Fearsome Foliage - An Overview of Toxic Plants
Spring has sprung... and so have many species of toxic plants! Poison centers across the United States receive over 100,000 reports of exposures to toxic plants annually. It is often difficult for Emergency Medicine providers to determine the quantity and time of exposure. Plant identification presents another challenge, and can even require the input of a botanist. Now that is an interesting consult! Thankfully, some of the more common and/or dangerous plant poisonings have been well-categorized, and are summarized in this post.
Spring has sprung... and so have many species of toxic plants! Poison centers across the United States receive over 100,000 reports of exposures to toxic plants annually. The most common reported effects of these exposures are skin irritation and gastrointestinal symptoms. The majority of ingestion cases occur in pediatric patients and are often minor due to low quantities of exposure. More serious poisonings typically involve adults who ingest plants in larger quantities for recreational, self-harm, foraging or medicinal purposes (1). These moderate-to-severe cases account for approximately 1% of all poisonings (2).
It is often difficult for Emergency Medicine providers to determine the quantity and time of exposure. Plant identification presents another challenge, and can even require the input of a botanist. Now that is an interesting consult! Thankfully, some of the more common and/or dangerous plant poisonings have been well-categorized, and are summarized below.
General Management
Manage airway, breathing, and circulation.
Address life-threats. Anaphylaxis, hypoglycemia, cardiotoxicity, and neurotoxicity can all be seen following exposure to poisonous plants.
Decontaminate. Exposed skin and mucous membranes should be irrigated. If a plant was ingested, activated charcoal can be used for GI decontamination at a dose of 50 mg (or 1 mg/kg in pediatric patients) depending on time since ingestion.
Supportive care is the mainstay of therapy for the majority of plant toxicities, and involves hydration, antiemetics, cardiac monitoring, and neurological monitoring.
Skin Irritants
Skin injury and irritation are some of the most common symptoms reported following exposure to poisonous plants, and can occur through a variety of mechanisms. Numerous plant species have specialized structures that may cause physical damage to the skin, such as needles and nettles. To add insult to injury, many plants, including those of the common Dieffenbachia and Philodendron species, produce calcium oxalate crystals that accumulate on the surface of the plant in bundles. Exposure to these needle-shaped crystal bundles causes further dermal injury in areas where the skin is already punctured.
Another mechanism of skin injury is carried out by phorbol esters found in the sap of Euphorbiaceae species. Phorbol esters are able to penetrate the skin upon contact, resulting in a contact dermatitis. Interestingly, these same compounds are also known for their tumor-promoting qualities.
A strong contender for the most notorious of the poisonous plants are those of the Toxicodendron species, known colloquially as poison ivy, poison oak, and poison sumac. The poisonous nature of these plants is owed to a urushiol, a resin that forms an antigenic complex with proteins present on the surface of the skin. After sensitization, subsequent exposures trigger a T-cell mediated (Type IV) hypersensitivity reaction that results in a pruritic, erythematous rash with vesicles and/or bullae within 12-48 hours of exposure. Treatment is generally supportive and the mainstays are soothing measures such as oatmeal baths, cool compresses, and ice packs. Oral antihistamines are an option, but are generally used for sedating purposes, as the resulting dermatitis is not histamine-mediated (3). Topical corticosteroids are sometimes prescribed, but there is little evidence that this changes the disease course once vesicles have been established. There is no indication for oral or topical antibiotics unless there are concerns for a superimposed bacterial infection (4).
Nicotinic Toxins
Fun fact: A form of transdermal nicotine poisoning has been described in farm workers who handle uncured tobacco plants, and is referred to as Green Tobacco Sickness, or GTS (5).
To better understand this toxicity, recall the location and function of the nicotinic acetylcholine receptor. Though this receptor normally carries out its functions by binding to acetylcholine, the receptor is named as such because it also binds to nicotine. These receptors are present at the neuromuscular junction of skeletal muscles and ganglia of the sympathetic and parasympathetic nervous systems. When nicotine binds these receptors at low doses, stimulatory effects are produced. However, at higher doses, inhibitory effects begin to predominate.
Exposure to nicotinic and nicotine-like toxins, like those found in hemlock, present on a spectrum of illness. Mild exposures present with nervousness and tremor due to activation of the sympathetic nervous system. More severe exposures present with a constellation of symptoms, including paralysis and more pronounced sympathetic and parasympathetic findings. Death may occur secondary to respiratory failure. Unfortunately, there is no specific antidote and treatment focuses on GI decontamination and supportive care.
Cardioactive Steroid Toxins
Fun fact: Foxglove was described in 1652 in The English Physician as a laxative and treatment for wound healing, epilepsy, and “scabby head” (6).
Emergency Medicine providers are likely familiar with the toxicity resulting from exposure to Foxglove, Oleander, and Lily of the Valley. All of these plants contain cardiac glycosides which function to inhibit myocardial Na+/K+ ATP-ase. Does that sound familiar? It should - this is the mechanism of action of Digoxin. As such, presenting symptoms resemble those of a Digoxin overdose; gastrointestinal symptoms, visual disturbances, and arrhythmia. Interestingly, this ingestion can be confirmed by obtaining a Digoxin level (given that the patient does not already take Digoxin). The benefit of that laboratory study ends there however, as it does not correlate with the toxin burden. Digoxin immune fab should be administered to patients who present with arrhythmia and/or a serum potassium greater-than five. Dosing should be empiric, and not based on the serum Digoxin level.
Lily of the Valley: https://commons.wikimedia.org/wiki/File:Convallaria_majalis_0002.JPG
Belladonna Alkaloid Toxins
Fun fact: What’s in a name? Atropa belladonna, known as Deadly Nightshade, was named by Carl Linneaus. The genus name “Atropa” comes from the Greek legend of The Three Fates, in which the Fate Atropos cut a person’s thread of life. The species name “belladonna” is a nod to the plant’s use as a cosmetic during the Renaissance period in which women used the juice of the berries to dilate their pupils (7).
Fun fact: Jimson Weed growing in its native ranges is noted to have up to 40 times the concentration of its toxic compounds when compared to plants growing in non-native ranges (8).
Deadly Nightshade and Jimson Weed are well known among the poisonous plants. Their toxic effects are caused by hyoscyamine and scopolamine. These atropine-like alkaloids produce an anticholinergic syndrome when smoked or ingested. Patients typically present with tachycardia, mydriasis hyperthermia, altered mental status, anhidrosis, and urinary retention. Severe cases may result in seizures or coma. Physostigmine, an acetylcholinesterase inhibitor, can be used to increase the concentration of synaptic acetylcholine in order to overcome the antagonism at muscarinic receptors responsible for this toxidrome. This is typically reserved for moderate-to-severe exposures, whereas mild symptoms can be managed with observation and supportive care. Of note, patients requiring pharmacologic therapy for management of agitation should receive benzodiazepines rather than antipsychotics, as antipsychotics may worsen their anticholinergic state.
Deadly nightshade: https://commons.wikimedia.org/wiki/File:Atropa_belladonna_001.JPG
References
Froberg B, Ibrahim D, Furbee RB. Plant poisoning. Emerg Med Clin North Am. 2007 May;25(2):375-433; abstract ix. doi: 10.1016/j.emc.2007.02.013. PMID: 17482026.
Chen BC, Nelson LS. Poisonous Plants. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. McGraw Hill; 2016. Accessed March 19, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=1658§ionid=109386389
Munday J, Bloomfield R, Goldman M, Robey H, Kitowska GJ, Gwiezdziski Z, Wankiewicz A, Marks R, Protas-Drozd F, Mikaszewska M. Chlorpheniramine is no more effective than placebo in relieving the symptoms of childhood atopic dermatitis with a nocturnal itching and scratching component. Dermatology. 2002;205(1):40.
Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. J Am Acad Dermatol. 1990;23(5 Pt 1):829.
Fotedar S, Fotedar V. Green Tobacco Sickness: A Brief Review. Indian J Occup Environ Med. 2017 Sep-Dec;21(3):101-104. doi: 10.4103/ijoem.IJOEM_160_17. PMID: 29618907; PMCID: PMC5868082.
Culpeper, Nicholas (1652). The English Physician, Etc (1st ed.). London: William Bentley. pp. 97–98. Retrieved 22 January 2023.
“U.S. Forest Service.” Forest Service Shield, https://www.fs.usda.gov/wildflowers/ethnobotany/Mind_and_Spirit/belladonna.shtml.
Castillo, Guillermo; Calahorra Oliart, Adriana; Núñez Farfán, Juan; Valverde, Pedro L.; Arroyo, Juan; Cruz, Laura L.; Tapia López, Rosalinda (23 August 2019). "Selection on tropane alkaloids in native and non native populations of Datura stramonium". Ecology and Evolution. 9 (18): 10176–10184. doi:10.1002/ece3.5520. ISSN 2045-7758. PMC 6787939. PMID 31632642.
Authorship
Written by: Colleen Arnold, MD, PGY-1 University of Cincinnati Department of Emergency Medicine
Expert Peer Review: Mel Otten, MD, Board Certified Toxicologist, Professor of Emergency Medicine
Additional Peer Review, Editing, and Posting: Jeffery Hill, MD MEd, Associate Professor of Emergency Medicine, University of Cincinnati Department of Emergency Medicine
Cite As
Arnold, C. Otten, M. Hill, J. (April 17, 2023) Fearsome Foliage - An Overview of Toxic Plants. TamingtheSRU. https://www.tamingthesru.com/blog/diagnostics/fearsome-foliage-an-overview-of-toxic-plants
Grand Rounds Recap 4.5.23
This week we start off with Dr. Mullen’s lessons from morbidity and mortality conference. This is followed by R1 Dr. Vaishnav with a diagnostics talk on hyperthermia. Dr. Adan walks us through the always terrifying world of laryngectomy patients and finally guest lecturer Dr. Ray Bignall gives an excellent talk on disparities in medicine and how we address them
M&M with Dr. Mullen
Diagnostic Errors
Diagnostic errors are often influenced by cognitive biases
Anchoring bias
Diagnostic momentum
Confirmation bias
Search satisfaction
Cognitive biases are not a reflection of knowledge
Obstructive Nephrolithiasis
Obstructive nephrolithiasis with UTI is a urologic emergency
Management of obstructive nephrolithiasis with UTI includes antibiotics (ceftriaxone or antipseudomonal coverage for patients with sepsis) and most often decompression strategies (i.e. stent, percutaneous nephrostomy) by urology or IR
Hypokalemia
evaluate for EKG changes
assess for underlying cause and factors that may influence ability to replete (i.e. medications)
consider using observation protocol or close outpatient follow-up with repeat lab for minor abnormalities
Transitions of Care
Transitions of care in the emergency department can be challenging and are not without risk of data loss or miscommunication
Reviewing Data at Signout
write your MDM at the time of signout
Use of the imaging report tab (under summary tab in epic) can easily condense imaging reports and make them easier to review
as the oncoming provider, reviewing all results rather than just those that were pending at the time of signout
Handoff checklists can be utilized
5 step process has been developed by ACEP
Record (offgoing provider fills out a paper form to identify key issues and pending tests)
Review (both teams sit at a computer and review the data)
Round (both teams go to the bedside)
Relay to the Team (communicate with nursing and other members of the team)
Receive Feedback (oncoming team completes the aforementioned record to update the outcome and give feedback to the offgoing team)
Signout checklist exists on TamingTheSRU
Status/acuity
Brief HPI
Pending
If/Then
Concerns
Questions
Re-cap
Minimize interruptions
Upper GI Bleed
can decompensate quickly
Specifically, variceal bleeding carries higher risk of morbidity and mortality
Consider a higher level of care for variceal bleeds as well as early consultation with GI for possible endoscopic intervention
PPI may decrease the size of post-endoscopic variceal band ligation ulcers
Prophylactic antibiotics provide mortality benefit (NNT 4) and are continued for 7 days. Ceftriaxone is often used
Octreotide can help by reducing risk of bleeding and blood product requirement, but does not necessarily confer mortality benefit
Ultrasonographic Findings in Cardiac Tamponade
Plethoric IVC is sensitive but not specific
RV collapse during diastole
Mitral inflow variation with respiration (this is the echo equivalent of pulsus paradoxus)
Physiology: there is increased preload during inspiration
Pulse wave doppler shows you these differences across the mitral valve during respiration
>25% variation across the mitral valve is concerning for tamponade
Hypertensive emergency
defined as >/= 180/120 with evidence of end organ dysfunction
ESRD patients are at risk for hypertensive crisis
Management strategies include diuresis, afterload reduction, NIPPV, and dialysis
Indications for emergent dialysis include acidosis, electrolyte derangements, ingestions, volume overload, and uremia
Recognize and expedite care for patients who need emergent dialysis
Atrial fibrillation with rapid ventricular response
Practice patterns vary regarding combination therapy with beta blockers and calcium channel blockers for atrial fibrillation with RVR
No great data on outcomes with this combination
Recognize potential bradycardia and hypotension that can result
R1 Clinical Diagnostics: Hyperthermia with Dr. Vaishnav
Hyperthermia: abnormally high body temperature due to thermoregulatory failure
Severe hyperthermia: temp greater than 40.5C
Fever: abnormally high body temp due to cytokine activation
Differential Diagnosis:
Infectious: sepsis, meningitis, encephalitis, brain abscess, tetanus, malaria
Neurologic: hypothalamic stroke, ICH, status epilepticus
Environmental: heat illness due to high temperature/humidity
Endocrine: thyroid storm, pheochromocytoma, DKA
Oncologic: lymphoma, leukemia
Drug/Toxin: malignant hyperthermia, NMS, serotonin syndrome, withdrawal syndromes (i.e. EtOH), sympathomimetic poisoning, anticholinergic poisoning
Heat load=heat dissipation
Methods of heat dissipation:
Evaporation
Radiation
Convection
Conduction
At high temperatures:
Increase in O2 consumption and metabolic rate
Blood shunted from splanchnic circulation to skin and muscles
MOSF and DIC
Production of heat-shock proteins
Hepatocytes, vascular endothelium, and neural tissue most sensitive
Oxidative phosphorylation uncouples
Risk Factors:
CV disease, DM
Neurologic or psychiatric disorders
Obesity, pregnancy, poor physical condition
Lack of air conditioning, social isolation
Extremes of age, physical disability
Use of recreational drugs (i.e. EtOH, amphetamines, or cocaine)
Prescription drugs (i.e. beta blockers decrease ability to dissipate heat through increase CO, diuretics predispose to dehydration, or anticholinergic agents can affect thermoregulation)
Clinical Presentation:
Temperature elevation, usually 40.5C with CNS dysfunction
Symptoms: weakness, nausea, dizziness
Vital signs: tachycardia, tachypnea, hypotension
Physical Exam: flushing, rales, ecchymosis, petechiae, AMS (agitation, somnolence, coma, seizures), ataxia, oliguria
Workup:
Labs: BMP, CBC, LFTs, INR, PT/OTT, VBG, lactate, CK, PO4, troponin, tox screen, blood cultures
Imaging: CXR, CT Head, consider EKG, LP
Management:
Airway: intubate and mechanically ventilate if unable to protect airway
Breathing: supplemental O2 if needed
Circulation: fluids and vasopressors
Get the patient naked, spray water on them, have fans blowing on moist skin
Ice packs, cooling blankets
Tarp assisted cooling oscillation (TACO), water ice therapy (WIT), pleural or peritoneal lavage, cool IV fluids
Management of shivering/agitation
ativan, propofol, fentanyl, rocuronium
Complications:
respiratory failure, arrhythmia and cardiac dysfunction, hypotension, seizures, cerebral edema, rhabdomyolysis, kidney injury, hepatic injury, DIC
Neuroleptic Malignant Syndrome:
Incidence: 0.02-3%
Seen in all ages but most cases occur in young adults, male>female
Mortality decreasing, now 10-20%
Most commonly associated with first generation antipsychotics (haloperidol, fluphenazine) but can occur in second generation antipsychotics (olanzapine, risperidone), or even in some antiemetics (promethazine, metoclopramide, prochlorperazine)
This can also be seen in withdrawal of L-dopa or other dopamine agonists
Pathogenesis: alterations in the autonomic and somatic nervous system caused by decreases in the function of central dopamine systems; muscle rigidity of NMS is secondary to loss of dopamine in the basal ganglia disrupting thalamocortical circuits; disrupted modulation of the sympathetic nervous system, manifesting in increased muscle tone and metabolism, inability to dissipate heat, labile BP and HR
Presentation: AMS, rigidity, hyperthermia, autonomic instability
Lab/Imaging Findings: elevated CK, leukocytosis, transaminitis, AKI, rhabdomyolysis, metabolic acidosis, EEG can show generalized slow wave activity
Management: discontinue offending agent, cardiorespiratory support, volume resuscitation as needed, cooling, benzodiazepines for agitation and muscle rigidity, dantrolene for moderate to severe rigidity with elevated CK, bromocriptine or amantadine for moderate to severe symptoms
Airway Grand Rounds with Dr. Adan
Laryngectomy
Larynx is surgically resected. Mouth and nasopharynx connect to the esophagus, and the trachea is sewn to the anterior neck stoma
Laryngectomy tubes are shorter, most often uncuffed, and some are fenestrated (to allow better airflow across a speaking valve if present). These are more often worn for comfort rather than for stoma patency
TEP speaking valve (voice prosthesis) aka Blom-Singer may be present and can clue you in to the fact that this is a laryngectomy
These patients cannot be oxygenated or intubated from above
Complications
Obstruction
mucous plugging: saline and deep suctioning
Granulation tissue
Strictures and stenosis (subacute)
Call for help (RT, ENT)
Apply oxygen over the stoma
Remove cover or tube
Pass suction catheter
Can bag using pediatric BVM or size 3 iGel placed horizontally over the stoma to create a seal
Can pass scope with ETT (i.e. 6.0 cuffed ETT) preloaded and intubate through the stoma if PPV needed
Infection (i.e. bacterial tracheitis)
Bleeding (skin irritation and bleeding at the stoma site)
Fistula (TEF or tracheocutaneous fistula), can perform fiberoptic scope to evaluate
Pulmonary (i.e. pneumonia)
MacSize-ICU study
Showed that the Macintosh 3 blade was statistically significantly better than Mac 4 for all comers regarding first pass success rate in direct laryngoscopy in a retrospective multicenter observational study in intensive care units in France. This showed no difference in Cormack-Lehane score.
2022 Pre-AeRATE Trial:
use of HFNC for preoxygenation and apneic oxygenation showed no difference in lowest SpO2 during first intubation attempt when compared with usual care. This did show that HFNC prolongs safe apnea time (~10 min) compared to NRB+NC (~7min), and decreased the risk of SpO2 falling below 90% compared to NRB+NC (RR 0.68).
