvent to account for drug volume, 3) withdraw more solvent to account for both overfill and drug volume. In our context, the rural ED with a crashing patient, we are most often choosing option 1, tolerating a minor inaccuracy in the infusion’s concentration in favor of ease and speed, and titrating our infusions to affect anyway. However, when the volume of drug you are adding is greater than 10% of the total volume of your solvent, we do recommend option 2, removing the volume of solvent equivalent to the volume of drug. For example, to mix a 1mg/mL diltiazem infusion using a 125ml bag of NS, remove 25mL NS from the 125mL bag, then add 125mg diltiazem reconstituted in 25mL sterile water (total volume 125mL).  Alternatively, you could use a 100mL bag of NS and add 125mg diltiazem in 25mL sterile water for a total volume of about 125mL (likely closer to 130mL due to overfill), and a concentration of about 1mg/mL, titrated to desired heart rate.

Disclaimer: These mixing and administration instructions provide rapid, general guidelines to assist in caring for critical patients with limited staff. Other compounding and dosing options may exist. It is ultimately the provider’s responsibility to make the best compounding and dosing for each patient. Compatibility lists include medications frequently used in critically ill patients but are not exhaustive.  We strongly recommending consulting a comprehensive reference such as Micromedex or Lexicomp as soon as possible.

Abbreviations: Normal saline (NS), Dextrose 5% in water (D5W), as needed (PRN), paroxysmal ventricular tachycardia (pVT), ventricular fibrillation (VF), diabetic ketoacidosis (DKA), Hyperosmolar hyperglycemic non-ketoacidosis (HHNK), Intracranial Pressure (ICP), Acute coronary syndrome (ACS), Pulmonary embolism (PE).

Take-Home Points

• Whether you work in a rural ED, a resource-limited ED, or a tertiary center filled with more sick patients than your ED pharmacists can cover, you need to be able to care for patients without the pharmacist, including mixing and dosing your own medication infusions. This can be very challenging when you are simultaneously caring for several sick patients, so preparation and practice are key.
• Familiarize yourself with the basic principles of mixing infusions and operating IV pumps.
• Review your hospital formulary and commit to memory the mixing instructions and dosing for a handful of your most essential resuscitation medications.
• Understand what resources (including this guide) are available to assist you when your next critical patient arrives and have them readily available. This will dramatically improve your efficiency, confidence, and cognitive load during these resuscitations.

References

General References for preparation, dosing, and compatibility: Micromedex, Lexicomp, Clinical Pharmacology

• micromedexsolutions.com
• https://www.wolterskluwer.com/en/solutions/lexicomp/resources/lexicomp-user-academy/trissels-iv-compatibility-databases 
• https://www.clinicalpharmacology-ip.com
• https://www.manuelsweb.com/McgPerMin.htm

Peer Reviewed Publications

1. Casey MM, Moscovice IS, Davidson G. Pharmacist staffing, technology use, and implementation of medication safety practices in rural hospitals. J Rural Health. 2006 Fall;22(4):321-30.
2. Bennett, Christopher L., et al. “National Study of the Emergency Physician Workforce, 2020.” Annals of Emergency Medicine. 2020 Dec; 76(6): 695–708.
3. Mk, Hall, et al. “State of the National Emergency Department Workforce: Who Provides Care Where?” Annals of Emergency Medicine. 2018 Sept; 72(3).

4. Walker SE, Law S, Garland J, Fung E, Iazzetta J. Stability of norepinephrine solutions in normal saline and 5% dextrose in water. Can J Hosp Pharm. 2010 Mar;63(2):113-8
5. Sharifi M, Bay C, Skrocki L, Rahimi F, Mehdipour M; “MOPETT” Investigators. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol. 2013 Jan 15;111(2):273-7.
6. Stemple K, DeWitt KM, Porter BA, Sheeser M, Blohm E, Bisanzo M. High-dose nitroglycerin infusion for the management of sympathetic crashing acute pulmonary edema (SCAPE): A case series. Am J Emerg Med. 2021 Jun;44:262-266.
7. Mathew R, Kumar A, Sahu A, Wali S, Aggarwal P. High-Dose Nitroglycerin Bolus for Sympathetic Crashing Acute Pulmonary Edema: A Prospective Observational Pilot Study. J Emerg Med. 2021 Sep;61(3):271-277.
8. Firestone RL, Parker PL, Pandya KA, Wilson MD, Duby JJ. Moderate-Intensity Insulin Therapy Is Associated With Reduced Length of Stay in Critically Ill Patients With Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State. Crit Care Med. 2019 May;47(5):700-705.
9. Dalziel SR, Borland ML, Furyk J, Bonisch M, Neutze J, Donath S, Francis KL, Sharpe C, Harvey AS, Davidson A, Craig S, Phillips N, George S, Rao A, Cheng N, Zhang M, Kochar A, Brabyn C, Oakley E, Babl FE; PREDICT research network. Levetiracetam versus phenytoin for second-line treatment of convulsive status epilepticus in children (ConSEPT): an open-label, multicentre, randomised controlled trial. Lancet. 2019 May 25;393(10186):2135-2145.
10. Glauser T, Shinnar S, Gloss D, Alldredge B, Arya R, Bainbridge J, Bare M, Bleck T, Dodson WE, Garrity L, Jagoda A, Lowenstein D, Pellock J, Riviello J, Sloan E, Treiman DM. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Curr. 2016 Jan-Feb;16(1):48-61.
11. Kapur J, Elm J, Chamberlain JM, Barsan W, Cloyd J, Lowenstein D, Shinnar S, Conwit R, Meinzer C, Cock H, Fountain N, Connor JT, Silbergleit R; NETT and PECARN Investigators. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus. N Engl J Med. 2019 Nov 28;381(22):2103-2113.
12. Alkazemi A, McLaughlin KC, Chan MG, Schontz MJ, Anger KE, Szumita PM. Safety of Intravenous Push Levetiracetam Compared to Intravenous Piggyback at a Tertiary Academic Medical Center: A Retrospective Analysis. Drug Saf. 2022 Jan;45(1):19-26.
13. Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, Decaux G, Fenske W, Hoorn EJ, Ichai C, Joannidis M, Soupart A, Zietse R, Haller M, van der Veer S, Van Biesen W, Nagler E; Hyponatraemia Guideline Development Group. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014 Feb 25;170(3):G1-47.
14. Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH, Thompson CJ. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013 Oct;126(10 Suppl 1):S1-42.
15. Maguigan KL, Dennis BM, Hamblin SE, Guillamondegui OD. Method of hypertonic saline administration: effects on osmolality in traumatic brain injury patients. J Clin Neurosci. 2017;39:147-150.
16. Cruz KCE, Churchwell MD, Mauro VF, Boddu SHS. Physical compatibility of levetiracetam injection with heparin, dobutamine, and dopamine. Am J Health Syst Pharm. 2018 Apr 15;75(8):510-512.

The post Rural ED DIY Pharmacy: Recipe Cards for Resource-Limited ED Teams Caring for Critical Patients appeared first on emDOCs.net - Emergency Medicine Education.

Author: Shane O’Donnell, DO (EM Resident Physician: UTSW – Dallas, TX); Zachary Aust, MD (Assistant Professor of EM/Attending Physician: UTSW – Dallas, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

Initial assessment on arrival includes vital signs BP 134/86, HR 94, RR 16, SpO2 98% on room air, and temperature 99.0F. He is speaking and mentating appropriately but in significant discomfort when you exam his pelvis. Blood is seen at the urethral meatus, and the pelvis is unstable. There is no obvious perineal ecchymosis at this time. The rest of the exam is unremarkable.

What type of injury should be considered with blood at the urethral meatus and suspected pelvic fracture?

