Managing the intubated patient with exacerbation of severe obstructive lung disease, especially asthma, can be very challenging as it carries higher risks of barotrauma due to higher pulmonary pressures and circulatory collapse due to auto-PEEP and decreased venous return. When measures such as medical therapy and noninvasive positive-pressure ventilation fail to prevent intubation, here are some tips to help:
1. Utilize a volume control ventilation mode to ensure a set tidal volume delivery / minute ventilation, as pressure-targeted modes will be more difficult due to the high pulmonary pressures in acute obstructive lung disease.
2. Set a low RR in order to allow for full exhalation, avoiding air-trapping / breath-stacking and circulatory collapse due to decreased venous return. This may require deep sedation and potentially paralysis.
3. Increase your inspiratory flow by shortening your inspiratory time (thereby increasing your time for exhalation.
4. Monitor for auto-PEEP:
5. Peak inspiratory pressures will be high -- what is more important is the plateau pressure, measured by performing an inspiratory hold at the end of inspiration. Provided your plateau pressure remains <30, you don't need to worry as much about the peak pressure alarms.
6. If your patient acutely decompensates in terms of hemodynamics and oxygenation -- first attempt to decompress their likely auto-PEEPed lungs by popping them off the ventilator and manually press on their chest to assist with exhalation of stacked breaths allowing venous return to the heart.
The American Diabetes Association requires a plasma glucose concentration greater than 250 mg/dL to diagnose diabetic ketoacidosis (DKA). However, with the new diabetic agents this is not always the case. With the introduction of SGLT2 inhibitors (canagliflozin [Invokana], dapagliflozin [Farxiga], empagliflozin [Jardiance]) there have been reported cases of DKA and patients being euglycemic.
Take Home Point
Patients with a low/normal blood glucose can still have DKA. Especially if they are taking newer medications, such as the SGLT2 inhibitors.
Hematologic toxicity (coagulopathy/bleeding) can occur with pit viper envenomation. Copperhead is the most commonly implicated pit viper envenomation in the U.S. However, the prevalence of hematologic toxicity from copperhead envenomation is variable, possibly due to regional variation in venom potency and species misidentification.
An observation study was performing using multi-center (Virginia Commonweath university, University of Virginia Medical Center and Eastern Virginia Medical medical center) electronic hospital/medical records (Jan 1, 2006 to Dec 31, 2016) of suspected copperhead bites. Authors state that copperhead snakes are "nearly exclusively endemic" to the VCU and UVA medical center region.
Results:
388 patients were identified but 244 met inclusion/exclusion criteria.
Hematologic toxicity: 14%
Conclusion
In a small sample of copperhead envenomation in Virginia, “subtle” hematologic abnormalities were observed but clinically significant hematologic toxicity was not observed (i.e. bleeding)
With increasing critical care boarding and the opioid crisis leading to more intubations for overdose, extubation - which was once a very rare event in the ED - is taking place downstairs more often. Prolonged mechanical ventilation is associated with a ton of complications, so it's important for the ED physician to be comfortable assessing extubation readiness. There is no single accepted set of criteria, but most commonly used are some variant of the following:
If the above criteria are met, two additional tests are frequently considered:
And don't forget to consider extubating high risk patients directly to BiPAP or HFNC!
Bottom Line: For conditions requiring intubation where significant clinical improvement may be expected while in the ED (e.g. overdose, flash pulmonary edema, etc), be vigilant about, and have a system for, assessing readiness for extubation.
Bone stress injury (BSI) in Adolescents
A BSI occurs along a pathology continuum that begins with a stress reaction and may progress all the way to a stress fracture.
Difficult to diagnose clinically.
Identifying risk factors as part of the history is very important.
Common sites for BSI are most frequently in the lower extremity and include the tibia, fibula, tarsals and metatarsals, calcaneus, and femur.
When considering this in an ED setting, image the involved area and if there is no fracture, advise discontinuing the activity until time of PCP/sports medicine follow up. For those with rest pain, pain with minimal weight bearing or in whom a fracture was suspected but not present, consider providing a walking boot or crutches.
BSIs occur more frequently in young athletes than in adults.
Almost 50% of BSIs occur in those younger than 20 years of age
Primary care and sports medicine providers are seeing more of these patients due to many factors.
Year-round training, sports specialization at younger ages and increase in training intensity/duration contribute to the increase incidence in adolescents.
Not surprisingly, participation in organized sports as an adolescent is a known risk factor.
Just as a change in sporting level from high school to college is a known risk factor for BSI, young “gifted” athletes who are promoted to competing with the varsity team may be at similar risk.
Shin pain lasting more than 4 weeks may represent a unique subset of MSK pain complaints increasing risk of BSI.
A prior history of BSI is a strong predictor of future BSI.
Inquire about night pain, pain with ambulation, and pain affecting performance.