DEI Visiting Lecturer: “What Kids and Kidneys can teach us about Racism in Cincinnati” with Dr. Ray Bignall
Race and racism works in tandem with other systems of inequality, such as residential segregation, housing and shelter, food insecurity, income inequality, education, environmental justice, policing, and health inequities
Systems of Inequality:
Segregation: the myth of “de facto” segregation exists, whereas in truth this segregation was legally enforced and federally directed. This impacted the ability to purchase homes in “red-lined” areas, and has had long standing impacts on generational wealth for their descendants
Housing: the byproduct of the new deal era housing policies often replaced neighborhoods with segregated housing projects. “Not in my backyard” movement has stifled attempts to expands low-income housing to address the housing crisis, and still, African Americans are 17.7% less likely to be offered rental property
Income: structural barriers also exist to prevent wealth-building in Black communities. Examples include wage inequality, 3x higher unemployment rate, banking and lending discrimination, racial disparities in home ownership, and little intergenerational wealth (as mentioned above)
Policing: differences in how people of different races interface with police
Defining Racism:
“I define racism as a system of structuring opportunity and assigning value based on the social interpretation of how one looks (which is what we call “race”), that unfairly disadvantages some individuals and communities, unfairly advantages other individual and communities, and saps the strength of the whole society through the waste of human resources.” - Dr. Camara Jones
Racism is disparity by design. This concept can be related to other marginalized groups such as women, immigrants, LGBTQ people, people with disabilities, people living in poverty, and other groups who experience social disadvantages.
How Racism Creeps into Medicine
Plantation physicians used spirometers to prove the “weak” lungs of “full blacks” or “mulattoes” compared to whites
Thomas Jefferson’s ‘Notes on the State of Virginia’ remarked that this data was valuable to prove that Black bodies were “fit for the field and little else”
This notion was reinforced as early as the 20st century medical literature (JAMA 1922)
To this day, race-based estimates of lung capacity have their basis in this history, and remains accepted practice, although recently there has been a push to re-evaluate this process
Using an example from pediatric nephrology:
20% of US households experience food insecurity
One study found that among children with ESRD, 64% were food insecure
higher healthcare utilization, increased infection rates, and lower health related quality of life
Nutrition and CKD/ESRD are inextricably linked and impact growth and transplant readiness
Food insecurity also ties back into historical redlining by the unavailability of nutritious foods and the existence of food deserts
Historically redlined neighborhoods that are overpoliced are also seen as less desirable for investment and are less likely to attract supermarkets and fresh food vendors
Housing insecurity is a major risk factor for food insecurity
Housing status can also impact dialysis options (peritoneal dialysis, which is preferred, becomes a much less accessible option)
How can we as physicians help to mitigate the health impacts of systemic racism?
Advocate for safe and affordable housing for all children, especially those living with CKD
Improve access to and education regarding healthy, nutritious, and kidney-friendly foods
Support institutional and societal policies that limit the influence of income on access to excellent kidney care
Improve patient education and health literacy to address adherence and psychosocial barriers to transplant listing
Advocate for safe and healthy environments for children and families to live that optimize kidney health
We need to be very intentional about our understanding of race and health outcomes. Are we seeing these disparities because of genetic or ancestral factors, or do these disparities exist due to systemic racism and its downstream impacts
Further, although some health conditions are related to ancestral factors, this can be difficult to determine. Many patients are mixed race, and unless genomic analysis is done, you cannot determine which genes may have been inherited from a particular ancestor
Ex. ApoL1 and its influence on risk for kidney disease among patients with African descent
Additionally, patients may appear to be of a certain race but identify differently, or may have ancestry that they are unaware of
Medical Mistrust among African Americans
Myths and conspiracy theories about the healthcare industry’s approach to Black communities are reinforced by personal experience
How can health professionals work to dismantle systems of inequality and injustice?
Acknowledge with our minoritized colleagues (and patients) the racism we see in the world around us.
Champion workforce diversity and inclusion through intentional recruitment, mentorship, and partnership
Screen for social determinants of health in encounters
Educate yourself by engaging with new voices
Encourage implicit (and explicit) bias training
Listen first, and don’t be afraid to ask questions
Develop sincere empathy for those who are crying to be heard and helped
Be an “active bystander” when confronting racist or intolerant language/behavior
Build trust through dynamic, “back bench” community partnership
Institutional statements must be backed by action and accountability
“Justice will not be served until those who are unaffected are as outraged as those who are”
-Benjamin Franklin
Annals of B Pod - Opioid-Associated Hearing Loss
Unfortunately, we are all familiar with the dangerous respiratory depression that can occur in opioid overdose; but did you know that opioids can also cause hearing loss? Dr. Kein takes us through two cases of opioid overdoses with associated hearing loss, as seen in B Pod.
Case 2
HISTORY OF PRESENT ILLNESS
The patient is a male in his 20s presenting after an unintentional opioid overdose. He was found down by his family. Per paramedics, the patient was responsive to 4 mg Narcan. He was found to have oxygen saturation in the low 80s by squad, with improvement to the 90s on nonrebreather mask. Patient is refusing to talk to staff and appears to have altered mental status, repeatedly stating “I can’t hear.”
PAST MEDICAL HISTORY: Chronic Hepatitis C, Polysubstance abuse, Hypertension, Hypothyroidism, Schizoaffective Disorder, Depression
PAST SURGICAL HISTORY: Non-contributory
MEDICATIONS: Clonidine, Ferrous sulfate, Fluoxetine, Invega Sustenna, Levothyroxine, Quetiapine, Risperidone
ALLERGIES: Hydroxyzine
Physical Exam
Vitals: BP: 87/58 mmHg HR: 92 bpm RR: 16 bpm Temp: 97.4° F O2 sat: 100% on NRB
Patient is slightly ill-appearing but in no acute distress. He has reactive pupils. His oropharynx is clear and his tympanic membranes appear normal bilaterally. His breathing appears non-labored and his breath sounds are clear bilaterally. Cardiac exam with regular rate and rhythm. He has a soft abdomen. There are needle track marks on his bilateral upper extremities. There is no skin rash noted. He is alert but unable to answer orientation questions and repeatedly tells provider “I can’t hear.” He does move all four extremities to command.
Diagnostics
WBC: 8.6 Hgb: 12.3 Hct: 37.2 Plt: 190
Na: 136 K: 4.4 Cl: 98 CO2: 24 BUN: 20 Cr: 1.56 Glucose: 78
CK: 1900
Alk Phos: 87 AST: 104 ALT: 90 Total bilirubin: 0.6
Acetaminophen: <10 Salicylate: <3
Troponin: 0.10
TSH: 18.04 T4: 0.95
UDS: positive for amphetamines, benzodiazepines, fentanyl, THC
EKG: Normal sinus rhythm, incomplete right bundle branch block, normal axis, normal intervals. J-point elevation in leads I, II, III, aVF, V5, V6.
CT head: no hemorrhage, mass, edema or hypodensity.
HOSPITAL COURSE
The patient was initially found to be hypotensive in the Emergency Department with a blood pressure of 87/58 mmHg. He was given an intravenous fluid bolus with minimal improvement in his blood pressure, but remained alert. Lab workup was remarkable for a troponin of 0.10 without signs of ischemia on EKG, an elevated CK of 1900, and a mild acute kidney injury with a creatinine of 1.56. His troponins remained slightly elevated during serial checks in the ED, peaking at 0.12. The cardiovascular ICU team was consulted and performed a bedside echocardiogram that demonstrated a dilated right ventricle. A CTPA was performed which was negative for pulmonary embolism, but did suggest pulmonary hypertension and left lower lobe opacities concerning for viral pneumonia or aspiration pneumonitis. Patient remained hypotensive after fluid resuscitation and was admitted to the CVICU for management.
During his admission, the patient’s blood pressure improved with correction of hypovolemia with crystalloid fluid resuscitation, and his CK and troponin trended downward. He had a complete echocardiogram, which demonstrated mildly dilated left and right ventricles, thought to be secondary to cardiomyopathy as a result of heavy drug use. He was treated for community acquired pneumonia with Ceftriaxone and Azithromycin and discharged to follow up with cardiology in 3-6 months. There is no further mention of the patient’s hearing loss in the inpatient notes.
Case 1
HISTORY OF PRESENT ILLNESS
The patient is a female in her 40s presenting after an unintentional opioid overdose. Patient was at a hotel with a friend and found to be unresponsive. She received 2 mg intranasal Narcan from paramedics with improvement in respiratory status, but in the emergency department (ED) she remains somnolent and is unable to provide further history.
PAST MEDICAL HISTORY: Chronic Hepatitis C, Polysubstance Abuse
PAST SURGICAL HISTORY: None
MEDICATIONS: None
ALLERGIES: No known allergies.
Physical exam
Vitals: BP: 112/68 mmHg HR: 112 bpm RR: 23 bpm Temp: 97.5° F O2 sat: 93% on RA
Patient is shivering and somnolent but becomes agitated with physical stimulus. She has pinpoint pupils bilaterally. Her tympanic membranes are clear bilaterally and her mucous membranes are moist. She is tachycardic with regular rate and rhythm. She has normal respiratory effort with scattered wheezes. Her abdomen is soft. Her skin is warm and dry. She is moving all 4 extremities.
DIAGNOSTICS
WBC: 27.2 Hgb: 12.7 Hct: 39.0 Plt: 259
Na: 137 K: 6.6 Cl: 98 Bicarb: 22 BUN: 36 Cr: 2.49 Glucose: 116
VBG: pH 7.19 pCO2: 59 HCO3: 23 BE: -6.1
Lactate: 5.3
CK: 496
High sensitivity troponin: 38
CXR: widespread bilateral airspace opacities, concerning for multifocal pneumonia, to include aspiration and viral etiologies.
EKG: Normal sinus rhythm with peaked T waves in V4, V5
UDS: positive for fentanyl
HOSPITAL COURSE
After initial evaluation in the ED, the patient’s respiratory rate dropped to 6-8 breaths per minute and she developed a new oxygen requirement. She was given an additional dose of Narcan 0.4 mg IV, with improvement in her mental status and respiratory effort, but she continued to require 4L oxygen via nasal cannula and had wheezing throughout all lung fields. The patient then reported inability to hear questions, which she stated had also occurred with previous opioid overdoses. Patient was able to respond to questions appropriately via writing.
Given the patient’s persistent oxygen requirement, chest X-ray was performed and showed bilateral airspace opacities. She was also found to have an acute kidney injury and hyperkalemia with EKG changes, for which she was treated with calcium gluconate, albuterol, insulin, and dextrose. She was started on a Narcan drip, placed on supplemental oxygen via nasal cannula, and admitted to the medical step-down unit.
During admission, the patient was treated for community-acquired pneumonia by the medicine team. Her oxygen requirement decreased throughout her hospitalization. Her acute kidney injury improved with hydration. There is no further mention of her hearing loss in the inpatient team notes. She was discharged to follow up with substance abuse resources and primary care.
Opioid-Associated Hearing Loss
Epidemiology
Opioid-associated hearing loss (OAHL) was first reported in 1979 associated with hydrocodone abuse. [1] Since then, this phenomenon has been reported with a variety of opioids including methadone, hydrocodone, hydromorphone, oxymorphone, propoxyphene, heroin, morphine, oxycodone, codeine, dextropropoxyphene, fentanyl, and tramadol.[1-7] The incidence of OAHL is unknown due to under-reporting, but it is believed to be a rare side effect. [1] OAHL has been reported after various dosages, administration routes, and lengths of opioid use. [5] There are reports of OAHL occurring after oral, intranasal, intravenous, and transdermal administration, as well as one case of intra-arterial administration. [5,7,8] Cases are most frequently reported after a single opioid overdose or after chronic use at high doses. [7,9]
Pathophysiology
As OAHL typically presents as sensorineural hearing loss, the etiology is believed to be secondary to damage to the cochlea. [2,6,7] The exact mechanism is poorly understood, but there are a few theories that are commonly cited. These include hypoxia to the cochlea or vestibulocochlear system, altered pharmacokinetics due to genetic polymorphisms of metabolic enzymes, and direct ototoxic effect to the cochlea. [1,2,5,7,9]
The cochlea is known to be sensitive to ischemia due to its high metabolic activity and intense energy requirements. [7,8] It is postulated that OAHL may be in part be due to hypotensive or hypoventilatory events that frequently occur due to respiratory depression from opioid overdose, leading to hypoxia and vasospasm of the spiral modiolar artery. [1,5,7,9] However, this theory has come into question, as some reports of OAHL involve no clear hypoxic event. [7] Another hypothesis suggests that toxic substances are generated during the metabolism of opioids, with genetic differences in oxidative enzymes of the P450 system leading to the formation of more or less of these ototoxic products. [2] However, since not all opioids generate the same metabolic products, this is considered to be less likely. [7,9] The theory that is currently the most widely accepted is direct opioid effect on receptors present in the cochlea. All three subtypes of opioid receptors (μ, δ, and κ receptors) have been found to be present on the cochlea, and overstimulation of cochlear opioid receptors is thought to lead to decreased activity of cochlear hair cells, perhaps via altered signal transduction and downregulation of adenylate cyclase. [1,7,9]
Figure. Diagram of the inner ear and the difference between conductive and sensorineural hearing loss.
Clinical Presentation
OAHL typically presents as bilateral hearing loss that is sudden in onset, although there are rare cases of unilateral hearing loss. [1,7,9] OAHL has been demonstrated to be sensorineural whenever audiometric testing has been performed on affected patients. [2,9] Severity can range from complete deafness to tinnitus to mild hypoacusis. [7] Though most have normal vestibular function on audiometric testing, there have been some cases that also have associated vertigo, suggesting possible extension of injury to the labyrinth. [2,5,7] In patients presenting after overdose, OAHL typically develops rapidly after the event and resolves spontaneously. In patients with chronic opioid use, hearing loss is usually slower in onset, but then becomes rapidly progressive and is often irreversible. [9]
Differential Diagnosis
Table. Differential diagnosis of acute sensorineural hearing loss.
Hearing loss can be categorized as conductive, sensorineural, or a combination of both (see figure). Conductive hearing loss occurs due to damage or obstruction of the mechanical components of the ear. The most common causes of conductive hearing loss include cerumen impaction, otitis media or externa, foreign bodies, or otosclerosis. [9] Sensorineural hearing loss, as seen in OAHL, is due to pathology with the pathway from the cochlea to the auditory cortex. [6] Other common causes of sensorineural hearing loss include cochlear injuries, cochlear ischemia, viral infections, autoimmune disorders, and ototoxic drug exposure (see table). [9,10] In suspected cases of OAHL, it is important to keep these other etiologies in mind and examine the patient’s medication list for possible concomitant ototoxic drug use.
Prognosis and Treatment
Prognosis of OAHL appears to be variable, with some patients recovering hearing after only a brief time and others with permanent hearing loss. [7] Most patients do appear to recover spontaneously. However, case reports seem to indicate that hearing loss associated with acute overdose is more likely to be reversible, usually within days to weeks, and that loss associated with heavy chronic use is much more likely irreversible. [4,7,9]
Treatment has been attempted with various interventions including naloxone, corticosteroids, and pentoxifylline. [4,5,7] However, there is little evidence of benefit from any of these interventions. In patients whose hearing loss persists at long-term follow-up, cochlear implants have been successful in restoring hearing. [5,7,9]
Summary
Sensorineural hearing loss is a known side effect of opioid class drugs in both acute overdoses and chronic high dose opioid use. The exact mechanism is unknown, but it is thought to be secondary to damage to the cochlea. Prognosis varies from rapid spontaneous resolution to long term hearing loss requiring cochlear implants. There is no evidence supporting any specific treatment to mitigate or treat OAHL.
AUTHORED BY Courtney Kein, MD
Dr. Kein is a PGY-3 in Emergency Medicine at the University of Cincinnati
Editing by the Annals of B Pod Editors
REFERENCES
Ghasemi S, Izadpanahi S, Yaghoubi MA, Brent J, Mehrpour O. Methadone associated long term hearing loss and nephrotoxicity; a case report and literature review. Substance Abuse Treatment, Prevention, and Policy. 2019;14(1).
Vorasubin N, Calzada AP, Ishiyama A. Methadone-induced bilateral severe sensorineural hearing loss. American Journal of Otolaryngology. 2013;34(6):735-738.
MacDonald LE, Onsrud JE, Mullins-Hodgin R. Acute Sensorineural Hearing Loss After Abuse of an Inhaled, Crushed Oxymorphone Extended-Release Tablet. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 2015;35(7).
Leache L, Aquerreta I, Moraza L, Ortega A. Morphine-induced hearing loss. American Journal of Health-System Pharmacy. 2016;73(22):1840-1843.
Orei M, Peyvandi AA, Mokhtarinejad F. Opioid Drugs and Sensorineural Hearing Loss. Addiction and Health. 2018;10(1).
Boyle KL, Rosenbaum CD. Oxymorphone Insufflation Associated with Acute Sensorineural Hearing Loss: Case Files of the University of Massachusetts Medical Toxicology Fellowship. Journal of Medical Toxicology. 2013;9(2):179-183.
Mozeika AM, Ruck BE, Nelson LS, Calello DP. Opioid-Associated Hearing Loss: A 20-Year Review from the New Jersey Poison Center. Journal of Medical Toxicology. 2020;16(4):416-422.
Lopez I, Ishiyama A, Ishiyama G. Sudden Sensorineural Hearing Loss Due to Drug Abuse. Seminars in Hearing. 2012;33(03):251-260.
Kopec KT, Nelson LS. Opioid-Induced Hearing Loss: A Trend to Keep Listening For? North American Congress of Clinical Toxicology. 2012:4-6.
Schattner A, Halperin D, Wolf D, Zimhony O. Enteroviruses and sudden deafness. Cmaj. 2003 May 27;168(11):1421-3.
Ultrasound of the Month: Severe Hydronephrosis in a patient with Horseshoe Kidney
This is not your average hydronephrosis… Join Dr. Olivia Gobble as she explores the sonographic and physiologic challenges presented by a horseshoe kidney.
THE CASE
An elderly female patient presents to the emergency department (ED) with 1 week of generalized weakness leading to numerous falls. She denies any fevers, abdominal pain, nausea, or vomiting. She has a history of previous episodes of nephrolithiasis, frequent urinary tract infections, and states she takes gabapentin for overactive bladder. She denies any current dysuria or hematuria. Her vital signs are within normal limits. Her cardiopulmonary exam is unremarkable and palpation of the back and abdomen reveals no significant tenderness. She is neurologically intact, with no gait abnormalities, intact cranial nerves and 5/5 strength in all extremities. She has no rashes or ecchymosis and otherwise her skin exam is unremarkable.
Given her age, history of nephrolithiasis, and frequent urinary tract infections, a bedside renal ultrasound was performed to assess for hydronephrosis due to concern her generalized weakness may be secondary to an infected stone or obstructive uropathy. Images are seen below.