Answer: Bladder Rupture

Background:

• The bladder is a hollow organ adjacent to the pelvic floor, situated posteriorly to the pubic ramus, anterior to the uterus in women, and anterior to the rectum in men.
• It is a primarily extraperitoneal organ. The dome of the bladder is lined by the peritoneum and is also the weakest part of the structure.
• Bladder injuries are uncommon, occurring in approximately 1.6% of blunt trauma.¹
• Injuries are primarily caused by blunt trauma and are most often associated with pelvic fractures. Penetrating trauma and iatrogenic injuries do occur but are much less common.²
• Motor vehicle accidents account for the overwhelming majority of bladder rupture presentations.³

Physical Exam

• Physical exam findings may not be conclusive and the absence of abnormalities on exam should not be used in solidarity to rule out bladder injuries.
• Pelvic instability should raise your suspicion of a bladder injury, as pelvic factures are the most common associated injury with bladder injury.⁴
• Blood at the urethral meatus/gross hematuria is an important finding and should also raise your suspicion for bladder injury (Sensitivity: 90%).⁴
• FAST exam is not sensitive enough to reliably detect solid organ injury, including bladder injury (Sensitivity 41-44%).^{5, 6}
• In delayed presentations, signs of peritonitis and/or ileus may be evident if urine is extravasating into the peritoneal cavity. This is often due to the vulnerability of the bladder dome and it’s anatomic location adjacent to the peritoneal cavity.⁶

Evaluation

• Gross hematuria, especially with a pelvic fracture, increases suspicion of injury along the GU tract, and coinciding urethral injuries must also be suspected. Therefore, a retrograde urethrogram (RUG) should be performed prior dedicated imaging for bladder injury.
  • To perform a RUG: Obtain a baseline KUB. After, insert a foley catheter a few centimeters into the urethra and gently inflate the balloon until a snug fit is achieved. Avoid overinflation and iatrogenic urethral injury. Instill 50-60mL of water-soluble contrast and obtain a second KUB while the last 10-15mL are being infused. Look for contrast extravasation as a positive finding for urethral injury.
  • A RUG is NOT a substitute for dedicated cystography.
• Pelvic fracture alone is not an absolute indication for dedicated bladder imaging.⁷
  • Gross hematuria + pelvic fracture = absolute indication for evaluation of bladder injury.
  • Microscopic hematuria + pelvic fracture = consider bladder imaging studies / urologic consultation especially if other concerning signs are present.⁸
    • Inability to void
    • Increased BUN & creatinine
    • Suprapubic pain
    • Low-density peritoneal fluid
•  Penetrating injury with pelvic trajectory + hematuria (gross or microscopic) requires radiologic or surgical evaluation.
• All life-threatening injuries should be identified and stabilized prior to evaluation of bladder injuries. This may require repeat imaging.
• Cystography is the gold standard for evaluation of bladder injury. Plain film and CT cystography both have sensitivities of 95%.^9,10
  • Empty bladder of urine using foley catheter.
  • Instill a dilute, water-soluble contrast until the patient feels the need to urinate or until you have injected >300mL of contrast.
  • CT slices should be thin cuts. Check with your institutional protocols for ordering.

Management/Disposition

• Urology consultation is necessary for all cases of confirmed bladder injury.
• Intraperitoneal Bladder Injury
  • Communication between the bladder and peritoneal cavity can lead to urine extravasation into the peritoneal cavity, progressing to peritonitis and possibly sepsis.
  • These injuries will almost always require surgical intervention, as they do not often heal spontaneously and can have devastating outcomes in left untreated.¹³
• Extraperitoneal Bladder Injury
  • Can often be managed conservatively with foley catheter drainage for 2+ weeks.^13,14
  • May require surgical repair in the setting of complex injuries in the surrounding area.¹³
    • Open pelvic fracture.
    • Associated rectal or vaginal injury.
    • Bladder neck injury.
    • Foley catheter drainage issues from persistent hematuria / blood clots.

Pearls

• Gross hematuria alone OR pelvic fracture + hematuria is an indication for evaluation of a bladder injury.
• Identification and stabilization of life-threatening injuries should take place prior to dedicated bladder imaging.
• Performing a RUG to evaluate for urethral injury is NOT a substitute for cystography.
• CT and Plain Film cystography and almost identical sensitivities and specificities.
• Bladder injury location will guide surgical vs conservative management.

Post MVC, the restrained passenger of an automobile presents to the ED with lower abdominal pain. There is blood at the urethral meatus. A FAST examination is negative for free fluid in the abdomen. Vital signs are stable. A CT scan of the abdomen-pelvis with CT cystography is thus obtained, revealing an extraperitoneal bladder rupture and fractures of the left inferior and superior pubic rami. Which of the following should be part of the management plan for this patient?

A) Admission to the trauma service for continued observation

B) Application of a pelvic binder

C) Immediate consultation to urology for placement of a suprapubic catheter

D) Surgical repair of the bladder rupture within 24 hours

Answer: A

Greater than two-thirds of bladder injuries result from blunt trauma. Most occur from motor vehicle collisions, with severe abdominal injury such as that which occurs with ejection from the vehicle or excessive compressive force from the seat belt on a distended bladder. Bladder injuries are classified as contusions, intraperitoneal ruptures, extraperitoneal ruptures, or a combination of intraperitoneal and extraperitoneal ruptures. The management of extraperitoneal bladder rupture is nonsurgical with Foley catheter urine drainage for one to two weeks to allow for spontaneous healing (assuming urethral injury has also been ruled out). None of the injuries sustained by this patient require an emergent procedure. However, given the reported mechanism and associated findings, it is reasonable to admit the patient for observation, serial exams, and urology consultation.

A pelvic binder (B) is used to reduce venous bleeding caused by sacroiliac joint disruption in open-book pelvic injuries; pubic rami fractures are considered stable and do not require such intervention. Insertion of a suprapubic catheter (C) is unnecessary in the management of extraperitoneal bladder rupture. In fact, the treatment is usually limited to Foley catheter drainage alone. Surgical repair (D) is necessary only for intraperitoneal bladder ruptures. Without operative intervention of an intraperitoneal bladder rupture, lower urinary tract contamination will infect initially sterile urine and promote the development of subsequent bacterial peritonitis. Bladder repairs are never emergencies and should be performed following operative intervention for more severe, life-threatening injuries.

Rosh Review Website Link

Further Reading:

#FOAMED

• http://www.emdocs.net/genitourinary-trauma-presentations-evaluation-and-management-updates/
• https://litfl.com/trauma-genitourinary-injuries/
• https://radiopaedia.org/articles/urinary-bladder-rupture?lang=us

References

1. Gomez RG, Ceballos L, Coburn M, et al. Consensus statement on bladder injuries. BJU Int 2004; 94:27.
2. Bjurlin MA, Fantus RJ, Mellett MM, Goble SM. Genitourinary injuries in pelvic fracture morbidity and mortality using the National Trauma Data Bank. J Trauma 2009; 67:1033.
3. Terrier JE, Paparel P, Gadegbeku B, et al. Genitourinary injuries after traffic accidents: Analysis of a registry of 162,690 victims. J Trauma Acute Care Surg 2017; 82:1087.
4. Teeluckdharry B, Gilmour D, Flowerdew G. Urinary Tract Injury at Benign Gynecologic Surgery and the Role of Cystoscopy: A Systematic Review and Meta-analysis. Obstet Gynecol 2015; 126:1161.
5. Körner, M., Krötz, M. M., Degenhart, C., Pfeifer, K.-J., Reiser, M. F., & Linsenmaier, U. (2008). Current role of emergency us in patients with major trauma. RadioGraphics, 28(1), 225–242. https://doi.org/10.1148/rg.281075047
6. Richards JR, McGahan JP. Focused assessment with sonography in trauma (FAST) in 2017: What Radiologists Can Learn. Radiology 2017;283:30–48.doi:10.1148/radiol.2017160107
7. Lumen N, Kuehhas FE, Djakovic N, et al. Review of the current management of lower urinary tract injuries by the EAU Trauma Guidelines Panel. Eur Urol 2015; 67:925.
8. Brown D, Magill HL, Black TL. Delayed presentation of traumatic intraperitoneal bladder rupture. Pediatr Radiol 1986; 16:252.
9. Quagliano PV, Delair SM, Malhotra AK. Diagnosis of blunt bladder injury: A prospective comparative study of computed tomography cystography and conventional retrograde cystography. J Trauma 2006; 61:410.
10. Morgan DE, Nallamala LK, Kenney PJ, et al. CT cystography: radiographic and clinical predictors of bladder rupture. AJR Am J Roentgenol 2000; 174:89.
11. Case courtesy of Dr Matt A. Morgan, <a href=”https://radiopaedia.org/?lang=us”>Radiopaedia.org</a>. From the case <a href=”https://radiopaedia.org/cases/41780?lang=us”>rID: 41780</a>
12. Case courtesy of Dr Vikas Shah, <a href=”https://radiopaedia.org/?lang=us”>Radiopaedia.org</a>. From the case <a href=”https://radiopaedia.org/cases/61059?lang=us”>rID: 61059</a>
13. Morey AF, Brandes S, Dugi DD 3rd, et al. Urotrauma: AUA guideline. J Urol 2014; 192:327.
14. Kotkin L, Koch MO. Morbidity associated with nonoperative management of extraperitoneal bladder injuries. J Trauma 1995; 38:895.

