Grand Rounds Recap 6.22.22
/Morbidity and Mortality - Social EM: Progress - Airway Grand Rounds - R1 Clinical Knowledge: asplenia - Taming the SRU: REBOA
Morbidity and Mortality WITH Dr. Frederick
Case 1: STREMI (new word) - Simultaneous STEMI and Acute Ischemic Stroke
Discuss concerning EKGs with the on call interventionist, even when EKG does not meet STEMI criteria. They may still offer LHC and may uncover intervenable disease.
Dynamic EKG changes are common in ACS presentations, obtain repeat EKGs
Simultaneous acute ischemic stroke (AIS) and acute MI is rare, 0.9 per 100,000
Shared risk factors, systemic inflammatory response, possible embolic sources may cause co-presentations
Left insular stroke is associated with adverse cardiac outcomes; RR 1.75
Management:
ACS
Thrombolysis indicated if no PCI available < 120 minutes presenting within 12 hours
Mechanical reperfusion is first line
Heparin recommended with poor evidence (1C for STEMI, 1B for UA/NSTEMI)
ASA and antiplatelets indicated within 24 hours
AIS
Thrombolysis indicated if < 4.5 hours
Mechanical reperfusion recommended in LVO
Heparin generally contraindicated
ASA and antiplatelets are indicated if no tPA administered
Combined presentation
Thrombolysis should be offered if indicated for stroke treatment
Mechanical reperfusion warranted for both AIS/ACS
Heparin risk may outweigh benefit depending on stroke characteristics and neurology recommendations
ASA and antiplatelets are indicated if not administering tPA
For combined presentations, neurocritical care can be helpful to coordinate advanced therapies
Case 2: Autoimmune Encephalitis
NMDA-R Encephalitis: Autoimmune disease in which autoantibodies are produced against synaptic NMDA receptors
Incidence is 1.5 cases per 1 million
Presents with prodrome fever, fatigue, headache (5-14d), followed by psychosis, attention difficulties, hallucinations, language difficulties, followed by seizures, catatonia and autonomic instability
Women present more with psychosis and hallucinations
Men present more with seizures, often focal
Workup
MRI
CSF
Pleocytosis
Increased protein
Oligoclonal bands
NMDAR autoantibodies
EEG abnormal in 90-100% of cases
Investigate for neoplasm; pelvic ultrasound often helpful
Treatment
IV steroids, IVIG, plasmapheresis
Those that do not respond may need targeted B cell-therapy with rituximab, cyclophosphamide, or intrathecal methotrexate
Prognosis
20% have significant deficits or progress to death
75-80% will recover
53% of patients show improvement within 1 month of starting immunotherapy and tumor removal
Typical hospital stay is 2-4 months
Case 3: Cardiac Arrest in the ED
ESI level dependent on vitals and resource utilization
Patients are under triaged ~17% of the time
Age > 70, bradycardia or tachycardia, tachypnea, syncope, chest pain, hypoxemia, arrival between 0100-1300 all have been shown to predispose to under triaging ESI levels
Clarify roles of resuscitation, especially when patients start in other care areas and are moved to the SRU
Be mindful of subconscious bias toward ‘difficult’ patients
Shown to have poorer pain control, fewer offers for admission, less time in the room communicating plans
Case 4: Acetaminophen Toxicity
Factors affecting toxicity
Acute alcohol intoxication
Decrease conversion to NAPQI, protective against toxicity
Chronic alcohol use
Decreases glutathione stores, increased risk of toxicity
Tobacco use increases CYP metabolism, increases risk of toxicity
Age < 5 is protective (underdeveloped CYP metabolism), age > 40 increases risk of toxicity
Fasting decreases carbohydrate reserves, decreases glucuronidation, increased risk for hepatotoxicity
Workup
Obtain APAP level 4 hours after (acute) ingestion, or on arrival if later
If ingestion time unknown, draw second level 4 hours after first
Treatment
NAC should be started within 8 hours, IV treatment is equivalent to PO
Indications for treatment
Supratherapeutic APAP (>150 ug/mL) at 4 hours
If unknown time of ingestion
Draw a level now and in 4 hours
If initial level is undetectable, treatment with NAC is decided based on laboratory or clinical signs of hepatotoxicity
If >8hrs from ingestion, NAC should be given empirically while awaiting APAP level.
