Clinico-pathologic Case Conference with Dr. Nicole Soria vs Dr. Bill Knight
The Case: A previously healthy young Asian college student wakes up with weakness in all extremities, lowers weaker than uppers. His college roommate had to help him out of bed. It started with some joint pain and nausea, minor muscle aches, fatigue and mild dyspnea as well. Review of systems is otherwise negative.
Exam: HEENT, CV, Resp, Abdominal, and MSK exams are normal. Skin normal. Neuro exam: Reveals 4 + strength in upper extremities, 4 - strength in lower extremities, decreased DTRs and down-going toes bilaterally, gait was unable to be assessed. Sensation intact to light touch. No cranial nerve deficits or other neurologic abnormalities.
Basic labs: Renal function normal, profoundly low potassium (2.1) and magnesium
EKG: Long PR interval, diffuse ST depressions
Dr. Knight's Gut Reaction: This sounds like Guillain-Barré - ascending weakness with decreased DTRs
- Onset (acute)
- Time course (days)
- Symmetry? (yes)
- Motor, sensory or both? (just motor)
- Proximal, distal or both (seems to be both)
- Fluctuating symptoms? (Associated with activity?) (no)
- Cranial Nerve involvement? (none)
- May be central or peripheral
- If there is a definitive sensory level think central
- If there are upper motor neuron signs (spasticity, hyperreflexia) think central
Our patient has none of the signs to suggest central cause of weakness.
Symmetric hyporeflexia differential:
- Peripheral Neuropathy
So the next question is why does a young male have hypokalemia?
Dr. Knight's Test of Choice: TSH/T4 - Predicted Diagnosis: Thyrotoxic Periodic Paralysis
The Diagnostic Test of Choice
TSH = 0.02
Thryotoxic Periodic Paralysis
- Complication of thyrotoxicosis in primarily Asian population
- More common in men than women
- This is an endocrine emergency
- Muscle paralysis and hypokalemia
- Potentially lethal: can result in arrhythmias
- Typically profound hypokalemia
- Can be precipitated by rest after exercise or after a carbohydrate rich meal
- Usually there are recurrent attacks and they occur more often at night
- Proximal muscles are weaker than distal, DTRs are decreased
- EKG findings
- Sinus tachycardia or sinus arrhythmia
- First degree AV Block
- High QRS Voltage
- U waves
Management of TPP
- Continuous cardiac monitoring
- Potassium supplementation
- Goal raise serum K and avoid rebound hyperkalemia (hypoK primarily from shift)
- IV or PO or both
- B-blockers, non-selective (blocks potassium uptake in cells)
- Treatment of hyperthyroidism
- Avoid precipitating factors
- Definitive therapy for hyperthyroidism
- B-blockers may be helpful long term
Cardiac Biomarkers with Dr. Matthew Scanlon
For an introduction, take a look through Dr. Scanlon's post from earlier in the week on troponins
Troponin assay: immunologic assay against different epitopes on the troponin molecule. Different troponin assays (e.g. I vs T) do not have physiologic significance and are simply focused on different parts of the troponin molecule.
Biokinetics of Troponin following Myocardial Infarction
- Troponin begins to rise in serum after 2-4 hours
- Detectable after 4-9 hours
- Peak in 12-24 hours
- Cleared in 7-10 days
Different Types of MI
- Type I: Occlusion of a coronary vessel due to thrombus or plaque
- Type II: Ischemic imbalance ("demand ischemia")
- Type III: Cardiac death due to suspected MI (no biomarker confirmation)
- Type IV: Myocardial infarction following PCI
- Type V: Myocardial infarction following CABG
Do troponin levels correlate with the extent of infarction?
- Yes, troponin levels provide a rough estimate of infarct size.
- Correlation strongest at 24 hours and for STEMI (NSTEMI correlated less)
Type II MI: Whats on the differential?
- Extreme catecholamine release
- Significant burn injury
- Perioperative period
- Exogenous catecholamine use
- Cerebrovascular accident
- Conditions precipitating oxygen supply/demand mismatch
- Pulmonary embolism
- Direct inflammatory/infectious insult to myocardium
- Unknown mechanism
- Chronic Kidney Disease
In a patient with a pulmonary embolism: is there a correlation between troponin and TTE findings?