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Here’s another case from Medical Malpractice Insights – Learning from Lawsuits, a monthly email newsletter for ED physicians. The goal of MMI-LFL is to improve patient safety, educate physicians, and reduce the cost and stress of medical malpractice lawsuits. To opt in to the free subscriber list, click here.

Chuck Pilcher, MD, FACEP

Editor, Med Mal Insights

#FOAMed

emDOCs – Aortic Dissection: Why do we miss it? 

emDOCs – Vascular Causes of Syncope

emDOCs – Syncope Mimics

The post Medical Malpractice Insights: Sudden collapse, hemiparesis & dysphasia – What’s the differential? appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Michael Andrew Tandlich, MD (EM Resident Physician, Northwestern University) and Timothy M. Loftus, MD, MBA (EM Attending Physician, Northwestern University) // Edited by: Bryant Allen, MD (EM Attending Physician, Carolinas Medical Center): Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case 1:

An 87-year-old male with history significant for chronic obstructive pulmonary disease, myelodysplastic syndrome complicated by anemia of chronic disease, obstructive sleep apnea, coronary artery bypass grafting, and percutaneous coronary interventions for coronary artery disease, with over a one-year history of exertional dyspnea, presented to the ED with one to two weeks of worsening dyspnea on exertion. Patient states he would feel his dyspnea worsen with any movement. In the ED, his vital signs were stable, and there was no hypoxia at rest, but upon standing upright, he was noted to have an abrupt oxygen desaturation on a pulse oximeter to 86% on room air. Laboratory studies were remarkable for a hemoglobin level of 8.2 g/dL, down from 9.6 g/dL two weeks prior. Chest x-ray and ECG showed no acute processes. The patient was transfused one unit of packed red blood cells and admitted to the hospital medicine floor for further management.

Case 2:

A 2-year-old female previously healthy with up-to-date immunizations presents to the ED with two days of lethargy, fever, rhinorrhea, and difficulty breathing. On exam, the patient appeared normal color with no increased work of breathing. Vitals notable for HR 137, RR 23, T 37.8, SpO₂ 65% on room air, improved to 78% on 15L NRB. Exam was notable for normal breath sounds and respiratory effort, normal heart sounds without auscultated murmurs, and an otherwise normal exam. An arterial blood gas was performed, demonstrating a true oxygen saturation of 96 percent.

What is hypoxia?

Hypoxia is the condition when body tissues receive inadequate oxygen. This leads to disruption in cellular function. There may be a switch to anaerobic metabolism and subsequent lactic acidosis. While low blood oxygen content, also known as hypoxemia, is a major cause of hypoxia, it is not the only cause.

What are the major etiologies of hypoxia?

Hypoxia can best be broken down into four major categories:

• Hypoxemia
• Anemic Hypoxia
• Ischemic/Stagnant Hypoxia
• Histotoxic Hypoxia

Hypoxemia

Hypoxia which refers to the state of low oxygen concentration in the blood itself, and largely depends on five key factors:

• Altitude: As one moves to higher altitudes, the barometric pressure drops, resulting in the amount of oxygen content inspired to be decreased despite a stable FiO₂. At the extremes of altitude, an otherwise healthy lung would not see enough oxygen in the inspired air to adequately supply metabolism of the body tissues.

• Ventilation: Ventilation refers to the supply of gases to the alveoli and is directly tied to clearance of CO₂. Hypoventilation leads to CO₂buildup, decreased CO₂ clearance, and subsequent decreased concentration of alveolar oxygen. In many disease processes, an increase in CO₂ itself may drive increased work of breathing and is correlated with lung compliance and airway resistance. For example, a patient with acute asthma exacerbation will have high airway resistance which will exacerbate work of breathing.

• Oxygen Diffusion: This is the ability of oxygen to cross the alveoli and surround capillary membranes effectively. Transport may be impaired because of a primary tissue disease process, such as in pulmonary fibrosis.

• Ventilation/Perfusion (V/Q) Matching: There is a balance between oxygenation of alveoli and blood flow through their capillaries. Mismatch between these two factors will occur when blood flows through alveoli with inadequate ventilation, or when blood does not reach alveoli that do have adequate ventilation. Examples of this is include pulmonary embolism, in which perfusion is obstructed, and status asthmaticus, in which airway collapse causes air trapping and ventilation obstruction. Mismatch may be corrected when excess oxygen is inhaled, since even poorly ventilated areas of the lung will receive adequate flow of oxygen. It is important to note that ventilation and perfusion matching is heterogeneous throughout different areas of the lung in normal state and is exacerbated by certain conditions affecting V/Q mismatch (e.g. asthma, pneumonia).

• Blood Shunting: Shunting of blood refers to the bypassing of the process by which blood receives oxygenation. In other words, blood enters systemic circulation before receiving adequate oxygenation. Classic examples of blood shunting occur with anatomic defects such as intracardiac septal defects. Mucus plugging of one mainstem bronchus is another example of shunt physiology. In either case, an increase fraction of inspired oxygen will not fill alveoli which are receiving blood, and classically will not correct hypoxemia.

Anemic hypoxia

Hypoxia may occur if there is a critically low blood oxygen carrying capacity. Acute changes in hemoglobin level (such as from acute blood loss anemia and hypovolemic shock) may result in decreased transport of oxygen to tissues. Hypoxia may also result from changes in the hemoglobin functionality such as during acute carbon monoxide poisoning, where there are plenty of hemoglobin molecules which simply are not able to bind oxygen.

Ischemic/stagnant hypoxia

Hypoxia may result from a critical decrease in the flow of oxygenated blood to peripheral tissues. Systemic conditions such as cardiogenic shock may lead to decrease oxygenation of blood during pulmonary gas exchange as well as inadequate global delivery of blood to central and peripheral organs. Localized conditions may impede cellular diffusion of oxygen (such as with severe tissue edema) or focally impede flow of oxygenated blood (such as with arterial damage or obstruction).

Histotoxic hypoxia

Hypoxia may result from low tissue utilization of oxygen. This may occur with direct cellular poison (cyanide, colchicine overdose) or abnormally high tissue oxygen demand (malignancy).

When should hypoxia be suspected?

While there is no single lab value to directly measure hypoxia, it should be suspected in any patient with anxiety, confusion, and restlessness, which may be early signs of hypoxia and may precede changes in vital signs³. Low SpO₂ is the hallmark of hypoxemia, one of the main causes of hypoxia, and may be suspected in any patient with oxygen saturation less than 90 percent (or less than 88 percent in patients with chronic lung disease). Lactic acidosis may develop in response to anaerobic metabolism from tissue hypoxia or from increased catecholamine surge and may be detected on blood gas⁴.

