Grand Rounds Recap 8.25.21
/MORBIDITY AND MORTALITY WITH DR. WALSH
Case 1: Bactrim-associated Acute Kidney Injury (AKI) and Abscess Imaging
Bactrim has been associated with transient increases in creatinine; however, previous studies have disputed whether this reflects a true decrease in renal function. More recent studies have re-demonstrated an association between AKI and Bactrim.
In one study, there was an 11.2% v. 0% incidence of AKI in patients who received Bactrim when compared with those who received Clindamycin, and AKI was further associated with AKI in those who received Bactrim and who were previously diagnosed diabetes, hypertension, and CKD.
Another study in Japan which used cystatin C (not tubularly secreted like Bactrim) demonstrated a 56% incidence of decreased GFR among those who received Bactrim; however, this study was poorly powered.
Two alternative regimens to Bactrim for gram positive coverage include: 1. Clindamycin OR 2. Doxycycline + Cephalexin. Both regimens perform adequately within our antibiogram at UC.
Several recent studies have demonstrated that point-of-care US for abscess has adequate sensitivity for diagnosis - 94.6% sensitivity, 85.4% specificity in 2010 meta-analysis, confirmed by testing, drainage, or revisit within 14 days.
When compared with CT, US of SSTI concerning for abscess was noted to have higher sensitivity (96.7% v. 76.7%) compared to CT, with no difference in sensitivity noted based on performer experience, though attendings did have superior image quality.
Take Home Points:
TMP/SMX Bactrim may lead to AKI, particularly in patients with DM and HTN.
Doxycycline is an appropriate alternative to TMP/SMX.
Ultrasound is more highly sensitive for abscess.
Ultrasound is more sensitive for abscess than CT.
Case 2: Tylenol (APAP) toxicity
Tylenol toxicity is the #1 cause of hepatic failure in developed nations with over 70,000 health care visits and 300 deaths annually in the US.
APAP toxicity occurs due to increased production of NAPQI, which saturates the glutathione metabolic pathway, with resulting NAPQI accumulation in hepatocytes causing hepatic damage. This pathway is adversely affected by alcohol use (chronic use is harmful, acute can be protective) and fasting.
Independent predictors of disease severity among individuals with acute liver injury with therapeutic doses (ALITD) of Tylenol include alcohol (OR 2.177), most impressively as well as duration (OR 1.014) and old age (1.026).
Treatment of acute overdoses relies on the Rumack-Matthew Nomogram. If a patient is supratherapeutically subacutely dosing, or reports chronic ingestion of APAP, then treatment with NAC should be considered for those with an APAP concentration over 20 ug/mL or if they are found to have elevated ALT and detectable APAP levels.
N-acetylcysteine (NAC) treatment regimen:
Oral: Load 140 mg/kg. Re-dose 70 mg/kg q4h x 17 doses.
IV: Load 200 mg/kg over 4 hours. Infuse 100 mg/kg over 16 hours (two dose regimen, also has a three dose option)
Take Home Points:
ALI can occur at therapeutic APAP doses.
Most of these patients have excess EtOH intake or are fasting.
Detectable APAP level with evidence of hepatic injury should be treated with NAC.
Case 3: Cerebral Venous Thrombosis (CVT) - Presentation and Diagnosis
CVT: Prevalence of 15.7 cases/million patient-years; 3:1 female to male predominance. Increased risk with malignancy, thrombophilias, nephrotic syndromes, and possibly COVID
Patient’s most commonly present with headache (80%), seizure (40%), or focal neurologic deficits (40%). They may have hallucinations or cranial nerve involvement - specifically CN IV or VI - with cavernous sinus involvement.
Pathophysiology: Venous occlusion leads to poor outflow and subsequently decreased cerebral perfusion pressure and hypoxia. With decreased concomitant CSF outflow, you have increased ICP. Finally, damaged vessel walls can lead to secondary subarachnoid hemorrhage.
Diagnostic evaluation:
When a D-dimer and risk stratification based on symptoms were used in concert, no single or combined factor had an adequate PPV or NPV to rule out CVT. In this study, D-dimer had a 26% false negative rate.
A non-contrast CT may demonstrate suggestive findings such as hyperdensity of a thrombosed sinus or deep vein (cord sign), edema, or hemorrhage secondary to venous congestion, but is not adequate with a sensitivity of 25-56% and 99.5% specificity.
