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Presentation of Dr.Yasser Zaghloul at ICEM Egypt 2012. ICEM Egypt 2012 is the leading medical conference and exhibition for Intensive Care and Emergency Medicine in Egypt.

Presentation of Dr.Yasser Zaghloul at ICEM Egypt 2012. ICEM Egypt 2012 is the leading medical conference and exhibition for Intensive Care and Emergency Medicine in Egypt.

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    Role of ICU in dcs Role of ICU in dcs Presentation Transcript

    • The Role of ICU inDamage Control Surgery Yasser Zaghloul Sheikh Khalifa Medical City – Cleveland Clinic Abu Dhabi – United Arab Emirates
    • Overview• Introduction.• Airway & Ventilation.• Hemodynamics & IVF.• Hemoststic Resuscitation.• Abdominal Compartment Syndrome.• Trauma & Immune response.
    • Introduction
    • What "Damage control" does mean ?• In navy, damage control term is used for the emergency control of situation that may hazard the sinking of a ship.• In medicine we have: - Damage control general surgery - Damage control orthopedics - Damage control neurosurgery
    • Damage Control• Damage Control Resuscitation in Military Medicine:* - Hypotensive resuscitation (SBP 90 mmHg) - Use of thawed plasma and RBCs rather than IVF. - Early and rapid correction of coagulopathy with component therapy. - Severely damaged victims receive warm whole blood as a resuscitative fluid. * Holcomb JB et al. J Trauma 2007; 62: 307
    • Why Damage Control Surgery?* Application of the skills used for elective surgery failed to obtain satisfactory results in the treatment of severely injured patients because of thedifferences in the physiology and anatomy. * Waibel BH, Rotondo MF. Crit Care Med 2010; 48:(Suppl.); S421
    • When DCS is indicated ?*• DCS should be employed in the severely injured patient presenting with: - Deep Hgic shock. - Signs of ongoing bleeding. - Coagulopathy. * Rossaint R et al. Critical Care 2010, 14:R52
    • DCS – European Guidelines 2010*• Additional factors that should trigger a damage control approach are: - hypothermia - acidosis - inaccessible major anatomical injury. - need for time-consuming procedures. - major injury outside the abdomen. * Rossaint R et al. Critical Care 2010, 14:R52
    • Components of DCS*• First: - An abbreviated resuscitative laparotomy for control of bleeding / contamination.• Second: - Intensive Care Management.• Third: - Definitive surgical repair. * Rossaint R et al. Critical Care 2010, 14:R52
    • AirwayManagement
    • Airway Challenges in Trauma Patients Urgency Full Head Stomach Injury C-Spines Airway Cardiovascular Injury Compromise ChallengesRespiratory AbnormalCompromise Anatomy Co-morbidities
    • Ventilation
    • Why the trauma patient may need ventilation?• Chest wall • Head Injury.• Lung contusion. • C-spine fractures.• Airway trauma • Severe shock.• Aspiration. • Diaphragm.• Inhalation injury. • Agitation. • TRALI. • Fat Embolism.
