11 NI Multysystem Injury Management DNA (1).pptx

Multysystem Injury Management

1. NEUROINTENSIVE CARE CHAPTER 11 MULTYSYSTEM INJURY MANAGEMENT Damar Nirwan Alby , MD Supervisor: Renindra Ananda Aman, MD, PhD

2. INTRODUCTION The intensive care management of complex, multisystem injury poses a challenge for even the most experienced clinician. The combination of neurological injury and abdominal, chest , or pelvic trauma often creates a particularly difficult situation in which the synergistic effects of shock , hypoxia , and ongoing hemorrhage may profoundly worsen the outcome from traumatic brain injury (TBI) or spinal cord injury (SCI)

3. RESUSCITATIVE PHASE Airway and Breathing For trauma case , c- spine control is the additional precaution Assesment begins : Is there any obstruction ? complete / partial Patient attempts of breathing , is there any effort ? retraction ? Intubation is indicated for respiratory failure or for airway protection in the setting of of altered conciousness Respiratory insufficiency or failure can be classified as either a ventilatory or oxygenation problem

4. RESUSCITATIVE PHASE Airway and Breathing Ventilatory failure May be due to neurological injury or a mechanical failure within thorax Ventilatory failure must be corrected with mechanical ventilation Oxygenation failure PO2 less than 60 mmHg or SaO2 less than or equal 90% Orotracheal intubation is the preferred route  if failed or patient with c- spine injury or craniofacial fracture , it can be done with bronchoscopy  it 3 attempts has failed or not possible  cricothryoidotomy

5. RESUSCITATIVE PHASE Reestablishing Perfusion : The Treatment of Shock States 4 types of shock : hypovolemic , cardiogenic , extracardiac obstructive , and extracardiac distributive ( neurogenic shock ) A loss of 20 – 30% blood will manifest with an increased HR, decresed blood pressure (BP), mental status change A loss of 30– 40% blood , RR rises , low urine output , pale/ cool skin > 40 % blood loss means almost certain death Children have the ability to maintain BP for a long time , therefore hypotension may present very late Internal blood loss must be ruled out

6. RESUSCITATIVE PHASE Reestablishing Perfusion : The Treatment of Shock States Patient takes b-blocker can be confusing because low BP without tachycardia Body’s protective mechanism : preserve blood flow to the heart and brain : Kidney perfusion is sacrificed  kidney failure Decreased gut perfusion  ischemic gut , acalculous cholecystitis , erosive gastritis Lactate as indicator of ischemia . Below a critical oxygen delivery level (8-10 ml O2/min/kg), anaerobic glycolisis only produces 2 ATP (versus 36 ATP in normal state )  ATP- dependent ion transport proteins unable to maintain transmembran gradient  intracellular acidosis and lactate production

7. RESUSCITATIVE PHASE Reestablishing Perfusion : The Treatment of Shock States First priority management of shock : ABC ECG, SaO2 Netral position Do not use any inotropic agents before restoring intravascular volume

8. RESUSCITATIVE PHASE Crystalloid Solutions NS 0,9 % and RL are the preffered ones NS 0,9% has a higher pH than RL. RL has additional bicarbonate , K , Ca, and lactate but offers no additional advantage over NS 0,9 %. Colloid Solutions Colloids stay in the intravascular space more readily than crytalloid . However there has been no difference in survival rates with the use of colloid .

9. RESUSCITATIVE PHASE Transfusion and Autotransfusion Transfusion of blood-banked products risk : viral infection and transfusion reactions Massive shed blood loss can be collected and retransfused to the trauma patients . Blood from hemothorax is normally depleted of fibrinogen, platelets , and clotting factors . It can be collected with chest tube  devices attached to a pleurovac system , the reservoir contains sodium citrate ( anticoagulation ) Blood shed from the repair of spinal , abdominal, retroperitoenal injuries contain high levels of clotthing factors

10. RESUSCITATIVE PHASE Hypothermia , Coagulopathy , and Metabolic Acidosis Temperature below 32 C is associated with 100% mortality in trauma patients Hypothermia is worsen by ressucitation cold fluids and evaporative heat loss from open body cavities during surgery . Hypothermia effect : coagulation , hemodynamics , and nervous system Coagulation : decreased platelet function and clotting factors . Normotemperature must be achieved before administering blood products . Brain injury resulting a release of thromboplastins  DIC Platelet counts < 50.000. 4 – 8 unit of platelet Fibrinogen < 100 mg /dl: cryoprecipitate PT > 1,5x or INR >: FFP Hemodynamics : negative inotropism

11. RESUSCITATIVE PHASE Hypothermia , Coagulopathy , and Metabolic Acidosis Metabolic acidosis caused by inadequate oxygen to meet metabolic demands Use of sodium bicarbonate is debatable because it can cause hypernatremia ( eg seizures , exacerbation of cerebral edema) and severe alkalemia Bicarbonate use is indicated if pH < 7,1 and renal tubular acidosis is the primary cause .