Approach to Hypoxia

1-Patient Stability – check general appearance, ABCs, vital signs

In the assessment of any patient in the ED, it is the cornerstone of our decision making as EM physicians to do a quick yet thorough “sick or not sick” assessment.

General appearance

How does the patient appear? Is the patient comfortable or in acute distress? Does the patient exhibit any behaviors which may be clinical signs however subtle of “badness?”

ABCs

Airway, Breathing, and Circulation assessment is the right place to start in any patient who may be experiencing critical illness, including from hypoxia.

Is the patient protecting her airway? Although rare, hypoxia may result from critical airway narrowing that can be audibly detected as stridor. In pediatric patients, laryngeal stridor should prompt a thorough evaluation of upper airway obstruction⁵. Hypoxia may be seen with severe smoke inhalation injury, which may present with rales and rhonchi and lead to imminent airway compromise⁶.

Are breath sounds present bilaterally? While tension pneumothorax is associated with classic symptoms of respiratory distress and tracheal deviation, only half of cases may present with frank hypoxia⁷. Does the chest rise and fall equally? Patients with significant rib fractures causing an unstable chest wall may become inadequately ventilated and develop hypoxia as well as hypercapnia and acidosis⁸.

Is the patient tachycardic? Are distal pulses present? Thready pulses may indicate intravascular volume loss. In the patient with blunt trauma, this may be a manifestation of hemorrhagic shock, in whom resuscitation is vital to prevent tissue hypoxia⁹. In the patient with severe infection, tachycardia may be the manifestation of inflammatory-mediated fluid shifts and subsequent end-organ hypoperfusion and ischemic damage¹⁰.

Vital Signs

Especially in any unstable patient, it is crucial to obtain a full set of vitals, which are likely to be abnormal and may help to elucidate an underlying etiology of the patient’s instability. Acute hypoxia is most likely to manifest with increased respiratory rate (RR>24) and increased heart rate (HR>100), but normal respiratory rate and heart rate should not exclude the possibility of hypoxia¹⁰. In diseases with hypoxemia and hypercarbia, the body will try to increase tidal volume in addition to respiratory rate, with the goal of increasing alveolar ventilation¹¹. Patients with brisk intravascular volume loss may develop tachycardia and hypotension, and as the hypovolemia worsens, the body compensates for the subsequent tissue hypoxia by increasing respiratory rate¹². Patients with hypotension may have hypoxia from malperfusion and warrants a prompt investigation of the underlying cause. Patients hypoxic from septic shock may be hyperthermic or hypothermic, and this may best be identified using core temperature measures such as rectal temperature. Pulse oximetry reading is prone to inaccuracies, especially in the unstable patient, and it should always be considered in a clinical context.

2-History and Physical Exam

In the unstable patient, the history may be limited. Yet, in the stable patient it is important to obtain a thorough history and physical exam. Taking a clear and thorough history is the first important step.

Does the patient have a history of cardiac disease or pulmonary disease? Patients with preexisting cardiovascular disease are more likely to develop dysfunctional perfusion of end organs and a subsequent hypoxic state¹³. Patients with underlying lung disease are prone to developing physiologic changes that increase the risk of hypoxemia and subsequent hypoxia, including decreased ventilatory drive, airway obstructive processes, intra-alveolar exudates, alveolar septal thickening, inflammation and fibrosis, and alveolar capillary damage¹⁴.

Any history of smoking? Cigarette smoking is well known for its detrimental effects on normal body physiology and is associated with increased risk of hypoxia. Carbon monoxide blood levels are often elevated in chronic smokers in whom severe elevations and symptoms of hypoxia have been reported.¹⁵

Recent surgeries? Patients in the post-operative period are generally more prone to atelectasis, pneumonia, and pulmonary embolism, all pathologies that may present with hypoxia¹⁶.

Review of Systems: Many patients with hypoxia will report dyspnea or increased work of breathing. Patients may also note confusion or feeling sluggish. Headache may the only symptom of hypoxia in patients with acute CO poisoning¹⁷.

Physical Exam

General appearance of a patient may give clues to underlying etiology. Cyanosis may first show on lips and distal fingertips and may be a sign of severe hypoxemia. Diffuse, dull, red skin discoloration may be a sign of cyanide toxicity. Pale appearance may be a sign of acute blood loss anemia. Crackles on auscultation of lung parenchyma may point to heart failure if bilateral or a lobar pneumonia if focal and unilateral. Absent breath sounds may point to an effusion or a collapsed lung. Distal extremities may be warm in distributive shock or cold and clammy in a patient with hemorrhage. Cherry red skin and mucous membranes are usual post-mortem findings in carbon monoxide poisoning which are in fact uncommon at presentation¹⁸. Patient may be altered and restless on neurologic exam. Rectal exam with gross blood may point to acute blood loss anemia.

3-Further Evaluation

Arterial oxygen saturation (SaO₂)

SaO₂ describes the amount of oxygen bound to hemoglobin, and normal values range between 95 and 100 percent¹⁹. A rapid means of evaluating this is with pulse oximetry. Based on the known absorption of light at particular wavelengths of oxygenated and deoxygenated blood, pulse oximetry uses spectrophotometry to calculate an estimated SaO₂ (SpO₂)²⁰. The accuracy of this measurement relies in part on accurate signal strength, which is demonstrated as a waveform and which should normally be sharp with a clear, dicrotic notch²⁰. Low perfusion states will have sinus wave forms with low amplitude; SpO₂ measurements must be taken with caution in these patients (such as those with low cardiac output, peripheral vasoconstriction, or hypothermia)²⁰. SpO₂readings should also be taken with caution in patients with nail polish, which may interfere significantly with light absorption at the wavelengths used by pulse oximetry, as well as in patients with darker skin pigmentation^21,22. It is also important to note that SpO₂ is often inaccurate in patients with carbon monoxide poisoning²³. In fact, since oxyhemoglobin and carboxyhemoglobin have similar absorptive properties for red light, pulse oximetry will often estimate true SaO₂ as normal or falsely elevated in patients with CO poisoning; this absorptive property is also the reason patients with CO poisoning would appear cherry red²⁴. Methemoglobinemia is another disease in which its absorptive properties of red light will make pulse oximetry unreliable and is the reason significant toxicity will often shift pulse oximetry estimations of SaO₂ toward approximately 85 percent²⁴. Also be cautious when using pulse oximetry to trend oxygen saturation in critically ill patients, in whom the effects of acidosis and amenia have been shown to interfere with the correlation of pulse ox estimates and true SaO2²⁵. New, multi-wavelength pulse oximeters designed to measure methemoglobin and carboxyhemoglobin may improve future oxygen monitoring capabilities²⁶.

Arterial Blood Gas (ABG)

Blood gas analysis provides information on alveolar ventilation, oxygenation, and acid-base balance²⁷. In the evaluation of these key physiologic processes, ABG analysis measures arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2), and compared with pulse oximetry, it is a more definitive tool in evaluating oxygenation and ventilation^28,29. Normal PaO₂is considered 80-100 mmHg, and lower values may indicate hypoxemia as the cause of hypoxia. Knowledge of its value also is useful in managing patients on ventilatory support³⁰.  Normal PaCO₂ is considered 35-45 mmHg, and its levels may be elevated in either situations of increased metabolism or decreased ventilation; in either case, acuity of the hypercapnia can be evaluated by assessing for any concurrent change in HCO₃³⁰. Elevations from baseline of PaCO₂ in respiratory distress with increased work of breathing may signal respiratory failure and serve as an indication for ventilatory support³¹. While most ABG analyses measures pH and PaCO₂ directly, HCO₃ and base changes are indirectly calculated; especially in critically ill patients, these latter calculations may be highly variable and should be interpreted with caution³². This prompt direct measurement of pH may be critical in patients with metabolic derangements, such as in severe sepsis, diabetic and alcoholic ketoacidosis, trauma, acute respiratory failure, cardiac arrest, and COPD; in these situations, venous blood gas (VBG) analysis, one which may be clinically preferred for numerous reasons, is also reliable³³.

