Carbon Monoxide Toxicity and Hyperbaric Oxygen Treatment
CO disrupts cellular function by several mechanisms at a
cellular/mitochondrial level. Ultimately, these disruptions are
manifested as tissue hypoxia and hypoperfusion.
Initial symptoms may be subtle and nonspecific. Be sure to ask about
CO exposure when evaluating “viral syndrome” or patients that present
with non-specific neurological complaints especially during fall and
winter months, when people first start using their heating, or after
power outages and generator use. Dysrhythmias, cardiomopathy, MI and
sudden cardiac arrest are reported in severe CO poisoning.
Lab studies- COHb, base excess, lactate and any other studies based on
presentation.
Supplemental oxygen is the cornerstone of treatment. Oxygen
delivered at hyperbaric pressure (as opposed to sea-level) will
increase the rate of CO dissociation from hemoglobin, and mitigate
damage to cellular and mitochondrial function.
Definite Indications for HBOT: Current evidence supports the use for
HBOT to reduce cognitive sequelae in CO poisoned patients who have:
LOC , seizure, exposure >23 hours, COHb of 25% or more, and age >36.
Relative Indications: persistent symptoms after 100% O2 or change in
mental status, pregnancy, persistent cardiac ischemia, increased COHb
levels.
Disposition: Clinical judgment should guide your decision. Most
patients with mild symptoms can be discharged after treatment. If
patient has a more concerning presentation with several risk factors
(extremes of age, CAD, unconscious at arrival in the ED, etc…)
consider admission.
Differentiating Central Retinal Artery vs. Vein Occlusion Fundoscopically
SAH and Electrolyte Disorders
5 year-old male with developmental delay presents with intractable non-bloody and non-bilious vomiting over 10 days; bowel movements are normal. Four weeks ago he was placed in a hip-spica cast following a motor vehicle crash. Abdominal x-ray is below. Diagnosis?
Elevated BNP levels are found in conditions besides acutely decompensated CHF. These conditions can include:
Older age
Renal failure
Severe sepsis
PE
Chronic CHF
These conditions will often produce BNP elevations in an intermediate range, but if the elevation is markedly positive, the acutely decompensated CHF is much more likely.
[adapted from ACEP speaker Matthew Strehlow, MD]
Sinus Tarsi Syndrome
Lisiteria Monocytogenes is typically transmitted from ingestion of contaminated food such as unpasteurized milk or cheese, raw foods, and recently cantaloupes; transmission from veterinary exposure, infected soil and water have also been reported.
Listeria has a predilection for the central nervous system (CNS) causing several infections including meningioencephalitits, brain or spinal abscess, cerebritis (infection of brain parenchyma), and rhomboencephalitis (encephalitis of the brainstem).
Risk factors include immunosuppression, advanced age, newborns, and pregnancy.
There is no clinical way to distinguish CNS infection with Listeria from other pathogens, therefore blood and cerebrospinal fluid (CSF) culture is required.
CSF analysis demonstrates pleocytosis, elevated protein, and low glucose. CSF gram stain has a low sensitivity (~33%), but consider Listeria in the differential if "diptheroid-like" bacteria are reported on gram stain.
Ampicillin is the drug of choice and should be continued for at least three weeks (sometimes longer). Adding gentamycin is sometimes recommended for synergy in severe infection.
ST depression in the right precordial leads can be anteroseptal ischemia, but it can also be a posterior STEMI. What are the clues to posterior STEMI?
Posterior leads (a couple of leads placed in the left mid-back area below the tip of the scapula) can help confirm posterior STEMI if there's STE in those leads. If there's no STE, call it just ischemia!
Anterolateral dislocation is most common (>85%)
As the tib/fib joint has its own synovial cavity, a knee effusion will not be seen
Mechanism: fall on the flexed knee with foot/ankle inversion
Hx: swelling, variable amount of lateral knee pain (anywhere from mild discomfort to inability to bear weight)
PE: Prominence of the fibular head, ankle motion exacerbates knee pain. no associated neurovascular issues
However with less common dislocations (posterior and superior) peroneal nerve injury may occur
Reduction: Place patient supine with knee flexed to 90 degrees. Ankle should be dorsiflexed and externally rotated.
REVERSE THE INJURY: Apply firm posteriorly directed pressure to the fibular head. May head an audible pop as fibular head reduces. Reassess collateral ligament function.
Peritoneal dialysis (PD) is a commonly used form of dialysis for pediatric patients with end-stage renal disease, particularly in children less than five years of age.