For repeated ingestions:
Ingestion of >7.5g in 24 hours, or >4g in 24 hours with factors that increase risk for hepatotoxicity
Supratherapeutic APAP Level (>20mcg/mL)
Elevated ALT/AST >50 on presentation
Elevated acetaminophen-aminotransferase multiplication product
APAP x ALT > 10,000 = Treatment
APAP x ALT < 1,500 = Toxicity unlikely to develop
Anaphylactoid reaction to NAC is possible in 8%, if this occurs then slow infusion rate. This is often not a true IgE mediated allergic response.
Typical clinical course:
0-24 hours = Symptomatic presentation
24-72 hours = Initial liver injury on labs
72-120 hours = Peak liver failure + mortality
1 week + = Recovery
See the 2021 Annals of B Pod article on this topic
Case 5: Pyoderma Gangrenosum
Pyoderma gangrenosum = neutrophilic inflammation of the skin often associated with underlying systemic illness
41% IBD
21% inflammatory arthritis
7% solid organ malignancy
6% hematologic malignancy
Treatment is local wound care and treat underlying disorder
Immunosuppressive therapy if no response with treatment of the underlying condition
Approach to rashes:
Primary morphology:
Macule, patch, papule, nodules, plaques, bullae, vesicle, pustule
Secondary morphology:
Erosion, ulceration, fissure, atrophy, excoriation
Crusting, lichenification, scaling
Modified lynch algorithm can help identify etiology of emergent rashes based on appearance
Be aware of varying appearances of rashes in patients with differing skin complexion
Resources: Brown Skin Matters, Mind the Gap
Social Emergency Medicine WITH Dr. Jarrell
The ED is the social barometer of its community. It is the confluence of social determinants of health and their deconstruction into pathology.
Update on SEM projects within UCMC
SEM Fellow - Dr. Pulvino
Public Health Leadership Academy - Dr. Pulvino, Dr. Berger, Dr. Laurence
Early Intervention Program RAMD - Dr. Gressick
SEM Electives offered
Advanced SEM
Human trafficking (in progress)
Medical Spanish
Advocacy
Our residents are involved in multiple national projects within the Social EM Education Subcommittee
Joint committee between SAEM, ACEP, EMRA
EMRA representation
Dr. Kimmel - SEM Committee Chair Elect
Dr. Yates - Health Policy Committee Assistant Vice Chair
ESL Workgroup
Appropriate use of interpreters - faculty and residents
Updating discharge resources in multiple languages
TamingtheSRU and Annals of B Pod articles - Dr. Stark
Reflections on path to SEM:
Not everyone has the same exposure to careers in medicine
We must be conscious of not only the availability of a resource within a community, but the ability to access this resource for specific members of a community.
Be mindful of ad hominem view of disease - focus on precipitants of disease in addition to the symptoms
Ex: Addressing underlying trauma that precipitates alcohol use disorder, leading to unstable housing
Ex: Diabetes may be uncontrolled because patients have no place to keep their insulin
Airway grand rounds WITH Dr. Carleton
Intubation is not a benign process:
Cardiac arrest 2-4%, desaturation rate 20-40%, hypotension rate 10-40%
Assess for physiologic difficulty
Hypoxia
Obesity, shunt physiology, oxygen consumption, anemia, low FVC
Hypotension
Positive pressure effects on the circulation, vasoactive drugs, differential RV, LV hemodynamics, hypovolemia
Risk of Apnea
Metabolic acidosis
Optimize patient prior to attempt
Hypotensive? IVFs, Blood, Pressors
Hypoxic? Upright, Maximize Pre-ox/Ap-ox
Acidotic? Pseudo-NIPPV, Awake technique
Preventing Desaturation = utilize NIPPV when possible
Optimize reservoir by maximizing FRC
De-nitrogenate/oxygenate volume in the reservoir
Make sure gas in reservoir is available for circulation
Utilize Ap-Ox
Strategies for high to refractory hypoxemia
Maintain spontaneous breathing
HFNO Preoxygenation
Upright position
iNO, epoprostenol (iNO faster to obtain in our ED)
Gentle transition to PPV
Strategies to mitigate hemodynamic instability:
Anticipate and assess hypovolemia/volume responsiveness and replete volume
Calculate the shock index
Prevent or reduce vasoplegia
Augment ventricular performance
Mitigate induction effects
Protect the RV
Ketamine may have high risk of immediate hemodynamic instability compared to etomidate; one study suggests etomidate has higher 7d mortality, but equal 28d mortality compared to ketamine
Considerations in acidosis
Recognize that apnea in RSI has physiologic consequences.
