A cura del Dott. Flavio Montinaro un video che mostra in maniera efficace i punti chiave per il posizionamento di un drenaggio toracico con tecnica chirurgica nei pazienti affetti da pneumotorace.
- UFH and LMWH
- Rivaroxaban, Edoxaban and Apixaban
- Antiplatelet drugs
Bleeding is the most common complication of antiaggregants and anticoagulants. The rate of major bleeding among users of vitamin K antagonists (VKAs) is 1.5% to 5.2% per year; low-molecular-weight heparin (LMWH) and intravenous unfractionated heparin (UFH) are associated with about 2% and 5.5% respectively of major bleeding complications [1-2]. Bleeding complications range from about 2% to 3% with direct oral anticoagulants (DOACs) .
Major bleeding is defined as:
- bleeding causing haemodynamic instability
- symptomatic bleeding in a critical organ: intracranial, intraspinal, intraocular, retroperitoneal, intraarticular or pericardial, or intramuscular (if causing compartment syndrome)
- bleeding causing a fall in hemoglobin > 2 g/dL or more
- bleeding leading to transfusion of ≥ 2 UI of packed red blood cells
- resulting in death
according to the ISTH criteria .
|LMWH||anti-factor Xa level||Protamine|
|Fondaparinux||anti-factor Xa level||No specific antidote|
|Dabigatran (Pradaxa)||ECT, Hemoclot® thrombin inhibitor assay, PT, aPTT.||Idracizumab|
|anti-factor Xa level||Andexanet alfa|
In patients with hypofibrinogenemia, cryoprecipitate may be used to keep fibrinogen levels above 100 to 150 mg/dL depending on the severity of bleeding.
For all patients with major bleeding administration of an antifibrinolytic agent like tranexamic acid or epsilon-aminocaproic acid is suggested.
Warfarin and other Coumarin derivatives act by inhibiting the synthesis of vitamin K dependent clotting factors, which include Factors II, VII, IX and X (FIG. 1), and the anticoagulant proteins C and S: The reverting agents act by restoring the synthesis of vitamin K dependent clotting factors or by providing vitamin K dependent clotting factors.
|SETTING||ASH Guideline – 2018||ACCP Guideline – 2012|
Vitamin K (intravenous)
Vitamin K (intravenous)
|(No recommendations given)||Vitamin K (oral)|
INR 4.5 to 10
No vitamin K
Vitamin K (low dose, oral) is optional
|Product||Time to Effect||Duration of Effect||Evidence of Efficacy for Warfarin Revesal||Risk of Thrombosis|
|Oral vitamin K||24 h||Days||++++||NS|
|Intravenous vitamin K||8–12 h||Days||++++||NS|
|Fresh frozen plasma||Immediate||12–24 h||++||NS|
|PCC||Immediate||12–24 h||+++||+ (Higher with activated PCC)|
|Recombinant factor VIIa||Immediate||2–6 h||+||++|
Vitamin K is indicated for warfarin reversal if (TAB. 2):
- INR of >10 or 4.5 to 10 in the presence of other risk factors for bleeding.
- INR is >10, NO active bleeding or minor bleeding (Vitamin K alone)
- In case of persistent INR elevation: Vitamin K administration can be repeated every 12 h
Fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) may be necessary in bleeding patients:
- In cases of major bleeding: PCC or FFP are given to reverse the immediate action of warfarin
- vitamin K is given to maintain the reversal effect against warfarin as the half-life for warfarin is 72 hours
Patients should repeat coagulation profile to ensure warfarin reversal. 3 – 5 units of FFP (10-15 mL/kg IV) are necessary to increase plasma coagulation factors by ∼15% to 25% .
PCC provides 3 (II,IX,X; does not contain factor VII) or 4 coagulation factors (Factors II, VII, IX, and X), depending on the preparation:
- is preferred to FFP in cases of major bleeding 
- In a clinical trial that randomly assigned 216 patients with warfarin-associated bleeding to receive PCC or FFP with intravenous vitamin K, PCC was found to be at least as effective as FFP with similar hemostasis (72% vs 65%) and similar length of hospital stay (median 4.5 vs 4.2 days).