A venographic study - either a CTV or MRV - should be performed in evaluation of DVST if the plain CT or MRI is negative or to define the extent of the CVT if plain CT or MIR suggests this as a possible diagnosis (Class I; Level C evidence).
Take Home Points:
Venous sinus thrombosis is rare and difficult to identify.
Symptoms and D-dimer cannot rule our CVT.
Non-contrast CT can rule in, but not out CVT.
MRV and CTV are equivalent, though MRV is considered the gold standard.
Case 4: Early initiation of pulmonary vasodilators in acute decompensated right heart failure
The right ventricular (RV) death spiral: Right ventricular dilation from acute or acute on chronic insult leading to increased RV wall tension, decreased RCA perfusion, RV ischemia, and RV overload with increased peripheral vascular resistance. RV overload also affects left ventricular (LV) function with RV septal intrusion into the LV and decreased LV filling, decreased cardiac output, and decreased RV perfusion.
Dr. Elwing’s recommendation for the peri-arrest known RV failure patient:
Pulmonary vasodilators such as Epoprostenol (increased cAMP and vasodilates) and Nitric Oxide (increased cyclic GMP and vasodilates;)
Restart home medications
Preference for inotropes like dobutamine before vasopressors
Norepinephrine> vasopressin
Alert ECMO team for possible cannulation
Nitric Oxide: Dosed at 20 ppm (max); can titrate down; able to obtain within 10 minutes
Epoprostenol: Dosed at 50 ng/kg/min (max), can titrate down, able to obtain in 30-40 minutes as it must be mixed
Take Home Points:
Decompensated pulmonary hypertension can progress rapidly.
Primary goal in pHTN is offloading the right ventricle.
iNO and Epoprostenol can be administered via CPAP/BiPAP or HFNC.
ECMO should be considered pre-arrest in decompensated pulmonary hypertension.
Case 5: Strategies to prevent cognitive bias and improve reflective practice
We all experience cognitive bias and can employ strategies to overcome or be more cognizant of it. These include:
Thinking about what you might be trying to “explain away”
Reviewing vital signs prior to disposition and historical vitals
Cognitive debiasing - in some studies, this method has been employed using a checklist of questions to prompt greater reflection.
Cognitive forcing is the implementation of a “hard stop” to make yourself reevaluate decisions and overcome cognitive shortcuts and biases that may have occurred before proceeding.
Example: SLOW mnemonic - Are you Sure about that? Look at the data and what it is Lacking and how it all Links together. What if the Opposite is true? Worst case scenario and What else could this be?)
In studies reviewed, cognitive debiasing and cognitive forcing demonstrated no change in the diagnostic outcome.
To keep an incessant watch (Acad Emerg Med. 2011) - single resident (and former Chief Resident at UCEM) review of >900 admission over course of residency to assess diagnostic accuracy, errors. Smith concluded that M&M does not catch all errors, particular near-misses, that your education is your responsibility, that self-evaluation combats learning plateaus, and that you don’t know you made a mistake, unless you look.
Take Home Points:
Cognitive biases affect all of us.
Increased awareness of biases and cognitive forcing are likely ineffective.
Bias can be fought through careful reflection of your performance.
Keep an incessant watch
Case 6: Outpatient Alcohol Withdrawal:
There is little to no evidence to support outpatient alcohol withdrawal treatment on discharge from the emergency department. Most studies focus on inpatient settings.
Consensus guidelines based on national practice patterns and expert opinions suggest that individuals who meet the following guidelines should be stable for outpatient treatment:
A CIWA < 8 at 1-2 hours apart
No other medical or psychiatric issues complicating ability to care for themselves
No prior history of complicated withdrawal
No seizures in the ED stay
Outpatient alcohol withdrawal regimens:
Chlordiazepoxide: 25-100 mg TID over 5-6 days
Diazepam: 20 mg qD over 5-6 days
Lorazepam 2 mg TID over 4-6 days
Consider hepatic function when deciding between lorazepam, which undergoes glucuronidation producing inactive metabolites and is preferred for those with known hepatic disease versus diazepam and chlordiazepoxide, which both undergo metabolism via CYP producing active metabolites.