Video 1: Left kidney seen in longitudinal view. Spleen coming into view on the left of the image and multiple hypoechoic structures seen on the right of the image. Difficult to appreciate renal parenchyma and inferior pole
Video 2: Left kidney seen in transverse view. Spleen coming into view on the right of the image. Multiple hypoechoic structures seen midline in the image. Difficult to appreciate renal parenchyma and inferior pole
Video 3: Right kidney seen in longitudinal view. Liver coming into view on the left of the image. Multiple hypoechoic structures (one smaller and the other significantly larger) seen immediately to the right of the liver edge with disruption of the renal parenchyma. Hypoechoic structures appear to be interconnected. No visualization of inferior pole of kidney.
Video 4: Right kidney seen in transverse view. Liver coming into view on the left of the image. Multiple hypoechoic structures seen, most interconnected, to the right of the liver. No visualization of inferior pole of kidney.
Overall impression: Numerous, bilateral, anechoic structures with disruption of the renal parenchyma and difficult to identify inferior poles bilaterally.
The patient’s presentation was concerning for hydronephrosis secondary to an obstructive process, such as a kidney stone. However, the bilateral nature of the anechoic structures raised some confusion. Other diagnoses considered included polycystic kidney disease, renal abscess, hematoma, infected stone, and malignancy. Her workup showed a urinalysis notable for large leukocytes and >100 WBC on microanalysis. Additionally, she was found to have an AKI on CKD with a creatinine of 4.10 (baseline Cr 1.3) and hyponatremia to 125.
The patient had never been seen in our medical system previously. Outside hospital records were obtained and upon review, it was noted that the patient had recently been diagnosed with a horseshoe kidney on CT imaging. On further discussion with the patient, she states she was told she had an abnormality with her kidneys but did not recall the specifics. This information explains why the inferior poles of her kidneys were difficult to identify bilaterally.
HORSESHOE KIDNEY PATHOPHYSIOLOGY
Image 1. Axial CT of a horseshoe kidney Hufeisenniere CT axial by Hellerhoff. Licensed under a Creative Commons Attribution-Share Alike 3.0 Unported license.
The horseshoe kidney is the most common renal fusion anomaly and is characterized by abnormalities with position, rotation, and vascular supply. A horseshoe kidney is identified by having functioning renal tissue on both sides of the vertebral column connected by an isthmus. The isthmus is made up of renal parenchyma in about 80% of cases, with the remainder made up of fibrous tissue. This isthmus is located either midline or laterally, with the lateral position resulting in an asymmetric horseshoe, 70% of which are left dominant [1].
Normally, the kidneys are located in the retroperitoneum, between T12 and L3, with the left kidney being located slightly higher than the right. The upper poles will typically be located medially and posteriorly when compared to the inferior poles. Comparatively, the horseshoe kidney’s ascent during development is limited by the inferior mesenteric artery, located around L3. The horseshoe kidney may also be found lower in the pelvis as seen in image 1 [2]. The fusion, which typically occurs in the inferior poles, causes these poles to be located medially, the reverse of the normal renal axis [3].
While about one third of patients with a horseshoe kidney are asymptomatic and diagnosis is made incidentally, the intrinsic anatomical defects associated with a horseshoe kidney predisposes patients to urologic complications such as ureteric obstruction and impaired urinary output [3].
IMAGING WITH ULTRASOUND
In patients with a horseshoe kidney, there are several differences that make point-of-care ultrasound (POCUS) evaluation difficult. The kidney will have a different axis as well as level of lie, so care should be taken to scan broadly if the renal cortex is not immediately apparent. The right side of the kidney can be evaluated with an anterolateral approach, using the liver as a window, with the patient either supine or in left lateral decubitus. The left side of the kidney should be evaluated with a posterolateral approach using the spleen as a window, with patient either supine or right lateral decubitus. Operators should take care to obtain clear images of the upper renal poles with the understanding that inferior pole evaluation will be limited from the isthmus. A midline approach, with the transducer over the umbilicus, is useful for identifying the isthmus itself [4]. It typically lies anterior to the inferior vena cava and aorta in most cases, although there are reports of the isthmus running posterior or even between the great vessels [2]. Ultrasonography is limited in some cases, particularly in patients who are obese or when the isthmus has a fibrous composition [5].
If a horseshoe kidney is not expected, the abnormal rotation and inferiorly located kidney can result in poor visualization of the inferior pole and underestimation of their length. Additionally, renal tissue located anterior to the aorta may be mistaken for retroperitoneal tissue, such as lymphoma or metastatic nodal enlargement [3].
POCUS FOR EVALUATION OF RENAL CYSTS AND HYDRONEPHROSIS
Determining whether the patient with numerous anechoic structures on renal ultrasound has hydronephrosis versus numerous renal cysts can be difficult, made trickier in patients with abnormal anatomy (such as a horseshoe kidney). In brief, hydronephrosis will appear as interconnected, branching anechoic areas, often with irregular contours indicative of renal collecting duct system. In contrast, parapelvic cysts will be thin walled, spherical and not connected to the ureter distally. However, given their anechoic nature and location near the renal collecting system, they can still be easily confused for hydronephrosis and vice versa [6]. Beyond parapelvic cysts, any large cyst can be confused for hydronephrosis if not viewed in both planes. Evaluation of the anechoic structure itself, as well as the relative location and communication with the renal pelvis is crucial. If there remains a question, further evaluation with CT imaging is indicated.
CASE RESOLUTION
The patient was started on intravenous fluids for her AKI and ceftriaxone for antibiotic coverage of her UTI. She had a foley placed and was admitted to the hospital. CT scans confirmed severe non-obstructive hydronephrosis and after several days of IVF and antibiotics, she had improvement of her weakness and creatinine. She was discharged with plans for follow-up with urology for foley removal.
AUTHORED BY OLIVIA GOBBLE, MD
Dr. Gobble (@oliviagobble) is a PGY-2 in Emergency Medicine at the University of Cincinnati.
PEER REVIEW BY Patrick Minges, MD
Dr. Minges (@mingespg) is an Ultrasound-trained and Clinical Faculty in Emergency Medicine at the University of Cincinnati.
EDITING AND LAYOUT BY MARTINA DIAZ, MD
Dr. Diaz (@martina_diazb) is a PGY-3 in Emergency Medicine at the University of Cincinnati and the current Resident Editor of Ultrasound of the Month.
REFERENCES
Kirkpatrick JJ, Leslie SW. Horseshoe Kidney. 2022 Nov 28. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 28613757.
Shah HU, Ojili V. Multimodality imaging spectrum of complications of horseshoe kidney. Indian J Radiol Imaging. 2017;27(2):133-140. doi:10.4103/ijri.IJRI_298_16
Niknejad M. Horseshoe Kidney: Radiology Reference Article. Radiopaedia Blog RSS. https://radiopaedia.org/articles/horseshoe-kidney?lang=us. Published October 7, 2022. Accessed December 13, 2022.
Clinical imaging. UT Southwestern Medical Center. https://www.utsouthwestern.edu/education/medical-school/departments/radiology/protocols/. Accessed December 13, 2022.
Sethi SK, Raina R, Koratala A, Rad AH, Vadhera A, Badeli H. Point-of-care ultrasound in pediatric nephrology. Pediatr Nephrol. 2022 Sep 26:1–19. doi: 10.1007/s00467-022-05729-5. Epub ahead of print. PMID: 36161524; PMCID: PMC9510186.
Koratala A. Parapelvic cyst mimicking hydronephrosis. NephroPOCUS. https://nephropocus.com/2019/06/05/parapelvic-cyst-mimicking-hydronephrosis/. Published July 14, 2022. Accessed December 13, 2022.
Grand Rounds Recap 3.29.23
We are back with an excellent grand rounds session, where we heard about a case of resuscitative hysterotomy from Dr. Stark, BRASH syndrome, and HIV screening in the ED. We also heard some life lessons from the Peace Corps and how they relate to emergency medicine.
R3 Taming the sru: resuscitative hysterotomy w/ Dr. stark
Indications: Maternal cardiac arrest > 20 weeks (at or above umbilicus)
Ideally, perform within 4 minutes of arrest
One study showed that this may be able to be extended to 10 minutes
Increases maternal cardiac output by 30%
No studies have proven improved maternal survival
Procedure:
Incision from umbilicus to pubic symphysis
Expose the uterus and retract bladder
Make vertical incision through lower uterine segment
Use scissors to extend incision
Deliver infant and clamp/cut cord
Deliver placenta
Pack abdomen
Give oxytocin
Other considerations:
Do not delay the procedure for the arrival of an obstetrician or neonatologist.
Do not evaluate for fetal cardiac activity or tocometry.
Do not prepare a sterile field (but be as clean as possible).
Do not transport to an alternative location.
Cardiac Arrest in Pregnancy
1 in 30,000 pregnancies
800 maternal deaths globally
Rates have nearly doubled between 1989 and 2009
Survival to hospital discharge after maternal in-hospital cardiac arrest 58.9%
Etiologies of arrest
Trauma is most common worldwide
Pulmonary embolism
Causes approximately 20% of maternal deaths
Risk factors:
Prior thromboembolism
Advanced maternal age
Increased parity
Obesity
Immobility, trauma, or recent surgery
Management
Thrombolytics
Pregnancy is relative contraindication to thrombolytics
Hemorrhage
Hemorrhage accounts for 17-38% of maternal deaths
Risk factors:
Hypertension
Preeclampsia or HELLP
Trauma to abdomen
Smoking
Cocaine use
Previous abruption
Management
Blood transfusion
Uterotonics
Pregnancy induced hypertension
Estimated 14.5% of maternal deaths attributed to preeclampsia and its variants
Can lead to arrest via
HTN → intracranial hemorrhage
Eclampsia → hypoxia or stroke
Pulmonary edema → hypoxia
Hepatic failure or rupture → hemorrhage
Management:
Delivery
Magnesium sulfate
AHA recommends magnesium in arrest thought to be secondary to eclampsia at the normal loading dose of 4-6g
Amniotic fluid embolism
Most common immediately following delivery
Anaphylactoid reaction → SIRS , DIC, and multi-organ failure
50% mortality within the first hour
Risk factors:
Difficult labor
Advanced maternal age
Multiparity
PROM
Amnioinfusion
Trauma
Abruption and rupture
Fetal death
Myocardial infarction
Infection/sepsis
Peripartum cardiomyopathy
Stroke
Anesthetic complications
R1 Clinical Knowledge: BRASH syndrome w/ Dr. wilson
Definition:
Bradycardia, Renal Failure, AV Nodal Blockade, Shock, Hyperkalemia
Etiology
AV nodal blockade (beta blockers, Ca channel blockers) + Renal injury
Renally-Cleared beta-blockers are: Atenolol, Nadolol, also bisoprolol, acebutolol
Ca channel blockers implicated are often the non-dihydropyridines (verapamil, diltiazem)
Renally cleared ACEi/ARB: Enalapril, Lisinopril, Ramipril, Benazepril
Hyperkalemia synergizes with AV nodal blockade to worsen bradycardia
Clinical Presentation
Hyperkalemia may not always be significantly elevated
Management
Hyperkalemia
Calcium, insulin/D50, albuterol, potassium binders, RRT if needed
Diuretics can be considered to remove potassium following fluid repletion
Bradycardia
Calcium, epinephrine, isoproterenol
Fluid resuscitation
Consider isotonic bicarb for patients with uremic acidosis and hyperkalemia
R4 Capstone w/ Dr. gressick
Life Lessons from the Peace Corps and the People that Taught Them
You can always give to others, you don’t need wealth to give
Children are universal
People change and personal growth is inevitable
Sometimes you don’t know what you want, embrace unexpected experiences
Adaptability is crucial, expand your comfort zone
r4 case follow-up: HIV Screening in the emergency Department w/ Dr. Kimmel
Locally, from 2014-2018, UCMC diagnosed 142 new cases of HIV, which represented 18% of all new cases of HIV in Hamilton County during this period.
In the year 2022, our department diagnosed 18 new cases, and linked over 50 patients with known HIV who were referred to care
Why this matters
⅓ of all US transmissions of HIV occurs in undiagnosed individuals
Early Intervention Program (EIP)
Follows up all ED HIV test at UCMC
Will contact patient to establish follow up, and will contact the health department to arrange contact tracing
EIP staff are usually available from 8a-12a every day of the week
Rapid HIV testing
Oral swab - 20 minute turnaround
Tests only for HIV antibody, if positive, requires additional confirmatory testing
Positive at about 30 days after exposure
Sensitivity 92-99%
Finger prick confirmatory test- 1 minute turnaround
ED HIV Serum Screen
Tests for HIV antibody and p24 Antigen
Will be positive around 18 days after exposure
Sensitivity ~99-100%
Disclosure of HIV Diagnosis
If you discharge a patient with a pending HIV test, consider the ramifications of having to deliver a positive diagnosis over the phone
Is English your patient’s primary language?
Does your patient have access to a phone and do you have the right phone number for the patient?
Is the patient hard of hearing?
What is the next step for follow up?
EIP Linkage Coordinator will make this call for you, and is trained to discuss this diagnosis with patients
Expedited Partner Therapy
If a patient’s partner is unable or unwilling to present to a medical facility for treatment, a provider can provide an additional prescription to a patient to treat their partner at the time of an STI diagnosis
For Chlamydia, doxycycline 100mg BID x7d, and for gonorrhea, cefixime 800mg PO once
Write “EPT” in the name line on a prescription pad and give the prescription to the patient
In Ohio, can print a paper prescription with the patient's name, and physically write “For EPT” next to their name for the partner’s treatment
EPT is legal in most states in the US
Resources
In EPIC, there are pre-populated discharge resources for many special patient groups:
Local needle exchanges
LGBT resources
Shelter resources
Look at “ED DC” under attachments in the discharge instructions
Add the health department to discharge instructions for patients with frequent STI
Caracole, a greater Cincinnati non-profit organization, can help patients with access to medications in situations of financial difficulty
EIP can help navigate
Grand Rounds Recap 3.15.23
What a packed week! We reviewed a harrowing case of massive bee envenomation (with insects in the airway) w/ Dr. Yates, R4 wisdom and philosophies with Dr. Mullen, an overview of hydrocephalus with Dr. Stothers, a CPC of a brain tumor presenting with aphasia with Dr. Glenn, a dive into hyperviscosity syndromes with Dr. Beyde, and a wonderful series of lectures on the Language of Being Well & Embracing Fear in EM with visiting professor Dr. Arlene Chung.
tamingthesru: Massive bee envenomation WITH dr. Yates
Anaphylaxis
Pathophysiology
Type 1 Hypersensitivity Reaction
IgE-mediated
Mast-cell degranulation of vasoactive materials
Reaction occurs in minutes
Clinical Definition:
Acute onset of illness with involvement of the skin, mucosal tissue or both + one of the following
Respiratory compromise
Reduced BP
Or, acute onset of illness with at least two of the following in the setting of a likely allergen:
Involvement of the skin/mucosal tissue
Respiratory compromise
Reduced BP (including hypotonia/collapse, syncope, incontinence)
Persistent GI symptoms
Anaphylaxis criteria can also be met with hypotension alone as a symptom if exposed to a known allergen
Treatment
Epinephrine
Alpha-1 Agonism
Vasoconstriction and increased PVR
Beta-1 Agonism
Increased chronotropy and inotropy cardiac output
Beta-2 Agonism
Decreased mucosal edema via pulmonary smooth muscle relaxation
Administration
0.01mg/kg IM
Max dose 0.5mg
Given every 5-15 minutes
If refractory hypotension epinephrine gtt
Can give 5-20ug IV boluses if needed while setting up gtt
Positioning
Passive leg raise
Fluid Resuscitation
H1 and H2 antihistamines
Steroids
No high quality data
Inhaled Beta-2 Agonists
Other treatment Considerations
Scene safety
Stinger removal
Africanized Bees
1957 – escaped lab in Brazil, subsequently colonized majority of Americas
1 sting: 140-150ug median dose delivered
Systemic symptoms typically > 50 stings
Lethal dose: 2.8-3.5mg/kg in human
Requires >1000 to be considered lethal
Includes melittin, phospholipase A2, hyaluronidase
Melittin: mainly responsible for the pain reaction
Phospholipase A2: responsible for large portion of allergic reactions
Hyaluronidase: Leads to faster distribution of toxin, also responsible for some of the allergic reactions seen
Melittin and PLA2 when form complex with melittin hemolytic factor which cleaves cell membranes, particularly hemoglobin, leukocytes, vascular membranes
Also individually and synergistically work together to break down skeletal muscle
Massive envenomation
> 50 simultaneous stings
Vague systemic symptoms
Complications:
Myocardial injury
Hypertension
Hepatic Injury
Rhabdomyolysis
Alkalinization of urine
Hemolysis
Acute Renal Failure
Disposition should be admission for observation given complications can be delayed for several hours with > 50 stings
R4 Capstone WITH Dr. Mullen
Cases and rants:
Marginalized patient populations deserve equitable treatment in the ED
Understand the triage note, but interview the patient with a clean slate to limit triage bias
Someone who normally walks and is not not walking is not normal – you must try and walk patients before discharge
PEs can look like anything; Sometimes luck brings the diagnosis
“Uncooperative” patients are not always behavioral and may portend real physiological distress
Meet EMS at the bedside – hearing information directly from the source is critical
Respect electrolytes
Understand and acknowledge the admitting physician’s comfort with accepting patients
Every patient is someone’s loved one
Life can be meaningful at any age
Parents are allowed to be concerned about their babies
Know your team member’s names
Protect your team and their wellness on shift
Give praise; we hear constructive feedback often but deserve to celebrate our successes
Hydrocephalus WITH dr. Stothers
Anatomy
CSF is produced in the lateral and third ventricle
Drains through the cerebral aqueduct into the fourth ventricle, then into the subarachnoid space
From here, CSF is absorbed into the venous system by arachnoid granulations
Physiology
Obstruction of flow of CSF between its production and drainage can cause increased ICP and symptoms of hydrocephalus
Obstruction can occur from tumors, intracranial bleeding, decreased drainage by arachnoid granulations, increased rate of CSF production
Monro-Kellie Doctrine = sum of the brain, CSF and blood is contained within a fixed volume within the skull
Clinical Presentation
Headache
Vision changes
Diplopia
Papilledema
Gait disturbances
AMS, coma, seizure
Death
Normal pressure hydrocephalus
Gait disturbances (94-100%), incontinence (78-98%), cognitive impairment (60-92%)
Diagnostics
CT Head
Enlargement of ventricles
Disproportionately enlarged subarachnoid space
Corpus callosal angle < 90 degrees
Evan’s Index
Ratio of the maximum width of the frontal horns of the lateral ventricles and the maximal internal diameter of the skull at the same level
Rough estimate of ventriculomegaly in NPH patients
CSF Tap for NPH
Remove 30-50cc’s
Wait 3-4 hours to evaluate response to therapy
Therapeutics
VP shunt
Catheter placed in the lateral ventricle with valve that can measure pressure
Distal tip empties into the RA or peritoneum
CPC: Brain tumor WITH Drs. Glenn and irankunda
Case: Isolated aphasia in a female patient diagnosed with a R parietal brain tumor on CT head
Brain tumor
Patients less than 30 - primary > metastatic
Presentation
Headache (50% of patients)
Worse in morning
Tension type 40-50%
Migrainous in 10%
Seizure
50-80% with primary brain tumors
10-20% metastatic brain tumor
Elevated ICP
Nausea/vomiting
Vision changes
Headache
Diagnostics
MRI Brain to characterize lesion
CT Chest/Abdomen and Pelvis to evaluate for primary tumors
In a case series of 227 patients, ~60% of patients with brain tumor had an identifiable primary tumor elsewhere
Management
Dexamethasone
Seizure prophylaxis is not indicated, but treat if patient presents with a seizure
Hyperviscosity syndromes (HVS) WITH dr. beyde
Hyperleukocytosis
WBC usually > 100k but symptoms can occur > 50k
5-30% of adult leukemias
Patients are functionally neutropenic
Infections are a leading cause of death
Sickle cell disease
Misshapen RBCs predispose to hyperviscosity
Simple transfusion cannot provide sufficient number of RBCs to lower percent of HgbS without causing hyperviscosity
Transfusion increases risk for autotransfusion
Waldenstrom Macroglobulinemia
Most common cause of HVS (up to 90% of all cases)
Rare type of NHL
More than 30% develop hyperviscosity
Malignant B cells secrete immunoglobulins
Presentation
Hyperviscosity triad
Mucosal bleeding, vision changes, neurologic symptoms
Mucosal bleeding is the most common
Mucosal bleeding
Naso-oral is most common, though GI and vaginal bleeding can occur
Platelet dysfunction
Neurologic Symptoms
Headache, stroke symptoms, ataxia, vertigo, hearing loss, coma, seizure, tinnitus
Vision changes
Painless vision loss, blurred vision, diplopia, fundoscopic changes
Optic nerve edema
Sausage link retinal veins
Hemorrhages
Exudates
Cardiopulmonary
Shortness of breath
High output heart failure
ACS
Acute kidney injury
Venous thromboembolism
Clues to increase suspicion
Cancer history
B symptoms
Lymphadenopathy
Mucosal bleeding
Dehydration
Ruddy complexion
Advanced age
Evaluation
CBC with differential
Evaluate cell lines
CMP
DIC labs (d-dimer, fibrinogen, coags)
Uric acid, LDH, phosphorus
UA
Peripheral smear
Rouleaux Formation
Serum viscosity
3-5 day turnaround
SPEP-UPEP
Imaging (CT head, CXR, MRI)
Treatment
Temporary
IV fluids
Phlebotomy
2-3 units replaced by 2-3L IVF
Definitive
Emergent plasmapheresis
Leukapheresis
Plateletpheresis
Anemia
Avoid transfusion before plasmapheresis
Will worsen symptoms
Broad spectrum antibiotics
Infection is a leading cause of death
Risk of Tumor lysis (10%)
Screen and treat electrolyte derangements
Hydroxyurea
50-100 mg/kg
Shown to reduce WBC by 50-60% in 24-48 hours
Chemotherapy
Only treatment proven to improve survival
The Language of being well WITH dr. arlene chung
Being able to accurately pinpoint how we are feeling is important and precision language is key
Burnout has been a longstanding issue, predating COVID
46% of physicians reported 1 or more dimensions of burnout (Shanafelt et al 2012)
72% of EM physicians reported 1 or more dimensions of burnout
Physicians in specialties at the front line of care access seem to be at the greatest risk
76.1% of emergency medicine residents report 1 or more dimensions of burnout (Lin Annals Emerg Med 2019)
Moral Injury with COVID
“We pushed aside our fear and frustration to focus on saving the patients in front of us; we kept our eyes open, and our feelings closed. As with soldiers in war, we know that as soon as we stop doing, we will start feeling.” (Dean Ann Emerg Med 2020)
Emotional Agility by Susan David, PhD
Being in touch with our inner emotional experience allows us to be more in touch with our lives in a more complex and intentional way
The readiness potential in our brains is activated and allows us to take action
Emotions are data and allows us to respond to them
Knowing what you’re feeling and knowing what to do about it (Barrett, Cogn Emot 2010)
53 subjects kept a diary of emotions over 2 weeks and their response to emotions
Ability to differentiate emotions is correlated with better emotional regulatory response
This was only true with negative emotions
Postulated to be adaptive response
Does not correlate with positive emotions
Emotional differentiation is a simple, easily trainable skill that is frequently overlooked
Plutchik’s Wheel of Emotions
Burnout
A job-related experience, characterized by emotional exhaustion, cynicism and reduced professional efficacy. Refers specifically to phenomena that occur in the occupational context and should not be applied to describe experiences in other areas of life.
Many think of burnout as a medical disease; this was never the intended use.
There are some emotions that are “okay” in medicine
Insecurity, depression, etc may not be viewed as “okay” emotions in a professional setting but may be labeled instead as “burnout”
Specific use of language is important
How to proceed
Mindfulness
Reflection
2800 physicians at Mayo were surveyed and found that leadership qualities of physician supervisors appear to impact the well-being and satisfaction of individual physicians working in health care organizations (Shanafelt, Mayo Clin Proc 2015)
Leadership score associated with decreased likelihood of burnout
Increased satisfaction with the department
Statistically significant correlation
Telling stories of our experiences in medicine is important and helps us to reflect, process and share emotions
“Stories are the avenue toward telling and, therefore, knowing of the self. Narratives trigger changes of many kinds in both the teller and the listener, yielding meanings that are reciprocally produced by each teller-listener dyad.” (Charon, Academic Med 2012)
embracing fear in emergency medicine WITH dr. arlene chung
What is fear?
Basic emotion
Social construct
Survival response
Personality
Physical Fear
Fear of heights, death, pain
Can have physical fear for someone else
Identity Fear
Fear of sense of self
Friend, leader, father/mother, daughter/son
Social Fear
Fear of isolation or being cast out
Fear of belonging
Fixed vs Growth Mindset (Mindset by Dweck 2006)
Fixed Mindset
We are born with all the abilities that we will ever have
Failure is a value judgment
Growth Mindset
Failure is another learning opportunity
I failed vs. I am a failure
Residency is an excellent time to cultivate the growth mindset
Hidden Curriculum
Doctors do not show weakness
The three most powerful words in emergency medicine are “I don’t know”
It takes courage to acknowledge deficits and limitations
Imposter syndrome
Imposter syndrome is fostered by fear of failure, fear of success and low self esteem (Traut-Mattausch Front Psychol 2016)
Leads to decreased career planning, career development, strive to succeed
The Armory (Dare to Lead, Brown 2018)
Mechanisms for self-preservation in the face of fear
Perfectionism
Numbing
Being right
Crush or be crushed
Cynicism/sarcasm
Absence of feeling fear does not lead to feelings of joy
Armor must be removed before we can embrace all emotions
Bravery
Quality or state of having the mental or moral strength to knowingly face fear, danger or difficulty
“It is not the critic who counts: not the man who points out how the strong man stumbles or where the doer of deeds could have done better. The credit belongs to the man who is actually in the arena, whose face is marred by dust and sweat and blood, who strives valiantly, who errs and comes up short again and again, because there is no effort without error or shortcoming, but who knows the great enthusiasms, the great devotions, who spends himself in a worthy cause; who, at the best, knows, in the end, the triumph of high achievement, and who, at the worst, if he fails, at least he fails while daring greatly” - T. Roosevelt
Courage is not a fixed trait and can be learned
Show up every day and do it again and again
Be prepared
Box breathing
Be human
It’s okay to feel a range of emotions
Be vulnerable
This is how we change the hidden curriculum
Be empathic
Be there for each other
Diastolic Shock Index: A clinically relevant predictor of poor outcome in septic shock?
Early recognition and resuscitation of patients in septic shock are critical skills for an emergency medicine physician. Many clinical decision-making tools have been developed and validated in their use to identify and define those who are in sepsis or septic shock, as well as predict a patient’s overall risk of morbidity and mortality, including tools like the SIRS criteria and SOFA score. The diastolic blood pressure is determined by vascular tone, and thus it can be assumed that a decrease in the diastolic blood pressure should correlate with the pathologic vasodilation in septic shock. As a result, the authors of this study hypothesized that the relationship between heart rate and the diastolic blood pressure (i.e. the diastolic shock index) could provide providers a tool to quickly identify patients that are at risk for unfavorable outcomes.
Ospina-Tascón GA, Teboul J-L, Hernandez G, et al. Diastolic shock index and clinical outcomes in patients with septic shock. Ann Intensive Care 2020;10(1):41. 10.1186/s13613-020-00658-8
P: A total of 761 patients from two separate cohorts found to have septic shock
I: Diastolic shock index
C: Comparison to a variety of well adopted markers of morbidity and mortality, including systolic shock index, SOFA score, APACHE II score, lactate, etc.
O: There was an association between increased diastolic shock index score and mortality at 90 days and performed similarly to more advanced measures of morbidity and mortality in septic shock including lactate levels and SOFA scores.
Background
Early recognition and resuscitation of patients in septic shock are critical skills for an emergency medicine physician. Many clinical decision-making tools have been developed and validated in their use to identify and define those who are in sepsis or septic shock, as well as predict a patient’s overall risk of morbidity and mortality, including tools like the SIRS criteria and SOFA score. However, in many cases, such tools require the combination of objective clinical and laboratory findings. In the setting of septic shock, hypotension is correlated with vasodilation that leads to altered blood flow (1). The pathologic vasodilation observed in sepsis is thought to result from failure of the vascular smooth muscle to constrict appropriately, leading to hypotension as well as tissue hypoperfusion (2). The diastolic blood pressure is determined by vascular tone, and thus it can be assumed that a decrease in the diastolic blood pressure should correlate with the pathologic vasodilation in septic shock. As a result, the authors of this study hypothesized that the relationship between heart rate and the diastolic blood pressure (i.e. the diastolic shock index) could provide providers a tool to quickly identify patients that are at risk for unfavorable outcomes.
Methods
This was a retrospective cohort study utilizing two separate patient cohorts. The first, considered the “primary cohort”, included 337 patients with septic shock requiring vasopressor support in a single ICU from a hospital in Columbia, South America. The second cohort included 424 patients with septic shock included in the recent randomized control trial, the ANDROMEDA-SHOCK trial (3). This cohort included patients from 28 hospitals in 5 different South American countries. Patients in the primary cohort were identified using the Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012 (4) while those included in the ANDROMEDA-SHOCK trial were identified using The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis 3.0) (5). Patients were excluded under the following criteria: patients <18 years old, pregnant patients, patients with liver failure (prothrombin time >15 seconds or INR > 1.5 and hepatic encephalopathy), advanced liver cirrhosis, atrial fibrillation, presence of ventricular dysrhythmia, use of pacemaker, and those with do-not-resuscitate orders.
The variable of interest was the diastolic shock index (DSI), calculated as the ratio between HR:Diastolic blood pressure. In the primary cohort, the DSI was calculated prior to the initiation of vasopressor therapy whereas the DSI was calculated at the randomization point for those in the ANDROMEDA-SHOCK cohort. In both populations, DSI was again calculated at the 2-hour, 4-hour, and 8-hour post vasopressor initiation. DSI levels were then distributed into 5 different quintiles. Researchers conducted a variety of different statistical analyses to calculate the relative risk of mortality associated with a given DSI quintile, as well as broke the DSI calculation into its components and studied the relationship of DSI, HR, and DAP with death at 90 days.
Results/Conclusion
A total of 761 patients were included in the analysis. The general characteristics between the two cohorts were comparable. Researchers found that increases in DSI were associated with increased risk of mortality 90 days in both study groups. When new partitions were performed using the components of DSI separately (diastolic blood pressure and heart rate), researchers found that there was a decrease in the relative risk of mortality as long as the HR decreased and/or the diastolic blood pressure increased or stayed the same (i.e., decreased DSI values). When compared to other measures of mortality in sepsis including lactate, SOFA, and APACHE II scores, DSI performance did not differ significantly. However, mean arterial pressure, isolated diastolic blood pressure, and the systolic shock index were found to be poor predictors of mortality. Researchers conducted a logistic regression model / Chi-Square test to evaluate early vasopressor initiation on 90-day mortality and found that early initiation of vasopressors was associated with more favorable outcomes in those with high DSI values.
Limitations
Though an interesting study, there are a variety of limitations that exist that may have contributed bias into the study. First, this study has a retrospective design. Though researchers attempted to control for a variety of variables, including volume of resuscitation prior to vasopressor initiation, volume of resuscitation from vasopressor initiation to 8 hours, initial arterial lactate, and a variety of additional variables, the retrospective nature of the study subjects it to bias. Additionally, this study lacks external validity and generalizability, as it took place on a single continent in a select few hospital settings. Similarly, the exclusion criteria are relatively strict, for example, researchers exclude patients with acute or chronic atrial fibrillation, an arrhythmia common in those who are acutely and critically ill. However, one may expect this to bias their results towards the mean, and by excluding these patients they may have lacked increased statistical power. Breaking up their DSI values into quintiles further suggests a lack of inherent statistical power in the study, and a study with a larger sample size is important in research moving forward. Last but not least, blood pressure measurements were obtained using noninvasive means, which may have led to inappropriate / inaccurate diastolic blood pressure measurements.
Takeaway
Further research on this topic should be considered in order to offer truly practice-changing evidence. However, the question asked by the researchers is one that has the potential to have a major clinical impact. The diastolic shock index is something that can be calculated less than 30 seconds after the patient enters the resuscitation bay. As such, it does not rely on various laboratory values in order to create a clinically beneficial prediction tool. If one’s index of suspicion is high enough for septic shock, and the patient has an elevated DSI, it may cause the provider to pause for a moment and consider aggressive resuscitation and possibly early vasopressor use. However, as was mentioned above, this study merely suggests a correlation between elevated DSI values and mortality, but it does not provide a practical cut off that can be universally applied to patients presenting with septic shock. This study should prompt the reader to think critically about the clinical and physiologic plausibility of the DSI and its utility in sepsis management. However, further research must be done to validate its clinical use.
References
Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-34.
Siegel JH, Greenspan M, Del Guercio LR. Abnormal vascular tone, defective oxygen transport and myocardial failure in human septic shock. Ann Surg. 1967;165(4):504-17.
Hernández, Glenn, Gustavo A. Ospina-Tascón, Lucas Petri Damiani, Elisa Estenssoro, Arnaldo Dubin, Javier Hurtado, Gilberto Friedman et al. "Effect of a resuscitation strategy targeting peripheral perfusion status vs serum lactate levels on 28-day mortality among patients with septic shock: the ANDROMEDA-SHOCK randomized clinical trial." Jama 321, no. 7 (2019): 654-664.
Dellinger, R. Phillip, Mitchell M. Levy, Andrew Rhodes, Djillali Annane, Herwig Gerlach, Steven M. Opal, Jonathan E. Sevransky et al. "Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012." Intensive care medicine 39 (2013): 165-228.
Singer, Mervyn, Clifford S. Deutschman, Christopher Warren Seymour, Manu Shankar-Hari, Djillali Annane, Michael Bauer, Rinaldo Bellomo et al. "The third international consensus definitions for sepsis and septic shock (Sepsis-3)." Jama 315, no. 8 (2016): 801-810
Authorship
Written by: Josh Ferreri, MD, PGY-3 University of Cincinnati Department of Emergency Medicine
Peer Review and Editing: Jeffery Hill, MD MEd
Cite As
Ferreri, J. Hill, J. (March 30, 2023). Diastolic Shock Index: A clinically relevant predictor of poor outcome in septic shock? TamingtheSRU. https://www.tamingthesru.com/blog/2023/3/30/diastolic-shock-index-a-clinically-relevant-predictor-of-poor-outcome-in-septic-shock
Grand Rounds Recap 3.8.23
We are back with a special grand rounds with visiting professor Dr. Arun Nagdev discussing a variety of ultrasound guided nerve blocks in the ED, CPC with Drs. Harward and Roche, and a review of multiple etiologies and management of pediatric seizure with our CCHMC PEM colleagues.
Ultrasound guided nerve blocks in the ed WITH Dr. Arun Nagdev
Visit http://highlandultrasound.com/ for in depth discussion of each block with accompanying ultrasound and anatomy images
Best practices for pain management in the ED
Active
Non-siloed
Should be available 24/7
Multimodal
Blocks, ketamine, NSAIDs, APAP
Goal is not 100% resolution with blocks, 50% is success with multi-modal treatment
Ketamine assisted blocks: 25mg ketamine in 100cc piggyback infused during block placement
Equipment
Blunt tip needles are best, lower risk of trauma to neurovascular structures
25g needle for local skin wheal
Inject saline first to dissect the tissue planes
Goal: All blocks are fascial plane blocks; do not need to surround the nerve
Bathe the nerve by filling the fascial plane
Do not inject within the epineurium
Complications
Peripheral nerve injuries
1-3 per 100,000
Mechanical trauma
Anesthetic toxicity
Microvascular ischemia
Instruct patients to call if still numb 24 hours after block
Intravascular injection
CNS and cardiovascular toxicity
Treat with intralipid infusion
Anesthetic Selection and duration of action
3% 2-Chloroprocaine (40-60 min)
1.5% mepivacaine (1-3 h)
1% lidocaine +/- epi (2-3h)
0.25% bupivacaine (2-3 h)
0.25-0.5% ropivacaine (4-10 h)
Always use calculator to determine maximum safe dose
Brachial Plexus Block
Interscalene and Supraclavicular
Indications:
Shoulder dislocation, humeral injury/abscess, elbow injury, forearm injury, distal radius, hand injuries
Above elbow = interscalene
Below elbow = supraclavicular
Anatomy
Lateral neck, at the level of the thyroid, between anterior and middle scalene muscles is the brachial plexus
C5-C8
Goal is to deposit anesthetic under prevertebral fascia
Slide distally, above first rib is the brachial plexus sheath where supraclavicular block is performed
Goal is to pop under pre-vertebral fascia
Setup:
Probe parallel to the clavicle to find supraclavicular brachial plexus, slide proximal up the neck to identify scalene muscles
Have patient look to contralateral side
Place a shoulder roll under shoulder to prevent needle from hitting the bed
Complications
With large volume of instillation, risk of phrenic nerve paralysis (max 10cc’s)
Do not perform with people at risk of respiratory depression (e.g. COPD patients)
Use color doppler to evaluate path of needle to make sure there are no vascular structures in the way
Superior Trunk Block
Regional anesthesia for analgesia of the shoulder
C5/C6 roots
Lower risk of hemidiaphragmatic paresis
Fascial plane is closer to the nerve sheath
More challenging block compared to interscalene/supraclavicular
Forearm Block
Supplies
Use short blunt tipped spinal needle
Control syringe (do not need a lot of volume, ~5-10ccs)
ED Indication
Hand wound debridement/laceration repair
Hand abscesses
Metacarpal fractures
Setup
Place machine across the bed/table from patient
Median Nerve
Mid-forearm, midline on volar forearm, surrounded by three fascial planes
Radial Nerve
Volar mid-forearm, radial to the radial artery, often difficult to visualize before hydrodissection
Ulnar nerve
Volar mid-forearm, ulnar to the ulnar artery, nerve will run with the artery but separates as you scan more proximally; Target the more proximal portion where the artery dives deeper into the arm and separates from the nerve.