12. ICU PHASE Acute Lung Injury and ARDS The normal ratio PaO2/FiO2 is 450 to 500. ARDS is equal or below 200, ALI is greater than 200 but less than 300. Causes is classified as two categories : Direct lung injuries : lung infection , traumatic thorax Indirect lung injuries : sepsis, pancreatitis Ventilator practices in ARDS: correcting PCO2, arterial pH,and oxygenation Maintain positive end-expiratory pressure (PEEP) and low near tidal volume (6 cc/kg) is the key in ARDS

13. ICU PHASE Ventilator Weaning First, gas exchange : PaO2/FiO2 > 200, FiO2 50%, PEEP 5 Second , hemodynamic is stable with no need of vasopressors . Third , adequate drive to breathe and protect the airway . Patient is not overly sedated . Neuromuscular blockade should be reversed . Severe metabolic alkalosis need to be corrected to provide drive to breathe . Head-injured patient must be adequately awake . Last , patient must be able to sustain alveolar ventilation with minimal support  

14. ICU PHASE Ventilator Weaning A popular method of weaning protocols is to gradually decrease mechanical support SIMV: ventilator rate is decreased gradually PS ( ex : CPAP) can also be added to SIMV and eventually reduced to minimal levels Another approach of weaning is spontaneuous breathing trials of increasing duration using a T-piece with flow-by oxygen , PS, or CPAP Tracheostomy should be considered it patients required prolonged intubation , timing is remain controversial , but should be a conideration after the first week if intubation and mechanical support continue to be necessity .

15. ICU PHASE Stress Ulcer 48 hour post onset critical condition Caused by decreased splanchnic blood flow Prevention : proton pump inhibitor Colonic Ileus Motility problem ( Ogilvie’s syndrome ) Sign : distended abdomen, decreased bowel sound , xray shows distended air- filled colon Management : fluid resuscitation , NGT, rectal tube assist decompression , prokinetic agent Treatment : exploratory laparotomy

16. ICU PHASE Nutritional Needs Should be implemented within 48 hours if possible Enteral feeding is preferable Direct stimulation mantains gut mucosa  enhances mucosal barrier Parentral nutrition (TPN) increases risk of central line infection

17. ICU PHASE DVT and Pulmonary Embolism (PE) Incidence of PE can vary from 1 – 10%, mortality 0,5% - 5% Sign of DVT: fever , leg edema, palpable thrombosed venous cord , Homan’s sign Diagnosis of DVT: doppler USG Management of PE: LMWH, stocking compression Sign of PE: not specific Diagnosis of PE: pulmonary angiogram , CT thorax with contrast > MRI Management of PE: intubation , mechanical ventilation , INR target 2-3 with heparin . Surgical embolectomy , thromboembolytic therapy and suction catheter embolectomy might be needed .

18. ICU PHASE Renal Failure and Renal Replacement Therapy Mortality up to 50%, if it is part of multiple organ failure , the rate is 100%. Caused by prerenal ( decreased renal perfusion ), renal, post renal ( obstruction ) Management : fluid ressucitation , dopamin , Renal replacement therapy is needed in condition of hypervolemia , electrolyte disturbances , refractory metabolic acidosis , and uremia

19. ICU PHASE Prophylactic Antibiotics in Trauma Classification of wounds : Clean : < 6 hours , no soilage (3% of infection rate ) Clean contaminated : clean wound with contaminating soilage (8% of infection rate ) Contaminated wound : > 8 hours (25% of infection rate ) Antibiotic choices : Abdominal trauma: gram negative and anaerobic Orhtopedic surgery with open fractures : cephalosporin and anaerobic ( depending on contamination ) Inappropriate us of antibiotics : MRSA Opportunistic fungi

20. ICU PHASE Sedation Agitation and anxiety control  decreases oxygen consumption Propofol is agent of choice is head trauma patient . Good for evaluating level of conciousness of patient Propofol is an amnestic and hynotic , but has analgesic properties Benzodiazepine , such as midazolam . Midazolam has a rapid onset , can be used as infusion Has a metabolite that can have an effect for several days Haloperidol can be useful in addition to benzodiazepines in controlling delusional , psycothic patients

21. ICU PHASE Pain Control Epidural analgesia : patient with chest trauma and abdomen Fentanyl : fast onset , little sedating effect , does not have adverse cardiovascular effect Morphine : has a longer duration , can respiratory depression NSAID: very limited role in the ICU setting

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