by: Kaitlyn Dixon M.D.

by: Kaitlyn Dixon M.D.
Allison Cash M.D.
HPI
Physical Exam
Work-up
Hospital Course
IBD complications pearls
References:
Author: Jordan Spaude M.D.
by Daniel Petrosky M.D.
HPI
PMHX
Physical Exam
Work-up
Case Conclusion
TCA Overdose Pearls
Classic Symptom Description | Physical Exam Manifestation |
“Mad as a Hatter” | Acute encephalopathy |
“Red as a Beet” | Erythroderma (in fair skinned patients) |
“Blind as a Bat” | Dilated and unresponsive pupils |
“Dry as a Bone” | Dry, cracked mucous membranes, no sweating |
“Tachy as a Leisure Suit” | Sinus tachycardia |
“Hot as Hell” | Hyperthermia |
References:
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, 1194-1199.
Author: Tara Knox M.D.
Author: Dan Harwood M.D.
HPI:
A 63 y.o. female with PMH of migraines and chiari malformation presents with headache. Patient reports that for the past 10 days, she has had a right-sided migraine that she describes as similar in quality to her prior migraines but longer-lasting. However, at 2 PM yesterday, she experienced an acute worsening of the severity of her headache – additionally, the pain became bilateral and occipital at this time. The patient reports dizziness, nausea, and photophobia, and her husband states that the patient has been slower to respond to questions for the past day. Denies vomiting, visual changes, or fever.
Vitals: BP: 133/90 | Pulse: 71 | Temp: 98.1F | Respiratory Rate: 18 | SpO2: 99%
Neuro exam is non-focal. Patient appears tired, but responds to questions appropriately.
Clinical Course:
Patient given Tylenol, 10 mg IV Compazine, and 1 L lactated ringers with significant improvement in symptoms. Given change in headache quality from prior migraines and acute worsening of headache, CT Head wo contrast ordered.
CT revealed a large hemorrhagic neoplasm in the right frontal region with associated mass effect and 1.2 cm leftward midline shift resulting in obstructive hydrocephalus. Patient subsequently noted to be increasingly somnolent compared to initial presentation. Neurosurgery was emergently consulted who recommended decadron, Keppra for seizure prophylaxis, and admission to the Neuro ICU.
Headache Pearls:
The majority of headaches are due to primary headaches such as tension headache, migraine, or cluster headache. However, as 18% of patients with chief complaint of headache may be experiencing a secondary headache disorder. Many of these secondary headaches represent life-threatening emergencies such as intracranial bleeding or CNS infection. The SNOOP mnemonic is a helpful tool for remembering “red flag” headache symptoms to identify headache patients who warrant further imaging/laboratory work-up in the ED. Additionally, improvement in symptoms with medication does not decrease the likelihood of a secondary headache disorder.
Systemic: Systemic signs or conditions such as fever, weight loss, immunocompromise, HIV, cancer
Neuro: Neurologic findings including mental status changes, vision changes, seizure, confusion, or focal neuro findings on exam
Onset: Onset that is acute with progression to worst severity within minutes
Older: Older patient (50 y.o. or older) with new headache or a progressive headache
Previous: No history of previous headaches, or in a patient with history of headaches, a change in severity/symptoms/location from prior headaches
Pregnancy: Headache in pregnant or post-partum patient
References:
Ashenburg Nick, Marcolini Evadne, Hine Jason. Approach to Headache. In: Mattu A and Swadron S, ed. CorePendium. Burbank, CA: CorePendium, LLC. https://www.emrap.org/corependium/chapter/rec8eRzSrPsVUiMuV/Approach-to-Headache#h.pq7xksb5a2qy. Updated October 8, 2022. Accessed December 22, 2023.
Dodick DW. Clinical clues and clinical rules: primary vs secondary headache. Adv Stud Med 2003;3:87–92.
Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
Author: Vincent Li M.D.
HPI
Vitals
T 98.4F, HR 99, BP 112/55, RR 18, O2 97% on 2L NC
Clinical Course
Pulmonary embolism pearls
References
1. Garrett, John S., and Anant Patel. “Pulmonary Embolism.” Edited by Jeremy Berberian. Corependium, 2023, Accessed 26 Dec. 2023.
2. Tintinalli, Judith E., et al. “Venous Thromboembolism Including Pulmonary Embolism.” Tintinalli’s Emergency Medicine, Ninth ed., McGraw Hill, New York, 2020, pp. 389–399.
Submitted by Kevin Anderson MD PGY1
HPI
A 63-year-old male with PMH diabetes type 2 and renal failure presents to the ED via EMS with AMS. The patient’s family noted the patient had been feeling ill over the last week, causing him to miss 2 dialysis sessions. Patient has been taking insulin as prescribed. Today, the patient was confused and lethargic with LOC. EMS noted the patient’s blood glucose to be >600.
Vitals HR: 90, BP: 110/70, RR: 30, SpO2: 100%, Rectal Temp: 94F
The patient has peaked T-waves on ECG
Patient is initially given calcium gluconate for suspected hyperkalemia and IVF for suspected Sepsis/DKA. Patient’s labs result:
VBG: pH 6.96, pCO2 20, pO2 41, HCO3 6, K 7.4
BMP: Glucose 1227, BUN 120, Cr 5.90, Na 123, K (hemolyzed), Cl 84, CO2 4, Anion Gap 35
Beta-Hydroxybutyrate: 8.18
Lactate: 2.2
Clinical Course
Patient given additional doses of calcium gluconate for hyperkalemia and IVF for worsening hypotension. Insulin bolus and drip started. Sodium Bicarbonate was given for severe acidosis. Patient started on broad-spectrum antibiotics for sepsis as suspected cause of DKA. Patient was admitted to the ICU for diabetic ketoacidosis and continued to receive insulin until anion gap closed. UTI secondary to urinary retention was identified as the cause of sepsis.
DKA Pearls
Diabetic ketoacidosis is usually secondary to insulin non-adherence or infection DKA is the result of decreased serum insulin, increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization. Utilizing fatty acid metabolism for energy production
Of note, whole-body potassium will be depleted through osmotic diuresis Serum levels may be normal due to large potassium shift into serum- except in patients with renal failure (like this one!) Potassium must be checked and replaced to >3.3 before giving insulin, otherwise patient may go into respiratory arrest, cardiac arrhythmias, or cardiac arrest!
Patients will be tachypneic (Kussmaul respirations), trying to breathe off CO2 to compensate for their metabolic acidosis! AVOID intubating these patients as even seconds of hypoxia will interrupt this crucial compensatory mechanism.
References
Diabetic Ketoacidosis
https://www.emrap.org/episode/icufundamentals/thefulltalk
Submitted by Rahul Gupta M.D.
HPI
Physical Exam
Vitals: BP 210/89, P 75, RR 18, SPO2 98%
DDx
Case course
Pearls:
References