Traumatic brain injury2

Views:
 
Category: Entertainment
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

By Dr. Magdy Aly Omera Prof. of Anesthesia & Intensive Care Faculty of Medicine Suez Canal University :

By Dr. Magdy Aly Omera Prof. of Anesthesia & Intensive Care Faculty of Medicine Suez Canal University Traumatic Brain Injury [TBI]

Incidence TBI is a major cause of death, disability, and economic cost to our society. In 2000, the economic impact of TBI in the United States (USA) was estimated to be $9.2 billion in medical costs and $51.2 billion in productivity losses. In USA approximately one million individuals are hospitalized for head trauma each year with mortality about 50,000 deaths annually. (1.5 million new cases in 2003) In adult, motor accident contributes about 2/3 of all head injuries, followed by falls then gunshot. In contrast, falls are the most likely mechanism of head injuries in the pediatric and elderly. Male has double incidence than female. :

Incidence TBI is a major cause of death, disability, and economic cost to our society. In 2000, the economic impact of TBI in the United States (USA) was estimated to be $9.2 billion in medical costs and $51.2 billion in productivity losses . In USA approximately one million individuals are hospitalized for head trauma each year with mortality about 50,000 deaths annually. (1.5 million new cases in 2003) In adult, motor accident contributes about 2/3 of all head injuries, followed by falls then gunshot. In contrast, falls are the most likely mechanism of head injuries in the pediatric and elderly. Male has double incidence than female.

Classification 1)Scalp injury 2)Skull injuries a) Linear fractures b) Depressed fractures c) Skull base fractures 3)Meningeal injuries a) Subdural hematoma b) Epidural hematoma c) CSF leakage 4)Brain injuries a) Focal brain injury -Contusion -Intracerebral hematoma b) Diffuse brain injury -Concussion -Diffuse axonal injury :

Classification 1)Scalp injury 2)Skull injuries a) Linear fractures b) Depressed fractures c) Skull base fractures 3)Meningeal injuries a) Subdural hematoma b) Epidural hematoma c) CSF leakage 4)Brain injuries a) Focal brain injury - Contusion - Intracerebral hematoma b) Diffuse brain injury - Concussion - Diffuse axonal injury

Slide4:

Concussion is defined as Diffuse injury to the brain without any evidence of structural alteration. Grade I concussion is one in which a person is confused temporarily but does not display any memory changes. Grade II concussion , brief disorientation and anterograde amnesia of less than 5 minutes' duration are present. Grade III concussion , grade II concussion plus retrograde amnesia and loss of consciousness for less than 5 minutes Grade IV concussion are similar to grade III, except that the duration of loss of consciousness is 5-10 minutes, Grade V concussion are similar to grade III, except that the duration of loss of consciousness is › 10 minutes .

Slide5:

About 30% of patients who experience a concussion develop postconcussive syndrome (PCS). PCS consists of a persistence of any combination of headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances Typically, PCS symptoms peak 4-6 weeks following the injury. PCS usually lasts 2-4 months. On occasion, PCS last for a year or longer. Approximately 20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently by PCS.

Causes 1) Penetrating trauma Missiles or stabbings by sharp instruments and impaled objects. 2) Blunt trauma Direct blow, rapid deceleration by vehicular collisions or falls.:

Causes 1) Penetrating trauma Missiles or stabbings by sharp instruments and impaled objects. 2) Blunt trauma Direct blow, rapid deceleration by vehicular collisions or falls.

Pathophysiology Primary injury It comprises the immediate effects of impact. It is the physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue. The impact initiates a series of events, including release of mediators, which cause injury over minutes to hours after impact.:

Pathophysiology Primary injury It comprises the immediate effects of impact. It is the physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue. The impact initiates a series of events, including release of mediators, which cause injury over minutes to hours after impact.

Slide8:

Secondary injury It is due to factors other than the direct impact & may begin almost immediately or some time later. Asphyxia or massive blood loss may cause overwhelming ischemic–hypoxic secondary damage, irrespective of the severity of the primary injury.