BZD have demonstrated a protective benefit against alcohol withdrawal symptoms, especially seizures, when compared with placebo, but we are unable to make definite conclusions regarding the effectiveness and safety of BZDs.
Take Home Points:
Evidence for outpatient treatment of withdrawal is poor.
Benzodiazepine taper may be considered for mild withdrawal.
No studies have demonstrated safety of benzodiazepine tapers.
Gabapentin is an emerging treatment for mild alcohol withdrawal.
R2 CPC WITH DRS. MARTELLA AND SHEWAKRAMANI
The Case: An elderly male patient with a history of DMT2, HTN, HLD, EtOH cirrhosis and esophageal strictures (s/p balloon dilation) who presents with 2 days of emesis and associated diaphoresis with solid food. He states that these symptoms are similar to when he was initially diagnosed with esophageal strictures. He is hypotensive on arrival to 86/57. Vitals otherwise notable for HR 81, O2 Sat 97%, 98.2 F. Exam unremarkable. Labs notable for mild anemia, hyponatremia at 131, AG 19, transaminitis. Patient received 1 L of LR with persistent blood pressure at 92/63. Expanded work up with STE in V2 and TWI in V2-V5, a troponin of 1.98, lactic acid of 2.4, VBG with pH 7.45, pCO2 34, HCO3 24, no BE. CT C/A/P with no evidence of PE and no acute intra-abdominal pathology save 1.5 cm fat attenuation lesion at the right hepatic dome. And then a test was ordered…
Deep T-wave inversions differential
Cardiac: ACS, Welllen’s, LVH, Takotsubo, myocarditis, BBB, PE
Neurologic: Intracranial lesions (bleeds)
Metabolic: electrolyte disturbances
Diagnostic test of choice: Point-of-care cardiac echo looking for left apical hypokinesis suggestive of Takotsubo’s cardiomyopathy
Takotsubo Cardiomyopathy (Octopus trap) aka Broken Heart Syndrome or Apical Ballooning Syndrome
Stress-induced (36% physical trigger such as ARF, operative intervention, 27.7% emotional trigger, 7.8% combo, 28.5% no obvious trigger)
Most often seen in women > 60 years of age
Commonly present with chest pain (in 75.9% of patients), dyspnea, syncope, shock
Mimics myocardial infarction with EKG changes of STE in anterior precordial leads observed the most frequently, but with ST depression, QT prolongation, and T-wave inversions also observed.
Pathophysiology: Catecholamine-induced dysfunction and spasm causing myocardial stunning by direct myocardial toxicity, though hypothesis based on animal studies and higher catecholamine levels observed in patients with Takotsubo’s vs. true MI.
Evaluation and diagnosis includes:
EKG with new changes (either STE or TWI) OR modest troponin elevation
Coronary angiography with non-obstructive CAD or coronary disease in areas that do not correlate with regional wall motion abnormalities
Absence of myocarditis, pheochromocytoma, significant head injury
Transient left ventricular apical hypokinesis, akinesis on echocardiogram.
Management:
If presenting with shock (observed in 5-10% of patients), consider small fluids (as warranted) versus inotropic resuscitation with dobutamine (tends to be less effective than usual)
If presenting with signs and symptoms suggestive of heart failure, then consider gentle diuresis +/- vasodilators
If evidence of thromboembolic disease, then initiate heparin. Patient with LV apical systolic dysfunction may develop a ventricular thrombus.
Prognosis:
Risk of in-hospital complications similar to ACS patients
Most common complications include heart failure and stroke
Recovered LV systolic function in 1-4 weeks
Risk of recurrence is 1.8% per patient year
NEUROLOGY CONSULTANT’S CORNER: PRO TIPS FOR THE ED PROVIDER WITH DR. LAPORTA
Forced Eye Version
New onset forced eye version can be a neurologic emergent suggesting stroke or status epilepticus. Look for bilateral eye gaze deviation.
“Look towards the stroke”
“Look away from the seizure”
Do not mistake forced eye version and dysconjugate gaze, which is single eye deviation (ie, “tropia”). This could be normal amblyopia (“lazy eye”) present in 3% of adults or suggest a toxic/metabolic process.
