Is the supine position associated with loss of airway patency in unconscious trauma patients? A systematic review and meta-analysis3 lug
Endovascular therapy in Stroke: the 2015 AHA/ASA Updated Guidelines establish new eligibility criteria.30 giu
New evidences aroused in treatment of ischemic stroke from early 2015. Large and well conducted trials demonstrated the benefit of endovascular therapy (in association with thrombolysis) on primary clinical endpoints.
Today AHA and ASA updated the 2013 Stroke Guidelines for the Early Management of Patients With Acute Ischemic Stroke regarding Endovascular Treatment on the basis of this recent evidences.
Let’s resume the recommendations on Endovascular Interventions:
- Patients who are elegible for intravenous r-tPA should receive r-tPA and in addition endovascular therapy with a stent retriever if they meet all the following criteria (Class I; Level of Evidence A). (New recommendation):
- Prestroke modified Ranking Scale score 0 to 1
- Acute ischemic stroke receiving intravenous r-tPA within 4.5 hours of onset according to guidelines from professional medical societies
- Causative occlusion of the internal carotid artery or proximal MCA (M1)
- Age ≥18 years
- NIHSS score of ≥6
- ASPECTS of ≥6
- Treatment can be initiated (groin puncture) within 6 hours of symptom onset
- To ensure benefit, reperfusion should be achieved as early as possible and within 6 hours of stroke onset (Class I; Level of Evidence B-R). (Revised from the 2013 guideline); if treatment is initiated beyond 6 hours from symptom onset, the effectiveness of endovascular therapy is uncertain (Class IIb; Level of Evidence C). (New recommendation)
- The benefits are uncertain, on carefully selected patients with acute ischemic stroke in whom treatment
can be initiated (groin puncture) within 6 hours of symptom onset and who have causative occlusion of the M2 or M3 portion of the MCAs, anterior cerebral arteries, vertebral arteries, basilar artery, or posterior cerebral arteries. (Class IIb; Level of Evidence C). (New recommendation)
- Endovascular therapy with stent retrievers may be reasonable for some patients <18 years of age with acute ischemic stroke who have demonstrated large vessel occlusion in whom treatment can be initiated (groin puncture) within 6 hours of symptom onset, but the benefits are not established in this age group (Class IIb; Level of Evidence C). (New recommendation)
Read the full text on AHA/ASA website:
2015 AHA/ASA Focused Update of the 2013 Guidelines for the Early Management of Patients With Acute Ischemic Stroke Regarding Endovascular Treatment
Medscape article: Groups Issue Guidance on Endovascular Repair of Ischemic Stroke (subscription required)
“Look-alike Drugs”is a present concern for all the emergency medicine professionals. EZDrugID Campaign address this topic with a petition a survey and suggesting strategies to prevent medication errors.
Go to the website http://ezdrugid.org/EZDrugID/About_EZDrugID.html and sign the petition, take the survey but most importantly introduce in your working place the awareness of “Look-alike drugs” danger for medication errors.
Busting new and old myths on treating ICH.
Highlits on new and revised reccomendation in patients presenting with Spontaneous Intracerebral Hemorrage (ICH).
Safety of Early Intensive BP-Lowering Treatment
For ICH patients presenting with SBP between 150 and 220 mm Hg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome (Class IIa; Level of Evidence B) (Revised from the previous guideline)
For ICH patients presenting with SBP >220 mm Hg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusionand frequent BP monitoring (Class IIb; Level of Evidence C). (New recommendation)
Glucose Management: Recommendation
- Glucose should be monitored. Both hyperglycemia and hypoglycemia should be avoided (Class I; Level of Evidence C).(Revised from the previous guideline)
- Treatment of fever after ICH is reasonable
Seizures and Antiseizure Drugs Recommendations
- Clinical seizures should be treated with antiseizure drugs (Class I; Level of Evidence A). (Unchanged from the previous guideline)
- Prophylactic antiseizure medication is not recommended (Class III; Level of Evidence B). (Unchanged from the previous guideline)
ICP Monitoring and Treatment: Recommendations
- Corticosteroids should not be administered for treatment of elevated ICP in ICH (Class III; Level of Evidence B). (New recommendation)
Those are just few of many changes introduced in this revision of the Guidelines. Discover more!
You can find the link to download the full text of this (and may other) guidelines on MEDEST at:
The 3-3-2 rule is part of the evaluation in a patient for a predicted difficult airway. This evaluation can be done on an unconscious patient in supine position and is reliable tool for the anticipation of a difficult BVM ventilation and intubation out of the hospital.
In the video you can see the 3-3-2- rule application on a patient with a predicted difficult airway. .
This patient was difficult to BVM ventilate (cause of the “sloopy” chin) and was intubated in VL with the aid of a bougie.
In this case the predicted difficulty of the airway, determined the choice of VL bougie aided intubation as first choice for the airway management, avoiding so multiple attempts. This choice was of more importance view the difficulty of BVM ventilation that would have conducted to a critical desaturation during the intubation attempts.