For each increase in pCO2 by 10mmHg, pH drops by 0.08
Be mindful of minute ventilation after intubation, match or exceed pre-intubation MV; requires us to measure it before intubation
Assuming normal VCO2, minute ventilation required to maintain pCO2 = 60 mL/kg/min
Estimate or quantify VE pre-intubation using Bi-PAP for pre-oxygenation
Consider an awake technique to maintain their minute volume
If using RSI, consider pseudo-NIPPV to attenuate worsening acidosis
R1 Clinical Knowledge: Asplenia WITH Dr. Negron
Anatomy
Receives 5% total cardiac output per minute
White pulp = Lymphatic nodules where T cells envelop B cells
Red pulp = Tight network of sinusoids and cells responsible for filtration and processing
Function
Differentiations of WBC/adaptive immune response, production of antibodies
Activation of innate immune response
Storage of WBC and platelets
Filtering of blood
Asplenia/Hyposplenia
Over 1 million people in the United States are asplenic
Cirrhosis, Celiac disease, Vasculitis, Spleen irradiation, Sickle Cell, Lupus, bone marrow transplant may produce functional asplenia
Complications
Risk of infection is 2-3 fold greater in asplenic patients compared to the general population
Risk is greatest in patients <5 y/o and >65 y/o
For anatomic asplenia, risk greatest in first 2 years
Overwhelming Post-splenectomy Infection (OPSI) is a potentially fatal condition with sudden decompensation from overwhelming bacterial infection, most often caused by S. pnemoniae
OPSI annual incidence among asplenic patients is 0.5% however mortality is up to 70%
Pulmonary hypertension exists at 8-11% in this population
Higher risk for VTE
Platelet activation, loss of platelet storage, endothelial lining dysfunction and damage
Risk of VTE after splenectomy of 10.7%, compared to 3.5% of patients undergoing other abdominal surgeries
Patients who underwent surgical splenectomy have RR of 2.2 for DVT, 2.2 for PE, and 4.5 for risk of death from PE
Approach to the asplenic patient
Complete H&P to assess for signs of infection
Broad spectrum antibiotics +/- Atypical coverage
Adults: cefepime + vanc
Children: ceftriaxone + vanc
+/- azithromycin if concerned for pneumonia
May consider IVIG
In vasopressor and fluid-resistant shock or concern for adrenal hemorrhage, treat for adrenal insufficiency with hydrocortisone
Higher risk for VTE
Platelet activation, loss of platelet storage, endothelial lining dysfunction and damage
Risk of VTE after splenectomy of 10.7%, compared to 3.5% of patients undergoing other abdominal surgeries
Patients who underwent surgical splenectomy have RR of 2.2 for DVT, 2.2 for PE, and 4.5 for risk of death from PE5
Taming the SRU: REBOA WITH Dr. Mullen
REBOA = Resuscitative endovascular balloon occlusion of the aorta
Zone 1 celiac trunk to left subclavian artery
Zone 2 celiac trunk to lower renal arteries
No indications for placement here
Zone 3 Iliac bifurcation to lower renal arteries
Indications
Hemorrhage due to trauma below the diaphragm
Suspected traumatic abdominal hemorrhage (Zone I REBOA)
Blunt pelvic injury or groin junctional hemorrhage (Zone III REBOA)
Placement considerations
Must know time of balloon tamponade = ischemia time
Confirm placement with X-ray
There is no high-grade evidence demonstrating that REBOA improves outcomes or survival compared with standard treatment of severe traumatic hemorrhage.
2019 consensus statement from American College of Surgeons: “REBOA should only be placed by a surgeon or interventionalist responsible for definitive hemorrhage control or by a physician trained and qualified in REBOA in direct consultation with the physician who will provide definitive hemorrhage control. In all circumstances, these trained clinicians should be integrated within an appropriate system of care.”
Revised language that does not limit this procedure to surgeons, but should be done in conjunction with trauma team that can facilitate definite care