Serratus Anterior Plane Block
ED Indications:
Anterior and lateral rib fractures
Stable chest tubes
Chest wall burns
Zoster
Anatomy:
Intercostal nerve branches between latissimus dorsi and pectoralis muscle and lies on top of the serratus anterior muscle
Setup:
Midaxillary line at level of the nipple, place probe in transverse orientation along ribs
Can inject anesthetic above the serratus anterior muscle, or deep to the serratus anterior muscle above the rib
Rib space does not matter, breathing will diffuse anesthetic along fascial plane
Takes ~30-45 minutes to take effect
Requires large volume of anesthetic (30ccs, inject slowly in 5cc aliquots every 30 seconds)
Distal Sciatic Nerve in the Popliteal Fossa
ED Indications
Ankle fractures
Achilles tear
Abscess drainage
Burns and amputations
Lower extremity wounds/lacerations
Anatomy:
Lower extremity except saphenous nerve
Posterior lower leg and foot except medial lower leg (saphenous)
Setup:
Place patient prone
Posterior midline leg proximal to popliteal fossa
Aim for the split of the distal sciatic into the common peroneal nerve and tibial nerve
10-20 cc's of anesthetic
If unable to lie prone, can elevate leg and place probe underneath leg
Do not block mid shaft tibial fractures due to risk of compartment syndrome
Novel approach: Crosswise approach to Popliteal Sciatic (CAPS)
Patient can lay supine, use curvilinear probe on the lateral leg, and needle inserts in the lateral leg
Transgluteal Sciatic Nerve Block (TGSNB)
ED indication
Sciatica
Anatomy
Nerve lies in the fascial plane below gluteus maximus
Find sciatic nerve in between ischial tuberosity (medial) and greater trochanter (lateral)
Place anesthetic in the fascial plane underneath the gluteus maximus
Setup:
Curvilinear probe
Needle comes from lateral to medial approach (inserts over greater trochanter)
10cc anesthetic
Steeper needle angle
Steeper angle may portend more difficult needle visualization
10% will get foot drop and foot numbness- expect this if performing this block
If it persists for >24 hours, return to ED
CPC: CO Toxicity WITH Drs. Harward and Roche
Carbon Monoxide Toxicity
Incidence
50,000 cases per year
Pathophysiology
Decreased O2 delivery by Hgb
250x greater affinity than O2
Stabilizes the high affinity conformation
Binds cytochrome C oxidase, inhibiting ATP production within the electron transport chain
Platelets and inflammation
Displaces NO from platelets
Triggers neutrophil degranulation
Neurologic and cardiac injury
Neurotoxicity
Reactive oxygen species
Hypoxia
Acidosis
Presentation
Neurologic: Dizziness, headache, confusion → somnolence, seizures
Cardiopulmonary: Dyspnea, cough, chest pain → syncope, MI, arrhythmias
Diagnosis:
CO Measurement
CO Hgb > 2% in nonsmokers, > 10% in smokers
Clinical severity does not correlate with level
Standard pulse oximetry is not helpful
CO-oximetry is specific but not sensitive
Hydroxycobalamin interferes with COHgb measurement
EKG to evaluate for ischemia
Lactate
Cardiac biomarkers
Treatment
Increased FiO2
Increased PEEP = CPAP, BiPAP
ETT if cannot participate
Hyperbaric oxygen therapy (HBOT)
Indications for HBOT = 13-15% for pregnant patients, 20-25% for nonpregnant patients
Pediatric simulation: Seizure WITH CCHMC PEM Faculty and fellows
Pediatric seizure
Benzodiazepine dosing:
Ativan: 0.1 mg/kg IV
Versed: 0.2 mg/kg IM, 0.2 mg/kg IN (may repeat to max of 0.4 mg/kg IN), 0.2 to 0.5 mg/kg buccal
Febrile Seizure
6 mo to 6 years
Simple:
Generalized tonic clonic seizure
< 15 minutes
1 per 24 hours
Complex:
> 15 minutes
More than 1 in 24 hours
Partial/focal seizure
Status
Seizure greater than 30 minutes
No return to baseline between seizures
If age < 2, likelihood of repeat febrile seizure is 30%, if greater than 2, likelihood is 50%
If child is < 6 mo, workup alternative causes:
NAT (consider CTH)
CNS infection (consider LP)
Infantile Spasms
Patients under 6 months will not have generalized tonic clonic seizures due to the absence of myelin
Usually 3-7 months, 90% present under 1 year
Portends very poor future neurologic outcome
Make sure to ask about prenatal history, birth history
Make sure to ask about regression of milestones
Ddx:
Benign myoclonus = 3-8 months of life
Benign sleep myoclonus = occurs during onset of sleep
Clinical Presentation
Usually involve neck, trunk and extremities
Last seconds at a time (initial contraction ~2 seconds followed by a tonic phase of 8-10s)
May look like crunches
Disposition
If infantile spasms is suspected, should be admitted to pediatric hospital for spell capture
Hypsarrhythmia on EEG
MRI
Treatment
ACTH
Vigabatrin
Blindness is a known side effect
Hyponatremic Seizures
Acute symptomatic hyponatremia (altered mental status, seizures) should be treated with 3% hypertonic saline 1 cc/kg
May repeat if seizures continue
Diagnostics: The Shunt Series
Ever palpate the scalp of an altered patient to find a VP shunt you weren’t expecting? Have a febrile patient and wondering if it could be the cause? Join Dr. Cody Stothers as he dives into a case-based review of Hydrocephalus and VP Shunts
Introduction
Hydrocephalus is an accumulation of cerebrospinal fluid (CSF) in the cerebral ventricular system secondary to a mismatch between CSF production and resorption. Excessive production of CSF is rare and occurs with choroid plexus papillomas or other tumors. Impaired drainage or resorption of CSF is a far more common cause of hydrocephalus and can occur due to congenital malformations, tumors, trauma, or infection. Rapid development of hydrocephalus in the acute setting presents with signs and symptoms of increased intracranial pressure and represents a surgical emergency because of the risk of herniation syndromes.
Treatment
If a patient is herniating in front of your eyes – hypertensive, bradycardic, altered, and not protecting their airway – secure the ABCs, provide hypertonic fluids (3% normal saline, mannitol), hyperventilate the patient, elevate the head of the bed and call neurosurgery. Definitive management in these, and less acute cases, is often the placement of a ventriculoperitoneal (VP) shunt.
More on this below as we work through a few cases….
Case 1
-
A 1-month-old (ex-34 week premature) infant comes to your emergency department for fussiness. He appears well and is triaged to an ESI 4. After waiting for several hours, the family arrives in an examination room and the child appears stuporous. He has a weak cry and you notice bulging fontanelles. After a several week NICU stay for prematurity, the infant has been generally healthy and this is his first trip back to the hospital since discharge. The symptoms started yesterday evening and have been getting worse. A broad infectious and metabolic workup is negative and you decide to obtain cross-sectional head imaging as part of your altered mental status workup. As you scroll through the images, you notice the lateral ventricles appear significantly enlarged.
As you await the formal read, you see an 80-year-old woman with urinary incontinence and confusion. She was brought in from her nursing home and is reported to “always act like this when she has a UTI.” Similarly, your infectious workup is negative and you note that all prior urine cultures failed to grow bacteria when she was treated for UTIs 4 times over the last 6 months. Collateral information from the family indicates that she has been progressively more forgetful, disinhibited, and combative. She is now near totally incontinent and wears a diaper 24 hours a day. You decide to obtain cross-sectional head imaging as part of your altered mental status workup. As you scroll the images, you again notice the lateral ventricles appear significantly enlarged…
What is going on? Who do we need to call?
-
Hydrocephalus (congenital vs. idiopathic). Consult neurosurgery!
In the first case, congenital hydrocephalus accounts for approximately 20% of all cases. Prematurity is a risk factor and the exact pathophysiology is poorly understood. Young infants will present with failure to thrive, poor weight gain, and increasingly worsening altered mental status as ICP continues to increase beyond critical values.
In the second case, adults (especially the elderly) are at risk for hydrocephalus that develops insidiously. Because the compensatory mechanisms that regulate ICP are able to calibrate for slowly enlarging ventricles, these patients will often have normal ICP and are therefore termed as having normal pressure hydrocephalus. The presentation is highly variable, but the classic triad of “wet, wild, and wobbly” (urinary incontinence, altered mental status, and gait instability) is rare. Diagnosis is made via CT scan and/or lumbar puncture.
A treatment option for both of these cases is placement of a VP shunt. The idea is over half a century old. Modern VP shunts have a programmable ball-ring valve that allows flow of CSF out of the ventricular system when intraventricular pressure exceeds a preset value. The drainage catheter is tunneled under the skin and terminates in the peritoneal cavity.
Case courtesy of Paul Simkin, Radiopaedia.org, rID: 30453
Case 2
-
A 19-year-old male is brought into your emergency department via EMS for witnessed seizure-like activity. The seizure abated with rectal diazepam given by the squad. The patient arrives hemodynamically stable and post-ictal, unable to answer any questions. On exam, you palpate a tube-like structure in the patient’s neck. His abdomen is soft. He is responsive to pain, but is not spontaneously moving his extremities. You notice a med-alert bracelet with the patient’s name and the word “SEIZURES.” You read about the patient’s history of VP shunt placement for aqueductal stenosis as a child and decide to order some imaging…
-
Obtain shunt imaging (“shunt series,” CTH non-con)
Shunt series shows no migration of the shunt catheters or fractures of the tubing. CTH demonstrates acute hydrocephalus despite the presence of a VP shunt.
Given the break-through seizures, hydrocephalus on CT, and benign abdomen, you are concerned for a proximal shunt occlusion. This occurs when brain parenchyma, clotted blood, inflammatory cells or cellular debris occludes the drainage catheter from the ventricular system. Shunt failures are quite common with the average patient requiring 2-3 shunt revisions over their first 20 years with the shunt. Amongst shunt mechanical failures, proximal occlusion is the most common cause.
Management of these patients in the emergency department is largely supportive. Shunt malfunction may cause seizures, nausea/vomiting, altered mental status, and headache which should all be treated symptomatically. Unfortunately, maneuvers to relieve a proximal occlusion in the emergency department are limited. Lumbar puncture is an option with limited data for success. Ultimately, definitive management is in the operating room with revision or replacement of the VP shunt.
Case 3
-
A 6-year-old boy is brought to the emergency department for a fever. His father states it has been as high as 104F at home, taken orally. It developed over the last couple of days and today the boy has been “loopy.” The father relates that the boy has spina bifida, and three weeks ago, he had a VP shunt placed after he suddenly regressed in physical therapy and was found to have hydrocephalus. At his first follow-up visit, he had regained his lower extremity motor function and had no complications from the surgery other than some minor pain.
You examine the boy and note a somnolent, but arousable, child in no acute distress. He has tactile warmth. He moans in pain when you flex his neck and you note an upgoing Babinski reflex. The rest of his exam is unremarkable. What are you most concerned for?
-
Acute shunt infection
Acute shunt infection is a rare complication that occurs nearly exclusively in the immediate (weeks-months) post-implantation period. The advent of antibiotic-impregnated shunts and refined placement technique have decreased the incident of shunt infections. However, a high index of suspicion must be maintained as children may present with range of symptoms from generalized malaise and fever to acute reaccumulating CSF and increased ICP to frank meningitis.
Broad infectious workup should be initiated. A normal leukocyte count on CBC does not exclude a shunt infection, which may be localized. Other sources of infection should be excluded with chest x-ray, urinalysis and a thorough skin exam. Blood cultures should be obtained and broad-spectrum antibiotics/antivirals initiated. Most shunt infections are from skin flora such as Staphylococcus epidermis, S. aureus, and gram-negative rods. Consultation with neurosurgery is essential as these patients need source control in addition to standard antimicrobial therapy for meningitis or encephalitis.
Case 4
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You are working as solo coverage in a critical access hospital. After one-too-many people says “it sure is quiet tonight,” a mother comes rushing in with her 3-year-old child who appears to be minimally responsive and erratically breathing. After getting the patient on the monitor, you see her vital signs to be HR 75 bpm, BP 145/98 mmHg, RR 12, O2sat 84% on room air. She is arousable to painful stimuli only. After securing your ABCs, you get more history from the mother.
The child was born with a Chiari II malformation and required a VP shunt placement at 8 months of life. The shunt matured with minimal complications. Her mom takes her to see a neurosurgeon in clinic every 6 months for a check in and remarks “the closest option we had was 2 hours away.” She was doing well, but recently has had the “stomach flu” with a couple weeks of abdominal pain, nausea and vomiting.
You arrange interfacility transport and provide temporizing measures for what you suspect is an acute increase in ICP. Unfortunately, your helicopter is still 45 minutes away and the clinical picture is worsening. What can you do?
-
Tap the shunt
This patient has likely developed an abdominal pseudocyst, which is a rare complication of peritoneal catheter placement. In the case of a distal shunt occlusion in the abdomen, tapping the shunt in the emergency department can be a life-saving maneuver. However, there are significant risks associated with the procedure and it should be reserved for cases with limited options or time, and under consultation of a neurosurgeon. Little data exists on the ideal emergent approach, but general concepts can be applied:
· Palpate the shunt reservoir, which will be cephalad/proximal either in cranium or neck
· Select an appropriate needle length for size of the child (reservoir will likely be just under the skin) with 22-25 gauge and, if possible, a three-way stopcock
· Proceed only in a sterile fashion (as we saw above, shunt infections are very real and deadly)
· Using analgesia and sedation as appropriate, access the reservoir with your needle tip and aspirate CSF, titrating to symptom management
· Collect CSF for laboratory evaluation if possible
In this case, you perform heroic measures and drain 40mL of CSF and the patient begins to stabilize. The secure the drain and close the three-way stopcock. Instructions on how to drain additional CSF are provided to the intrepid flight team when they arrive and the patient is whisked away to a tertiary care center with pediatric neurosurgery.
Post by Cody Stothers, MD PhD
Dr. Stothers is a PGY-1 in Emergency Medicine at the University of Cincinnati
Peer Editing by Carl Goff, MD and Ryan LaFollette, MD
Dr. Goff is a PGY-4 at the University of Cincinnati and Dr. LaFollette is an Associate Professor and Co-editor of TamingtheSRU
References
Andersson et al. Prevalence of idiopathic normal pressure hydrocephalus: A prospective, population-based study. PLos One. 2019.
Bothwell, Janigro, Patabendige. Cerebrospinal fluid dynamics and intracranial pressure elevation in neurological disease. Fluids and Barriers of the CNS. 2019.
Crossman. Neuroanatomy. 6th ed., 2020.
Griffiths. VP SHUNTS. Don’t Forget the Bubbles. 2020.
Kazui H, Miyajima M, Mori E, Ishikawa M: SINPHONI-2 Investigators: Lumboperitoneal shunt surgery for idiopathic normal pressure hydrocephalus (SINPHONI-2): an open-label randomized trial. Lancet Neurol. 2015.
Marmarou, Young, Aygok. Estimated incidence of normal pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities. Neurosurg Focus. 2007.
Marmarou et al. Diagnosis and management of idiopathic normal-pressure hydrocephalus: a prospective study in 151 patients. J Neurosurg. 2005.
Nakajima et al. Guidelines for Management of Idiopathic Normal Pressure Hydrocephalus (Third Edition): Edited by the Japanese Society of Normal Pressure Hydrocephalus. Neurol Med Chir (Tokyo). 2021.
Pitetti. Emergency department evaluation of ventricular shunt malfunction: is the shunt series really necessary? Pediatr Emerg Care. 2007.
Rosenberg. Brain Edema and Disorders of Cerebrospinal Fluid Circulation. Bradley and Daroff’s Neurology in Clinical Practice. 88, 1327-1344.e2.
Sasaki et al. Narrow CSF space at high convexity and high midline areas in idiopathic normal pressure hydrocephalus detected by axial and coronal MRI. Neuroradiology. (2008)
Shprecher, Schwalb, Kurlan. Normal Pressure Hydrocephalus: Diagnosis and Treatment. Curr Neurol Neurosci Rep. 2008.
Wallace et al. Imaging Evaluation of CSF Shunts. Amer J Rad. 2012.
Zhou and Xia. Application of Evans Index in Normal Pressure Hydrocephalus Patients: A Mini Review. Front. Aging Neurosci. 2022.
Grand Rounds Recap 2.15.23
Check out this week’s MASSIVE recap with Dr. Connelly’s poignant lessons from her time with Sydney HEMS, Dr. Broadstock’s R4 case follow up of HIV myositis, Dr. De Castro’s extensive Vitamin deficient review, Small Groups on task saturation and ITE review and a Palliative Medicine lecture by dual trained Dr. Kiser.
EMS Grand Rounds WITH Dr. ConnelLy
What I learned in my time with Sydney HEMS
The area of NSW is nearly twice the size of Ohio
Staffing model
Rotor wing
Fixed wing
Clinical Capabilitis
Limb Escaratomies
Peripheral nerve blocks
FIberoptic intubations
Craniotomies
Clamshell thoracotomy
On-Boarding
All staff go through a 2 week onboarding training induction
2 months before hand there are hours of videos, SOPs
High fidelity simulations to reinforce learning done before arrival
Learning
Lesson 1
Assess and optimize yourself, your team, your environment, and your patient.
This is the Zero Point Survey - referring to the zero point or time zero on the mission clock.
Often we think of patient care as starting with a primary survey.
The idea with the zero point survey is that you do it *before* your primary survey and it provides a framework for consciously optimizing the non-clinical or non-technical aspects of a mission.
STEP-UP
Self
Physical and Psycological
IM-SAFE
Illness
Medications
Stress
Alcohol
Fatigue
Eating
Psychological
Cognitive Threat/Challenge appraisal: PERCEIVED demands vs. resources
Threat appraisal - stress levels excessive, performance impaired – vapor lock (autonomic arousal, tunnel vision, auditory exclusion, loss of time awareness, impaired memory recall and decision making)
Challenge appraisal - stress levels optimally matched to task, performance enhanced – flow state
External locus of control vs. internal locus of control
Tools
Beat the Stress Fool
Breathe - tactical “box” breathing, control your physiology
Talk - positive self talk - reframing a situation to focus on a positive outcome
See - visualize the procedure or resuscitation
Focus - code phrase or ritual to center yourself e.g. basketball free throw (“Cutting skin” before a cric, “This is what we train for” “I am the best possible person to care for this patient.”)