It is imperative to always interpret ABG within the clinical context of the patient. Accuracy of the data collected with an ABG sample is particularly susceptible to errors, and care must be taken to confirm the blood sample is truly arterial in nature (and not venous), completely and promptly rid of any air bubbles, inspected for any clots, and analyzed within thirty minutes of the collection time³⁴. ABG samples are even more prone to error in patients with high PaO₂ such as those with high levels of supplemental oxygen or in whom shunt physiology is suspected, as well patients with leukocytosis or thrombocytosis, and should have ABG analysis performed within five minutes³⁴.

Venous Blood Gas (VBG)

Compared with ABG, the VBG puncture is often quicker to perform, less painful, and carries a lower risk of complications such as arterial injury and arterial thrombosis^35,36. Given these potential benefits, VBG should be considered in establishing acid-base state and assessing respiratory function, two key purposes for which blood gas analysis is used in the ED. VBG is noninferior in its ability to screen for acid-base abnormalities in critical illnesses such as DKA and acute COPD exacerbations^34,35. Numerous studies and meta-analyses have confirmed this^35,37,38. Caution should be taken in severe hemodynamic compromise such as in severe shock or cardiac arrest, when VBG analysis of lactate and pH has been shown to be less reliable^38,39. Furthermore, while VBG may be helpful in screening for arterial hypercarbia, it has poor correlation with ABG results in pO₂ and pCO₂ analysis and is too clinically unpredictable³⁹.

Imaging

Imaging studies of the chest can aid in determining the underlying cause of hypoxia. Chest x-ray can be useful in diagnosing focal airway abnormalities, such as pneumonia, acute respiratory distress syndrome, lung hyperinflation, and pulmonary edema. An initial chest x-ray may not always elucidate an underlying etiology. Chest computed tomography (CT) can be useful in giving more detail. Evidence of smoke inhalation injury may be absence on initial chest x ray imaging but nonetheless will serve as a baseline evaluation in such cases⁴⁰.

Differential Diagnosis of Hypoxia

HYPOXEMIC:

– High altitude: high altitude, high altitude pulmonary edema

– Hypoventilation: central nervous system depressants (opioids), hypothyroidism, neuromuscular (myasthenia gravis, Guillain-Barre syndrome), nerve disease (cervical spine injuries, phrenic nerve injuries), chest wall injury (flail chest)

– Low Diffusion: pulmonary edema, pulmonary contusion, chronic obstructive pulmonary disease, interstitial lung disease

– V/Q Mismatch: pulmonary embolism, chronic obstructive pulmonary disease, asthma, mucus plugging, pulmonary hypertension

– Shunt: Intracardiac, arteriovenous malformation, pneumonia, atelectasis, acute respiratory distress syndrome

ANEMIC:

acute blood loss anemia, hemorrhagic shock, carbon monoxide poisoning, methemoglobinemia

ISCHEMIC:

global: cardiogenic shock (STEMI, ADHF), distributive shock (anaphylaxis, severe sepsis), obstructive shock (tamponade, tension pneumothorax), increased demand (seizure, shivering)

local: arterial obstruction, interstitial edema

HISTOTOXIC:

cyanide poisoning, hydrogen sulfide

4-Management

Maintain Patent Airway

The first step in managing an airway is to evaluate whether the airway is patent. Hypoxic patients with respiratory failure or altered consciousness may not be able to protect their airway patency in which endotracheal intubation may be warranted⁴¹. Patients in respiratory failure exhibiting signs of fatigue (such as lethargy, increasing use of accessory muscles, decreased rate and depth of respiration) may decompensate without ventilatory support in whom intubation may also be warranted⁴². Airway management is particularly important in inhalation injuries and thorough evaluation and risk stratification for impending airway compromise may be performed with fiberoptic bronchoscopy⁴³.

Increase Oxygen Content of Inspired Air

Supplemental oxygen is the cornerstone of therapy for many cases of hypoxia and can be divided into devices which provided low flow of oxygen, high flow of oxygen, and positive pressure ventilation. Supplemental oxygen at 100% FiO2 should be administered to any patient with suspected inhalation injury in whom the physiologic goal is to quickly reverse and displace carbon monoxide from hemoglobin binding sites⁴⁴.

The post Hypoxia in the ED Setting: Systematic Approach and Management appeared first on emDOCs.net - Emergency Medicine Education.

The post Journal Feed Weekly Wrap-Up appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Matthew Cravens, MD (Emergency Medicine Resident, Atrium Health’s Carolinas Medical Center); Christine Murphy, MD (Emergency Medicine Attending, Medical Toxicologist, Atrium Health’s Carolinas Medical Center) // Reviewed by: James Dazhe Cao, MD (@JamesCaoMD, Associate Professor of EM, Medical Toxicology, UT Southwestern Medical Center, Dallas, TX); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Case:

A 78-year-old man presented to the emergency department after ingesting six boxes of old rat bait he found in his garage (active ingredient: 0.005% brodifacoum) over the past few days in a suicide attempt. He had no active bleeding. Initial vital signs were: BP 96/43, HR 98, T 97.4°F, RR 16.

Questions:

1. What are superwarfarins, and how do they cause toxicity?
2. What labs should be ordered for this patient?
3. Should the patient be given empiric vitamin K prior to lab result?

Background:

• Developed in the 1950s and 1960s, anticoagulant rodenticides have been used for years to help control rodent infestations.
• Anticoagulant rodenticides cause death by internal bleeding and inhibited coagulation several days after ingestion.
• There are two generations of anticoagulant rodenticides:
  • First generation:
    • Hydroxycoumarins (e.g., warfarin)
    • Indandiones (e.g., diphacinone, chlorophacinone)
  • Second generation: superwarfarins or long-acting vitamin K antagonists (e.g., brodifacoum, bromadiolone)¹
• Superwarfarins were developed as more potent and longer-acting rodenticides in the 1970s after rodents evolved warfarin resistance.²
  • In mice given one-half the lethal dose 50 (LD50), the plasma elimination half-life of brodifacoum was 92 days compared to 15 days for warfarin.³ Of note, warfarin’s elimination half-life was longer than expected in this study due to a bi-phasic decline – warfarin reached very low concentrations within 5 days of administration, then entered a second, much slower elimination phase.³
  • In humans, the elimination half-life of brodifacoum has been estimated between 16 and 62 days,⁴ compared to 35 hours for warfarin.⁵
  • Superwarfarins are vitamin K epoxide reductase (VKOR) inhibitors with the same mechanism of action as warfarin (Figure 1). They cause anticoagulation by preventing the recycling of vitamin K, depressing the hepatic activation of factors II, VII, IX, and X.¹

• While the U.S. Environmental Protection Agency (EPA) banned the sale of superwarfarins from use in residential consumer products in 2011:⁶
  • Warfarin and indandione rodenticides are still sold in the U.S.
  • The threat of superwarfarin exposure from pre-2011 stored rat bait persists.
• In the early 2000s, prior to the EPA ban, about human superwarfarin exposures occurred annually in the U.S. Most unintentional exposures are pediatric, and of these, less than 1% have a moderate or major effect.⁷
• Superwarfarins may be ingested, inhaled, or absorbed topically, and possess bioterrorism potential.⁸
• In 2018, inhalation of superwarfarin-contaminated synthetic cannabinoids (“spice”) affected 300 patients and caused 7 deaths in an outbreak centered in Illinois, U.S.⁸

Clinical Presentation and Diagnosis:

• Symptoms of easy bruising or bleeding do not develop for several days after exposure.
• Patients naïve to vitamin K antagonists presenting on the day of exposure, like a child with a witnessed ingestion, are asymptomatic and have normal INRs.
• Patients presenting after an intentional ingestion can have major bleeding
  • Most commonly a genitourinary source, with flank or abdominal pain and hematuria.
  • Gastrointestinal and intracranial hemorrhage are also seen.
• No confirmatory laboratory testing is necessary to make the diagnosis if history suggests superwarfarin exposure.
  • Can consider sending a laboratory test to assess for superwarfarin exposure if patient without known exposure develops persistent unexplained INR elevation.
    • This is a send out test that takes several days to weeks to result.