- The dose of PCC varies depending on INR, ranging from 25 to 50 units/kg. Higher dose: 5000 UI. If rFVIIa is used to supplement 3-factor PCC, a lower dose is preferred (20 mcg/kg).
- Recombinant-activated factor VIIa (rFVIIa) is used off-label for warfarin reversal: it corrects INR but not fully restore hemostasis .
Two case series have reported thromboembolism rates ≥10% with rFVIIa [10,11]; a randomized trial compared two doses of rFVIIa (80 and 20 mcg/kg) with placebo: thromboembolic events were similar in the three groups, but severe events were more common in those who received high-dose rFVIIa .
|1. 4-factor PCC (4F PCC) is the preferred approach:|
|1. Give 4F PCC 1500 to 2000 Units IV over 10 min. Check INR 15 minutes after completion of the infusion. If INR is not ≤1.5, give additional 4F PCC.[Body weight-based and INR-based dosing: 25 UI/kg for INR 2 – 4; 35 UI/kg for INR 4 – 6; 50 UI/kg for INR >6 (maximum: 5000 UI)]|
|2. + vitamin K 10 mg IV (in 10 – 20 min).|
|2. If 4F PCC is not available: 3-factor PCC (3F PCC)|
|1. Give 3F PCC 1500 to 2000 units IV over 10 minutes. Check INR 15 minutes after completion of the infusion. If INR is not ≤1.5, give additional 3F PCC.|
|2. + Factor VIIa 20 mcg/kg IV OR FFP 2 units IV.|
|3. + vitamin K 10 mg IV (in 10 – 20 min).|
|3. If neither is available: FFP.|
|1. 2 units IV by rapid infusion Check INR 15 minutes after completion of infusion:- If INR ≥1.5: 2 additional units of FFP IV rapid infusion. Repeat process until INR ≤1.5.|
|2. + vitamin K 10 mg IV (in 10 – 20 min)|
3. UFH AND LMWH
Heparin binds reversibly to ATIII and leads to instantaneous inactivation of factors IIa and Xa. The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin. The antithrombotic effect of heparin is correlated to the inhibition of factor Xa (FIG. 2).
First: Discontinue heparin.
Protamine sulfate is a reversal agent that completely reverses UFH:
- 1 mg of protamine sulfate neutralizes 100 units of heparin (eg 4000 UI : 40 mg of Protamine)
- The number of heparin units to be corrected depends on the heparin units administered and the time since the last administration (Heparin half-life: 1-2 h): if 4000 units was given 2 h ago, the number of units would be 2000 and the dose of protamine would be 20 mg).
- Alternatively a fixed dose of 50 mg or 25 mg may be given: someone give 50 mg while others give 25 mg followed by 25 mg if needed (eg, persistently prolonged aPTT).
- Protamine must be given by slow intravenous infusion (infusion rate < 20 mg/min or 50 mg/10-minute), because rapid infusion cause hypotension, particularly at high doses. Other related adverse effect are: cardiovascular collapse, noncardiogenic pulmonary edema, catastrophic pulmonary vasoconstriction, and pulmonary hypertension.
- In case of persistently high aPTT levels repeat doses may be given
- Protamine is derived from fish sperm and may elicit an allergic reaction, especially in previously exposed.
Protamine sulfate completely reverses the action of UFH but not of LMWH. A potential reversal agent for LMWH, aripazine is under development:
- Andexanet is preferred rather than protamine: efficacy was demonstrated in the ANNEXA-4 study where a small group of 16 people received LMWH .
- Protamine is less effective in reversing the effect of LMW heparin: Protamine only reverses ∼ 60 % due to decreased binding to the shorter heparin chains. (is a reasonable treatment option if LMWH have been administrated within the previous 12 hours):
- LMWH administered < 8 h: 1 mg protamine per 1 mg of enoxaparin.
- LMWH administered ≥ 8 h, or if it has been deemed that a second dose of protamine is necessary: 0.5 mg protamine per 1 mg of enoxaparin.
Fondaparinux is a synthetic heparin pentasaccharide with a sequence identical to that found in heparin which acts by binding to antithrombin and inducing a conformational change that causes inhibition of factor Xa (half-life: 17-21 h).