    • Lung Protective Strategy*• The lowest possible FiO2 (PaO2 > 60 - 70 mmHg)• Low TV ( 6 ml/kg).• Peak Airway Pressure < 30 cmH2O.• Assist-synchronized Mode.• PEEP 5 -10 cmH2O. * ARDS Network. NEJM 2000; 342: 1301 * Papadakos PJ et al. Curr Oponion Anesthesiology 2010; 23: 228
    • Titration of PEEP - Acute lung injury - Lung contusion - Non-cardiogenic pulmonary oedema- High ICP. - TRALI- Haemodynamic instability High PEEPLow or no PEEP
    • TraumaticBrain Injury
    • Secondary Brain Damage - Hypotension. - Hypovolaemia. •High ICP, Seizure- Hypoxia.- Hyper- & Hypo- CO2 •Haemoglobin, low- Hyperthermia.- High H+ ions (Acidosis) •Hyper & Hypoglycaemia
    • Haemodynamics
    • Target Blood PressureA target SBP 80-100 mmHg untilmajor bleeding has been stopped inthe initial phase following trauma without brain injury.* * Rossaint R et al. Critical Care 2010, 14:R52
    • Do not wait for  BP ....!!!In the absence of hypotension, when shock is suggested by history and physical examination, a marker of inadequate perfusion should be measured.* ed SvO2 ed blood Lactate Perfusion-related low pH ed Base Deficit* Antonelli M et al. Intensive Care Med 2007; 33: 575
    • • Lactate levels should be checked to identify patients with occult tissue hypoperfusion.• The use of lactate clearance may be as beneficial as mixed venous oxygenation in selected patient populations and should be viewed as a resuscitation target.* * Fullera BM, R. Dellinger P. Curr Opin Crit Care 2012, 18:267
    • IV Fluids
    • Current Controversies ...!!!• Which fluid? (Colloids Vs crystalloids)• End points of resuscitation• Low (delayed) volume Vs High volume IVF.• Target Haemoglobin ?
    • A Comparison of Albumin and Saline for Fluid Resuscitation in ICU The SAFE Study Investigators . 2004; 350: 2247 Saline Vs Albumin Fluid Evaluation
    • Kaplan–Meier estimates of the probability of survival Saline Vs Albumin Evaluation – SAFE Trial
    • • Randomized, controlled, double-blind study of severely injured patients requiring 3 liters of fluid resuscitation.•• Blunt and penetrating trauma were randomized separately.• Patients were followed up for 30 days. * James MFM et al. British J Anaesth 2011: 107: 693
    • • Conclusions: - In penetrating trauma, HES provided significantly better lactate clearance and less renal injury than saline. - No firm conclusions could be drawn for blunt trauma.• Low volume does NOT mean delayed resuscitation.
    • Colloids versus crystalloids for fluid resuscitation in critically ill patients (Review)** Pearl P, Roberts I. Cochrane Database of Systematic. Reviews 2012, Issue 6 Art. No.: CD000567. DOI: 10.1002/14651858.CD000567 Published on line on 14th November 2012
    • Colloids versus crystalloids for fluidresuscitation in critically ill patients (Review)*• Conclusion: There is no evidence from RCTs that resuscitation with colloids reduces the risk of death, compared to resuscitation with crystalloids, in patients with trauma, burns or following surgery.
    • Low Volume Resuscitation• Contraindicated in:* Elderly patients? Hypertension? Spinal injuries Traumatic brain injury * Rossaint R et al. Critical Care 2010, 14:R52
    • End Points of IVF Resuscitation*Parameter Goal Notes MAP > 65 mmHg - TBI > 70 PaO2 ≥ 80 mmHg - Lowest PEEP (Saturation ≥ 95%) - FIO2 < 0.6 UOP > 0.5 ml/Kg/h > 1.0 ml/Kg/h in paediatric patientsHaemoglobin ≥ 9 gm/dL -Higher in CV and resp. disorders Lactate < 2.1 mmol/L -  in 1st 6 h - Clearance in 24h * Garcia A. Surg Clin North Am 2006; 86: 1359
    • Complications of large volume fluids resuscitation• Pulmonary oedema.• Abdominal Compartment Syndrome.• es tissue oedema and es perfusion.• Dilution Coagulopathy.
