Grand Rounds Recap 9.12.18
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QI/KT: COPD WITH Dr. Lane and Dr. Hall
Pathophysiology and Epidemiology
Chronic obstructive pulmonary disease patients suffer persistent respiratory symptoms linked to airway and/or alveolar abnormalities that limit airflow. PFTs show FEV1/FVC <0.7
Acute exacerbations of COPD (AECOPD) are marked by worsened symptoms and also increased inflammation that perpetuates proteinase/anti-proteinase imbalance and further lung injury
AECOPD are most commonly caused by infectious etiologies, of which bacterial infections including H. flu predominates
In our institution, about 40% of patients are admitted, about 40% are discharged, and about 20% are placed in ED Observation; more patients are admitted during winter months
Evidence for Evaluation in COPD
VBG is adequate for most patients: McKeever et al (2016) showed ABG/VBG correlated well for mild acidemia/acidosis, as well as showed SaO2 and Pulse ox correlated well if pulse ox >80%
While limited evidence is available to support chest x-ray, most experts recommend using CXR in evaluation of AECOPD
Multiple protocols have been proposed for using ultrasound to evaluate dyspneic ED patients, including the LuCUS protocol (Russell et al 2015); however, the evidence is not year clear that typical emergency physicians performing US increase diagnostic accuracy (Papanagnou et al 2017)
PEs are reasonably common in admitted AECOPD patients (16%; 95%CI 8-26%) according to a recent meta-analysis (Aleva et al 2017)
Consider PE when pleuritic CP, lower limb asymmetry, history of VTE/PE, malignancy, immobility, heart failure, absence of typical URI symptoms, obesity, or a decrease in PaCO2 from baseline are present
Multiple studies of predictors of admission in ED COPD patients including Tsai et al 2007; however, no validated scale/clinical decision making tool to assist disposition decisionmaking
Evidence for Acute Interventions in COPD
Oxygen:
Titrated O2 saturation of 88-92% has been shown to have lower mortality, hypercapnia, and respiratory acidosis (Austin et al. 2010)
Bronchodilators:
In stable COPD, duo-neb has been shown to increase FEV1 more significantly than albuterol or ipratropium alone
In acute exacerbations of COPD, evidence for bronchodilators is poor but short acting beta-2 agonists and short-acting muscarinic antagonists produce similar responses in FEVI and adding them in combination does not necessarily increase the response (Geffen et al 2016).
Despite poor evidence, they are a mainstay of treatment and should be used in acute exacerbations.
Bronchodilators given by metered-dose inhaler +spacer vs nebulizer have no difference in FEV1 after one hour, safety, hospital admission, or subjective symptoms. The medication cost of nebulizers is much cheaper than the inhalers at UC.
Corticosteroids:
Should be given in acute exacerbations as they have number needed to treat of 9, improve FEV1, decrease treatment failure, and shorten hospital durations (Walters et al 2014).
Shorter courses of PO steroids are non-inferior to longer tapers with IV steroids (Leuppi et al 2013).
Antibiotics:
Reduce the need for intubation, in-hospital mortality, treatment failure, and prolong time to next exacerbation (Rothberg et al 2010).
Consider antibiotics in all patients with acute exacerbations of COPD except in mild exacerbations without increased sputum purulence or production.
Which antibiotics to use should be guided by local resistance patterns. A good 1st line agent are the macrolides. Azithromycin 1st line for added anti-inflammatory activity in respiratory illnesses.
Non-Invasive Ventilation:
Number needed for beneficial outcome of 12 (Osadnik et al 2017).
Significantly decreases need for intubation with number needed to prevent intubation of 5 (Osadnik et al 2017).
Decreased mortality (Osadnik et al 2017).
Consider NIV for severe dyspnea, respiratory acidosis, and the initial mode of ventilation for respiratory failure
Magnesium
Some studies show marginal improvement in FEV1 at early times points and when given with beta-2 agonists. No effect on other clinical outcomes.