One well known complication to this mode of dialysis is PD-associated peritonitis.
Children may present with fever, abdominal pain and a cloudy dialysate.
If peritonitis is suspected, obtain sample of dialysate fluid and send for cell count, Gram’s stain and culture.
Cell count in PD-associated peritonitis is usually WBC >100 with >50% neutrophils.
Both gram-positive and gram-negative organisms are involved with PD-associated peritonitis . Keep both MRSA and Pseudomonas in mind.
In the ED, empiric therapy should cover both gram-positive and gram-negative organisms. Initiate antibiotic therapy with vancomycin and either a third-generation cephalosporin (ceftazidime) or aminoglycoside, respectively.
For PD-associated peritonitis, intraperitoneal (IP) administration of antibiotics is preferred over IV.
There are an increasing number of intranasal medications commercially available for use, which is opportune as more and more intravenous medications become scarce.
These now include:
| Generic name | Brand Name | Usage |
| Fentanyl | Instanyl | Opiate analgesic |
| Ketorolac | Sprix | NSAID analgesic |
| Desmopressin (DDAVP) | Stimate | Bleeding |
| Vitamin B12 | Nasobal | Anti-migraine (yes!) |
| Sumatriptan | Imitrex | Anti-migraine |
| Zolmitripran | Zomig | Anti-migraine |
*******In addition, you can administer glucagon, midazolam and narcan intranasally as well.
Fever and ICH
Question: 50-year-old diabetic female s/p foot burn several weeks ago, now presenting with pain and discharge from a poorly healing wound. Diagnosis?
Hostile behavior appears to be a predictor of ischemic heart disease and myocardial infarction. Prior studies have demonstrated this association, and now one more study has supported this. In short, researchers from Nova Scotia demonstrated that observed hostility was a predictor of ischemic heart disease and myocardial infarction (2-fold), independent of age, sex, Framingham Risk Score, and other psychosocial risk factors.
The key takeaway point of this fun, but validated concept, is that in addition to exercising and eating right, we all just need to relax a bit more. And the next time you have to deal with an angry consultant, just tell him to chill out or he'll die!
An acute increase in the INR over 3 in patients with chronic kidney disease (CKD) is often associated with an unexplained acute increase in serum creatinine and an accelerated progression of CKD.
Kidney biopsy in a subset of these patients showed obstruction of the renal tubule by red blood cell casts, and this appears to be the dominant mechanism of the acute kidney injury. This has been termed warfarin-related nephropathy (WRN).
In 15,258 patients who initiated warfarin therapy during a 5-year period, 4006 had an INR over 3 and creatinine measured at the same time. A presumptive diagnosis of WRN was made if the creatinine increased by over 0.3 mg/dl within 1 week after the INR exceeded 3 with no record of hemorrhage. WRN occurred in 20.5% of the entire cohort, 33.0% of the CKD cohort, and 16.5% of the no-CKD cohort. Other risk factors included age, diabetes mellitus, hypertension, and cardiovascular disease. The 1-year mortality was 31.1% in patients with WRN compared with 18.9% in those without WRN, an increased risk of 65%.
Take home message: Although the mechanisms are not clear, be very wary of even a small creatinine bump in patients presenting with an INR > 3 on warfarin therapy. Yet another reason to fear warfarin...
You are seeing a high school football player following a head injury. After your exam or head CT, you determine the child to have had a mild traumatic brain injury (aka concussion). You are ready to discharge him home when the parents or coach ask you when he can return to playing football.
A concussion is a form of functional, rather than structural, brain injury that displays no evidence of injury on structural neuroimaging. Symptoms include transient loss of consciousness, amnesia, vomiting, headache, poor school work, sleep changes, and emotional lability. Remember that children’s brains (even adolescents) are still developing, and are more prone to prolonged recovery following injury.
Recovery of symptoms usually follows a sequential course. Current guidelines recommend a stepwise return to play (aka concussion rehabilitation) involving both physical and cognitive rest (e.g. no texting, video games, limited school work). Once asymptomatic, the patient goes through each stage with at least 24 hours between stages. If symptoms return during a stage, then the patient is expected to return to the previous stage for 24 hours before attempting the higher stage again.
Return to Play Guidelines:
| Rehabilitation stage | Functional Exercise |
| Complete physical and cognitive rest |
| Walking, swimming, stationary cycling at 70% maximal heart rate, no resistance exercise |
| Specific sport related drills but no head impact |
| More complex drills, may start light resistance training |
| After medical clearance, participate in normal training |
| Normal game play |
References:
