Grand Rounds Recap 10.6.21


Morbidity and Mortality with Dr. Laurence

Case 1 Mesenteric Ischemia and Atrial Fibrillation 

  • Mesenteric ischemia can be occlusive and nonocclusive

    • 50% due to mesenteric arterial embolism

    • 25% due to acute mesenteric arterial thrombosis. These patients typically present chronically.

    • 20% due to non-occlusive mesenteric ischemia (hypotensive states)

    • <10% due to venous thrombosis

  • The small bowel can tolerate 50-75% reduction in blood flow for up to 12 before becoming ischemic.

  • Mortality is 70% if time to diagnosis is greater than 24 hours, but this decreases to 14% if surgical intervention occurs within 12 hours of symptom onset.

  • Patient presentation: usually starts with visceral abdominal pain followed by a 3-6 hour pain free interval due to hypoperfusion of visceral pain receptors.

  • No single symptom or finding is diagnostic of mesenteric ischemia.

  • Biomarkers have been evaluated as diagnostic tools:

    • Lactate has a sensitivity of 86%, a specificity of 44%, and -LR of 0.20

    • D-dimer has a sensitivity of 96%, specificity of 40%, and -LR of 0.12

  • CT angiography:

    • Highly sensitive and specific for presence of mesenteric ischemia

    • Repeat imaging demonstrated worse findings in 30% of cases of ongoing symptoms. Patient factors did not predict worsening of CT findings

    • Current guidelines suggest that delay in CT and diagnosis causes elevated mortality rates and this risk greatly outweighs risk of CIN, radiation exposure, and cost from repeat imaging.

  • Atrial fibrillation with RVR: 

    • Determine whether the atrial fibrillation with RVR is primary or secondary before attempting rate control.

    • Patients with RVR and a different primary process at time of admission have short and long term mortality rates that were three times that patients admitted with similar diagnoses

    • Patient with underlying medical illness and RVR who received rate or rhythm control had a 6-fold increase in adverse events (need for inotropic support, intubation, volume expansion)

Take Home Points:

  1. Acute mesenteric ischemia (AMI) can have variable presentations. A high level of suspicion should be maintained, especially in the elderly.

  2. No laboratory studies are sufficiently accurate to rule in or rule out AMI.  

  3. CTA should be performed as early as possible for any patient with suspicion for AMI.

  4. Consider underlying medical etiologies in any patient who presents in Atrial fibrillation with RVR and address likely causes before administering rate or rhythm control. ​

Case 2: HIV Post-Exposure Prophylaxis

  • 63% of the HIV positive population in the US is either undiagnosed or not retained in care, and 91% of new HIV infections come from this population

  • The HIV care continuum outlines the stages from diagnosis to achieving viral suppression

    • Diagnosis with HIV -> linkage to care -> receipt of medical care -> retention in care -> achievement and maintenance of viral suppression

    • We can intervene at many points in the ED, particularly surrounding diagnosis and linkage with care

  • Of patients seen in the emergency department

    • 27% were a new diagnosis

    • 43% were linked to care

    • Only 22% of those who were linked to care were virally suppressed

  • Patients with an occupational exposure  are more likely to receive PEP than those with non-occupational exposures, leading to an increase in seroconversion in this population

  • While a large proportion of providers are aware of the responsibility to prescribe PEP, 57% or less were confident in their ability to appropriately prescribe a PEP regimen.

  • CDC criteria for prescription of HIV PEP

    • Risk stratify by: exposure type, body fluid, source, time from exposure. More information here. https://www.cdc.gov/hiv/pdf/programresources/cdc-hiv-npep-guidelines.pdf

    • If patients meets one of each of these criteria and is within 72 hours of exposure they qualify for PEP

    • Prescriptions: Tenofovir 300 mg daily/Emtricitabine 200 mg daily, Raltegravir 400 mg twice daily or Dolutegravir 50 mg daily for 28 days

    • First dose can be given in the ED

    • Consider prescribing zofran as nausea is likely

    • Medication assistance consult is available at Hoxworth

    • For occupational exposures, UC pharmacy can provide three days of medication 

    • Patients should follow-up in the ID clinic, and can request an urgent appointment for PEP

    • CDC consult service for clinicians is available 0900-0200 ET and can be reached at 1-888-448-4911

Take Home Points:

  1. Prescription of postexposure prophylaxis (PEP) is an important part of HIV prevention and treatment and is a well-accepted part of emergency medicine practice.

  2. Knowledge of indications for PEP is critical and may influence confidence in prescribing and counseling.

  3. Typical HIV PEP regimens include Tenofovir + Emtricitabine and Raltegravir or Dolutegravir and are generally well-tolerated, though they can cause nausea, headache, and dizziness.

  4. Many opportunities exist to positively intervene on the HIV continuum of care in the ED, including counseling on risk mitigation and harm reduction, providing linkage to care, and reinforcing retention and ART. 

Case 3: Targeted Temperature Management and Neuroprognostication 

  • Indications for TTM at UCMC

    • Cardiac arrest with ROSC

    • Not following commands

    • Trauma is not the cause of the arrest

    • No DNR/DNI

  • Exclusions for TTM at UCMC

    • Patient is currently following commands

    • Trauma is the cause of the arrest

    • Patient is age <= 15 (consider transfer to CCHMC)

    • Known intracranial hemorrhage or stroke

    • Existing DNR or DNI orders

    • Hypothermia as the cause of the patient’s cardiac arrest (should actively rewarm)

  • Ability to follow commands after ROSC is very promising from a neuroprognostication standpoint. Other findings are suggestive of, but not adequate to neuroprognosticate

    • Myoclonus still may have 9-16% chance of good neurologic outcome

    • No response to pain or extensor posturing still may have 8-52.5% chance of good neurologic outcome

    • Absent corneal reflexes still may have 25% chance of good neurologic outcome

    • Absent pupillary light reflex still may have 15-63% chance of good neurologic outcome

  • Neuroimaging as a neuroprognostication tool:

    • Early head CT (in the ED) may demonstrate changes in grey-white matter differentiation. These findings are suggestive of poorer outcomes, but are not diagnostic.

  • MIRACLE2 score

    • Points for: unwitnessed arrest, non-shockable rhythm, non-reactive pupils, age, change in rhythm, pH < 7.20, administration of epinephrine

    • MIRACLE2 score < 3 has NPV of 94.4% for poor neurologic outcome

    • MIRACLE2 score >4 has PPV of 92.3%% for poor neurologic outcome

    • Validation studies are ongoing

    • Criticisms include: use of pupillometry, accuracy of pre-hospital data, retrospective cohort used for derivation, and concern for self-fulfilling prophecy

  • Overall, no single tool or combination of tools can be used for accurate neuroprognostication in the ED, and no prognostication should be performed this early in the patient's course. 

Take Home Points:

  1. TTM should be initiated for all patients unless:

    1. Patient is following commands

    2. Cause of arrest is trauma or hypothermia

    3. Found to have ICH or stroke

    4. Age ≤ 15

    5. Current DNR/DNI

  2. There is no reliable way to prognosticate neurologic recovery in the ED, and physicians should be conscious of the bias that tests, exam findings may introduce.

Case 4: Aortic Stenosis

  • Aortic stenosis is the third leading cause of cardiac disease. 10% of patients over 80 have aortic stenosis. Classic symptoms include: syncope, angina, and dyspnea. Once symptomatic, the one-year mortality rate is about 25%.

  • Pathophysiology: decreased valve cross section and increased leaflet stiffness cause increased pressure gradient across the valve. This leads to increased afterload to the LV and hypertrophy that beget diastolic dysfunction. Ultimately this causes decreased myocardial and cerebral perfusion and symptomatology. 

  • Ultrasound is the mainstay of diagnosis. The most important aspects for EM docs is the presence of flash pulmonary edema and whether the valve appears normal or not.

  • Treatment options: The cornerstone of treatment is aortic valve replacement. There is a lower risk of operative mortality and death with early surgery (15% vs 1%). Watchful waiting is associated with increased risk of death and increased operative mortality.

  • Acute management of hypotensive patients

    • Small aliquots of fluid (500cc) if they do not appear volume overloaded

    • Phenylephrine is the ideal vasopressor as it does not cause tachycardia or increased myocardial demand from increased inotropy. Phenylephrine will increase diastolic blood pressure without increasing myocardial demand significantly, improving coronary perfusion in diastole. Reflex bradycardia further decreases demand. Epinephrine and norepinephrine are not first line agents for hypotension here due to increased myocardial demand

    • Study of 1 ug/kg bolus: increased peak early flow velocity with overall improvement in LV filling dynamics

    • Preserve sinus rhythm to capitalize on atrial kick. Consider cardioversion early.

    • If pulmonary edema is present NC O2 and NPPV are the mainstays. Nitroglycerin is controversial.

    • If in frank shock, inotropes can be useful, but valve replacement is necessary

Take Home Points:

  1. Symptomatic aortic stenosis (AS) is a highly morbid condition that can rapidly progress. 

  2. Asymptomatic patients with AS may benefit from early evaluation for surgical intervention and deserve additional scrutiny and guidance in the ED.