Hand Complaints with Dr. Faryar
Boxer’s Fracture: This is a fracture of the 5th metacarpal. It is commonly associated with punching an object, but rarely occurs with proper punching form. Diagnosis is made with xray, but there are several physical exam findings that help determine management. It is important to look for any open wounds. As these are often “fight bites”, retained teeth in the wound is always a possibility. Any open wound should be copiously irrigated. The fingers should also be examined to look for any rotational misalignment. When flexing at the MCP and PIP joints, imaginary lines extending from the digits should converge at the scapho-lunate junction. If they don’t this may indicate some degree of misalignment. Finger “scissoring” is another sign of misalignment. When in doubt, always compare to the unaffected digit. On xray, calculating the fracture angulation can determine if reduction is needed. The acceptable degree of angulation can be remembered using the 10,20,30,40 rule:
2nd digit: 10 degrees angulation acceptable
3rd digit: 20 degrees angulation acceptable
4th digit: 30 degrees angulation acceptable
5th digit: 40 degrees angulation acceptable
If there is >40 degrees of angulation or misalignment, the fracture should be reduced. This can be accomplished using a hematoma block or ulnar nerve block. One technique for reduction is the Jahss Maneuver, where you flex the MCP and PCP joints, then use the proximal phalanx to push up the metacarpal head. There are many images and videos of this maneuver online. The patient should then be splinted with 70-90 degrees flexion at the MCP joint. Hand surgery should be consulted with open fractures and fractures with malrotation as these may need open reduction with internal fixation.
Extensor Tendon Injuries: The dorsum of the hand is separated into several zones, which helps to determine management.
Zone 1: mallet finger, should be splinted, no tendon repair necessary
Zone 2-4: these may be repaired, but often do well with simple splinting
Zone 5: if not a fight bite, it can be repaired
Zone 6: these all may be repaired in the ED
Zone 7-8: do not repair these as there is a high risk of complications
It is important to fully evaluate the tendon through range of motion to look for laceration. Use finger tourniquets to make a bloodless field. If you cannot see a tendon injury: splint, close skin, follow up with hand in 1-3 days. If a tendon laceration is seen and it is in an appropriate zone, can be repaired using either a figure of 8 suture or a “grasping” suture technique (modified Kessler or Bunnell). Typically a braided non-absorbable suture is used. Ethibond or mersline sutures are preferred, but if they are not available nylon or prolene can also be used. Splint all these patients in 30 degrees of wrist extension and have them follow up with hand surgery.
Felon: This is a pulp space infection of the pad of the finger. Complications include ischemic necrosis, osteomyelitis, flexor tenosynovitis, and septic arthritis of DIP joint. These need I&D; a lateral incision is preferred as it avoids the digital artery/nerve and tendons. Splinting can be performed and antibiotics should be given for 5-7 days.
atrial fibrillation in chf WITH DR. fermann
These patients are complex and there isn’t much good literature on how to manage these patients acutely. Often we have questions of if they are AF because their HF has gotten worse, or are they in HF because of their AF? Unfortunately, this is a difficult question to answer and we probably won’t be able to reliably figure this out in real time.
There are many reasons why these conditions often occur together: abrupt changes in rate can impair filling, tachycardia mediated cardiomyopathy, atrial kick important for patients with HFpED, increased sympathetic tone occurs in patients with CHF.
Atrial fibrillation occurs in >15% in patients with HF, and its prevalence increases as HF worsens:
Mild CHF: 5-10% have atrial fibrillation
Moderate CHF: 10-26% have atrial fibrillation
Severe CHF: up to 50% have atrial fibrillation
In chronic atrial fibrillation management, the goal HR is 80-100. However, in an acute exacerbation, we want this in the 100-120 range. Lowering the rate too quickly can worsen cardiac output.
Rate Lowering Agents:
Calcium Channel Blockers: these medications result in excellent rate control. However, they are negative inotropes. Verapamil is worse in this regard than diltiazem. These are probably not the best agents in patients with heart failure. But this study, although only 37 patients, suggested that diltiazem may be safe in patients with moderate to severe CHF.
Beta Blockers: these reduce risk of hospitalizations or death chronically in patients with CHF. They can be effective in the acute setting as well.
Digoxin: this medication increases parasympathetic tone on the AV node and may have some benefits with inotropy. However, it has a slow onset, and high sympathetic tone (such as that in acute heart failure) may overcome its effects.
Amiodarone: the increases likelihood of conversion to sinus rhythm and may cause less hypotension than diltiazem. However, it has many non-cardiac side effects that may limit its use.
ACCF/AHA Guidelines recommend either beta blockers or calcium channel blockers as first line. However, if patient has decompensated heart failure (EF < 40%), they recommend against using a beta blocker or calcium channel blocker.
It is important to remember to not just treat the heart rate, but to treat the heart failure as well. Do not forget to diurese these patients if they appear volume overloaded. This can help to break the cycle leading to atrial dilation and atrial fibrillation.