- Protamine sulfate is ineffective for fondaparinux reversal.
- Andexanet is a reasonable option if it is available: It is a catalytically inactive form of factor Xa able to bind and sequester direct factor Xa inhibitors and is likely to be effective also for reversing indirect-acting factor Xa inhibitors like fondaparinux. [14,15].
- aPCC and rFVIIa may provide reversal against fondaparinux activity: clinical data are limited to in vitro studies rather than management of patients with bleeding [16,17]; aPCC better normalize thrombin generation time than rFVIIa. The high thrombotic risk of these agents should always be kept in mind and weighed against the bleeding risk.
Dabigatran reversibly binds to the active site on the Factor II (Thrombin), preventing thrombin-mediated activation of coagulation factors.
Dabigatran has an emergency reversal agent: Idarucizumab. It is an anti-dabigatran monoclonal antibody fragment. Other options, If Idarucizumab is not available, are PCC and FFP.
If idarucizumab if available this is the drug of choice, rather than clotting factor products (aPCC, PCC, or plasma).
Unabsorbed dabigatran can be removed from the gastrointestinal tract using oral activated charcoal if the last dose was within 2 h. Dabigatran can also be removed by hemodialysis.
- The dose is 5 g, administered either as two consecutive infusions (2.5 g + 2.5 g) or as a bolus. Repeat dosing may be appropriate in selected cases as overdose or persistently prologed aPTT.
- Use idarucizumab alone: Do not combine with PCC, aPCC, or rFVIIa.
- Thrombosis were more common with idarucizumab: These are associated with due to the patient’s underlying thrombotic risk factors.
- Activated PCC: dose of 50 to 80 units/kg. The aFVII activates the free factor X and may bypass dabigatran effect and promote clotting.
- Alternatively, 4-factor or 3-factor PCC at a dose of 50 units/kg would be reasonable. Three-factor PCC may be supplemented with rFVIIa or plasma.
- Activated charcoal and dialysis
6. RIVAROXABAN, EDOXABAN and APIXABAN
Apixaban, Edoxaban and Rivaroxaban are direct inhibitor of free and clot-bound factor Xa.
For patients with major bleeding and anticoagulation with a factor Xa inhibitor, andexanet alfa or 4F PCC are indicated. These agents have not been directly compared in a randomized trial.
- Discontinue factor Xa inhibitor
|ANDEXANET||In patients who received a lower dose of factor Xa inhibitor (rivaroxaban ≤10 mg, apixaban ≤5 mg, edoxaban ≤30 mg) or ≥ 8 h since the last dose of factor Xa inhibitor: bolus of 400 mg at 30 mg/min over 30 minutes, followed by an infusion of 480 mg given at 4 mg/min for up to 120 minutes.|
For those who receives a higher dose of factor Xa inhibitor, unknown dose or <8 h: bolus of 800 mg at 30 mg/min over 30 minutes, followed by an infusion at 960 mg given at 8 mg/min for up to 120 minutes
Do not combine andexanet with PCC, aPCC or rFVIIa.
|4F PCC||50 units/kg, or a fixed-dose regimen (2000 – 2500 units)|
Unabsorbed anticoagulant can be removed from the gastrointestinal tract using oral activated charcoal.
7. ANTIPLATELET DRUGS
The AABB (American Association of Blood Banks) developed this guidelines on appropriate use of platelet transfusion in adult patients:
|Recommendation 1||The AABB recommends that platelets should be transfused prophylactically to reduce the risk for spontaneous bleeding in hospitalized adult patients with therapyinduced hypoproliferative thrombocytopenia. The AABB recommends transfusing hospitalized adult patients with a platelet count of 10 × 10^9 cells/L or less to reduce the risk for spontaneous bleeding. The AABB recommends transfusing up to a single apheresis unit or equivalent. Greater doses are not more effective, and lower doses equal to one half of a standard apheresis unit are equally effective. (Grade: strong recommendation; moderate-quality evidence)|
|Recommendation 2||The AABB suggests prophylactic platelet transfusion for patients having elective central venous catheter placement with a platelet count less than 20 × 10^9 cells/L. (Grade: weak recommendation; low-quality evidence)|
|Recommendation 3||The AABB suggests prophylactic platelet transfusion for patients having elective diagnostic lumbar puncture with a platelet count less than 50 × 10^9 cells/L. (Grade: weak recommendation; very-low-quality evidence)|
|Recommendation 4||The AABB suggests prophylactic platelet transfusion for patients having major elective nonneuraxial surgery with a platelet count less than 50 × 10^9 cells/L. (Grade: weak recommendation; very-low-quality evidence)|
|Recommendation 5||The AABB recommends against routine prophylactic platelet transfusion for patients who are nonthrombocytopenic and have cardiac surgery with cardiopulmonary bypass. The AABB suggests platelet transfusion for patients having bypass who exhibit perioperative bleeding with thrombocytopenia and/or evidence of platelet dysfunction. (Grade: weak recommendation; very-low-quality evidence)|
|Recommendation 6||The AABB cannot recommend for or against platelet transfusion for patients receiving antiplatelet therapy who have intracranial hemorrhage (traumatic or spontaneous). (Grade: uncertain recommendation; very-low-quality evidence)|
Due to the low level of evidence it was not possible to establish clear guidelines regarding the transfusion of platelets during therapy with antiplatelet agents.
|DEVELOPMENT OF REVERSAL AGENTS FOR ANTIPLATELET THERAPY IS AN AREA OF UNMET NEED|
- Platelets should be transfused in patients with a low platelet count (less than 50,000/microL) who are receiving antiplatelet agents (APT).
- In patients with intracerebral hemorrhage (ICH) who are receiving antiplatelet agents, the decision to transfuse platelets is based on: size of the bleeding, patient’s level of consciousness and clinical factors. For neurosurgery, platelets are transfused prophylactically for a preprocedure platelet count less than 80 – 100 × 10^9 cells/L (low-quality data supporting this threshold) >>> Patients with ICH taking antiplatelet therapy should be transfused platelets only if planned for neurosurgical intervention but not if receiving medical management .
- Patients with upper gastrointestinal haemorrhage on APT do not benefit from platelet transfusions. They benefit from urgent endoscopic control of bleeding and proton pump inhibition only .
- The optimal dose of platelets and the timing of transfusion in patients on antiplatelet therapy are currently unknown; however, it must be borne in mind that:
- Clopidogrel or prasugrel: wait at least 6 -8 hours after the last dose.
- Ticagrelor: consider transfusion especially if the last dose was >24 hours prior.
- Aspirin half life: 20 min
- Platelets should not be transfused in patients with normal platelet counts who are on antiplatelet medications .
- Platelet and plasma transfusions should be considered in patients who receive massive RBC transfusions (>3 units of packed RBCs within one hour).
- Consider the use of pre-operative intravenous tranexamic acid which proved to improve the platelet function of those exposed to APT, resulting in a reduction in bleeding and transfusion.
- rFVIIa may limit bleeding (Off -label): it acts by reversing the effects of APT on thrombin generation . The increase the risk of arterial thromboembolic events is a major side effect: rFVIIa should be considered only as a last source.
- Desmopressin may be a useful agent to reduce bleeding and transfusion requirements for people with platelet dysfunction or with a history of recent antiplatelet drug administration (GRADE quality of evidence: very low to moderate) .
Dr. Lorenzo Pelagatti
Emergency Department – Nuovo Ospedale di Prato S. Stefano – Prato, Tuscany, Italy
High Dependency Unit – AOU Careggi – Florence, Tuscany, Italy
Dr. Franco Lai
Emergency Department – Nuovo Ospedale di Prato S. Stefano – Prato, Tuscany, Italy
- Dhakal P, Rayamajhi S, Verma V, Gundabolu K, Bhatt VR. Reversal of Anticoagulation and Management of Bleeding in Patients on Anticoagulants. Clin Appl Thromb Hemost. 2017 Jul;23(5):410-415. doi: 10.1177/1076029616675970. Epub 2016 Oct 26. PMID: 27789605.
- Chai-Adisaksopha, C, Crowther, M, Isayama, T, Lim, W. The impact of bleeding complications in patients receiving target-specific oral anticoagulants: a systematic review and meta-analysis. Blood. 2014;124(15):2450–2458.