    • Blood Transfusion
    • What is the Target Hb in Poly-trauma Patients? Target haemoglobin 7 - 9 gm/dl ...!!!** Rossaint R et al. Critical Care 2010, 14:R52
    • Factors Affecting Anaemia Tolerance**  Tolerance: *  Tolerance:•  FiO2 • Hypovolemia • Hypoxia.• Hypothermia. • Poly-trauma. • Acute Brain Injury.• Sedation. •  Metabolism (Burn) • CAD.• Inactive muscles. • Sepsis. * Pape A, Habler O. Best Practice & Research Clinical Anesthesiology 2007; 21: 221
    • HaemostaticResuscitation
    • Lethal Triad Acidosis Bloody Vicious CycleHypothermia Coagulopathy
    • Lethal Quad Acidosis Low Hb Bloody Vicious CycleHypothermia Coagulopathy Hypocalcaemia
    • Are RBCs important for haemostasis?• Erythrocytes are involved in the biochemical activation of platelets and thrombin generation  haemostasis.* * Peyrou V et al. Thromb Haemost 1999; 81: 400• Presence of elastase on surface of RBC, activates F IX triggering blood coagulation. * Iwata H et al. Biochem Biophys Res Commun 2004; 316: 65
    • Hypothermia & Coagulation• Between 37 – 33 C, haemostasis defects result from a defect in platelets adhesion and aggregation. * Lier H et al. J Trauma 2008 ; 65: 951• Each  1 C   15% in Thromboxane production. * Valeri CR et al. Crit Care Med 1995; 23: 698• Below 33 C, altered enzymatic activity is an additional factor. * Wolberg AS et al. J Trauma. 2004; 56: 1221
    • Hypocalcaemia & Trauma• Hypocalcaemia frequently ( > 50%) occurs on arrival at the hospital in severe trauma patients.*• Ionized Ca++ < 0.9 mmol/L was associated with ed mortality. * * Vivien B eta l. Crit Care Med 2005; 33: 1946
    • Should we treat all major trauma patients with IV Ca?• Ionized Ca++ should be ≥ 1.0 mmol/L.• Should be given when citrate-containing blood products (FFP & Platelets) are infused @ high rate.• Either Ca gluconate (9.3 mg/ml) or CaCl2 (27 mg/ml). * Lier H et al. J Trauma 2008; 65: 951 * Rossaint R et al. Critical Care 2010, 14:R52
    • Blood Products• FFP.• Platelets.• Cryoprecipitate.
    • Fresh Frozen PlasmaFFP should be used in patients with massive bleeding or significant bleeding complicated coagulopathy. * (PT or aPTT > 1.5 control) FFP : RBCs = 1:1 (With the 4th Unit of RBCs) * Rossaint R et al. Critical Care 2010, 14:R52
    • Platelets Transfusion• Platelets should be maintained > 50,000 /dl. - Multiple trauma with severe bleeding and/or traumatic brain injury > 100,000.* Platelets should be given with the 6th – 8th unit of RBCs in a 1:1 or 1:1.5 ratio. * Rossaint R et al. Critical Care 2010, 14:R52
    • CryoprecipitateFibrinogen concentrate or cryoprecipitate should be given if there is bleeding & fibrinogen < 1gm/l.* * Rossaint R et al. Critical Care 2010, 14:R52
    • Haemostatic Drugs• Tranexamic Acid• Activated factor IIV.
    •  20.211 patients, 174 hospitals, 40 countries Tranexamic acid safely reduced the risk of death and should be considered for use in bleeding trauma patients. * CRASH-2 Trial Collaborators (www.crash 2.LSHTM.ac.uk) Published online first on 15th June 2010 http://www.thelancet.com/crash-2
    • The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratoryanalysis of the CRASH-2 randomized controlled trial• Tranexamic acid should be given as early as possible (< 3h) to bleeding trauma patients.• For trauma patients admitted late after injury, tranexamic acid is less effective and could be harmful.* The CRASH-2 collaborators. Lancet (March) 2011; 377:1096
    • • In view of efficacy and safety of this relatively cheap and simple drug, it may be recommended to put tranexamic acid in the first (may be even pre-hospital) line of management of patients with severe traumatic hemorrhage.* * Levi M. Curr Opin Anesthesiol 2012, 25
    • Tranexamic Acid• CRASH-2 (June 2010) - 1 gram IV loading, then 1gm over 8 hours (infusion).• European Guidelines (April 2010) - 10-15 mg/kg followed by infusion 1-5 mg/kg/h.
    • AbdominalCompartment Syndrome
    • Pathophysiology CENTRAL NERVOUS SYSTEM Intracranial pressure  Cerebral perfusion pressure Idiopathic intracranial hypertension (obesity) CARDIOVASCULAR SYSTEM RESPIRATORY SYSTEM Difficult preload assessment RENAL SYSTEM Intrathoracic pressure  Wedge pressure  Renal blood flow  Pleural pressure  Central venous pressure  Diuresis  Functional residual capacity  Intra thoracic blood volume index = Tubular dysfunction  All lung volumes  Extra vascular lung water = Glomerular filtration rate  (~restrictive disease)Right ventricular end-diastolic volume Renal vascular resistance  Auto-PEEP  ? index = Renal vein compression  Peak airway pressure  Cardiac output  Compression ureters  Plateau pressures  Venous return  Anti-diuretic hormone  Dynamic compliance  Systemic vascular resistance  Adrenal blood flow = Static compliance  Venous thrombosis  Chest wall compliance  Pulmonary embolism  Hypercarbia  Heart rate  = GI SYSTEM PaO2  Mean arterial pressure  = Celiac blood flow  PaO2/FiO2  Superior mesenteric artery blood flow  Dead-space ventilation  Pulmonary artery pressure  Blood flow to intra-abdominal organs  Intrapulmonary shunt  Mucosal blood flow  Lower inflection point  Mesenteric vein compression  Upper inflection point  HEPATIC SYSTEM Intramucosal pH  Prolonged ventilation ? Hepatic arterial flow  Regional CO2  Portal venous blood flow  Difficult weaning ? CO2-gap  Portocollateral flow  Success enteral feeding  ? Lactate clearance  Intestinal permeability  ABDOMINAL WALL Glucose metabolism  Bacterial translocation  ? Compliance  Mitochondrial function  Multiple organ failure  ? Rectus sheath blood flow Cytochrome p450 function  Wound complications  Gastro-intestinal (re)bleeding  Incisional hernia  Malbrain. Current Opinion Crit Care 2004; 10(2): 132-145
    • Management of ACS*Grade Bladder Pressure Management (mmHg) I 12 -15 Maintain Normovolaemia II 16 – 20 Hypervolaemia III 21- 30 Decompression VI > 31 Decompression + re-exploration* Modified from Bailey J, Shapiro MJ. Crit Care 2000; 4: 23
    • Medical Management of ACS*• Evacuate intra-luminal contents. - NGT - Rectal tube . - Prokinetic agents -  or D/C Enteral feeding. - Enema - ?? Colonoscopic decompression• Evacuate intra-abdominal space occupying lesions. - Percutaneous catheter drainage. * Adapted from Intensive Care Medicine 2006;32(11):1722 & 2007;33(6):951 2009 World Society of the Abdominal Compartment Syndrome. www.wsacs.org
    • Medical Management of ACS*• Improve abdominal wall compliance. - Sedation / relaxation. -  Dressing• Optimize fluid administration. - Zero or negative balance by day 3. - ?? Diuresis - HD• Optimize regional & systemic perfusion. - Abdominal Perfusion Pressure > 60 mmHg. * Adapted from Intensive Care Medicine 2006;32(11):1722 & 2007;33(6):951 2009 World Society of the Abdominal Compartment Syndrome. www.wsacs.org
    • Trauma andImmune Response
    • Trauma & Immune ResponseGiannoudis PV. Pape HC. Injury, Int. J. Care Injured 2007; 38: 1333
    • Trauma & Psychological Stress NorepinephrineCoagulation Fibrinolysis NF-ќB Inflammation
    • Insult - No inflammation - Good HomeostasisPro-inflammatory - Good Recovery Innate Immune Response Day 1 7 days 14 daysAnti-inflammatory Adaptive Immune Response Natural course of inflammatory mediators* * Pape HC et al. Injury, Int J Care Injured 2007; 38, 1358
    • Other Therapies• DVT Prophylaxis.• Early Enteral Nutrition.• Renal Replacement Therapy• Control of Blood Sugar.• Stress Ulcer Prophylaxis.
    • Thank YouYasser Zaghloul