Athletes with BSIs have a significantly lower BMI than controls (<21.0 kg/m2).
Athletes with BSIs sleep significantly less than controls.
Athletes with BSIs have significantly lower dairy intake than controls.
Inquire about components of the female athlete triad (low energy availability, menstrual dysfunction and low bone mineral density)
The incidence of empyema as a complication of pneumonia has been increasing since the 1990's and source control requires removing the pus from the chest as soon as possible, but how large should the drain be? The American Association for Thoracic Surgery (AATS) released the most recent guidelines for identifying and managing empyema in June 2017 and at the time had no certain evidence to guide the choice of large-bore vs small-bore catheters. Most studies to guide us are flawed (not randomized), but no recently published randomized studies exist to provide a definitive answer.
Bottom line: a small-bore pigtail catheter is a reasonable choice to drain empyema and flushing it every 6 hours has been shown to prevent clogging.
-Benzodiazepines alone are effective in terminating status epilepticus in 40 to 60% of pediatric patients
-The guidelines for second line agents are based on observational studies and expert opinion
-Adverse effects of phenytoin include hepatotoxicity, pancytopenia, Stevens-Johnson syndrome, extravasation injuries, hypotension and arrhythmias
- Levetiracetam has a reduced risk of serious adverse events, greater compatibility with IV fluids and can be given in 5 minutes versus 20 minutes for phenytoin.
Bottom line: In a recent randomized control trial they found that levetiracetam was not superior to phenytoin as a second line agent for management of convulsive status epilepticus in children. There was no difference between efficacy or safety outcomes between the two groups.
Pulmonary complications - aspiration, pulmonary edema, etc. are frequently reported in both heroin intoxication and in reversal of opioid overdose with naloxone.
Suspected opioid overdose victims (N=1831) who received naloxone from EMS providers were studied retrospectively. Pulmonary complications were defined as pulmonary edema, aspiration pneumonia and aspiration pneumonitis.
Results
Conclusion
Higher out of hospital naloxone administration is associated with increased odds of developing pulmonary complications
POCUS in the Critically Ill Pregnant Patient
Long head of biceps tendon (LHBT) Testing
Overhead activities can cause anterior shoulder pain due to LHBT instability. A review of 3 physical exam maneuvers for bedside evaluation.
Speed test
Shoulder at 90° of flexion with arm fully supinated and elbow extended
Patient attempts to fwd. elevate arm against a downward force
Positive test is pain localized to bicipital groove.
Sensitivity 54% and specificity 81% for biceps pathology
Yergason test
Elbow at 90° of flexion with arm fully pronated and held against thoracic wall. Examiner grips patient’s hand and resists attempts at supination.
Positive test is pain localized to bicipital groove or LHBT subluxation.
Sensitivity 41% and specificity 79% for biceps pathology
Upper Cut test
Shoulder neutral with Elbow at 90° of flexion, arm fully supinated and hand in a fist. Patient moves hand toward chin in an uppercut motion like a boxer. Examiner places hand over patient’s fist and resists upward movement.
Positive test is pain localized to bicipital groove or LHBT subluxation.
Sensitivity 73%, specificity 78%, +LR 3.38 for biceps pathology
“Push dose pressors” – administration of small doses of vasopressors in the emergency room has become a common practice. A recently published study investigated the incidence of human error and adverse hemodynamic events.
Push dose pressors were defined as:
Adverse hemodynamic event was defined as:
249 out of 1522 patients were identified and analyzed from Jan 2010 to November 2017
Adverse event
Errors
Conclusion
With a shortage of push dose epi, this may be an opportune time to review alternative options (see also Ashley's email on the subject).
The dose of vasopressor required to reverse hypotension has been most studied in pregnant women undergoing c-section who get epidurals and experience spinal-induced vasoplegia and hypotension (not necessarily our patient population, but we can extrapolate...)
Phenylephrine was found to reverse hypotension 95% of the time at a dose of 159 micrograms (a neo stick has 100 ug/mL, so around 1-2 mL out of the stick)
Norepinephrine reversed hypotension in 95% of patients at a dose of 5.8 ug. The starting dose for our norepi order in Epic is 0.01 ug/kg/min, so if you have a levophed drip hanging and have an acutely hypotensive patient, you may want to briefly infuse at a higher rate such as 0.1 ug/kg/min (for a typical weight patient), or bolus approximately 3-7 ug for a typical patient. Of course the degree of hypotension, particular characteristics of your patient and clinical context should be taken into consideration. When your a lucky enough to have this resource, always consult your pharmacist.
Bottom Line: To reverse acute transient hypotension you may consider:
-A bolus of phenylephrine 50-200 ug (0.5-2 mL from neo-stick)
-A bolus of norepinephrine 3-7 ug
-Briefly increasing your norepinephrine drip (if you have one) to something around 0.1 ug/kg/min in a typical weight patient
-Always search for other causes of hypotension and consider clinical context.