- Juergens, CP, Semsarian, C, Keech, AC, Beller, EM, Harris, PJ. Hemorrhagic complications of intravenous heparin use. Am J cardiol. 1997;80(2):150–154.
- Granger CB, Alexander JH, McMurray JJ, Lopes RD, Hylek EM, Hanna M, Al-Khalidi HR, Ansell J, Atar D, Avezum A, Bahit MC, Diaz R, Easton JD, Ezekowitz JA, Flaker G, Garcia D, Geraldes M, Gersh BJ, Golitsyn S, Goto S, Hermosillo AG, Hohnloser SH, Horowitz J, Mohan P, Jansky P, Lewis BS, Lopez-Sendon JL, Pais P, Parkhomenko A, Verheugt FW, Zhu J, Wallentin L; ARISTOTLE Committees and Investigators. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011 Sep 15;365(11):981-92. doi: 10.1056/NEJMoa1107039. Epub 2011 Aug 27. PMID: 21870978.
- Witt DM, Nieuwlaat R, Clark NP, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: Optimal management of anticoagulation therapy. Blood Adv 2018; 2:3257.
- Holbrook A, Schulman S, Witt DM, et al. Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141:e152S.
- Ansell, J, Hirsh, J, Hylek, E, Jacobson, A, Crowther, M, Palareti, G; American College of Chest Physicians . Pharmacology and Management of the Vitamin K Antagonists: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133(suppl 6):160S–198S.
- Huttner, HB, Schellinger, PD, Hartmann, M. Hematoma growth and outcome in treated neurocritical care patients with intracerebral hemorrhage related to oral anticoagulant therapy: comparison of acute treatment strategies using vitamin K, fresh frozen plasma, and prothrombin complex concentrates. Stroke. 2006;37(6):1465–1470.
- Garcia, DA, Crowther, MA. Reversal of warfarin: case-based practice recommendations. Circulation. 2012;125(23):2944–2947
- Diringer MN, Skolnick BE, Mayer SA, Steiner T, Davis SM, Brun NC, Broderick JP. Thromboembolic events with recombinant activated factor VII in spontaneous intracerebral hemorrhage: results from the Factor Seven for Acute Hemorrhagic Stroke (FAST) Trial. Stroke. 2010; 41:48–53.
- Robinson MT, Rabinstein AA, Meschia JF, Freeman WD. Safety of recombinant activated factor VII in patients with warfarin-associated hemorrhages of the central nervous system. Stroke. 2010; 41:1459–1463.
- Mayer SA, Brun NC, Begtrup K, Broderick J, Davis S, Diringer MN, Skolnick BE, Steiner T; FAST Trial Investigators. Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. 2008 May 15;358(20):2127-37. doi: 10.1056/NEJMoa0707534. PMID: 18480205.
- Connolly SJ, Crowther M, Eikelboom JW, Gibson CM, Curnutte JT, Lawrence JH, Yue P, Bronson MD, Lu G, Conley PB, Verhamme P, Schmidt J, Middeldorp S, Cohen AT, Beyer-Westendorf J, Albaladejo P, Lopez-Sendon J, Demchuk AM, Pallin DJ, Concha M, Goodman S, Leeds J, Souza S, Siegal DM, Zotova E, Meeks B, Ahmad S, Nakamya J, Milling TJ Jr; ANNEXA-4 Investigators. Full Study Report of Andexanet Alfa for Bleeding Associated with Factor Xa Inhibitors. N Engl J Med. 2019 Apr 4;380(14):1326-1335. doi: 10.1056/NEJMoa1814051. Epub 2019 Feb 7. PMID: 30730782; PMCID: PMC6699827.
- Lu G, DeGuzman FR, Hollenbach SJ, Karbarz MJ, Abe K, Lee G, Luan P, Hutchaleelaha A, Inagaki M, Conley PB, Phillips DR, Sinha U. A specific antidote for reversal of anticoagulation by direct and indirect inhibitors of coagulation factor Xa. Nat Med. 2013 Apr;19(4):446-51. doi: 10.1038/nm.3102. Epub 2013 Mar 3. PMID: 23455714.