Team
Environment
Own the Resuscitative Real Estate
Set up how you want the resuscitation to go
Organize your space in the way that will wrok best for you and the patient
Patient
Special circumstances
Peds
Pregnant
Mechanical circulatory support
Update
Partner
Priorities
Clear and well defined
Lesson 2
Lead with kindness
Being liked is a powerful tool of persuasion
We also want prehospital teams or other hospitals to call us back for the next patient
Tricks
Be nice
Ask pointed questions that lead to the answers you want
Embed Presuppositions
Example
Do you want your team or my team to set up for intubation
This does not ask if the patient should be intubated but instead assumes this as fact
Ask for help
Use the group
Push a different button is not getting the results you would like
Be Authoritative
CUSS framework
Concerned
Uncomfertable
Safety issue
Stop
Lesson 3
Actively direct mission workflow. Perform an early primary assessment, prioritize meaningful interventions, and build momentum to destination.
Lesson 4
Leadership and individual priorities (i.e. task focus vs. situational awareness) are fluid. Communication is essential.
Gazelle - constant state of hyper vigilance and broad situational awareness (every sound = omg it’s a lion!)
Cheetah - hyperfocused on goal - catch lunch! - but might miss things like the poacher taking aim
In our world
Pilot eyes in - eyes out
Our pilots provide a great example of this
During normal ops, they’re looking out, scanning the horizon, watching for obstacles, and maintaining broad situational awareness
Sometimes, they need to enter coordinates into the GPS or look at something on their iPad or whatever – they switch to task focus
pilot and the nurse sitting up front switch from Situational Awarness to task focus, they clearly announce it, “My eyes are in.” the nurse will answer something like, “I’m eyes out.”
there’s closed loop communication around the pilot’s shift in attention to ensure someone up front is maintaining situational awareness so that we don’t fly into a cell tower, or a bird, or another helicopter.
using a “standard lexicon,” meaning there’s an agreed-upon and mutually-understood set of terms they’re using to communicate.
Sydney makes this explicit “Eyes on / Eyes off patient” - closed loop communication
Lesson 5
Choose deliberate pause points and share your mental model with your team.
A pause to assess in the beginning
A pause before leaving to check everything is stable, accounted for, and plan going forward is agreed upon
Lesson 6
Everyone brings different skill sets to a call. Make smart and deliberate choices when delegating tasks.
Lesson 7
Add value by prioritizing meaningful interventions – those that are time-critical, preserve life/limb/sight, or impact clinical course.
Prioritize tasks that are time critical
Do the diagnostics or procedures that ensure the patient resieves the most timely care possible
Lesson 8
Cognitively offload in stressful situations. The importance of checklist use increases with the urgency of airway intervention.
There’s a temptation to skip the checklist when there’s an urgent need to act – but using the checklist is actually MORE important when you’re under high cognitive load.
Lesson 9
Decide to do the high-stress procedures now so you won’t hesitate in the moment.
Have the confidence and belief in yourself to do the right thing for your patient, and to do it in a meaningful timeframe and without hesitation.
Make the commitment now – know how to do the procedures (mentally rehearse them) and know what your line in the sand is, then COMMIT.
Lesson 10
Details matter and marginal gains accumulate.
doing the little things right, with the understanding that small gains are additive, and that details can be the difference between a good outcome and a poor one.
Lesson 11
Find what you love to do and surround yourself with people who make you better at doing it.
R4 Case Follow up WITH Dr. Broadstock
Case
Young male patient presenting with weakness for 2 weeks. Intermittent fevers, chills and body aches
Chest pain, shortness of breath and some hemoptysis
Found to have a significant AKI, Hyperkalemia, Leukocytosis, elevated Transaminases, low retic count, urinalsyis with 69 WBCs
Postive HIV test
CK 9000
Interventions
HyperK treated, Antibiotics and imaging
Imaging showed Pneumomediastinum
Postive HIV Testing
HIV RNA Day 10-33
P24 Antigen +7 Days
HIV 1 or 2 Antibodies +12 days
We test for P24 and antibodies for HIV 1 or 2
This patient had an active acute HIV infection without seroconversion
Diagnosis
HIV myositis
HD for his acute rhabdomyolysis
Anemia leading to transfusions
Discharged to IPR
Acute HIV Infection
Acute, self-limited viral infection, including fever, fatigue, sore throat, pharyngitis, lymphadenopathy, muscle aches, diarrhea, and a rash (often maculopapular). They can occur within a few days of exposure or up to 6 weeks after, and usually last about 14 days. Can cause transient drop in CD4 count (like in our patient) which can lead to opportunistic infection. No antibodies have been produced, so viral loads are usually very high and patients transmit the infection disproportionately at this stage.
HIV Myositis
Multiple forms of myositis can occur with HIV infection. Polymyositis, infectious pyomyositis (usually GAS, can be salmonella or sometimes toxoplasma), inclusion body myositis have all been described. Polymyositis is not typically associated with significant immunosuppression and might occur at any stage during the course of the disease. Typically, polymyositis presents with a subacute, progressive, proximal muscle weakness associated with an elevated creatine kinase level. The cause remains unknown. Some nucleoside reverse transcriptase inhibitors, notably azidothymidine, are known to cause myositis as a side effect.
HIV related renal disease
HIV Associated Nephropathy (HIVAN)
Form of FSGS
Renal recovery can occur with ART
Can occur prior to HIV seroconversion
HIV Immune Complex Kidney Disease
Less common than HIVAN
Develops later in disease course
Better prognosis
Dermatologic Manigfestations of HIV
HIV Associated
Facial molluscum in an adult
Proximal subungual onychomycosis
Herpes zoster scarring
Oral hairy leukoplakia
Bacillary angiomatosis
Widespread dermatophytosis
Severe seborrheic dermatitis
AIDS defining
Chronic herpes simplex virus ulcers
Extrapulmonary tuberculosis
Kaposi sarcoma
Extrapulmonary cryptococcosis
Disseminated mycosis
Atypical disseminated leishmaniasis
Disseminated non-TB mycobacterial infection
R1 Clinical Knowledge: Vitamin Deficiencies WITH Dr. de Castro
Vitamin Deficiency
Water Soluble
Exctred in the urine, common to have deficiencies, less common toxicity
Fat Soluble
Stored in fat or liver, uncommon to have deficiencies, more common to have toxicities and can have deficiencies if there is fat malabsorption
Conditions that can lead to malabsorption
Infections
HIV
Parasites
Tropical sprue
Whipples disease
GI
IBD
Crohn’s
Short Bowel Syndrome
Gastric Bypass
Chronic Diarrhea
Biliary Obstruction
Systemic
Infiltrative disease like amyloidosis
Cystic fibrosis
Kidney disease
Liver disease
Pernicious anemia
Other
ETOH use
Anorexia
Diet
Vitamin A
Function
Assists in corneal and conjunctival development
Helps with the processing of light perception
Deficiency:
Night blindness (nyctalopia)
Dry, scaly skin
Xerophthalmia - spectrum of eye disease characterized by pathologic dryness of conjunctiva and cornea manifested by Bitot spots (keratin debris)
Corneal degeneration and erosion (keratomalacia) → scarring and blindness
Sources - eggs, sweet potato, green leafy vegetables, yellow/orange veggies with carotene like carrots, tomatoes, cantaloupes, bell peppers
Rarely seen in the US or resource-rich countries
Prevalence of vitamin A deficiency is approximately 30% among children under age 5 worldwide and nearly 50% in young children in South Asia and sub-Saharan Africa
World’s leading preventable cause of childhood blindness
Vitamin D
Function
Calcium homeostasis
By promoting calcium absorption, bone resorption, and maintaining calcium and phosphate levels
Important in bone remodeling
Deficiency
Can be seen in people who have inadequate exposure to sunlight
Rickets in children cause growth impairment and long bone deformities
Osteomalacia in children and adults, which is a bone-thinning disorder
Osteoporosis, Bone pain and tenderness, muscle weakness, fracture, and difficulty walking
Symptoms of hypocalcemia include Muscle aches, weakness, and twitching
Mood disorders and depression
Sources
Very few foods naturally contain Vitamin D, major source is through synthesis in the skin that is dependent upon sun exposure
Can also be found in fortified foods such as cereals and supplemented in milk
Vitamin E
Function
Protects RBCs and membranes from free radical damage
Plays a role in gene expression as well as activities of multiple enzymes
Deficiency
Very rare
Hemolytic anemia from oxidative damage
Neuromuscular disorders causing neuropathy and myopathies
Sources
Cooking oils, especially olive and sunflower
Nuts and seeds like almonds, sunflower seeds, pine nuts
Vitamin K
Function
Necessary for clotting factors II, VII, IX, X, and proteins C and S
Deficiency
Increased bleeding risk causing bruising, petechiae, hematomas, melena, hematuria
Labs show increased PT and INR, PTT is normal or only mildly prolonged
Overall rare, with the exception of newborns who receive a Vitamin K injection to prevent life threatening hemorrhage
Sources
Green vegetables like spinach, broccoli, and green leafy vegetables
Meats, cheeses, and eggs
Produced by gut bacteria
B1 Thiamine
Function
Involved in TCA and pentose phosphate pathway
Cofactor for enzymes involved in metabolism of carbohydrates and amino acids
Important role in synthesis of GABA and glutamate, as well as myelin sheath maintenance
Beriberi
Infantile - fulminant cardiac syndrome with cardiomegaly, tachycardia, cyanosis, pulmonary HTN; older infants may have neurological symptoms resembling aseptic meningitis (agitation, altered consciousness, seizure)
Dry - symmetrical peripheral neuropathy with sensory and motor impairments, mostly of distal extremities
Wet - cardiac involvement with cardiomegaly, cardiomyopathy, heart failure
Wernicke-Korsakoff
Wernicke - nystagmus, ophthalmoplegia, ataxia, confusion (acute syndrome requiring emergency treatment to prevent death and neurologic morbidity)
Korsakoff - impaired short-term memory, confabulation and confusion (chronic neurologic condition)
Sources - pork, legumes (beans, soybean, chickpeas, peanuts, lentils), enriched cereal or whole grain,
B2 Riboflavin
Function
Essential component of coenzymes involved in cellular metabolic pathways including TCA and beta-oxidation of fatty acids
Redox reactions - FAD
Deficiency
Sore throat, cheilitis (inflammation of lips, causing dryness and cracking), angular stomatitis (sores on corner of mouth), glossitis (inflammation and swelling of tongue)
Seborrheic dermatitis particularly affecting ear, nose, eyelids → red, scaly, greasy
Sources - milk, eggs, meats, green leafy vegetables, fortified cereals
B3 Niacin
Function
Involved in the synthesis and metabolism of carbohydrates, fatty acids, and proteins
Associated with coenzymes NAD and NADP+
Deficiency
Carcinoid syndrome is a paraneoplastic syndrome that occurs secondary to a neuroendocrine tumor
Causes metabolism of tryptophan into serotonin rather than niacin
Hartnup disease - autosomal recessive genetic disorder caused by a defect in a membrane transporter that is responsible for tryptophan absorption as well as other neutral amino acids
Drugs - isoniazid, azathioprine, 5-fluorouracil, 6-mercaptopruine, pyrazinamide
Pellagra - dermatitis, diarrhea, dementia
Dermatitis - symmetric, hyperpigmented photosensitive rash located in sun exposed areas
Diarrhea and vomiting
Dementia - irritability, poor concentration, fatigue, encephalopathy
4 D’s = death
Sources
Meats and fish, nuts/legumes/seeds, fortified foods and cereals
Tryptophan, which is an amino acid, can be converted into niacin in the liver
B5 Pantothenic Acid
Function
Required in order to synthesize coenzyme A, used in TCA
Essential for fatty acid metabolism, as well as proteins and carbohydrates
Deficiency is very rare and has not been studied well, cases of deficiency are mostly from prisoners of war during World War II, victims of starvation, or limited volunteer trials
Impaired energy - irritability, fatigue
Numbness and paresthesias in hands and feet
Animal studies of B5 deficiency showed growth failure, changes in coat color particularly graying, alterations in metabolism, other nervous, GI, and immune system alterations
Sources - eggs, dairy, chicken, beef, potatoes, whole grain
B6 Pyridoxine
Function
Involved in amino acid and lipid metabolism, neurotransmitter synthesis, histamine synthesis, hemoglobin synthesis, steroid hormone modulation
Coenzyme for many reactions including decarboxylation, transamination, elimination
Deficiency
Certain drugs are associated with vitamin B6 insufficiency because they interfere with pyridoxine metabolism, including isoniazid, hydralazine, and levodopa/carbidopa
Seborrheic dermatitis
Atrophic glossitis, cheilosis
Microcytic anemia due to impaired heme synthesis
Neurologic symptoms including somnolence, neuropathy due to impaired myelin synthesis, and seizures
Sources
Meats and fish, veggies, whole grains, nuts
B7 Biotin
Function
Essential cofactor for several carboxylase enzyme complexes which are involved in carbohydrate, amino acid, and lipid metabolism
Involved in protein synthesis and cell replication
Deficiency - rarely occurs because the daily requirement is low, contained in a lot of different foods, and intestinal bacteria synthesize a small amount
Deficiency can occur particularly with egg white consumption due to avidin, a protein that binds biotin
Other risk factors include long term TPN use
Thin, brittle hair → alopecia
Dermatitis, particularly around the eyes, nose, and mouth
Neurological symptoms - changes in mental status, lethargy, hallucinations, and paresthesias
Sources
Egg yolk, organ meats particularly liver, nuts and seeds, meats and fish, yeast
B9 Folate
Function
Essential for the synthesis of DNA, the modification of DNA and RNA, the synthesis of methionine from homocysteine, and various other chemical reactions involved in cellular metabolism
Particularly important for red blood cells
Deficiency
Macrocytic, megaloblastic anemia - large, immature red blood cells
Women with folate deficiency are more likely to give birth to infants with low birth weights, neural tube defects, spina bifida or other brain defects
Vague GI symptoms like diarrhea and anorexia
No neurological symptoms (unlike B12)
Deficiency can be caused by several drugs such as phenytoin, sulfonamides, methotrexate
Sources
Leafy green vegetables
Fortified grain products
Legumes and peanuts
B12 Cobalamin
Function
Cofactor in DNA synthesis
Involved with fatty acid and amino acid metabolism
Involved in myelin synthesis as well as red blood cell formation
Deficiency
Can be caused by
Deficiency in intrinsic factor, which must bind B12 for absorption - pernicious anemia
Decrease in stomach acids which also aid in absorption, therefore can be at risk when taking long term PPI, H2 blockers, or antacids
Megaloblastic, macrocytic anemia
Glossitis (pain, swelling, tenderness, hyperpigmentation)
Non-specific GI symptoms like diarrhea and constipation
Neurological symptoms
Symmetric paresthesias or numbness and gait problems
Subacute combined degeneration - progressive weakness, ataxia, and paresthesias that may progress to spasticity and paraplegia
Non-specific depression, irritability, insomnia, cognitive slowing and dementia
Sources
Meats
Dairy products and eggs
Fortified products like cereals and plant-derived milk substitutes
Strictly in animal products, so diets of vegetarians and vegans may not provide sufficient B12 unless a dietary supplement is consumed
Vitamin C
Function
Involved as a coenzyme in many enzymatic reactions, specifically wound healing and collagen synthesis
Helps with bone, teeth, skin and tendon
Deficiency - scurvy is a disease process that results from vitamin C deficiency
Symptoms are due to unstable collagen and collagen fragility, which can cause leaking of vascular structures
Gingival bleeding, petechiae, easy bruising, hemarthrosis
Coiled and brittle hair with perifollicular hemorrhage
Poor wound healing
Non-specific including weakness, fatigue, muscle cramping, mood disturbances and cognitive impairment
Sources
Citrus fruits
Vegetables like tomatoes, brussel sprouts, cauliflower, broccoli
R3 Small Groups Tox,Tasks,Rashes WITH Dr. Fabiano, Dr. Kein, and Dr. Martella
Task switching
Four responses to an interruption (from cognitive psychology research)
Task-switching: Suspending the primary task to attend to a secondary task
Multitasking: Continuing the primary task while also attending to the secondary task
Acknowledging: Responding to certain prompts with a brief word or gesture
Deferral: Delaying the secondary task until a later time or avoiding the need to deal with it by indicating unavailability, delegating it, or ignoring it entirely
Task Switching vs Multitasking
Task switching is devoting attention sequentially to two tasks that are occurring in parallel.
Multitasking is performing two tasks simultaneously
In studies of emergency physicians, around 70% of responses to an interruption result in a task switch
Multitasking accounts for only 8% of responses to interruption
Multitasking is only truly possible for manual tasks (hand-washing, gathering equipment, etc.) performed in simultaneously with verbal tasks
Costs of Task Switching
Switch cost – a task takes longer to perform than if there was no preceding task switch and the error rate is higher
Mixing cost – completion of the primary task remains slower after a switch than when just one task is performed, even when accounting for the time lost while performing the secondary task
Long-term priming cost – even when performing only one task, responses are slower if another task had just been performed in the previous few minutes
Asteroids and EKGs
Proof of concept one-group pre-test/post-test design done at Ohio State with emergency medicine residents
Comparing resident performance on ECG interpretation with no distractions to their performance on ECG interpretation while playing Asteroids
Attending to the Asteroids game as if it were an important clinical task yielded substantially lower ECG reading scores for everyone, regardless of their Asteroids score or experience with gaming
100% of residents said the game made ECG reading more difficult, most (91.7%) thought task-switching was difficult, and more than half (53%) thought they could improve with practice
Summary
Task switching in the ED is unavoidable and should be considered a core competency of emergency medicine
Task switching has negative consequences for efficiency and increases chance of errors
Deliberate practice may reduce the costs associated with task switching
Palliative Medicine Consultation WITH Dr. Kiser
What is Hospice
A special kind of care that focuses on the quality of life for people (and caregivers) who are experiencing an advanced, life-limiting illness
Life expectancy of 6 months or less
Affirms life, does not seek to hasten or postpone death
Goal to reduce visits to hospital
Hospice care can be provided in several different locations
Levels of Hospice Care
npatient Unit (IPU)
Like an ICU for hospice patients
Acute management of uncontrolled symptoms
Can not stay there indefinitely until death unless they are actively controlling symptoms that cannot be managed in a decreased level of care setting
Home/Long Term Care Facility
Significant burden on family/care providers
Respite Stay
Up to 5 overnights in an IPU or LTC facility
Palliative Medicine Services
HPM teams have time to get to know patients/families and fully explore patient and family goals of care
Multidisciplinary team
MD/DO
APP(s)
Social Worker(s)
Chaplain(s)
Pharmacist*
The Impact
Inpatient - decrease readmissions and cost per day
Outpatient - outpatient decrease admissions and ED visits
Skilled Nursing decreases hospital/ED transfers
Home-based Decrease the total cost of care
P-Cares
Palliative Care and Rapid Emergency Screening Tool
Content validation 2015
Designed to be completable by ED providers using routinely obtained information in an ED encounter to screen for unmet palliative needs
Recognizes that a brief, focused screening tool needed
Should not require additional patient interviews
Recent studies
Palliative Care and Rapid Emergency Screening Tool and the Palliative Performance Scale to Predict Survival of Older Adults Admitted to the Hospital from the Emergency Department. Paske et al. 2021.