Alteplase may be considered in some patients with a presumed or confirmed pulmonary embolism. Below is a list of the different patient populations and the associated alteplase dosing.
-Hemodynamically Stable/Submassive: Alteplase usually not indicated.
-Hemodynamically Unstable/Massive: Alteplase IV 100 mg as an infusion over 2 hours.
-Cardiac Arrest: Alteplase IV/IO 50 mg bolus over 2 minutes. Can repeat a second 50 mg bolus 15 minutes later if unable to achieve return of spontaneous circulation.
Volatile inhalants such as glue, lighter fluid, spray paint are abused by "sniffing" (from container), "huffing" (poured into rag), or "bagging" (poured into bag). "Dusting" is the abuse of canned air dust removal products. These inexpensive easliy accessible products are so dangerous that manufacturers include product warnings regarding lethal consequences from misuse and even may indicate that a bitterant is added to discourage use. Common duster gases include the halogenated hydrocarbons, 1,1-difluoroethane or 1,1,1-trifluroethane which are highly lipid soluble and rapidly absorbed by alveolar membranes and distributed to CNS. Desired effect of euphoria and disinhibition rapidly occur but unwanted side effects include confusion, tremors, ataxia, pulmonary irritation, asphyxia and, rarely, coma.
"Sudden sniffing death" is seen within minutes to hours of use and is due to ventricular arrhythmias and cardiovascular collapse. Available experimental evidence postulates the following mechanisms: Inhibition of cardiac sodium, calcium, and repolarizing potassium channels hERG and I(Ks) causing reduced conduction velocity and altered refractory period leading to reentry arrythmias or myocardial "sensitiization" to catecholamines resulting in after depolarizations and enhanced automaticity. Treatment should include standard resuscitation measures but refractory arrythmias to defibrillation have been reported and use of amiodarone and beta blockers should be considered.
Bottom Line:
Wound botulism presents as descending paralysis when Clostridium botulinum spores germinate in anaerobic necrotic tissue. There have been hundreds of cases in the last decade, but it is poorly reported outside of California.
Black tar heroin and subcutaneous injection (“skin popping”) carry the highest risk, but other injected drugs and other types of drug use suffice. C botulinum spores are viable unless cooked at or above 85°C for 5 minutes or longer and this is not achieved when cooking drugs.
Early administration of botulism anti-toxin (BAT) not only saves lives but can prevent paralysis and mechanical ventilation. An outbreak of 9 cases between September 2017 and April 2018 cost roughly $2.3 million, in part because patients didn’t present on average until 48 hours after symptom onset and it took an additional 2-4 days before the true cause of their respiratory depression and lethargy were understood. One patient died.
PEARL: talk to your injecting drug users about the symptoms of botulism: muscle weakness, difficulty swallowing, blurred vision, drooping eyelids, slurred speech, loss of facial expression, descending paralysis, and difficulty breathing. Consider botulism early in your patients who inject drugs but who do not respond to naloxone or who exhibit prolonged symptoms. Testing at the health department is performed with mouse antibodies to Botulism Neurotoxin (BoNT) combined with the patient’s serum.
Cyanide poisoning, while uncommon, is frequently fatal. Current antidotes include methemoglobinemia inducers (nitrites), sulfur donators (thiosulfate), and hydroxocobalamin. Each has risks and benefits that must be considered. Three new potential antidotes, including sodium tetrathionate, have recently been evaluated in swine models.
Intramuscular sodium tetrathionate1
Advantages:
Bottom line:
Primary headaches (not secondary to a life-threatening disease) can be challenging to manage. Remember the following pearls:
Things that DO NOT work: IV fluids, 5-HT3 Antagonists (aka Zofran), diphenhydramine (aka Benadryl), opioids
Things that KINDA work: oxygen for all headaches, sphenopalatine ganglion block (4% lido spray)
Things that PREVENT recurrence: dexamethasone for migraine headaches
Children are prone to inflammation and infection of the intervertebral discs
-Mean age 3-5years at presentation.
Lumbar region frequently involved
Although disc biopsy is not necessary for diagnosis, as many as 60% of biopsied discs grow bacteria
-Usually Staphylococcus aureus.
Untreated - may spontaneously resolve or progress to vertebral osteomyelitis or abscess
Chief complaint: Back pain and irritability, often associated with a limp or refusal to crawl or walk.
Fever is absent or low grade.
Physical examination findings are nonspecific and may include a tendency to lie still and percussion tenderness over the involved spine.
Blood culture is generally sterile,
WBC count can be normal early in the disease course
However, the ESR is elevated in >90% of patients.
Plain radiographs are normal at the start of the illness, and generally take 2-3 weeks to demonstrate narrowing of the intervertebral space.
Therefore imaging study of choice is MRI.