Complications (EXTRACRANIAL) Cardiovascular *Hypertension *Arrhythmia *ST-segment depression Respiratory *Neurogenic pulmonary edema *ARDS Metabolic *Hyperglycemia *Diabetes insipidus *SIADH Syndrome Coagulation *DIC Gastrointestinal *Stress ulcer :

Complications (EXTRACRANIAL) Cardiovascular * Hypertension *Arrhythmia *ST-segment depression Respiratory * Neurogenic pulmonary edema *ARDS Metabolic * Hyperglycemia *Diabetes insipidus *SIADH Syndrome Coagulation * DIC Gastrointestinal * Stress ulcer

Management of patient with traumatic brain injury A) Initial resuscitation (ABC). B) Primary survey. C) Radiological assessment. D) Secondary survey for definitive diagnosis E) Surgical intervention. F) Conservative medical treatment. :

Management of patient with traumatic brain injury A) Initial resuscitation (ABC). B) Primary survey. C) Radiological assessment. D) Secondary survey for definitive diagnosis E) Surgical intervention. F) Conservative medical treatment.

A) Initial resuscitation ABC Advanced Trauma Life Support (ATLS) guidelines. A-Airway patency with cervical spine immobilization -Chin left or jaw thrust -Oropharyngeal airway -Endotracheal intubation if *Compromised airway *Ventilatory failure *Oxygenation failure *GCS <9 *Sustained Seizures -Surgical airway (cricothyrotomy or tracheostomy):

A) Initial resuscitation ABC Advanced Trauma Life Support (ATLS) guidelines. A- Airway patency with cervical spine immobilization -Chin left or jaw thrust -Oropharyngeal airway -Endotracheal intubation if *Compromised airway *Ventilatory failure *Oxygenation failure *GCS <9 *Sustained Seizures - Surgical airway (cricothyrotomy or tracheostomy)

NEVER hyperextend, hyperflex, or rotate the neck. If immobilizing devices must be removed , stabilize head and neck with manual, in-line immobilization B-Breathing (ventilation& oxygenation) -Seal open pneumothorax -Alleviate tension pneumothorax -Stabilize flail chest -Administer oxygen -Ventilate with Ambu bag -Attach pulse oximeter:

NEVER hyperextend, hyperflex, or rotate the neck. If immobilizing devices must be removed , stabilize head and neck with manual, in-line immobilization B - Breathing (ventilation& oxygenation) -Seal open pneumothorax -Alleviate tension pneumothorax -Stabilize flail chest -Administer oxygen -Ventilate with Ambu bag -Attach pulse oximeter

C-Circulation -Control external bleeding -Insert 2 large bore iv canulae -Obtain blood sample for analysis &cross matching -Initiate warmed iv fluid (saline) -Use colloid or blood if required -Insert urinary catheter after exclusion of urethral injury -Insert CVP (if required and avoid neck lines) -Attach the patient to ECG & NIBP monitor :

C - Circulation -Control external bleeding -Insert 2 large bore iv canulae -Obtain blood sample for analysis &cross matching -Initiate warmed iv fluid (saline) -Use colloid or blood if required -Insert urinary catheter after exclusion of urethral injury -Insert CVP (if required and avoid neck lines) -Attach the patient to ECG & NIBP monitor

Urinary Catheters No transurethral catheter until genitalia, perineum, and rectal exam. Urethral injury indicators: Meatal blood, shaft hematoma, perineal or scrotal ecchymosis, non-palpable prostate, pelvic fracture. Suspected urethral injury requires: Retrograde urethrogram (RUG) prior to transurethral catheter insertion. :

Urinary Catheters No transurethral catheter until genitalia, perineum, and rectal exam. Urethral injury indicators: Meatal blood, shaft hematoma, perineal or scrotal ecchymosis, non-palpable prostate, pelvic fracture. Suspected urethral injury requires: Retrograde urethrogram (RUG) prior to transurethral catheter insertion.