Six month survival showed lower survival in those that are P-Cares Positive
Inferred Hazard Ratio increased with those that are Pcares positive
How to Get palliative Care involved
Discuss concerns with patient/family
Consult from the ED
In hospital M-F 0800-1630
Available by phone consultation at other times
ED Contact: Palliative Care
Inpatient Consult to Palliative Care order*
ED social workers/case managers can place hospice referrals for dispo to hospice
Patient being admitted
Suggestion to admitting provider
Offer to place IP consult order
Patient being discharged
Suggestion to outpatient provider(s)
ED Social Worker/Case Manager can place hospice/palliative referrals
Grand Rounds Recap 2.1.23
This week in Grand rounds, we had some case reflection from R4 Dr.Zalesky reminding us to avoid anchoring, be aware of our biases for or against patients, and avoid creating a rude work environment. Dr. Moulds and Dr. Goel had a CPC showdown with a case of Cecal Diverticulitis, while Dr. Artiga gave us the low down on Lung Ultrasound in the ED. We wrapped up the day with an R4 lead simulation on a case of Thyrotoxicosis.
R4 Case Follow-Up WITH Dr. Zalesky
Humility Hubris and Healing
Case 1
A case of a patient who presented during the height of covid with signs of sepsis. Patient was resuscitated and admitted. After they were admitted they were noted to have worsening shock and it was found that they had a necrotizing infection of their leg.
Learning points
Don’t anchor on pressure ulcers as they often are not the source of sepsis
Look at the feet of all sick patients as infections often can hide there
Be smooth and methodical in your clinical actions. Think about an economy of motion in all actions. Slow is smooth and smooth is fast.
Dogma
Rudeness has been shown to degrade team performance in the clinical setting. Creating a rude or hostile care environment can impact the quality of care delivered to patients. Seeking to avoid this and instead building an environment of collaboration creates a place that is better to work in and better for our patients
Case 2
Patient initially presented for back pain with a history of significant IVDU and discitis. After a prolonged ED course the patient eventually received a non-contrast MRI spine which was not the initial plan to evaluate for possible spinal epidural abscesses. This was negative. Patient was discharged. He returned a few days later in septic shock with endocarditis.
Learning points
Respect signout and ensure every patient still gets an honest moment of thought and review before final decisions are made.
Know your own biases and work to counterbalance them in the clinical environment. Don't let your pathology become your patients pathology
Closing
For this is the day you know too little
against the day when you will know too much
For you will be invincible
and vulnerable in the same breath
which is the breath of your patients
For their breath is our breathing and our reason
For the patient will know the answer
and you will ask him
ask her
For the family may know the answer
For there may be no answer
and you will know too little again
or there will be an answer and you will know too much
forever
- Excerpt from Gaudesmus Iggituar, John Stone MD
R2 CPC:Cecal Diverticulitis WITH Dr. Moulds and Dr. Goel
Diagnosis: Cecal Diverticulitis
Test of Choice: CT abd/pelvis - Cecal (right-sided) Diverticulitis
Accounts for 1.5% of diverticulitis in Western countries
Up to 75% of cases of diverticulitis in Asian countries
Initially thought to be separate disease process from left-sided diverticulitis
Pathophysiology
Fiber hypothesis
Genetic predisposition
Connective tissue degradation
Presentation
More common in younger patients
Less likely to be complicated than left sided
Differential: appendicitis, typhlitis, crohn’s disease, gynecologic, testicular torsion
Treatment
No clear treatment guidelines
Can be managed medically with antibiotics or surgically with colectomy or diverticulectomy with similar success rates
Recurrence risk is higher with medical management (16% vs 2%)
R1 Clinical Diagnostics: Lung Ultrasound WITH Dr. Artiga
Fundamentals
Artifacts depend on:
Hardware itself
Tissue harmonics
Spatial compounding
Frequency
Persistence
Post bandwidth
MI range
Operator-dependent factors
Use the correct preset
Use the correct probe
Linear probe
Superficial anatomy
Absolute best for PTX
Pleural line at 1/3-1/2 of screen
Curvilinear or Phased Array
Deeper structures to ~15cms
Adjust settings for gain and focal point
Image the correct area
PTX: One of each anterior lung
Pleural effusion: PLAPS-point of each lung
parenchymal disease: More views needed for localization
No standard protocol for every clinical context
Our protocol: 5 views + PLAPS
Anterior superior/middle/inferior
Lateral middle/inferior
PLAPS-point
Findings
A lines
Parallel to pleural line
Equidistant
Depth at multiples of distance between probe and pleural line
Attenuate
B-Lines
Originates at the pleural line
Does not attenuate
Traverses entire depth of scan
Moves synchronously with pleural sliding
Must obliterate A-lines
Evaluating B lines
Density
Semiquantitative: ≥3 within an ICS, ≥2 regions of lungs
Extent over lung surface
Laterality
Diffuse vs Focal
Sparing
Homogenous vs Heterogenous
Gradient
Gravitational-component
Intensity
No correlation to severity!
Pneumothorax
Look for Lung sliding or lung point
Linear probe
Pearls
M-mode
Subcutaneous emphysema
False lung points
Lung pulse
Pulmonary edema
Look for B lines
~6 views of the lungs total
Pneumonia
Newly infected tissue
Edematous → B-lines
Subpleural consolidations
~90% PNA involve visceral pleura
Shred sign
Consolidated lung tissue = subpleural hypoechoic region, irregular (shredded) border against normally aerated lung
Tissue-like sign
Hepatization
Air bronchograms
Static Air Bronchograms
Air trapped by fluid on both sides of a collapsed airway
Fluid bronchograms
Effusions
Effusion Types
Anechoic
Transudates
Homogeneously echogenic
Hemothorax
Complex non-septated
Complex septated
Pearls
Spine sign
Jellyfish sign
Plankton sign
Sinusoidal sign
R4 Simulation: THyrotoxicosis WITH Dr. COmiskey, Dr. Mullen, and Dr. Frankenfeld
Overview
Acute, life-threatening diagnosis of hyperthyroidism with multi-system involvement
Technically a clinical diagnosis
if the clinical suspicion is high enough, you should not wait to initiate treatment
Usually caused by a superimposed precipitating factors in the context of diagnosed or undiagnosed hyperthyroidism
Epidemiology
Rare presentation of hyperthyroidism, approx. 0.57-0.76 cases per 100,000 per year
Mortality estimated to be 8-25%
Most common with Grave’s disease
Pathophysiology
Underlying mechanism is not well understood, but thought to be caused by a surge of catecholamines and thyroid hormone
No correlation between the severity of disease and the level of hormone
Clinical findings
Hemodynamic consistent with sympathetic surge (tachycardia, hypertension, hyperpyrexia, tachypnea, may see hypoxia due to increased metabolic O2 demand and pulmonary edema)
Lab findings may be:
Hypercalcemia
Hyperglycemia (inhibition of insulin release and increased glycogenolysis)
Abnormal LFTs
Low or high WBC
Abnormal TFTs
· Several scoring systems: all based on clinical findings
Burch-Wartofsy Point Scale
>45 = thyroid storm
25-44 = less likely
< 24 = unlikely
Japanese thyroid association
CXR may help identify CHF/cardiomegaly
Head CT helps to rule out other CNS pathology
EKG useful to detect and monitor for arrhythmias
Treatment
Supportive measures
Treatment of underlying precipitating factors
Thyroid storm specific treatment:
1. Beta blocker
40-80mg of propranolol q4-6hrs
Chose cardiac beta-blockers in patients with underlying asthma (atenolol or metoprolol)
May also use diltiazem if there is an absolute contraindication
2. Thionamide
PTU: loading dose of 500-1000mg
Followed by 250mg q4hrs
Favored due to blocking of peripheral conversion of T4 to T3
Methimazole: 20mg q4-6hrs
Both drugs can cause agranulocytosis and should be monitored with routine CBCs
If initially started on PTU, the patient should be transitioned to methimazole due to hepatotoxicity of PTU
Pregnant women should be started on PTU and then transitioned to methimazole as well due to the teratogenic effects of methimazole in early pregnancy
3. Iodine solution
One hour after administration of thionamide, give 5 drops of supersaturated potassium iodide PO q6hrs
Must administer thionamide prior to iodine to prevent significant surge of thyroid hormone
4. Block peripheral conversion
Hydrocortisone 100mg IV q8hrs or Decadron 2mg q6hrs
5. Block enterohepatic recycling (severe cases)
Oral cholestyramine 4g q6hrs
Thyroidectomy may be the mainstay of treatment if the patient does not tolerate or has contraindications to medical management
Definitive treatment is radioactive iodine or surgical management
Will need to be treatment with exogenous hormone afterwards for iatrogenic hypothyroidism
Surgical complication of hypocalcemia (accidental removal of parathyroid glands)
Some refractory cases of been managed with plasma exchange
Disposition
Patients with confirmed or highly suspected thyroid storm should be admitted to the ICU for close monitoring
Will need frequent labs and medication administration
Diagnostics: TEG and Blood Products
Need a quick reminder of what the MA means as you’re watching your TEG tick by? Join Dr. Della Porta for a quick hit review of Thomboelastography, aka TEG.
Infographic by Alessandra Della Porta, MD (@MedEdTweeter)
Dr. Della Porta is a PGY-1 in Emergency Medicine at the University of Cincinnati
Peer Editing by Simi Mullen, MD and Ryan LaFollette, MD (@lafoller)
Dr. Mullen is a PGY-4 and Chief Resident at the University of Cincinnati, Dr. LaFollette is an Associate Professor and Co-Editor of TamingtheSRU.com
Grand Rounds Recap 2.8.23
During Grand Rounds this week, we had the pleasure of hosting our Brian Gibler visiting lecturer Dr. John Deleda who Spoke about Henry Ford Hospitals COVID-19 response and the leadership lessons he learned over his career. Dr. Della Porta then gave us the rundown on different blood products and using TEG. We discussed PPROM, Breech delivery, and neonatal resuscitation with Dr. Crawford. The CPC showdown with Dr. Minges and Dr. Brower ended as a case of Hyperleukocystosis and Leukostasis. We ended the day with a talk from our PEM colleagues on inborn errors of metabolism.
Dr. Brian Gibler Visiting Lecture WITH Dr. John Deedda
The 1st Surge COVID-19 at Henry Ford Hospital
ED and ICU front line
The operational framework of having a robust EM/CCM faculty made a continuous operational unit between EM and ICU care.
MICU, SICU, CVICU, NSICU
Opened first ICU COVID pod in MArch
Opened 17th COVID ICU pod in april
Lessons Learned
We can adapt
New medications
New policies
New processes
New covid units
We are agile
Surge Planning
Build capacity
Surge team
ED,ICU physician and Nursing leadership
Daily Surge call
Resource needs
Expand capacity(where, when,who)
We are Collaborative
Routine calls with Wuhan, Barcelona, and Milan
Critical Care Clinical Standardized COVID-19 Management across all ICUs in the Henry Ford System
We are innovative
Creating novel care spaces
Changing how care is delivered to conserve resources
We are Compassionate
A lot of isolation with no visitors and the stay at home order
Lots of donations and care from around the hospital and the city
We are Courageous and Strong
We worked
Long hours
High volume
Tough conditions in PPE
We are supported
Massive outpouring of support from the community and from within the hospital system
We are Human
Range of emotions
Lots of death, saves,and tragedies
Grief, hope, and everything in between
We are proud
Pride in the work they were doing help sustain incredibly difficult work conditions
We will Endure
Sprint became a marathon
Physical and emotional strain of vaccination politics
Three more surges after the initial surge
Crisis that spawned more crises
Vaccination as a term of employment
Premium labor crippling finances
Healthcare will forever be more costly
Personal wellness
Leadership I've learned from shoe repair, the caddyshack, the c-suite and places in between
Emotional Intelligence
Discuss Various styles
Leadership styles are strategic choices not personalities
Self Awareness
Self management
Social awareness
Social skill
Successful leaders can flex between leadership styles
Leadership actions that motivate engagement
Discuss courage the challenges of employing it in the workplaces that cultivate it
Courage is taking worthy actions despite the potential risk
Works when
Excel at their job
Engaged in the organization
even handed
Pick your battles
Is it critical
Is it the right time
Does the battle aid or hinder winning the war
Focus on
Frame the issue
Effective use of data
Managing emotions in the room
R1 Clinical Diagnostics on TEG WITH Dr. Della Porta
Blood Products
General
“A therapeutic substance derived from human blood, including whole blood and other blood components for transfusion, and plasma derived medicinal products.”
Disparities in Quality and Access
There is a marked difference in the level of access to blood between low- and high-income countries. The whole blood donation rate is an indicator for the general availability of blood in a country.
Transfusion related transmission of Hepatitis B is 2.81 in Low income countries and 0.02% in high income countries
Components of Blood
pRBCs 45% of Whole blood
12 million units/year in the US
1500 per month at UC
Shelf life of 42 days at 4C (fridge)
70% Hct in pRBC compared to 40% Hct in whole blood
Increases Hct 3-4% or increases Hgb 1g/dL
Can be washed or leukoreduced
Indicated for patients needing red cells for oxygen carrying capacity rather than for volume replacement (i.e. sickle cell, symptomatic anemia, Hgb < 7), or as part of MTP
Plts <1% of Whole blood
Pooled from donated blood (ie. 5 donors= 1u)
Shelf life of 5 days at 22C (room temp)
A unit can increase plt count by 30-50k platelets
Transfuse SLOWLY to avoid hypotension
Indicated or patients with plt counts <10k prophylactically, known platelet disorders with associated signs of bleeding, or patients with thrombocytopenia prior to planned invasive procedure (i.e. <20k prior to CVC placement), as part of MTP
Plasma
Water 92% of Plasma
Protein 7% of plasma
Albumin
Clotting factors
Products
FFP
Portion of whole blood that remains after platelets and RBC are removed
1000u/month at UC
Increases each clotting factor by 2-3%
Takes 45 minutes to thaw, pre-thawed available for emergency use
Shelf life of 12 months at -25C
Indicated for patients with INR > 1.7 and planned invasive procedure, >1.4 and need for oral anticoagulant reversal, as part of MTP
Cryoprecipitate
Contains factor VIII, XIII, fibrinogen and vWF, ADAMTS13
1u/5-7 kg can increase fibrinogen levels by 100 mg/dL
Shelf life of 12 months at -25C
Indicated for the correction of hypofibrinogenemia, usually levels < 100-150 mg/dL in conditions such as hemophilia, vWD, DIC, and HELLP
Whole Blood Transfusion
More than the sum of its parts
Whole blood has more Hct (40 vs 30%), more Plts, representation of all factors, and more fibrinogen than component resuscitation.
Coagulation measurement
TEG (Thromboelastography) and ROTEM (rotational Thromboelastomotry)
TEG components
R time - clot initiation which is heavily dependent on clotting factors and fibrinogen
If long consider FFP
Alpha Angle and K - Clot propagation dependent on clotting factors and fibrinogen
If prolonged K or shallow alpha angle consider FFP and Cryoprecipitate
Max Amplitude - the strength and size of the clot which is dependent on platelets
If low consider giving platelets
Lys30 which assess fibrinolysis
If long consider giving TXA
R4 Case FOllow up:PPROM and NRP WITH Dr. Crawford
PROM Premature rupture of Membranes:
Rupture of membranes before the onset of labor
PPROM = Preterm PROM
complicates 2-3% of pregnancies in the US
a leading cause of neonatal morbidity and mortality and is associated with 30% of preterm deliveries.
Pre-Term
The onset of labor before 37 weeks gestation.
Signs and Symptoms including:
regular uterine contractions
effacement and dilatation of the cervix
Accounts for 10% of all deliveries
Perform an ultrasound for fetal position
Monitor mother and fetus
Consult an obstetrician for admission
Consider tocolytics, antibiotics and steroids
Risk Factors
History of preterm birth
Infections
Vaginal bleeding
Smoking
Short cervix
Multiple gestations
Diagnosis is confirmed by: (AVOID digital exam to help decrease infection risk (chorioamnionitis)
finding a pool of fluid in the posterior fornix
pH greater than 7.0
Ferning pattern on smear.
Commercial Assays (Amnisure)
US looking for oligohydramnios
Treatment (is controversial in OB!)
Antibiotics
Steroids
Betamethasone 12 mg 2x
Consider RhoGam
Expectant management vs intervention
Treatment overall depends on:
Gestational age
Presence or absence of maternal/fetal infection
Presence or absence of labor
Fetal presentation
Fetal well-being
Expectation of fetal lung maturity based on gestational age
Umbilical Prolapse
Umbilical cord prolapse is when the umbilical cord exits the cervical os before the fetal presenting part
It is dangerous because compression of the cord results in decreased blood flow and fetal hypoxia
Risk Factors:
Malpresentation (breech, transverse, oblique, or unstable lie)
Preterm gestational age
Low birth weight
Rare 0.1%
Management involved elevating the presenting part
Minimize manipulating a prolapsed cord and avoid exposing it to the cold environment, which may exacerbate poor perfusion
Gently replace an overtly prolapsed cord in the vagina and keep it moist with wet gauze
Prompt delivery: c-section
Breech
Represents about ~4% of singleton deliveries at term, about 25% of cases before 30 weeks
Prematurity, small fetal size, excessive amniotic fluid, multiple pregnancies
Delivery
For frank and complete breech delivery
Let the delivery progress naturally, pulling too early can cause the fetal head to go into extension which will cause issues with the delivery later on
Allow the baby to be delivered until the umbilicus
Usually baby is face down and their back is flat
After spontaneous expulsion to the level of the umbilicus, external rotation of each thigh with pressure in the popliteal fossa with delivery of the foot
A towel is wrapped around the fetus for better traction
Apply pressure to the pelvis
Don’t grab the abdomen
When the scapula appears under the symphysis, the operator reaches over the left shoulder, sweeps the arm across the chest and delivers the arm
You may have to rotate side to side to get arm out
If arms are crossed, there is a good chance the arms will delivery spontaneously
Delivery of the head is accomplished with continued expulsive forces from above, suprapubic pressure, and gentle traction.