The invasive airway management is a critical skill in out of hospital emergency medicine and, when indicated, not avoidable. Predicting in advance the difficulty is important to choose the right plan and avoiding multiple attempts.
47 ysr old male collapsed on the field. First ALS unit found him arrested in VF.
Shocked 3 times he regained a palpable central pulse.
When we arrived the patient arrested again. VF on the monitor. Shocked 4 times. Mechanical chest compression and tracheal intubation on board. He received Epi, Amio (300+150), Calcium Gluconate and Bicarb (suspected iper K in kidney insufficiency) before the ROSC.
15 minutes passed from the collapse to ROSC, 7 of wich were of “no flow” (no chest compressions, no AED from bystanders).
PMH: Hypertension, kidney insufficiency, heavy smokers. Medication history unknown.
He had chest pain before collapsing, as referred from bystanders.
Vitals at ROSC: GCS 3 T, RR 10 MV, SaO2 100%, EtCO2 35, HR 70 bpm. NIBP 100/70 12 lead EKG at ROSC is shown below
An echo of the heart performed on the field (in the ambulance running to the ED, so I apologize for the low quality of the images) confirmed the lateral wall MI and shown distended IVC, B lines in both lungs and no sign of aortic dissection. No free fluid was present in the abdomen.
After administration of Heparin and Aspirin the patient arrived in ED and taken straight to cat-lab where a PTCA was performed 50 min after the collapse.
I think that increasing the use of ultrasonography on the field, and using it when really makes the difference, with a Point Of Care approach, is a big step for the care of critical patients out of the hospital.
Every prehospital emergency system have to instruct their professionals on how to use POC Ultra Sonography on the field and need specific “problem solving” protocols to help it’s diffusion.
Drug-to-drug interaction. New evidences on Morphine and delayed onset of action of antiplatelet agents.11 mag
A recently published article entitled “Chest pain relief in patients with acute myocardial infarction” (European Heart Journal: Acute Cardiovascular Care April 22, 2015) address in a very well documentrd way the topic about drug-to-drug interactiono between morfine and antiplatelets agents in STEMI patients.
Guido Parodi, a lead interventional cardiologist in Cardiovascular and Thoracic Department of Careggi Hospital in Florence, (Italy) author of the article, highlights the fact that “despite the complete absence of rigorous studies designed to assess the impact of morphine administration in patients with AMI, clinical practice guidelines for the management of patients with STEMI strongly recommend the use of morphine for analgesia.”
As indicated in the article recent literature indicates an increased risk of mortality in STEMI patients treated with Morphine.
The analysis of CRUSADE registry in 2005 has shown how patients treated with morphine had a higher adjusted risk of death than patients not treated with morphine even after using a propensity score matching method. This is a non randomized trial and so influenced from potential bias, and the hypothesis that morphine was administered to higher-risk patients is also to be considered. But an additional potential explanation of morphine’s negative impact on AMI outcome may be related to drug-to-drug interactions.
Biologically a cause effect relation can be explained, because morphine inhibits gastric emptying, delaying absorption and so decreasing peak plasma levels of orally administered drugs in general and antiplatelet agents in this particular case.
This was very well demonstrated in a 2015 study from the same author “Morphine is associated with a delayed activity of oral antiplatelet agents in patients with ST elevation acute myocardial infarction undergoing primary PCI” (Parodi G, Bellandi B, Xanthopoulou I, et al. Circ Cardiovasc Interv Epub ahead of print January 2015) in whom the negative impact of morphine on platelet inhibition was not only limited to patients who vomited (patients with vomiting were excluded), but morphine-treated patients clearly showed higher residual platelet reactivity compared with patients who did not receive morphine.
In ATLANTIC Trial (Montalescot G, van ‘t Hof AW, Lapostolle F, et al.; ATLANTIC Investigators. Prehospital ticagrelor in ST-elevation myocardial infarction. New Engl J Med 2014; 371: 1016–1027), STEMI patients who did not receive morphine had a significant improvement in the ECG-based primary end point (ST-segment resolution), reflecting better myocardial reperfusion,with a significant “p” value for interaction between morphine use and time of ticagrelor administration. Professor Montalescot one of the lead authors of this Trial noted:“Co-administration of morphine in the ambulance may have delayed ticagrelor’s onset of action. To what extent this interaction may have affected our results remains unknown at this stage.”
So what to do with analgesia strategy in STEMI patients?
Given the key importance of platelet inhibition in patients treated by PPCI for STEMI and the absence of data that may support a potential clinical benefit of morphine in patients with acute myocardial infarction, more caution should be used regarding morphine administration in STEMI patients, and a restricted morphine use seems to be reasonably recommended.
Morphine administration has to be reserved, as suggested in the article, just for level of pain ≥ 7 on the base of a numerical rating scale (NRS) related value.