Management:

• Unintentional, acute ingestions
  • Asymptomatic patients with acute ingestions (<24 hrs) do not require admission to the hospital.
  • With small ingestions (e.g., < 1 mg), patients may be monitored at home for two weeks for signs of bleeding of bruising.
  • For larger or unknown ingestions, patients should have PT/INR at 48-72 hrs with their primary care physician to further dictate management.
  • Report should be made to local poison control center (1-800-222-1222) for follow-up.
• Intentional or chronic ingestions
  • Require initial PT/INR and evaluation for co-ingestants (e.g., acetaminophen concentration).
  • Charcoal may be useful if administered to prevent absorption in the first 1-2 hours after ingestion.
  • Whole bowel irrigation may be considered for an acute massive ingestion or ingestion of intact packets of bait.
• Use the INR to guide management.
  • Vitamin K₁ should not be administered empirically but only in response to elevated INR.
    • If given prior to detecting an elevated INR, vitamin K₁ may delay INR elevation and underestimate severity of exposure.⁹
  • If INR is normal at 48-72 hrs, clinical toxicity can be safely ruled out with very rare exceptions.⁹
  • For INR > 2.0 with minor or no bleeding, initiate oral vitamin K₁ 10-50 mg every 6-12 hours, which may be rapidly titrated up to 50-100 mg every 6 hours. Dosing for children should be 0.4 mg/kg/dose every 6-12 hours.⁹
  • After INR normalizes, vitamin K₁ dosing may be titrated down.
  • Large superwarfarin ingestions may require outpatient treatment for several months.
• For patients with major bleeding
  • Blood products should be administered in a similar fashion to serious bleeding with warfarin, including protein complex concentrate, fresh frozen plasma, and packed red blood cells.
  • Oral vitamin K₁ should be administered as above, unless the patient is critically ill, in which case IV vitamin K₁ at a dose of 0.3 mg/kg (max 10 mg) should be administered initially. This carries a risk of anaphylactoid reaction.¹⁰ Continued oral vitamin K₁ will be required after initial IV dose(s).

Case Follow-up:

The patient’s blood pressure normalized after 1L of crystalloid. His EKG had normal intervals, and acetaminophen and salicylate concentrations were undetectable. Prothrombin time resulted >100 seconds, with INR 12.7, and partial thromboplastin time was 79 seconds. He remained without symptoms. He was administered oral vitamin K₁ 40 mg every 6 hours. His INR decreased to 1.9 after 3 days of therapy, and he was continued on oral vitamin K₁ titrated to an INR of <2 for the next several months.

Clinical Pearls:

• Superwarfarins are extremely potent and long-lasting inhibitors of vitamin K epoxide reductase.
• Most accidental ingestions do not cause significant injury, including in pediatric ingestions.
• Normal INR at 48-72 hours can reliably rule out clinical toxicity with very rare exceptions.
• Vitamin K₁ is the mainstay of treatment but should not be started empirically in a stable patient, only in response to INR elevation.
• Resuscitation of serious bleeding is not different from warfarin-induced coagulopathy, comprising blood products in addition to IV vitamin K.
• Patients often need PO vitamin K₁ supplementation for months after large ingestion.
• While unnecessary if the history is clear, can consider sending superwarfarin panel to make the diagnosis in unexplained INR elevation.

References:

1. Chong YK and T Wing-Lai Mak. Superwarfarin (Long-Acting Anticoagulant Rodenticides) Poisoning: from Pathophysiology to Laboratory-Guided Clinical Management. Clin Biochem Rev. 2019 Nov; 40(4): 175–185.
2. Feinstein et al. The emerging threat of superwarfarins: history, detection, mechanisms, and countermeasures. Ann N Y Acad Sci. 2016 Jun; 1374(1): 111–122.
3. Vandernbrouke V, Bousquet-Melou A, De Backer P, and Croubles S. Pharmacokinetics of eight anticoagulant rodenticides in mice after single oral administration. J. Vet Pharmacol Therap. 2008 31:437-445.
4. Yip L, Stanton NV, Middleberg RA. Vitamin K₁ treatment duration in patients with brodifacoum poisoning. N Engl J Med 2020; 382:1764-1765.
5. Holford NH. Clinical pharmacokinetics and pharmacodynamics of warfarin. Understanding the dose-effect relationship. Clin Pharmacokinet. Nov-Dec 1986; 11(6): 483-504.
6. EPA Takes Major Actions to Reduce Americans’ Risks from Mouse and Rat Poisons / Move will better protect children, pets and wildlife. U.S. Environmental Protection Agency, 2011. Available at: https://archive.epa.gov/epapages/newsroom_archive/newsreleases/5689a230c1490219852578a80053a4b7.html. [Accessed May 18, 2022]
7. Caravati EM, Erdman AR, Scharman EJ, et al. Long-acting anticoagulant rodenticide poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicology 2007;45(1):1-22.
8. Kelkar et al. An Outbreak of Synthetic Cannabinoid–Associated Coagulopathy in Illinois. N Engl J Med 2018; 379:1216-1223.
9. Recognition and management of pesticide poisonings, 6^th U.S. Environmental Protection Agency, 2013. Chapter 18: Rodenticides. Available at: https://www.epa.gov/pesticide-worker-safety/recognition-and-management-pesticide-poisonings. [Accessed July 16, 2021.]
10. Britt RB and JN Brown. Characterizing the severe reactions of parenteral vitamin K1. Clinical and Applied Thrombosis/Hemostasis 2018, Vol. 24(1) 5-12.

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Today on the emDOCs cast with Brit Long, MD (@long_brit), we look at updates in Clostridioides difficile infection.

Episode 54: Clostridioides difficile infection updates

Background:

• Clostridioides difficile is an anaerobic Gram-positive, spore-forming, enterotoxin-producing bacterium. It’s transmitted by fecal or oral route and leads to tissue injury and death of intestinal cells, particularly epithelial and inflammatory cells of the GI system (resulting in diarrhea, GI symptoms).
• While CDI rates have decreased since 2010, domestic rates still average approximately 500,000 cases annually.
• Current data suggest 10% of patients in the ED with diarrhea are ultimately found to have CDI, and a recent 8-year search of the Nationwide Emergency Department Sample found over 900,000 emergency department (ED) visits with the primary diagnosis of CDI.
• In 2014, CDI replaced methicillin-resistant Staphylococcus aureus (MRSA) as the most common hospital-acquired infection in the U.S.

Risk Factors:

• Focus on 2 components: exposure and increased susceptibility to C. difficile.
• Exposure risks center on contact with contaminated individuals or clinical settings
• Susceptibility is the other risk factor. One of the most important risk factors is antibiotic exposure. Abx disrupt normal gut microbiota and enable C. difficile seeding in newly-exposed individuals as well as germination of pre-existing dormant C. difficile spores in carriers.
  • Fluoroquinolones (OR 5.5-16.7), beta-lactam and beta-lactamase inhibitors (OR 2.7), third- and fourth-generation cephalosporins (OR 1.6-14.9), carbapenems (OR 1.5-5.7), and clindamycin (OR1.8-31.8).
  • While 10 days of antibiotics classically associated, may occur in even single doses.
  • Recent use includes those receiving antibiotics within 3 months of CDI presentation.
  • Up to 40% of CDI patients lack a history of recent antibiotic use.
• Age > 65 years increased risk (5-fold).
• Recent healthcare exposure, IBD (3% risk in 5 years), and immunosuppression are risks.
• HIV, recent GI surgery, tube feedings, malnutrition, obesity, female sex, and low serum albumin.
• Proton pump inhibitor use likely increases risk, but many confounders in the available evidence.