- Desmurs-Clavel H, Huchon C, Chatard B, Negrier C, Dargaud Y. Reversal of the inhibitory effect of fondaparinux on thrombin generation by rFVIIa, aPCC and PCC. Thromb Res. 2009 Mar;123(5):796-8. doi: 10.1016/j.thromres.2008.07.007. Epub 2008 Sep 3. PMID: 18771795.
- Frontera JA, Lewin JJ 3rd, Rabinstein AA, Aisiku IP, Alexandrov AW, Cook AM, del Zoppo GJ, Kumar MA, Peerschke EI, Stiefel MF, Teitelbaum JS, Wartenberg KE, Zerfoss CL. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for Healthcare Professionals from the Neurocritical Care Society and Society of Critical Care Medicine. Neurocrit Care. 2016 Feb;24(1):6-46. doi: 10.1007/s12028-015-0222-x. PMID: 26714677.
- G. Gómez-Moreno, A. Aguilar-Salvatierra, M. Ángel Martín-Piedra, J. Guardia, J. L. Calvo-Guirado, M. Cabrera, C. López-Gallardo, T. Castillo. Dabigatran and rivaroxaban, new oral anticoagulants. new approaches in dentistry. J Clin Exp Dent. 2010;2(1):e1-5. doi:10.4317/jced.2.e1.
- Kaufman RM, Djulbegovic B, Gernsheimer T, Kleinman S, Tinmouth AT, Capocelli KE, Cipolle MD, Cohn CS, Fung MK, Grossman BJ, Mintz PD, O’Malley BA, Sesok-Pizzini DA, Shander A, Stack GE, Webert KE, Weinstein R, Welch BG, Whitman GJ, Wong EC, Tobian AA; AABB. Platelet transfusion: a clinical practice guideline from the AABB. Ann Intern Med. 2015 Feb 3;162(3):205-13. doi: 10.7326/M14-1589. PMID: 25383671.
- Swan D, Loughran N, Makris M, Thachil J. Management of bleeding and procedures in patients on antiplatelet therapy. Blood Rev. 2020 Jan;39:100619. doi: 10.1016/j.blre.2019.100619. Epub 2019 Oct 15. PMID: 31648803.
- Zakko L, Rustagi T, Douglas M, Laine L. No Benefit From Platelet Transfusion for Gastrointestinal Bleeding in Patients Taking Antiplatelet Agents. Clin Gastroenterol Hepatol. 2017 Jan;15(1):46-52. doi: 10.1016/j.cgh.2016.07.017. Epub 2016 Jul 25. PMID: 27464591
- Altman R, Scazziota A, M DELH, Gonzalez C. Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation. J Thromb Haemost. 2006;4(9):2022 -7
- Desborough MJ, Oakland KA, Landoni G, Crivellari M, Doree C, Estcourt LJ, Stanworth SJ. Desmopressin for treatment of platelet dysfunction and reversal of antiplatelet agents: a systematic review and meta-analysis of randomized controlled trials. J Thromb Haemost. 2017 Feb;15(2):263-272. doi: 10.1111/jth.13576. Epub 2017 Feb 8. PMID: 27893176.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
MINOCA, questa nuovo acronimo ci mancava! già in alcuni studi di una decina di anni fa emergeva che in corso di IMA era possibile riscontrare delle coronarie con un flusso sanguigno preservato o addirittura assenza di ostruzione significativa al punto tale che spesso questi pazienti con un’iniziale diagnosi di IMA venivano successivamente considerati come dei “falsi positivi”.
Si stava delineando il MINOCA , di cui la Drssa Balzarini ci presenta una eccellente disamina.
Quante volte amici, segretarie, farmacisti inviano in PS persone perchè “hanno la pressione alta“?
Tante volte !! Spetta al medico di emergenza collocare nel corretto percorso il paziente , utilizzando correttamente ed appropriatamente le risorse che un PS moderno offre
Un excursus esaustivo della Drssa Daghini vi condurrà ad un nuovo approccio all’ Emergenza ipertensiva”!
Il Dr Lai medico di emergenza con esperienza puriennale sia nel setting pre ospedaliero che ospedaliero propone una visitazione su “La Morte Improvvisa” , tema per eccellenza della disciplina di pronto soccorso e 118