B) Initial assessment A) History *Past history (allergy, medications, last meal) *Details of injury *Symptoms (loss of conc., vomiting, headache, memory loss or convulsion) :

B) Initial assessment A) History *Past history (allergy, medications, last meal) *Details of injury *Symptoms (loss of conc., vomiting, headache, memory loss or convulsion)

B) Examination Completely undress the patient to facilitate thorough examination and assessment. Cover with warm blankets or use an external warming device to prevent hypothermia. Hypothermia has several deleterious effects including coagulopathy, cardiac dysrhythmias, impaired renal function, and poor wound healing. Apply appropriate splinting devices. :

B) Examination Completely undress the patient to facilitate thorough examination and assessment. Cover with warm blankets or use an external warming device to prevent hypothermia. Hypothermia has several deleterious effects including coagulopathy, cardiac dysrhythmias, impaired renal function, and poor wound healing. Apply appropriate splinting devices .

Slide17:

Vital signs (BP, HR, RR, Temp, SaO2) CNS (GCS, pupil, cranial nerves, motor, sensory) Head (scalp, eye, ear, nose, mouth) Neck (injury, trachea, spine) Chest (inspect, palpate, percuss, auscultate) Abdomen (inspect, palpate, percuss, auscultate) Perineum/rectum/vagina Musculoskeletal (UL, LL, spine, chest, pelvis)

C) Radiological assessment 1) Plain x-ray Chest & Pelvis Skull (for penetrating head injury) Spine (pain, tenderness, parathesia, coma) Long bone (If Q. fracture) 2) Computed Tomography CT Brain if a) Coma (GCS<9) after resuscitation b) Focal neurological signs c) Skull fracture with GCS<15 d) Multiple trauma patient not fully oriented e) Previous known intracranial pathology Spine if +ve plain x-ray 3) Abdominal US if Q. internal hemorrhage :

C) Radiological assessment 1) Plain x-ray Chest & Pelvis Skull (for penetrating head injury) Spine (pain, tenderness, parathesia, coma) Long bone (If Q. fracture) 2) Computed Tomography CT Brain if a) Coma (GCS<9) after resuscitation b) Focal neurological signs c) Skull fracture with GCS<15 d) Multiple trauma patient not fully oriented e) Previous known intracranial pathology Spine if +ve plain x-ray 3) Abdominal US if Q. internal hemorrhage

D) Secondary survey *Continuous monitoring. *Maintain normothermia *Continue ventilation and oxygenation. *Apply appropriate splinting devices. *Maintain adequate immobilization. *Adequate consultation (neurosurgery, surgery). *Judicious use of analgesic. *Administer antitetanic serum. Persistence hypotension indicates extracranial injury.:

D) Secondary survey * Continuous monitoring. * Maintain normothermia * Continue ventilation and oxygenation. * Apply appropriate splinting devices. * Maintain adequate immobilization. * Adequate consultation (neurosurgery, surgery). * Judicious use of analgesic. * Administer antitetanic serum. Persistence hypotension indicates extracranial injury.

SITES of BLOOD LOSS in TRAUMA OBVIOUS Scalp lacerations Facial injuries Open Fractures HIDDEN Intra/retroperitoneal Hemothorax Pelvic hematoma Long-bone fractures Aortic disruption :

SITES of BLOOD LOSS in TRAUMA OBVIOUS Scalp lacerations Facial injuries Open Fractures HIDDEN Intra/retroperitoneal Hemothorax Pelvic hematoma Long-bone fractures Aortic disruption

E) Surgical intervention Indications for urgent neurosurgery: 1) Extra or Subdural hematoma with a) Midline shift 5-10 mm b) Transtentorial herniation c) Signs of lateralization d) GCS <9 2) Depressed fracture with a) More than 1 cm b) Gross contamination c) Presence of CSF or brain tissue d) Undue bleeding 3) Penetrating head injury Indications for late neurosurgery: 1) Chronic Subdural hematoma 2) Hydrocephalus (often after 7 days) 3) Persistent CSF leak:

E) Surgical intervention Indications for urgent neurosurgery: 1) Extra or Subdural hematoma with a) Midline shift 5-10 mm b) Transtentorial herniation c) Signs of lateralization d) GCS <9 2) Depressed fracture with a) More than 1 cm b) Gross contamination c) Presence of CSF or brain tissue d) Undue bleeding 3) Penetrating head injury Indications for late neurosurgery: 1) Chronic Subdural hematoma 2) Hydrocephalus (often after 7 days) 3) Persistent CSF leak