- It's not completely clear: some studies suggest there is not a good correlation.
- Troponin elevations in PE are prognostic for higher mortality.
Prognostication using troponin:
- It's not clear why baseline troponin is elevated in many patients who have CKD, however elevated troponin predicted an increased risk of mortality.
- Elevated troponin in patients with CHF with or without exacerbation also predicted an increased risk of mortality.
Troponin Elevation following PCI:
- Troponin can remain elevated for 7-10 days
- The trend (rise or fall) is more likely to be helpful than the absolute number following very-recent MI
- Elevated troponin in a patient post-MI is prognostic of morbidity and mortality
Case Follow-Up Master's Class: Dr. Natalie Kreitzer
HPI: Middle aged male who was transferred from an outside hospital with an ICU. Symptoms included dizziness and vomiting. On CT scan he has a small basal ganglia hemorrhage but has developed hydrocephalus due to local swelling.
PMH: DVT, HTN, Gout
Meds: Atenolol, HCTZ, Coumadin
Labs: INR - 4.7, the only abnormal lab (no reversal given prior to arrival in the ICU)
Learning Point 1: Reverse the anti-coagulation at the outset, even if you plan to transfer the patient.
Vitals: 97.7 F, HR 74, RR 20, 165/110
The patient was given Prothrombin Complex Concentrate and vitamin K for rapid INR correction to facilitate EVD placement.
PCCs vs FFP
- PCCs are effective at reversing anticoagulation
- PCCs reduced hemorrage size but not mortality (when controlled for hemorrhage size and location)
- PCCs reduced mortality and severe disability at 3 months
PCCs: Pros and Cons
- Pros: effective, no risk of transfusion reactions, lower volume needed
- Cons: expensive, risk of thrombotic events (~1.4%)
Shortly after receiving PCCs and vitamin K: the patient suddenly declines and becomes bradycardic, hypotensive, and hypoxic.
Learning Point 2: When your patient suddenly, unexpectedly declines, start over.
- Hematoma expansion: Brott et al. described hematoma expansion in 26 percent of patients within one hour
- Seizure: Incidence of seizure in ICH is 1.7% up to 17%
- Thrombotic complication: such as PE
- Anaphylaxis from Vitamin K
- Primary cardiac etiology (MI precipitated by PCCs)
Patient course: intubated and lined. EKG concerning with atrial flutter and ST segment depressions. Neurologic exam improved with better blood pressure. CT Head did not show any significant progression. CTPA negative. Chemically cardioverted out of atrial flutter with amiodarone. Troponin begins rising and peaks at 24.
He eventually was extubated and received a VP shunt after a failed EVD wean. Left heart cath showed no CAD.
Diagnosis: Takotsubo Cardiomyopathy
- From the Japanese word for Octopus Pot
- Most common finding on ECHO there is apical ballooning of the LV (81%)
- More than half of these cases occur due to an acute neurologic or psychiatric disorder
- Most frequently SAH
- Typically LVF improves rapidly
- Therapy is mostly supportive but ACE-i or ARB can be beneficial
Air Care Grand Rounds
Case Presentation with Dr. Liz Powell
HPI: Young male - pedestrian struck by motor vehicle
Exam: Obese male, guppy breathing - gasping respirations, secretions. Breath sounds are present but diminished bilaterally. Bruising and ecchymosis over the lower abdomen and pelvis. Evidence of head trauma on exam.
BP 76/40, saturations in the low 90s but with poor pleth
Neuro exam: GCS 3
How do you intubate this patient?
- Consider resuscitation before intubation in the hypotensive trauma patient. Remember to use your airway adjuncts.
- Resource utilization is key:
- Figure out what tasks are critical and need to be done by you
- Delegate tasks that can be done by others
- For use in pediatric patients in a can't intubate, can't oxygenation scenario.
- This is a temporizing measure - a definitive airway will still need to be established.
- Classically for patients under 5 years of age and the majority of patients under 10 years of age.
- See our taming the SRU post about needle cric for more details on the procedure.