  3. With hypotensive AS patients, consider careful volume replacement and phenylephrine or norepinephrine as your vasopressor of choice. Avoid epinephrine.

Case 5: Seizure presentations in patients with known epilepsy

  • CT scans are performed on 13-42% of patients with recurrent seizures. Overutilization of CT imaging contribute to length of stay, overcrowding, treatment delays, radiation exposure, and cost.

  • CT scans rarely change management in patients with a history of seizures, but intracranial abnormalities are more common in:

    • Infants < 6 mo of age (55% found to have abnormality on CT)

    • AIDS patients (28% found to have abnormality on CT)

    • Children with immediate post-traumatic seizures (5% found to have abnormality on CT)

  • Factors that are associated with neuroimaging changing management

    • Prolonged post-ictal period > 60 minutes: OR 6.5

    • Head trauma: OR 6.2

    • Abnormal neurologic exam: OR 4.0

    • History of brain tumor: OR 5.88

  • 29-66% of individuals with epilepsy are not adherent to their medications

    • Associated with increased seizures, ED visits, hospitalization, fractures, head injuries, and premature mortality

    • Medication adherence is a complex issue: 

      • Patient specific barriers

      • Medications specific barriers

      • Healthcare and system factors

    • Patient adherence to medication does fall within our wheelhouse. And we should be counseling patients during their ED visit.

Take Home Points:

  1. ED physicians should be good stewards of ED neuroimaging when caring for patients with recurrent seizures, weighing monetary, individual patient, and systems costs.

  2. Imaging may be indicated in a subgroup of patients, including those with reported trauma, history of brain tumor, persistent alteration of consciousness, or focal neurologic deficits.

  3. AED nonadherence is associated with increased morbidity and mortality. ED physicians, staff should educate patients on medication use, importance to improve adherence.

Case 6: Heterotopic Pregnancy

Take Home Points:

  1. Keep heterotopic pregnancy on your differential for abdominal pain and pregnancy.

  2. Don't stop ultrasounding after finding an IUP, consider RUQ view for free fluid (FF). 

  3. If concerned for ectopic, scan for IUP, FF in pelvis, and FF in RUQ. 

  4. If your suspicion is high, call your consultants for definitive diagnostic laparoscopy.


R4 Case Follow-up: Aortic Dissection with Dr. Roblee

Pathophysiology: Tear in the tunica intima allows dissection of blood into the tunica media, leading to creation of false and true lumens. The false lumen can expand and cause compression of the true lumen. The dissection flap can occlude branching vessels and this can occur in a static or dynamic fashion. Dissections can also extend into the aortic valve leading to aortic regurgitation. Dissection into the coronaries causes cardiac ischemia. Rupture of the aorta, proximally, can cause hemopericardium and tamponade physiology. 

Classification:

  • Type A: Any dissection involving the ascending aorta. This is a surgical emergency.

  • Type B: Any other type of dissection. Many of these can be managed medically, depending on location. 

Epidemiology:

  • 2.5-3.6 per 100,000 person years

  • 66% male

  • Median age 63 years

  • 27% mortality

Risk factors

  • Hypertension is present in 77% of patients, leading to increased shear forces.

  • Stimulant use can cause rapid increases in blood pressure that precipitate dissections.

  • Connective tissue diseases, such as Marfan syndrome, cause a weakening of the tunica media.

  • Aortic aneurysms, in which the walls of the aorta are weakened, and bicuspid aortic valves, which cause abnormal flow patterns in the aorta, are also associated with aortic dissection

Presentation

  • 95% present with pain that is severe and abrupt in onset

  • 31.6% have a diastolic murmur 2/2 aortic regurgitation

  • 15% have an upper extremity pulse deficit

  • 9.4% present with syncope

  • 4.7% present with neurologic deficits

Diagnosis

  • EKG abnormalities in 30% with changes 2/2 hypertension or ischemia

  • CXR with widened mediastinum in 80% of patients

  • TEE is 98% sensitive and 95% specific

  • CT angiography is 100% sensitive and 98% specific

  • MRI is 98% sensitive and 98% specific

  • D-dimer plus Aortic Dissection Detection Risk Score (ADD-RS)

    • Looked at patients with score of one or zero (considered low risk) plus D-dimer

    • Sensitivity was 98.8%, Specificity of 57.3%, NLR 0.02

    • Reduced CT scans by 60%

    • This has not been externally validated

Treatment: 

  • Pain control

  • Beta blocker (esmolol or labetalol) for HR < 60 and SBP < 120

  • Cardiothoracic surgery consult


QI/KT: Hypotension in ESRD with Drs. Kletsel and Ferreri

Stable hypotension in Kidney Disease

Peri-dialytic hypotension can be due to a number of factors:

  • Excessive ultrafiltration

  • Predialtytic volume loss (GI loss, decreased PO intake)

  • Post dialytic volume loss (blood from vascular access)

  • Medication effects (antihypertensives)

  • Decreased vascular tone (sepsis, low dialysate temperature)

  • Cardiac dysfunction (LV hypertrophy, hypoxia, arrhythmia, pericardial tamponade)

Intradialytic hypotension is defined as SBP drop > 20 mmHg or MAP drop > 10 mmHg, symptoms of end organ ischemia, or hypotension requiring intervention during dialysis. Hypotension complicates 70% of dialysis treatments. This is likely multifactorial and due to decrease in blood volume with ultrafiltration that exceeds the vascular refilling rate from interstitial fluid, vascular tone (RAAS dysfunction and thermoregulatory vasodilation), and cardiac compensation. Furthermore, end organ ischemia leads to cardiac stunning and increased release of nitric oxide.

Treatment options:

  • Midodrine is a alpha-1 agonist that prevents venous pooling to increase BP

    • Dose: 2.5-10 mg TID

    • Most useful in the first hour of dialysis to prevent hypotension, so may not be helpful in the emergency department unless the patient has missed a dose.

  • 250-500cc bolus of fluid

    • Normal saline is as effective as albumin at improving blood pressure.

Sepsis Induced Hypotension in ESRD

  • 100-300% increase in mortality from sepsis in ESRD patients, accounting for 12% deaths in ESRD patients per year

  • Immune dysfunction in ESRD is due to: elevation in proinflammatory cytokines, increased monocyte activity, impaired T-cell activation and T-reg function, impaired Ig production and function, increased granulocyte activity. These patients also have a decreased response to immunizations.

  • Infection associated with vascular access complicates 2.5% of fistulas and 10% of grafts. Atypical pneumonia, C. Diff, UTI, and peritonitis are also common

  • S. aureus is the most common pathogen, followed by GNRs and enterococcus

  • These patients also have decreased response to immunizations

Determination of fluid responsiveness with ultrasound:

  • IVC collapsibility via ultrasound is a surrogate of central venous pressure, but current data suggests that CVP is a poor predictor of fluid responsiveness. IVC collapsibility can also be affected by intrathoracic pressures (respiratory effort) and intra-abdominal pressures (obesity)

  • LVOT VTI is effective in predicting fluid responsiveness in septic shock, particularly when coupled with passive leg raise

  • Lung ultrasound can help determine fluid tolerance by evaluating for existing pulmonary edema

How much fluid should be administered?

  • ESRD patient receive much less fluid in the first 6 hours and overall.

  • Those who receive 30 cc/kg have lower mortality regardless of ESRD diagnosis

  • Goal directed fluid therapy did not appear to confer greater risk of volume overload.

Which type of fluid should be administered?

  • Balanced crystalloids such as Lactated Ringers or Normosol are preferred and have been shown to decrease mortality

  • Normal saline is associated with worsened acidosis and hyperkalemia

  • Additional lactate from LR is likely beneficial as a fuel source in sepsis and has been shown to improve cardiac output

  • Lactated ringers has not been shown to contribute to hyperkalemia

pH guided fluid resuscitation:

  • ESRD patient have impaired pH regulation as they back the ability to generate bicarb and to excrete hydrogen ions

  • Bicarbonate administration improves pH, improves hyperkalemia, and can be used to temporize emergent dialysis

  • pH guided fluid resuscitation may reduce mortality and decrease incidence of organ failure

  • Calculate the patients bicarbonate deficit and aim to replete 80% of it

  • Isotonic bicarb (150 mEq/L) can be made by adding three 50 mEq ampules of bicarb to 1L of sterile water or D5W


R1 Clinical Diagnostics: Fungal Skin Infections with Dr. Davis

 The most important question: Is this patient immunocompromised?

Tinea is the most common fungal skin infection and comprises three main dermatophytes (Trichophyton, Microsporum, and Epidermophyton). These organisms are highly contagious and spread via direct contact (person-person, person-animal, or person-object). The diagnosis is primarily clinical and they are generally treated with topical antifungals (with a few exceptions).

Tinea Capitis

  • Epidemiology: Most common in toddlers and school age children

  • Exam: Scaling plaques w/ alopecia and black dots (breakage of hair at base), gray patches (fungus coating hair follicles), or kerion (boggy, pustular, painful mass with alopecia). These findings are often accompanied by posterior lymphadenopathy. 