F) Conservative medical treatment According to GCS: 1) Mild TBI GCS (15—13) 2) Moderate TBI GCS (12—9) 3) Severe TBI GCS (8—3) :

F) Conservative medical treatment According to GCS: 1) Mild TBI GCS (15—13) 2) Moderate TBI GCS (12—9) 3) Severe TBI GCS (8—3)

Glasgow Coma Scale 3-15 :

Glasgow Coma Scale 3-15 Eye Opening Never 1 To pain 2 To verbal 3 Spontaneous 4 Best Verbal Response None 1 Sounds 2 Inapp. words 3 Confused 4 oriented 5 Motor Response None 1 Extensor 2 Flexor Posture 3 Withdrawal 4 Localization 5 obeys 6

Management of Mild TBI [No ICU admission] Bed rest Observation Mild analgesic Patients with acute spinal cord injuries appear to be best managed in ICU for the first 7-14 days after injury, the time frame during which they appear most susceptible to significant fluctuations in cardiac and pulmonary performance.:

Management of Mild TBI [No ICU admission] Bed rest Observation Mild analgesic Patients with acute spinal cord injuries appear to be best managed in ICU for the first 7-14 days after injury, the time frame during which they appear most susceptible to significant fluctuations in cardiac and pulmonary performance.

2) Management of Moderate TBI [ICU admission] Bed rest Monitoring Analgesic Positioning Normalization Antiseizure prophylaxis Prophylactic antistress Prophylactic antibiotic Prophylaxis for DVT Treatment of associated complication Nutritional support Nursing Care :

2) Management of Moderate TBI [ICU admission] Bed rest Monitoring Analgesic Positioning Normalization Antiseizure prophylaxis Prophylactic antistress Prophylactic antibiotic Prophylaxis for DVT Treatment of associated complication Nutritional support Nursing Care

Position Patients are usually nursed 30° head up with neutral neck position after head injury and intracranial surgery in order to reduce ‘venous congestion’ and ‘brain swelling’. In most patients ICP is lower in this position. It was found that in many patients, although ICP fell with head elevation, there was also a significant fall in CPP. A fall in CPP was less likely when circulating volume was adequate. :

Position Patients are usually nursed 30° head up with neutral neck position after head injury and intracranial surgery in order to reduce ‘venous congestion’ and ‘brain swelling’. In most patients ICP is lower in this position. It was found that in many patients, although ICP fell with head elevation, there was also a significant fall in CPP. A fall in CPP was less likely when circulating volume was adequate.

Normalization Normotensive MAP>70mmHg or SBP> 90mmHg Euvolemic CVP = 8-10 mmHg Normothermic Temp = 36.5± 0.5 C Euglycemic RBS = 80-130 mg/dl Normocapnic PaCO2 = 40-36 mmHg Normoxia PaO2>85 mmHg or SaO2>95% Hemoglobin [Hb] >10 g/dL, or Hematocrit [Ht] >30:

Normalization Normotensive MAP>70mmHg or SBP> 90mmHg Euvolemic CVP = 8-10 mmHg Normothermic Temp = 36.5± 0.5 C Euglycemic RBS = 80-130 mg/dl Normocapnic PaCO 2 = 40-36 mmHg Normoxia PaO 2 >85 mmHg or SaO2>95% Hemoglobin [Hb] >10 g/dL, or Hematocrit [Ht] >30

Slide28:

Isotonic crystalloids , specifically normal saline, are the fluid of choice for fluid resuscitation and volume replacement. Norepinephrine , a pure alpha-agonist vasoactive agent, is recommended in TBI patients with tachycardia. Phenylephrine is recommended if HR>120. Avoid hyperglycemia particularly during the early 48h and give insulin if glucose level>150mg/dl. Avoid hypoglycemia and give glucose only if glucose level <60mg/dl Fever should be aggressively treated. Achieve normoxia Pulse oximetry (SpO2) of 95% or greater and/or PaO2 of 80 mm Hg or greater . Eucapnia with PaCO2 35 to 40 mm Hg.