Case 1: The Twitchy Guy in the Corner
Distinguish between negative myoclonus (involuntary relaxation of muscles, sequela of disruption of nerve transmission by toxins, infection such as UTI, metabolic insults such as DKA, hypercarbia, hyperammonemia causing asterixis) and positive myoclonus (involuntary activation of muscles, also related to toxins typically but could represent a seizure)
Case 2: Posterior Reversible Encephalopathy Syndrome
Vasoregulatory syndrome of the CNS that causes the vessels to become “leaky” often in the posterior circulation distribution. Classic MRI findings demonstrate vasogenic edema in the posterior region. Excessive edema can lead to cortical irritation and seizures. Malignant hypertension is the most common and treatable cause, though you can also consider pre-eclampsia, immunosuppressants, chemotherapy, and autoimmune disease.
Management is similar to hypertensive emergency with blood pressure management (decrease BP by 10-25% within 2 hours). Should ensure that this is not a stroke before doing so that you do not drop compensatory autoregulation. If focal neurologic deficits (beyond vision loss) are present, then should consider stroke as more likely etiology.
Case 3: Myasthenic crisis
A focused exam is critical - look for fatigable weakness, ptosis, diplopia on prolonged upgaze, strength of cough, neck flexors, extensors (ability to raise head off bed)
Diagnostic considerations
Breath count is clutch. Patient counts as high as possible on one breath (normal > 50). Around 30 is concerning and should be in step down. If 20, then consider elective intubation. If 10-15, then consider elective but emergent intubation.
Negative Inspiratory Force (NIFs) also helpful in measuring inspiratory strength as is forced vital capacity.
Check a VBG
Consider precipitants for MG crisis including antibiotics, beta blockers, antiarrhythmics, magnesium, avoid using depolarizing neuromuscular blocking agents (eg, Succinylcholine) when intubating.
Treat with IVIG and plasma exchange
Case 4: Peripheral v. Central Vertigo
HINTS exam can be used to differentiate, but has only demonstrated good sensitivity and specificity in those who are well trained. Controversial and lacks convincing evidence when used by ED providers.
Head impulse - Eye lag with corrective saccade suspicious for a peripheral process
Nystagmus - Central process suggested by vertical, bidirectional, occasionally rotary nystagmus in contrast to unidirectional or horizontal nystagmus
Test of Skew - Central process suggested by vertical skew deviation
Case 5: Low back pain with bilateral leg weakness and feet numbness
Remember to check reflexes in certain patients
Hyperreflexia and clonus suggest UMN whereas hyporeflexia and areflexia suggest a LMN.
Back pain is an under discussed but common manifestation of Guillain Barre Syndrome, especially in concern with lower extremity motor/sensory changes and areflexia
More GBS patients die from dysautonomia (heart block, hypotension) than respiratory failure.
Case 6: Acute Dystonic Reaction
Dystonia is abnormal sustained muscle contractions that can be related to disease, congenital, or medication side effects
Acute dystonic reactions typically involved retrocollus, upward eye deviation (oculogyric crisis), and forced jaw opening
Offending meds are those that block dopamine such as typical antipsychotics, antiemetics like metoclompramide and prochlorperazine, or dopaminergic agent withdrawal.
Treat by withdrawing the offending medication and administered anticholinergic agents - Benadryl, benztropine or trihexyphenidyl, monitor for status dystonicus
Case 7: Double Trouble Diplopia
Are symptoms monocoular or binocular?
Monocular diplopia means that the double vision occurs in one eye or only when that one, bad eye is open. This is an ophthalmologic issue and often an issue of refraction
Binocular diplopia means that the double vision occurs when both eyes are open and resolves when either eye is closed. This is a primary neurologic issue, most often due to misalignment likely caused by a cranial nerve palsy
Same concept with vision loss. Monocular vision loss generally occurs as a result of a primary ophthalmologic issue, and binocular vision loss often results from disruption at a level of the visual pathways (eg, early decussation, optic chiasm, visual cortex, etc)
One exception is optic nerve pathology such as optic neuritis from MS and NMO, which can result in monocular vision loss; however, an ophthalmologic exam is still a reasonable first step.
Case 8: Recently diagnosed ALS with acute decompensation
ALS is a fatal disease, but one that progresses in an insidious fashion (typical life span is 3-5 years, though there are fast and slow progressors). If a patient with ALS decompensates rapidly, then certainly have an informed discussion with decision makers and patient as able, but also consider pursuing a full infectious/metabolic work up.