For lower chest pain intensity (NRS ≤ 7) alternative strategies has to be persecuted.
The author indicates paracetamol (1 g) or aspirin (≥300 mg) as alternative of choice to reduce chest pain as well demonstrated in letterature.
It has also to be considered how first line agents, currently indicated from STEMI guidelines, as Beta- blocker and Nitrates are able to reduce AMI-related chest pain until the definitive pain relief effect obtained with myocardial mechanical reperfusion.
The first impact to reduce chest pain has to be reserved to Nitrates or B-blockers (where all contraindications are excluded).
After this NRS has to be evaluated and the use of Morphine is indicated only for values above 7. For lower values Paracetamol or Aspirin are the agents of choice.
Parodi G. Chest pain relief in patients with acute myocardial infarction. Eur Heart J Acute Cardiovasc Care. 2015 Apr 22. pii: 2048872615584078. [Epub ahead of print] Review.PMID:25904757
Meine TJ, Roe MT, Chen AY, et al. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J 2005; 149: 1043–1049.
Parodi G,Valenti R, Bellandi B, et al. Comparison of prasugrel and ticagrelor loading doses in ST-segment elevationmyocardial infarction patients: RAPID (Rapid Activity of Platelet Inhibitor Drugs) primary PCI study. J Am Coll Cardiol 2013; 61: 1601–1606
Parodi G, Bellandi B, Valenti R, et al. Comparison of double (360 mg) ticagrelor loading dose with standard (60 mg) prasugrel loading dose in STEMI patients: The Rapid Activity of Platelet Inhibitor Drugs (RAPID) primary PCI 2 study.Am Heart J 2014; 167: 909–914.
Nimmo WS, Heading RC, Wilson J, et al. Inhibition of gastric emptying and drug absorption by narcotic analgesics. Br J Clin Pharmacol 1975; 2: 509–513.
Parodi G, Xanthopoulou I, Bellandi B, et al. Ticagrelor crushed tablets administration in STEMI patients: The MOJITO study. J Am Coll Cardiol 2015; 65: 511–512.
Montalescot G, van ‘t Hof AW, Lapostolle F, et al.; ATLANTIC Investigators. Prehospital ticagrelor in ST-elevation myocardial infarction. New Engl J Med 2014; 371: 1016–1027
Duggan ST and Scott LJ. Intravenous paracetamol (acetaminophen). Drugs 2009; 69: 101–113.
Zijlstra F, Ernst N, de Boer MJ, et al. Influence of prehospital administration of aspirin and heparin on initial patency ofthe infarct-related artery in patients with acute ST elevation myocardial infarction. J Am Coll Cardiol 2002; 39: 1733–1737
Yusuf S, Sleigh P, Rossi P, et al. Reduction in infarct size and chest pain by early intravenous beta blockade in suspectedacute myocardial infarction. Circulation 1983; 67: 132–141.
Kim YI and Williams JF Jr. Large dose sublingual nitroglycerin in acute myocardial infarction: Relief of chest pain and reduction of Q wave evolution. Am J Cardiol 1982; 49: 842–848.
22 years old male hit from a car on the roadside of an urban area.
The ground EMS ambulance (physician, nurse staffed), dispatched on scene, find the patient alert, oriented and spontaneously breathing. His vitals are:
GCS 15 , RR 20, SaO2 95, HR 85, SBP 110
No mention of head trauma.
Chest no sign of trauma, bilateral and equal expansion and air entry.
Pulse is strong.
He has a profound laceration with loss of substance but not evisceration on left flank and no external bleeding from the wound.
The abdomen is painful and resistant to palpation in left flank.
There is an open fracture to left tibia (VNS 9).
The ground team, after the primary survey, activates the local medical helicopter.
The place is 10 k from a level 1 Trauma Center on a local road in an urban area and the helicopter is at 10 minutes flight distance. There is a safe landing space at 500 mt from the point of the accident.
A Level 2 hospital (general surgery, orthopedics, anesthesiologist, radiology and laboratory 24/7) is at 2 km distance from the scene.
Is this a proper activation for HEMS?
What international litterature says about advantages of air medical service vs ground medical service?
So what about the case?
Severity: The patient is slightly tachycardic, and the mechanism of trauma give us some clue on possible abdominal injuries, so he need a quick transport to an hospital with a general surgery (and orthopedics naturally for the tibial fracture)
Speed: non simultaneous activation. This kind of missions become competitive on long distances (45 miles) from Level 1 Trauma center (or the appropriate hospital). So GEMS is faster anyway.
Trauma center access: no difference between HEMS and GEMS and even there is doubt on the fact that this patient really need a Level 1 Trauma Center
Crew: this patient does not need an over skilled staff for some particular procedure.
We can conclude that for the standard HEMS activation criteria, this is not an appropriate activation and the best way to reach the hospital for this patient is a ground ambulance.
Any suggestion on the theme treated is, as usual, very welcome