If the patient is unstable, and you feel it is due to the atrial fibrillation (elevated heart rate), cardioversion is reasonable. However, it often is not effective. Cardiogenic shock in this setting has a high mortality. Inotropes (milrinone, dobutamine) and pressors (vasopressin) can be considered, but come with their own set of risks and side effects. Once you are in this setting, there are not a lot of good literature to guide management.
r3 taming the sru WITH DR. banning
The Case: EMS was called to the house of a teenage female after having a seizure. Initial vitals per EMS were notable of a BP greater than 200/100. Patient had another seizure en route to the hospital and was given 5mg of IM midazolam. Oh and one other thing to mention… the patient was clearly in her third trimester of pregnancy but did not know it. When she arrived in the emergency department she was extremely agitated and altered with initial vitals of BP 86/49, HR 192, RR 30, O2 100%.
Differential Diagnosis for seizures in pregnancy:
Eclampsia
Central Venous Thrombosis
Stroke
ICH
Drug (ethanol or benzo) withdrawal
Hypoglycemia
Hyponatremia
Infection
Primary Epilepsy
In a pregnant patient with hypertension, assume eclampsia until proven otherwise. If symptoms not resolving continue to evaluate for other etiologies.
Eclampsia: Development of seizures in a woman with pre-eclampsia. This is thought to be caused by systemic endothelial dysfunction from both maternal and fetal factors.
To know whether this patient has eclampsia, we must define pre-eclampsia:
SBP >140 or DBP >90 on two occasions four hours apart after 20 weeks of gestation in a previously normotensive patient AND the new onset of one of the following:
Protein/creatinine ratio > 0.3 or +1 protein on urine dipstick
Platelet count < 10,000
Serum creatinine > 1.1 or doubling of baseline creatinine
Liver transaminases 2x upper limit of normal
Pulmonary edema
Cerebral or visual symptoms
Labs to evaluate for pre-eclampsia:
Urinalysis, CBC, BMP, Hepatic Panel, LDH, Uric acid (supplementary marker of renal clearance), Coagulation panel (if indicated based on other labs)
Complications of Pre-eclampsia:
Eclampsia, stroke, pulmonary edema, DIC, acute renal insufficiency, HELLP Syndrome
Treatment:
Magnesium: unclear mechanism, possible acts as a smooth muscle relaxer
Loading dose: 6g IV over 30 min
Maintenance dose: 2g IV per hr over 24 hours
For any additional seizures: additional 2g IV bolus over 5-10 min
Intramuscular dose if unable to obtain IV access: 5g IM x2 (in each buttock)
Blood Pressure Management:
Hydralazine: 5-10mg IV every 20 min
Labetalol: 20-40mg IV every 10-15 min
This particular patient it was very difficult to obtain IV access, begging the question what are the best medications to sedate pregnant patients if needed:
Benzodiazepines
Crosses placenta, but much lower doses in fetus
Can cause respiratory distress in fetus at high doses
Probably safer options to use
Ketamine
In high doses shown to be teratogenic
Randomized control trial showing no change in apgar scores when used as induction agent
Caution with HTN and tachycardia
Anti-psychotics
Avoid in first trimester as can cause deformities
Can be considered safer than physical restraint late in pregnancy
Use minimal doses to reduce agitation
Still unclear if this patient truly has eclampsia given these patients are usually hypertensive. During resuscitation, it is important to evaluate for other causes of shock.
Review of the causes of shock in pregnant patients:
Cardiogenic:
Peripartum cardiomyopathy
Arrhythmia (this patient was initially thought to be in SVT and was cardioverted without improvement)
Hypovolemic:
Dehydration
Hemorrhage: specifically do not forget placenta previa, placental abruption, uterine rupture (associated with trauma)
Obstructive:
Pulmonary Embolism
Tamponade
Tension PTX
Distributive:
Sepsis
Amniotic Fluid Embolism: when amniotic fluid enters mother’s blood stream and triggers cardiovascular collapse and coagulopathy. Most often seen during childbirth, but can be seen with trauma.
Other key principals to treating shocky pregnant patients:
Left lateral decubitus to increase preload
All code medications are category B/C medications, but should not be withheld from mother for life saving measures
If unclear gestational age, consider administration of betamethasone for lung maturity in fetus
Back to our patient …. Improved with magnesium load and IV fluids. Final diagnosis: likely eclampsia with unclear cause of hypotension. Possibly reaction to midazolam, possibly hemodynamic compromise from severe tachycardia or positioning given patient was on her back. Patient ended up going for stat C section with OB with good outcome for both fetus and mother.
r1 clinical diagnostics: Toxic alcohols WITH dr. Frederick
When dealing with patients who have ingested toxic alcohols remember to consider both the effects of the parent alcohol and the toxic metabolite. Ethanol co-ingestion may obscure and delay the presentation of toxic alcohol ingestions.
Isopropanol:
More intoxicating than ethanol
In severe ingestions may cause hemorrhagic gastritis and cardiovascular compromise
Causes significant ketosis without acidosis
The metabolite (acetone) is less toxic than the parent alcohol, so don't use alcohol dehydrogenase inhibition, instead just let them metabolize while providing supportive care
Methanol:
Presentation can be delayed in onset
Damages the myelin of the optic nerve leading to visual symptoms including central scotoma, "snowstorm" sensation, and complete blindness
Ethylene Glycol:
3 stages of presentation:
CNS Depression: mimics ethanol intoxication
Cardiovascular stage: HTN, tachycardia, tachypnea, hypocalcemia (tetany, cranial nerve palsies, arrhythmias)
Renal Failure: glycolic acid leads to ATN and calcium oxalate deposition in the renal tubules. This AKI can then delay clearance of ethylene glycol, furthering its toxicity.
Evaluation:
Be wary of labs as they can vary greatly based on the time from ingestion and may mislead you
All alcohols initially cause an osmolar gap
Methanol and Ethylene Glycol also cause anion gap acidosis as metabolism occurs
Treatment:
Isopropanol:
Supportive care is typically all that is needed
Methanol and Ethylene Glycol:
ABCs!
ADH inhibition - allows the alcohol to be excreted unchanged before it is metabolized to it's toxic counterpart
Ethanol: readily available, difficult to regulate (goal is >100mg/dL), adds to the patient's CNS depression, requires a central line and ICU admission
Fomepizole: easy to dose, less monitoring
Adjunctive Therapies - accelerate the clearance of toxic metabolites and shunt them through less toxic pathways
Methanol: treat with leucovorin or folic acid
Ethylene Glycol: pyridoxine and thiamine
Sodium Bicarbonate
Alkalinization decreases the ability of toxic metabolites to cross into tissues and cause damage
Target a pH >7.3
Hemodialysis
Indicated when signs of end organ damage are present (vision changes or renal failure) or there is severe acidosis (pH<7.1)
pediatric simulation WITH DR. valentino
Pediatric Trauma: Initial evaluation similar to adults. Starts with ABC’s. Do not get distracted just because it is a child. Make sure you have Broselow Tape or some other resource to help with dosing/equipment sizes.
Airway: pediatric patients are more prone to desaturating quickly or becoming acidotic
Breathing: needle decompression and chest tubes are placed in similar locations to adults
Circulation: if hypotensive, give crystalloid/blood as appropriate
GCS: consider hypertonic saline
Other interventions:
Thoracotomy: studies in blunt trauma show virtually no survival, consider in penetrating trauma
Pediatric Cases with the Pediatric Fellows
Case 1: Hemolytic Uremic Syndrome: characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Most cases occur due to shiga-toxin producing E Coli (90% of cases); another common cause is infection with strep pneumo (higher mortality). It is thought that the shiga toxin causes damage to the renal glomerular cells leading to cytokine activation, microthrombi, and hemolysis. HUS classically presents with a diarrheal illness, followed by acute kidney injury. However, other organ systems are often involved and many patients have neurologic symptoms. This makes differentiating this condition with TTP difficult in many cases. Antibiotic use with diarrheal illnesses may increase risk as antibiotics lyse bacteria releasing shiga toxin. Treatment for HUS is mainly supportive care. These patients can get pRBCs for Hgb less than 6-7. Most of the other treatments (dialysis, steroids, IVIG) have little evidence and will be mainly directed by specialists.
Case 2: Kawasaki Disease: this is a vasculitis of unknown etiology that occurs mainly in ages 4 months to 5 years. Diagnosis is primarily clinical (see below).
Diagnostic Criteria: Fever for at least 5 days PLUS 4-5 of the following:
Lymph node > 1.5cm (typically cervical)
Mucous membrane changes (cracked lips, strawberry tongue)
Rash (any rash)
Ocular (limbic sparing conjunctivitis)
Extremity Changes (swelling, erythema, skin peeling)
Incomplete Kawasaki: 2-3 criteria with 5 days of fever plus lab criteria (mix of ESR/CRP and some other labs). The cardiac complications can still happen with these patients.
The feared complication of Kawasaki’s disease is coronary aneurysm. This typically occurs in the 3rd-4th week of illness and can lead to MI.
Treatment: These patients will get IVIG (2g/kg IV) and ASA (80mg/kg/day). All of these patients need to be admitted. They will get a baseline echo and then will be followed by cardiology for repeat echos to look for coronary aneurysm.
