Hot off the press! FANTASTIC conference this fine Wednesday morning. Special thanks to all of our speakers, and everyone else for being present. We kicked this morning off with an M+M from none other than Dr. Shang:
M+M with Dr. Shang
EMS arriving with an unresponsive woman in her third trimester at 33 weeks gestation, actively seizing. They had called L+D directly to notify them of patient’s arrival.
What is your differential?
Eclampsia is highest. But important to consider other causes: Metabolic, Infectious, structural, toxicologic, hypoxia, epilepsy, pseudoseizure
Pregnant and seizing with ______?
Seizure and low BGM? Glucose.
Na 110: 3% hypertonic or sodium bicarb
Being treated for Tb: B6
Pregnant: magnesium
Recent space shuttle launch: Also vitamin B6
Returning to the case. Initial vitals: Pulse 149, Resp: 32, BP: 164/125, O2 99% on NRB. She is actively seizing. BGM 117
HPI: 26 year old F g1po, 33 weeks gestation, husband heard fall and saw her seizing. No prior seizure history. Patient found seizing on arrival. Possibly seizing up to 30-40 min at this point.
PE otherwise normal.
Interventions in ED: 4g magnesium, 6mg Ativan, intubated with propofol and rocuronium
CTH: to rule out intracranial hemorrhage. READ: Was some white matter hypodensities. Likely PRES, seizure related changes, or less likely embolic infarct.
Went to OR for STAT C section
Still hypertensive in the ED: given 15mg labetalol and 20mg hydralazine given without improvement
Seizure controlled.
Labwork: WBC 22.5, Electrolytes wnl. LFTs normal.
Course:
Patient had C section, baby delivered and intubated in NICU
Patient admitted to SICU, EEG later showed no epileptiform activity
Extubated without difficulty, transferred to floor, discharged 1 week later.
CT READ: Was some white matter hypodensities. Likely PRES, seizure related changes, or less likely embolic infarct.
MRI read several days later: PRES syndrome: subcortical hypodensities, not involving gray matter: suggestive of vasogenic edema. Patchy parietooccipital cortical/subcortical edema without associated DWI. Obtain CT dry followed by MRI with and without contrast when possible.
Hypertensive Disorders in Pregnancy:
Less severe to more severe: gestational htn, preeclampsia, eclampsia, HELLP syndrome
Gestational HTN: new onset htn at 20 weeks gestations or more
SBP > 140, DBP >90
Absence of proteinuria, signs of end organ dysfunction
10-50% develop preeclampsia
Severe if persistently SBP 160, DBP> 110
Plan is for good follow up with OB, if severe, then treat with antihypertensives in ED
Preeclampsia:
SBP >140, DBP 90 WITH
Proteinuria, platelet count, creatinine >1.1, elevated LFTs, pulmonary edema, new onset and persistent headache, visual symptoms.
Can occur after delivery as well.
Red flag symptoms: severe headache, visual abnormalities, epigastric/abdominal pain, AMS, dyspnea, orthopnea: if these present: considered severe preeclampsia. Give magnesium.
Eclampsia: preeclampsia and seizure
HELLP Syndrome: hemolysis, elevated liver enzymes, low platelets. Unclear if this is a part of preeclampsia or its own disease.
Hemolysis: transfuse if hb less than 7
Elevated Liver enzymes: chance of hepatic bleeding, liver rupture, hematoma
Low platelets: transfusion controversial, but consider if actively bleeding, <20,000, <50,000 with plan to operate
Why do we care?
10-15% maternal deaths attributed to pre/eclampsia
Abruptio placentae
Fetus: they may have growth restriction, prematurity, stillbirth
Treatment: Severe HTN SBP 160, DBP >110
Treatment: Seizure:
Magnesium sulfate for ppx (preventing preeclampsia to eclampsia), and for breaking seizure as well. Initiated at onset of labor or prior to and during C section.
If seizing past 15-20 min, proceed down normal status epilepticus pathway
Magnesium Pharmacology
4-6mg IV loading over 15-20 min
Repeat seizure can give additional 2g over 3-5 min
2g/h maintenance OR 10mg IM (5mg each buttock)
Side effects: diaphoresis, flushing, hypotension
Severe side effects: cardiotoxicity and cardiac arrest
Definitive treatment: Delivery
PRES: Posterior Reversible Encephalopathy Syndrome (though not always reversible, not always posterior)
Clinical radiographic syndrome of heterogenous etiologies that are grouped together based on neuro imaging studies
Symptoms: HA, visual disturbance, ams, seizures
Related to htn encephalopathy and eclampsia
Treat the htn and seizure, same as you would eclampsia patient
These patients can be difficult regarding airway management, given normal changes in pregnancy.