  • Treatment: Oral antifungals for all cases, as topical treatment will not penetrate hair follicles. Terbinafine is first-line for all except Kerion, which should be treated with Griseofulvin.

Tinea Corporis

  • Epidemiology: Most often children and adolescents, but common in adults

  • Exam: Annular patch or plaque, 1-5 cm in size. Plaques have raised, well demarcated borders and central clearing. Mucosal involvement generally rules out tinea infections.

  • Treatment: Topical Butenafine or Terbinafine daily for two weeks. Should be applied to the surrounding 2cm of skin. Consider oral antifungals if disease is extensive.

Tinea Cruris

  • Epidemiology: Most common with occlusive clothing or high perspiration activities

  • Exam: Annular patch or plaque with central clearing to bilateral thighs that spares the scrotum and labia. 

  • Treatment: Topical Terbinafine for 1-3 weeks, or 1 week after lesion resolves. Oral Griseofulvin or Terbinafine for extensive disease or involvement of hair follicles.

Tinea Pedis

  • Epidemiology: Most common with occlusive footwear or those with warm, wet feet

  • Exam: Interdigital scaling, erythema, fissuring

  • Treatment: Topical butenafine twice daily for one week. 

Onychomycosis:

  • Epidemiology: Athletes and those with arterial or venous insufficiency

  • Exam: Thickened, brittle, discolored nails, most common on 1st & 5th digits

  • Diagnosis: Requires scraping and laboratory confirmation

  • Treatment:

    • Topical: 48 weeks of daily Efinaconazole (15% cure rate)

    • Oral: 12 weeks of daily Terbinafine (70% cure rate)

High Risk Fungal Skin  Infections in the Immunocompromised Patient

Immunocompromised: organ and hematopoietic cell transplant, HIV, chronic high dose steroid, TNF-alpha inhibitors, 2nd/3rd trimester pregnancy,

Rash is often a marker of dissemination

Blastomycosis

  • Epidemiology: Endemic in Mississippi and Ohio River Valleys, Great Lakes and St. Lawrence River Valley. Immunocompromised patients are at the highest risk of cutaneous blastomycosis. 60% of disseminated disease presents on the skin. 

  • History and Exam: Pneumonia symptoms often precede the rash. The rash is comprised of verrucous lesions with raised irregular borders and crusted appearance that primarily appear on the arms and face. 

  • Diagnosis: Urine antigen or skin microscopy are readily available, but culture is the gold standard. Chest X-ray should also be obtained to evaluate for pulmonary disease. 

  • Treatment: Liposomal amphotericin B then step-down to triazoles (fluconazole, itraconazole, voriconazole) for 12 months. 

Histoplasmosis

  • Epidemiology: Endemic in Mississippi and Ohio River Valleys

  • Exam: Diffuse papulonodular or pustular lesions

  • Diagnosis: Urine and serum antigens readily available, but culture is the gold standard

  • Treatment: Immediate liposomal amphotericin B, then Itraconazole for 12 months. AIDS patients stay on therapy until CD4 > 200.

Coccidiomycosis

  • Epidemiology: Endemic in Southwest US (AZ,CA) and most often in people working outside

  • Exam: Nodular rash involving chest wall, face, & neck. The nasolabial fold is a very common site

  • Diagnosis: Serology for IgG and IgM, but culture is the gold standard

  • Treatment: Disseminated disease (non-meningeal) can be treated with itraconazole or ketoconazole for 3-6 months or amphotericin B if severe. Meningeal disease requires high dose itraconazole then step-down therapy for life. Can also consider acute intrathecal amphotericin B.

Cryptococcus

  • Epidemiology: Cell mediated immunodeficiency (transplant patients); AIDS w/ CD4 <100

  • Exam: Umbilicated papules or abscesses. Close inspection may reveal draining sinus tracts that may herald deep or bony disease.

  • Diagnosis: Crypto polysaccharide antigen plus lesion biopsy. India ink stain if concerned for meningeal involvement.

  • Treatment: HIV patients require amphotericin B + flucytosine x2 weeks then follow with fluconazole for another 8 weeks before maintenance fluconazole.

Mucormycosis

  • Epidemiology: Burn/trauma patients, diabetes, hematologic cancers

  • Exam: Black eschars with surrounding edema

  • Diagnosis: Biopsy and culture required for definitive diagnosis. Coccidioidomycosis antibodies is specific and relatively sensitive

  • Treatment: Surgical resection of devitalized tissue in combination with liposomal amphotericin B for all cases. Consider colony stimulating factors in hematologic or solid organ malignancies. Glucose control in diabetic patients.