Categories and Presentation

• CDI can cause a spectrum of manifestations ranging from an asymptomatic carriage to fulminant disease with toxic megacolon.
• Overall: abdominal pain (6-90%), fever (21-50%), bloody stools (5-21%), and watery diarrhea (55-84%).
• Classified into nonsevere, severe, and fulminant. Classification based on labs (Cr, WBC) and patient hemodynamics.
  • Classic presentation: diffuse, watery stools and recent antibiotic use and/or hospitalization.
• Nonsevere disease: Watery diarrhea (≥3 loose stools in 24 hours) is the cardinal symptom of CDI. Other manifestations include lower abdominal pain and cramping, low-grade fever, nausea, and anorexia. Diarrhea may be present with mucus or occult blood, but melena or hematochezia are rare. Fever >38.5°C is associated with CDI in about 15% of cases.
  • Diarrhea usually lasts weeks to months. Diarrhea may not be isolated. CDI may present with nausea and vomiting in 2-30% of patients.
  • Cr < 1.5 mg/dL and WBC < 15,000.
• Severe colitis: Clinical manifestations include diarrhea, lower quadrant or diffuse abdominal pain, abdominal distention, fever, hypovolemia, lactic acidosis, hypoalbuminemia, elevated Cr, leukocytosis (WBC of 40,000 cells/mL or higher), elevated lactate.
  • Defined by Cr > 1.5 mg/dL, WBC > 15,000.
• Fulminant colitis: Abdominal distention, shock or early vasopressor requirement.
  • In 1-3% of CDI cases, patients can have a delayed presentation resulting in a fulminant colitis; these numbers may be increasing due to hypervirulent strains.
  • Ileus can occur in severe forms. Present in 20% of CDI patients with fulminant colitis in a single 12-year study.
  • Megacolon should be suspected in patients with severe systemic toxicity together with radiographic evidence of large bowel dilatation (>6 cm diameter in the colon and/or >12 cm diameter in the cecum).
  • Radiographic findings of ileus and toxic megacolon should raise concern for CDI in at-risk patients, regardless of whether diarrhea is present.
• Recurrent disease: Defined by resolution of CDI symptoms while on appropriate therapy, followed by reappearance of symptoms within 2-8 weeks after treatment has been stopped.

Evaluation/Testing

• CBC, electrolytes, lactate, LFTs can assist in assessing disease severity and evaluate for other conditions/complications.
• IDSA guidelines recommend CDI testing in patients with 3 or more unformed stools in a 24-hour period.
• Use presentation and risk factors to determine need for testing, especially for diarrhea lasting over 1 week and there’s no other explanation.
• CDI testing centers on detection of the organism itself and the toxins (A and B) produced. We used to use the cell cytotoxicity neutralization assay (CCNA) for detecting toxin B as the diagnostic “gold standard,” but this is no longer used.
• Organism detection: nucleic acid amplification tests (NAAT) detect toxin genes.
  • This includes PCR.
  • Highly sensitive but cannot distinguish infection from asymptomatic colonization. NAATs may lead to overdiagnosis of CDI.
  • Glutamate dehydrogenase (GDH) enzyme immunoassays (EIA): Detects the metabolic enzyme that is found in all strains of C. difficile, but this has low specificity. Can’t differentiate between toxigenic/nontoxigenic strains.
• Toxin production: Toxin EIA.
  • Toxin EIA for A and B sensitivity ranges between 51-88%. Specificity is 99%.
• General consensus is lacking as to which laboratory test is best. IDSA emphasizes using a two or three step algorithm as agreed upon between individual institutions and their clinical laboratory (e.g., EIA for GDH plus EIA for toxin; EIA for GDH plus EIA for toxin plus NAAT; NAAT plus EIA for toxin).
• One sample algorithm: Start with NAAT/PCR. If NAAT/PCR negative, you can rule out disease. If NAAT/PCR positive, proceed with toxin EIA testing. If this is positive, treat patient. If negative, isolate patient but don’t treat. This is likely a carrier.
• Caveat: If immunocompromised and NAAT/PCR positive, treatment is warranted.
• If a patient can’t provide a stool specimen, send them home and have them bring back the sample.

Severity assessment

• Several scoring systems can be used to assess the severity of CDI and guide initial treatment.
  • The ATLAS scoring system includes 5 parameters that are each scored as 0-2 points:
    • Age (<60 y, 0 points; 60-79 y, 1 point; ≥80 y, 2 points)
    • Treatment with systemic antibiotics – yes 2 points; no 0 points
    • Leukocytosis (<16,000, 0 points; 16,000-25,000, 1 point; >25,000, 2 points)
    • Albumin (>35 g/L, 0 points; 26-35 g/L, 1 point; <25 g/L, 2 points)
    • Serum Creatinine (<1.3mg/dL 0 points; 1.4-2.0mg/dL 1 points;>2.1mg/dL 2 points)
  • Ghosh identified several indicators of moderate to severe CDI:
    • Leukocytosis (white blood cell count >20 × 10⁹/L)
    • Albumin level <30 g/L
    • Creatinine level >50% baseline
    • Vital sign instability (SBO <100 mm Hg, temperature >38°C)
    • Abdominal pain/distension
    • Ascites, colonic distension, or ileus on radiology studies
  • Summary: Use hemodynamics, systemic toxicity, elevated WBC/Cr/lactate, presence of megacolon.

Imaging:

• No clear recommendations on when diagnostic imaging should be used in CDI.
• The World Society of Emergency Surgery recommends CT “for patients with clinical manifestations of severe-complicated C. difficile colitis” without formerly defining “severe-complicated”.
• Patients with evidence of severe disease (severe abdominal pain, abdominal distention with apparent ileus, fever, hypovolemia, lactic acidosis, hypoalbuminemia, and/or marked leukocytosis), concern for another condition, history of abdominal surgery/obstruction, medical complications (such as diabetes, ulcerative colitis, or Crohn’s disease) should undergo CT imaging.
• CT may show pronounced colonic wall thickening and low-attenuation mural thickening (due to mucosal and submucosal edema, which may be visible as a “target sign” or “double halo sign” consisting of two or three concentric rings of different attenuation). Pericolonic stranding and ascites may occur but are not specific.
• Toxic megacolon: colonic dilatation (>6 cm in diameter) is diagnostic; other findings include small bowel dilatation, air-fluid levels (mimicking an intestinal obstruction or ischemia), and “thumb printing” (scalloping of the bowel wall) due to submucosal edema.

Therapy

• Empiric treatment without confirmation testing is not recommended.
• If confirmed positive, stop unnecessary antibiotics. First line used to be metronidazole. This is no longer the case due to increasing resistance (rates as high as 18%).
• First line is fidaxomicin per 2018 IDSA guidelines, or oral vancomycin if fidaxomicin not available.
  • In 2011, fidaxomicin was FDA-approved for the treatment of CDI and is currently supported by IDSA guidelines in treatment of an initial episode of CDI.This recommendation is supported by two large-scale RCTs involving over 1100 patients and demonstrating near-equal efficacy of oral vancomycin vs. fidaxomicin on clinical resolution of symptoms at 10 days.
  • Unfortunately, fidaxomicin is very expensive, and most use oral vancomycin.