Cephalic flexion is maintained by pressure (heavy arrow) on the fetal maxilla (not mandible!).
Pull up at a 45 degree angle
If this is unsuccessful there is a : symphysiotomy to help increase the diameter of the canal
Zavanelli maneuver – the child is replaced back into the uterus to allow for emergent C-section.
Neonatal Resuscitation Program
Cornerstone of NRP is respiratory support, with is different than PALS and ACLS
If the answer is no the initial assessment the baby should be brought the the radiant warmer , clamp and cut cord
The Algorithm
Position the baby with head in sniffing position to open the airway, consider a shoulder roll
If needed clear secretions from the airway , suction, mouth before nose (M comes before N in the alphabet)
Dry and stimulate
If HR > 100 and breathing OK continue to observe
If there is labored breathing or cyanosis
Reposition airway and clear airway
Apply pulse-ox- remember O2 sats are low at birth and slowly rise
Administer O2 as needed 21-30% FiO2, may need oxygen blender depending on pulse ox
Usually starting at 21% and titrating up as needed, 10 LPM to meet target saturations
If the baby as persistently low O2 sats or labored breathing, move on to CPAP
If there is apnea or gasping or the HR is less than 100
Prepare for PPV
Using ”breath” two three, administering a breath each time you say breath
If HR remained less than 100, MR SOPA, considering a more advanced airway, laryngeal mask or ETT
If HR less than 60
Intubate
Starting chest compression , and then administering epinephrine
Epi every 3-5 minutes with CPR and ventilations
R2 CPC: Blast Crisis and Leukostasis WITH Dr. Brower and Dr. Minges
Hyperleukocytosis WBC > 50K- 100K
Leukostasis = symptomatic hyperleukocytosis (aka Hyperviscosity syndrome)
Pathophys
thought to be secondary to two mechanisms: hyperviscosity and local hypoxemia
Increased blood viscosity occurs as a direct complication of a large population of leukemic blasts that are less deformable than mature leukocytes resulting in plugs in the microcirculation
Local hypoxemia then may be exacerbated by the high metabolic activity of the dividing blasts and the associated production of various cytokines
Presentation
the main clinical symptoms of leukostasis and causes of early death are related to involvement of the central nervous system and lungs, which affect ~40% and ~30% of patients, respectively
Neurologic
visual changes, headache, dizziness, tinnitus, gait instability, confusion, somnolence, and coma
increased risk of intracranial hemorrhage that persists for at least a week after the reduction of white cell count, possibly secondary to reperfusion injury to areas of the brain that were ischemic from leukostasis
Pulmonary
dyspnea and hypoxia with or without diffuse interstitial or alveolar infiltrates on imaging studies
~80 percent of patients are febrile, which may be due to inflammation associated with leukostasis or concurrent infection
Less common signs or symptoms
electrocardiographic signs of myocardial ischemia or right ventricular overload, worsening renal insufficiency, priapism, acute limb ischemia, or bowel infarction
Management
In addition to ABC’s and supportive care, the goals of management are cytoreduction, prevention of tumor lysis syndrome, and antibiotics
Cytoreduction
achieved via induction chemotherapy, hydroxyurea, and/or leukapheresis
Induction chemotherapy or other immunologic agents is the preferred treatment for symptomatic hyperleukocytosis with leukostasis and typically substantially reduces the WBC count within 24 hours, though also increases the risk of precipitating tumor lysis syndrome
Hydroxyurea is typically reserved for patients with asymptomatic hyperleukocytosis who are unable to receive immediate induction chemotherapy
leukapheresis remains a controversial adjunct for treatment, with several retrospective analyses demonstrating conflicting evidence on early mortality rates. However, this treatment remains an option for critical patients
Prevention of tumor lysis syndrome primarily involves IV fluids, allopurinol or rasburicase for hyperuricemia, correction of electrolyte abnormalities, and potentially renal replacement therapy
Patients should be treated with broad-spectrum antibiotics as they are functionally neutropenic. Cefepime monotherapy or in combination with vancomycin is typically the preferred regimen
Pediatrics lecture: Inborn Errors of Metabolism WITH Dr. Yu
In-Born Errors of Metabolism
Defect in an enzyme or pathway leads to a deficit in the necessary product, build up of toxic substrate or activating of a different or secondary pathway leading to build up of other toxic compounds
Consider in any neonate/infant who is critically ill without known etiology
Often have a period of normalcy, progressing to poor feeding, frequent vomiting, failure to thrive, lethargy, seizures, hypothermia, ALTE/BRUE
Crisis caused by a variety of catabolic stress: acute illness, fever, vomiting/diarrhea, surgery
Types
Protein*
Amino acidopathies
Tyrosinemia
Phenylketonuria
Organic acidemias
Maple syrup urine disease
Urea cycle defects***
Glucose***
Carbohydrate intolerance disorders*
Galactosemia
Fructosemia
Carbohydrate production/utilization disorders
Glycogen storage diseases
Fat
Fatty acid oxidation defects***
Mitochondrial disorders
Lysosomal Disorders
Peroxisomal Disorders
* present in crisis (catabolic state) before 1 month of age
***present in crisis after 1 month of age
Evaluation and Management
NPO (don't know what substrate is the culprit)
IV fluids with electrolytes and treatment of hypoglycemia
Normal saline (no lactate ringers because some patients have profoundly elevated lactate)
D10 bolus for hypoglycemia (<40 for newborn, <50 for infants or older, or symptomatic)
"rule of 50"
D10 x 5ml/kg
D25 x 2ml/kg
D50 x 1ml/kg
D10 1/2 NS for infants at 1.5x maintenance fluids to maintain BG with goal 120-170
Need this continuous source of fuel regardless of whether or not they are hypoglycemic to avoid catabolic state
Treatment of acidosis
NPO and Dextrose containing fluids still first line
If need acute stabilization can administer sodium bicarb, but this is a temporary bandaid and will not impact the underlying derangements
Avoid too-rapid correction of acidosis
Treatment of hyperammonemia
NPO
Dextrose and intralipids
Consider ammonia scavengers
If >300, can require dialysis or ECMO
Antibiotics to cover for infection (sepsis always on ddx for these kids, or may be the trigger for the crisis)
Labs
ISTAT, glucose, CBC, CMP, ammonia (increase indicates issue with protein metabolism - urea cycle defect), lactate, urinalysis
Resource for metabolic emergencies
Vadamecum Metabolicum: https://evm.health2media.com/#/start
Contains info about acute presentation, emergency management, lab workup, specifics about different disorders
Ultrasound of the Month: Radial Pseudoaneurysm
Abscess? Cyst? Hematoma? Join Dr. Tillotson and review the unique images obtained that led to a diagnosis of a radial pseudoaneurysm!
The Case
Figure 1: Clinical image of wrist swelling
An elderly patient presents to the emergency department (ED) for left wrist mass/swelling. The patient has a past medical history of coronary artery disease, diabetes (type 2) on metformin, and carotid stenosis s/p carotid endarterectomy. He underwent a right heart catheterization (RHC) 2 months prior to his first ED visit with placement of stents. His heart cath was accessed using his right radial artery. After his RHC, he was placed on Plavix. Over the preceding six weeks, he noted swelling of his left wrist which was tender to palpation without redness, warmth, or drainage.
On evaluation, the patient is hemodynamically stable with a 5 cm mass overlying the left palmar radial wrist (Figure 1). There is a pulsatility with palpation of the mass. No overlying erythema, warmth, or induration but there is mild fluctuance. No other abnormalities are noted on the remainder of his exam.
The patient's presentation raises concern for a pseudoaneurysm. Other differential diagnoses include hematoma, abscess, or cyst. Point of care ultrasound (POCUS) was used to evaluate the mass. The acquired images are shown in Figures 2-5.
Figure 2: Cystic structure
Figure 3. Color doppler image of cystic structure showing “yin-yang” sign
Figure 4. Swirling of blood in the pseudoaneurysm
Figure 5. Neck of the pseudoaneurysm visualized under color feeding the pseudoaneurysm. From the left radial artery
The findings led to concern for pseudoaneurysm formation. Vascular surgery was consulted for pseudoaneurysm management.
Pseudoaneurysm Pathophysiology
Pseudoaneurysms are tears in arterial walls leading to a sac communicating with the artery. As opposed to true aneurysms, pseudoaneurysms (i.e. false aneurysms) are not encapsulated by all 3 layers of the artery, but rather only by the media or adventitia. Pseudoaneurysms communicate with the artery via a channel or “neck” which allows blood to flow into a saccular space. Pseudoaneurysms can be seen in arteries (femoral being most common), viscera, and the aorta. Arterial pseudoaneurysms result from iatrogenic arterial cannulation for endovascular procedures, trauma, infection, or anastomotic failure (1). Iatrogenic pseudoaneurysms are a rare but concerning complication of procedures requiring arterial access. The large pulsatile sac may compress on neurovascular structures in proximity, cause thromboembolism, necrosis of overlying tissues, or rupture leading to life threatening bleeding (1, 2). Typical causes include multiple puncture attempts to achieve vascular access, inadequate post procedure compression, accidental arterial dilation during venous procedures, and failure of closure devices. Patients on anticoagulation are at increased risk of this complication. Radial artery pseudoaneurysms are an extremely rare complication of arterial cannulation occuring in <1% of arterial cannulations. In fact, the radial approach has been favored in recent years due to its low complication rate (including pseudoaneurysms rate) as well as being an area relatively easy to access and compress (3).
Imaging Recommendations
Given that pseudoaneurysms are fairly superficial and require visualizing fine details, a high frequency probe should be used. Imaging should show a saccular lesion with some pulsatility or movement. Images of the mass should be obtained in a longitudinal and transverse plane. Pseudoaneurysms may be anechoic in the absence of thrombi or partially hyperechoic if partially thrombosed. For diagnosis, images must show a communicating channel between the artery and the mass through which blood is flowing. Due to the different velocities of blood entering and exiting the pseudoaneurysm, swirling may be seen on grayscale ultrasonography. Increasing the gain may better visualize the swirling of blood in the sac. Using color doppler, one should see bidirectional, turbulent blood flow with red color flow towards the probe and blue color flow away from the probe (2). This creates the “yin-yang” sign characteristic of larger pseudoaneurysms as seen in Figure 3. Using color, one should also see the blood flowing through the communicating channel, or neck, of the pseudoaneurysms as seen in Figure 4. These findings separate pseudoaneurysms from hematomas and cysts (2).
Management
Prevention of pseudoaneurysms formation is noted in the literature as first line management. Post procedure, prolonged compression of the puncture site with limb rest is typically sufficient to prevent pseudoaneurysm formation (3,4,5). In anticoagulated patients, the length of compression is extended. If these measures fail, secondary treatment is needed. Historically, surgical management was the gold standard treatment for pseudoaneurysms. However, in recent years, less invasive treatments have been preferred by vascular surgeons with excellent clinical outcomes. For small pseudoaneurysms, compression of the mass typically resolves the pseudoaneurysm. In medium to large size pseudoaneurysms, direct visualization using ultrasound is used to create thrombosis inside the pseudoaneurysm (3,4). Ultrasound guided compression of the pseudoaneurysm neck until thrombosis of the pseudoaneurysm is considered the first line treatment. Alternatively, ultrasound guidance may be used for thrombin injections. In this procedure, ~300 IU of thrombin is injected under ultrasound guidance into the pseudoaneurysm until thrombosis of the pseudoaneurysm is achieved (6). Thrombin injections carry a small risk of embolization and are thus not attempted in very small pseudoaneurysms (1). Should these methods fail, open operative management is then pursued.
Case Resolution
Vascular surgery evaluated the patient and offered thrombin injection into the pseudoaneurysm which he accepted. The patient was taken to the vascular lab for an urgent thrombin injection. Post procedure, he was noted to be neurovascularly intact with minimal pain and good indices of perfusion. The patient was discharged after a brief period of observation.
AUTHORED BY KELLY TILLOTSON, MD
Dr. Tillotson (@kellytillotson2) is a PGY-3 in Emergency Medicine at the University of Cincinnati.
PEER REVIEW BY Lori Stolz, MD
Dr. Stolz (@sonostolz) is an Associate Professor of Emergency Medicine at the University of Cincinnati and Director of the Ultrasound Fellowship.
EDITING AND LAYOUT BY MARTINA DIAZ, MD
Dr. Diaz (@martina_diazb) is a PGY-3 in Emergency Medicine at the University of Cincinnati and the Resident Editor of Ultrasound of the Month.
References:
Rivera PA, Dattilo JB. Pseudoaneurysm. [Updated 2022 Mar 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542244/
Chun EJ. Ultrasonographic evaluation of complications related to transfemoral arterial procedures. Ultrasonography. 2018 Apr;37(2):164-173. doi: 10.14366/usg.17047. Epub 2017 Aug 25. PMID: 29145350; PMCID: PMC5885482.
Cauchi MP, Robb PM, Zemple RP, Ball TC. Radial artery pseudoaneurysm: a simplified treatment method. J Ultrasound Med. 2014;33(8):1505-1509. doi:10.7863/ultra.33.8.1505
Kongunattan V, Ganesh N. Radial Artery Pseudoaneurysm following Cardiac Catheterization: A Nonsurgical Conservative Management Approach. Heart Views. 2018
Grand Rounds Recap 1.11.23
Join us for our 1.11.23 Recap with Dr. Wolski covering caustic skin injuries, Dr Shaw taking on Dr. Hughes with a CPC case of trophoblastic disease with thyrotoxicosis and finally peds sim cases with our CCHMC PEM colleagues
R1 Clinical diagnostics: caustic skin injuries WITH Dr. wolski
Severity of caustic skin injuries depends on physical state of substance, concentration, strength, amount, skin characteristics, time of exposure
Algorithm to manage most caustic skin injuries
Safety: scene safety, PPE
Strip: remove clothing
Shower: 45-60 minutes of irrigation time
Size: attempt to estimate the burn size and depth
Sedate: adequate pain control
Stabilize
Chemicals can be associated with systemic toxicity so monitor electrolytes and telemetry
Do not neutralize substances due to possible exothermic reaction
Cement
Typically delayed presentation. Several hours after exposure, patients will develop burning pain, erythema, and vesicles. 24-48 hours after exposure, wounds will ulcerate and develop black necrosis
Treatment: extensive irrigation, debridement, and hydrocolloid dressing
Hydrofluoric Acid
Glass etching/cleaning, ceramic manufacturing, rust removal, automobile wheel cleaners, air conditioner cleaners, germicides, insecticides, tile cleaning, laundry powders, semiconductor production, plastic production
Distinct characteristics
Pain out of proportion to burn appearance
Progressive tissue destruction, with maceration, erythema, edema, ulcers, necrosis, eventually whitish/silvery-gray discoloration
Delay in presentation depending on HF concentration
Systemic effects
Acidemia, hypocalcemia, hypomagnesemia, hyponatremia, hyperkalemia, hyperphosphatemia → cardiac arrhythmias
Tenosynovitis and osteolysis can occur due to depth of HF penetration. Patients may also have nausea, abdominal pain, muscle fasciculations
Pulmonary edema, bronchopneumonia, and tracheobronchial hemorrhage also possible
Treatment
Copious irrigation followed by administration of calcium
All cases: topical calcium gluconate gel
Deep wounds: above plus subeschar calcium gluconate injection
Digital burns: topical treatment + arterial infusion after identifying arterial supply to injury
IV calcium for hypocalcemia
Phenol
Found in soaps, sprays, ointments, as well as industrial production of explosives, fertilizers, rubber
Distinct characteristics: sweet odor, numbness over burns due to anesthetic properties of phenol, dark-colored burns
Systemic effects
Direct damage to renal tubules and glomeruli leading to renal failure
CNS stimulation (hyperreflexia, convulsions) or CNS depression (lethargy, respiratory arrest)
PNS demyelination
Cardiovascular toxicity
Erythrocyte lysis
Central lobar hepatic necrosis
Treatment
DO NOT RINSE. Irrigation with inadequate amounts of water increases risk of absorption by exposing more body surface area to the phenol. Instead, you should wipe phenol off with polyethylene glycol. Alternative solvents include soap and vegetable oil
White Phosphorus
Most frequently used in military, fireworks, insecticides, fertilization as well as illicit methamphetamine production
Combined thermal and chemical burn
Distinct characteristics: yellow flame with white smoke, burn appears yellowish, waxy, and necrotic
Systemic effects
Hypocalcemia, hyperphosphatemia → bradycardia, QT prolongation, ST/T wave changes
Erythrocyte hemolysis
Renal damage
Hepatic necrosis
Treatment
Extensive irrigation, particle removal, and dressing with saline-soaked pads.
Beware
Dry dressings can ignite
Removed particles should be placed in cold water to prevent combustion
Examine debrided wounds twice daily for smoking and missed particles
Of note, you can use a Wood’s lamp for particle visualization
R2 CPC WITH Dr. Shaw and Dr. Hughes
Case: Middle aged female with recent history of molar pregnancy with chief complaint of abdominal pain, vaginal bleeding. Found to have a temperature of 101.2 and tachycardia.
Diagnosis: Gestational trophoblastic disease with secondary hyperthyroidism
Test of Choice: Thyroid Studies
Premalignant: hydatidiform mole (partial, complete)
Malignant: Gestational trophoblastic neoplasia
Gestational Trophoblastic disease: abnormal proliferation of trophoblastic cells
Trophoblasts provide nutrients to the embryo and develop into a large part of the placenta
Secrets hCG early in pregnancy
Clinical signs and symptoms
Hyperemesis
Elevated BP
Enlarged uterus
Vaginal bleeding
Diagnostics
Ultrasound
Laboratory testing
Thyrotoxicosis
Can be complication of GTD
Treatment
Beta-blockers
Glucocorticoids- prevent conversion of T4 to T3
Definitive management: Dilation and curettage
Post-operatively: methimazole, birth control
pediatric simulation
Consider congenital cardiac etiology in a newborn with poor feeding, vomiting, cyanosis, or mottling.
Coarctation typically presents with sudden symptoms of heart failure and shock due to closure of the PDA that has been bypassing the coarc for systemic circulation, so they are often pale, mottled, irritable with hepatomegaly and diminished or absent femoral pulses. Four extremity BPs demonstrate hypotension in bilateral LEs +/- LUE depending on the location of the coarc
In addition to other supportive measures, prostaglandins are administered to keep the PDA open to allow for systemic circulation. The starting dose is 0.05 mcg/kg/min but can be titrated up to 0.1 mcg/kg/min
Risks of prostaglandins include apnea and hypotension, which increase with increasing doses. Be prepared to secure the airway and provide resuscitation as needed. This is a patient you would want to talk to peds cardiac ICU very early in the process to coordinate transfer and care