Always be set up for intubation in case things go wrong with this type of patient
Increased edema and hyperemia
Decreased caliber upper airways
Consider smaller ET tube when intubating
Decreased FRC
They have increased O2 consumption
Decreased safe apnea time for patient- importance of early preoxygenation
IVC compression by gravid uterus
Increased likelihood of post intubation hypotension
Decreased lower tone of LES, increased risk of vomit
Increased intraabdominal pressure from uterus
Minimize BVM, intubate semi-upright position if possible
Prefer rocuronium over succinylcholine in the seizing patient in case there is associated rhabdo/electrolyte abnormality
Don’t use ketamine- can increase BP in this patient
EKGs with Dr. Weizberg
EKGs- ISCHEMIA
EKGs measures vectors. If electricity coming at sensor, registers upward deflection. If going to lead and then passes by, get biphasic deflection.
Lead 2 3 avf- inf wall
V1-v6: anterior wall. 1 and 2- interventricular septum. V5-6-avl: lateral wall
Coronary anatomy: in most patients:
QRS complex
Q wave: can recognize old MI
-ST segment: whatever connects QRS complex to t wave
Ischemia:
Ischemia
Acute MI
ST elevations
means 100% occlusion of respective coronary artery
Old MI
EKG 1: normal
EKG 2: T wave inversions of inferior wall. Neighbors are V2 and AVF: also has inversions. Inferior wall ischemia
3: lateral wall ischemia
Normal T wave inversions: 3, AVR, V1. Not a sign of ischemia.
EKG 4: normal
EKG 5: st depressions with more significant ischemia. Compare to baseline.
ST depressions v2-v5: anterior wall ischemia
EKG 6: lateral wall v4-v6 ischemia
Acute MI: ST elevations.
EKG 7: anterior and septal elevations
EKG 8: inferior wall MI
Old MIs.
EKG 9: Lead 2 Q wave. Is this normal? Look at neighboring leads. Same in neighboring leads in inferior wall. Old inferior wall MI
How to determine if q waves are normal? Width and depth. Normal q waves small and narrow.
Bad Q waves >1box wide, depth >25% size of qrs complex
EKG 10: anterior septal wall q waves, old MI V1-V2
Get V4R EKG if concerned about involvement/to detect R ventricular MI.
When we have both ST elevations and Q waves in same leads, represents EVOLVING MI.
Myocardium starts to die from inside out: inside dies first: representing Q waves, and outer layer dies last represented with ST elevations. This is still salvageable with reperfusion.
See isolated ST depressions in anterior wall? Get R sided EKG to check for posterior wall MI
Small Groups with Drs. Chung, Eng, Evans
Rheumatologic and Collagen Vascular Diseases with Dr. Chung
High Yield Kahoot!
Lupus is more common in women
SLE with hip pain, xrays negative: Obtain MRI. Concern for avascular necrosis
SLE patient with fever, remains hypotensive despite fluids and pressors. Give 100mg hydrocortisone
Scleroderma with elevated BP and respiratory distress? Renal crisis. ACE inhibitors
Alveolar hemorrhage associated with lupus: hemoptysis, pulmonary infiltrate, new anemia. Triad. Give steroids.
72 year old with progressive R sided headache x 1 week. CT head negative. Consider Giant cell arteritis, treat prednisone
What is not a treatment for Raynauds disease? Lisinopril. You can use nifedipine, topical nitroglycerin, sildenafil.
Hypersensitivity- Allergies, Angioedema & anaphylaxis with Dr. Eng
Patient with “panic attack”
Tachycardic, tachypneic.
Oral boards case: First thing is what do I see, hear smell? Obtain ABCs
Patient looks like she is panicking, holding chest, SOB. Talking normally, BL breath sounds with bit of wheeze
Obtain monitor, O2, large bore IVs x 2, labs
Differentials: PE, ACS, pneumonia, DKA, asthma, anxiety/panic attack, thyroid
Next ask HPI: PMH of history and anxiety attacks. On beta blocker. Patient was sitting eating lunch, 30 min later had palpitations and feeling BL hands, globus feeling throat. Started 30 min ago. Was eating at new sushi restaurant. No GI symptoms.
Allergic to PCN.
Start with fluids and Benadryl
Secondary exam: wheezing, non-stridulous, some mild mucosal swelling in aiway. Mild distress. Swelling upper lip. Managing secretions.
Patient in anaphylaxis: IM epi, solumedrol, Benadryl, albuterol, O2, famotidine, NS
Refractive to additional IM injection. Use glucagon for beta blocker. Consider epi drip, prepare for awake intubation.
Could use fiberoptic, video laryngoscopy
ICU consult, admission
Transplant Related Problems with Dr. Evans
40 year old TIDM htn, 11 months post kidney transplant. Has epigastric tenderness, UA positive for 6-10 wbc, positive for bacteria, large protein. Creatinine 3.4. T 100.1. Elevated BP
High on differential: infection, rejection, toxicity of transplant meds, vascular such as thrombosis
Infection:
UTI of native kidney, transplanted kidney
Patients are immunocompromised. May not have “true” fever. May not have leukocytosis
Basic labs, UA, get US and possibly CT
IV abx, look at prior urinary cultures/hospital biogram
Rejection:
Elevated Cr, elevated BP, pain over transplanted kidney, protein in urine
May need biopsy at some point
Tx: steroids high dose
Toxicity transplant meds:
When is patient at highest risk at opportunistic infection? What are most common infection?
1-6 months
1st months: consider regular post op issues, infections from donor
>6 months: increased susceptibility to common infections
How would you determine if there is transplant medication toxicity?
30 year old male s/p lung transplant 10 months ago. Dry cough, SOB, low grade fevers. Mildly tachypneic. Breath sounds with crackles. CXR shows BL small effusions, perihilar opacities and diffuse infiltrates.
Workup/Differential/Treatment:
-ekg cxr basic labs, chest CT, IV abx
Ddx: transplant rejection, infection
Lung transplant Complications
Infection
Labs, blood cultures, cxr, bronchioalveolar lavage, possibly transbronchial biopsy
Donor infection manifesting in recipient immunocompromised patient
Consider bacterial, fungal, viral
Rejection
Lung transplant patients have higher incident of chronic rejection
Cellular
Humoral
Chronic
Restrictive allograft
40 year old s/p pancreatic transplant
How frequently are pancreas only transplant done? Not very.
How do they present? DKA, abdominal pain, n/v, asymptomatic, elevated lipase/amylase
Agitation and Psychiatric meds with Pharmacy: Matt Williams Pharm D
Agitation:
Etiology and Incidence:
Variety of causes:
Incidence
Agitation Severity Assessment: AMS Score AMSS
Rapid sedation for acutely agitated patients: ACEP guidance
BZRD or conventional antipsychotic (Haldol, droperidol)
If rapid sedation required, consider droperidol over Haldol
Either atypical or typical antipsychotic effective if known psychiatric diseases
Ketamine added recently as treatment option
Antipsychotics:
Pharmacokinetics
Side effect profiles:
Droperidol:
Black box warning long ago for QTC prolongation
But more recently deemed safe and more effective than Haldol
Obtain EKG if possible before (or after) use if possible
QTC prolongation effect present in very high doses
Onset of action 5 min compared to 20 min for Haldol
AAEP: no EKG for doses < 2.5, up to 10mg is safe and effective in patient with agitation
QTCs
Olanzapine least qtc prolonging
In patients with prolonged qtc, haloperidol, olanzapine, or benzo may be preferred to droperidol or ziprasidone
First vs Second gen antipsychotics
Benzodiazepines
Benzodiazepines or Antipsychotics?
Strongest efficacy with combination therapy Haldol and midaz
Midaz/droperidol, droperidol, or olanzapine
Droperidol vs ziprasidone vs Ativan
Ketamine
NMDA antagonist
Dissociative Sedation: 1-2mg/kg 4-6mg/kg IM dose
Onset: IV 30seconds, IM 3-4 minutes; similar bioavailability
Hepatic metabolism
Extremely efficacious in violently agitated patients
Adverse effects ketamine
Research Recap with Dr. Motov
Started off with a reminder of the vast resources we under utilize:
Use the hospital library and our knowledgeable librarians!!
MMC Sharepoint-->
Institutional research library has a ton of useful resources- be sure to use it!
Has templates, resources on statistical analysis, access to published research
Followed by an extensive and awe-inspiring list of our attendings, fellows, and residents hard at work with their emergency medicine publications throughout 2021.
Thank you all and have a wonderful Wednesday!
-SD