• Metronidazole is an option for initial treatment of CDI if vancomycin and fidaxomicin are unavailable.
• Oral antibiotic regimens for a duration of 10 days resolve symptoms in the majority of CDI patients but can be extended to 14 days if symptoms are slow to improve.
• Fulminant: Consult surgery due to concern perforation, peritonitis, and septic shock. Surgical treatment can include total abdominal colectomy or a diverting loop ileostomy with colonic lavage.
  • High doses of oral/NG and rectal vancomycin should be administered in ED, contacting not only surgery but also GI. Endoscopic stool transplant having been shown to be surgery-sparing and life-saving and can be tried initially.
  • IDSA – For fulminant CDI*, vancomycin administered orally is the regimen of choice (strong recommendation, moderate quality of evidence). Most experts recommend rectal administration as well as a suspension enema, and this will be the primary route tf ileus is present. The vancomycin dosage is 500 mg orally 4 times per day and500 mg in approximately 100 mL normal saline per rectum every 6 hours as a retention enema. Metronidazole should also be given IV in doses of 500 mg every 8 hours with the oral and rectal vancomycin.

Prevention/Isolation

• Alcohol-based hand sanitizers are less effective than handwashing with soap and water.
  • C. difficile spores are resistant to alcohol solutions and have been shown in some instances to be equivalent to no hand hygiene at all.
• Gowns and gloves are required whenever entering the room of a patient in enteric precautions isolation to prevent contamination of garments/skin and the spread of disease.
• Hand washing with soap and water is the most effective strategy to prevent transmission; this is done after removing gown and gloves.
• Disinfect shared equipment such as stethoscopes, wrist band, ID scanners and others with bleach
• Frequently touched surfaces in the room and equipment removed from the room should be disinfected with bleach wipes. Terminal cleaning includes Ultraviolet light treatment.

Further Reading: 

• emDOCs
• WikEM

The post emDOCs Podcast – Episode 54: Clostridioides difficile infection updates appeared first on emDOCs.net - Emergency Medicine Education.

Author: Christopher J. Nelson, MD (EM Resident Physician, UTSW, Dallas, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

Answer: Finger Amputation

Background:

• An average of over 46,400 finger amputations occurred in the US from 1997 to 2016²
• Bimodal distribution – below the age of 5 year and over the age of 65 years²
• Doors and power saws are the most common mechanisms²
• Goals of treatment are to restore function, sensation, durability, and proper nail growth
• Improper treatment may lead to loss of function, pain, and poor cosmetic outcome³

Anatomy:

• The hand consists of phalanges, metacarpal bones, and carpal bones
• Each finger has a distal, middle, and proximal phalanges
• The thumb has distal and proximal phalanges
• Finger joints (distal to proximal):
  • Distal interphalangeal joints (DIP)
  • Proximal interphalangeal joints (PIP)
  • Metacarpophalangeal joints (MCP)
• Thumb joints
  • Interphalangeal joint
  • Metacarpophalangeal joint
  • Carpometacarpal joint
• Neurovascular components run on the lateral aspects of the digits
• Naming digits is less likely confused than numbering – Thumb, index, long, ring and pinky
  • Varying numbering systems can otherwise lead to miscommunication

History and Exam:

• Mechanism of injury
• Time of injury
• Other signs of injury (amputation may be a distracting injury to other injuries)
• Amputated digit cold vs. warm (important for reimplantation time)⁵
• Tetanus status
• Dominant hand
• History of blood thinners
• History of diabetes and smoking, which are predictors of poor wound healing⁷
• Examination of each digit’s sensation and strength
  • Isolating and examining extension/flexion of MCP, PIP, and DIP to assess flexor and extensor tendon involvement
• Careful examination of nailbed/subungual hematoma
  • Treatment of nailbed injuries important to avoid cosmetic and functional loss in fingertip injuries⁶

Differential:

• Finger amputation, fingertip amputation, finger laceration, nail/nailbed laceration, ring avulsion injury, crush injury

ED Evaluation:

• Hand and finger x-rays, including amputated part
• Consider preop labs
  • CBC, BMP, PT/INR, PTT
• Time of amputations to guide reimplantation viability
  • Time between amputation/loss of blood supply to the digit prior to surgery
    • 12 hours of warm ischemia⁵
      • Time without cooling of amputated digit
    • 24 hours of cold ischemia⁵
      • Cooling of the digit
        • Covered in saline-moistened gauze in a sealed bag on ice

Management:⁷

• Stabilize patient and perform primary and secondary survey
• Irrigate amputated part and injury site with saline and wrap in moist sterile gauze
  • Palpate for obvious foreign body
  • Place amputated part in bag; place this in water with crushed ice
    • Direct contact with ice can cause irreversible damage to cells⁷
  • Limit handling of amputation when possible
  • Administer cefazolin 2 grams or clindamycin for penicillin allergy^7,8
    • No difference in infection rates (antibiotics vs. none) if injury is a fingertip amputation with planned surgical management⁹
  • Tetanus prophylaxis
  • Analgesics – Local vs. systemic
    • Local
      • Digital blocks
        • Lidocaine 1% vs. Bupivacaine 0.5%
    • Systemic
      • May consider when multiple injuries or insufficient analgesic effect with digital blocks
      • Fentanyl, hydromorphone, or morphine
  • Early hand surgery consultation
  • General indications for replantation¹⁰
    • Thumb
    • Multiple digits
    • Single digit distal to the insertion of the flexor digitorum superficialis tendon
    • Pediatric amputations
  • General contraindications for reimplantation¹⁰
    • Severe crush/avulsion injuries
    • Single digit proximal to the insertion of the flexor digitorum superficialis tendon
    • Prolonged ischemic time
  • Reimplantation counseling
    • 80% viability after reimplantation¹⁰
    • ~50% motion compared to normal¹⁰
    • Requires prolonged physical therapy (PT)

Disposition:

• Admit for patients with infection or if patient will undergo reimplantation
• Discharge those with controlled bleeding and distal phalanx amputation

Pearls:

• History involves mechanism, cold/warm ischemic time, tetanus, hand dominance, medical issues
• Imaging should include amputated part
• Place amputated part in moist gauze, avoid direct ice contact
• Consider both systemic and local analgesics
• Early surgical consult
• Council patient on realistic outcomes, 80% viability, 50% motion and prolonged PT

The post EM@3AM: Finger Amputation appeared first on emDOCs.net - Emergency Medicine Education.

Author: Alex Koyfman, MD (@EMHighAK) // Reviewed by: Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER)

Welcome back to the EM Educator Series. These posts provide brief mini-cases followed by key questions to consider while working. The featured questions provide important learning points for those working with you, as well as vital items to consider in the evaluation and management of the specific condition discussed.

This week has another downloadable PDF document with questions, links and answers you can share with learners as educators in #MedEd. Please message us over Twitter and let us know if you have any feedback on ways to improve this for you. Enjoy!

Case 1:

A 35-year-old male presents with tachycardia and hypoxia. His lungs are clear, and his cardiac exam is normal other than the tachycardia. ECG demonstrates sinus tachycardia, and chest x-ray is normal.

Case 2:

A 57-year-old female presents with chest pain that worsens with inspiration. She is also tachypneic and has dyspnea with exertion.

Case 3:

A 28-year-old female G2 P1 at 32 weeks presents with pleuritic chest pain and shortness of breath that has worsened over 3 days. Her vital signs are normal, but the ECG reveals right heart strain.

Considerations:

• What are the major risk factors for PE?
• What are the various types of PE, and how can PE present?
• What is the differential for shortness of breath and normal lung exam/unexplained hypoxia?
• What does risk stratification entail, and what tools are available?
• What diagnostic tools do we have in the ED?
• What is the ED management of PE?
• Who can be discharged, and who requires admission?

Suggested Resources:

• Articles
  • EM Basic
  • Emergency Medicine Cases Respiratory Emergencies
  • Emergency Medicine Cases PE Part 1
  • Emergency Medicine Cases PE Part 2
  • IBCC PE
  • EMCrit ECG
  • EMCrit PERT
  • emDOCs
  • emDOCs Outpatient Therapy
• Journal Articles
  • JEM Risk Factors
  • JEM Diagnostic Approach
  • US RV Strain
  • EMJ PE Management

The post The EM Educators Series: Pulmonary Embolism appeared first on emDOCs.net - Emergency Medicine Education.