Antiseizure prophylaxis Indications of Antiseizure prophylaxis: 1) GCS <9 2) Cortical contusion 3) Intracerebral hematoma 4) Subdural hematoma 5) Epidural hematoma 6) Depressed skull fracture 7) Penetrating brain injury 8) Ventilated sedated paralyzed patient :

Antiseizure prophylaxis Indications of Antiseizure prophylaxis: 1) GCS <9 2) Cortical contusion 3) Intracerebral hematoma 4) Subdural hematoma 5) Epidural hematoma 6) Depressed skull fracture 7) Penetrating brain injury 8) Ventilated sedated paralyzed patient

Antiseizure medications in the first week after TBI are recommended to prevent early posttraumatic seizures (e.g. with phenytoin, carbamazepine, valproate or phenobarbital) Prophylactic treatment with anticonvulsants beyond the first week after TBI has been not shown to prevent the development of new seizures, and is not recommended. Phenytoin loading dose of 15 mg/kg (I.V. over 30 min) followed by 100 mg (I.V. every 8 h for 7 days). :

Antiseizure medications in the first week after TBI are recommended to prevent early posttraumatic seizures (e.g. with phenytoin, carbamazepine, valproate or phenobarbital) Prophylactic treatment with anticonvulsants beyond the first week after TBI has been not shown to prevent the development of new seizures, and is not recommended. Phenytoin loading dose of 15 mg/kg (I.V. over 30 min) followed by 100 mg (I.V. every 8 h for 7 days).

Slide31:

Prophylaxis for DVT 1) Mechanical thromboprophylaxis (if no CI) a) Graduated Compression Stockings (GCS) b) Intermittent Pneumatic Compression (IPC) 2) Pharmacological thromboprophylaxis It is used in combination with mechanical prophylaxis after 48-72h if there is no CI . a) Low molecular weight heparin b) Low dose unfractionated heparin Thromboprophylaxis should be continued until patients are ambulatory.

Prophylactic antibiotic Indications 1) Scalp wound 2) CSF leakage 3) Some depressed skull fracture 4) Penetrating brain trauma 5) Postoperative:

Prophylactic antibiotic Indications 1) Scalp wound 2) CSF leakage 3) Some depressed skull fracture 4) Penetrating brain trauma 5) Postoperative

Treatment of associated complication:

Treatment of associated complication S.I.A.D.H. Posterior pituitary secretes ADH to regulate water balance Too much ADH causes S.I.A.D.H. where kidneys will retain H2O and blood serum will be hypotonic Signs and symptoms: Changes in L.O.C., headache, nausea and vomiting and decreased urinary output. Treatment of S.I.A.D.H. Fluid restriction 500cc or less in 24 hrs. IV saline (3% or 5%) with appropriate electrolyte replacements (K, Mg) Diuretics (Lasix)

Slide34:

Diabetes Insipidus Failure of ADH secretion and failure of kidneys to store H2O. Signs and symptoms: Urinary output increased with specific gravity of urine decreased Client will have dehydration Treatment: Use of Vasopressin (Pitressin), given I.M. or s.c.

Nutritional support DER = REE X AF X SF AF=1.15 for bedridden SF=1.25 for minor trauma 1.50 for multiple trauma Route: Enteral or Parentral Start: Enteral after 24h or Parenteral after 48h Full caloric req. by day 7 Hyperglycemia is associated with high brain lactate levels and possibly greater cerebral cellular injury, particularly in the early phases of brain injury. :

Nutritional support DER = REE X AF X SF AF=1.15 for bedridden SF=1.25 for minor trauma 1.50 for multiple trauma Route : Enteral or Parentral Start: Enteral after 24h or Parenteral after 48h Full caloric req. by day 7 Hyperglycemia is associated with high brain lactate levels and possibly greater cerebral cellular injury, particularly in the early phases of brain injury.

Nursing Care:

Nursing Care Assessment Feeding Positioning Raising head of bed to 30° Turning the patient regularly Keeping the head and neck in a neutral position Care of eye, mouth and skin Care of ETT Care of Bowel Care of Bladder Break up activities (Performing physiotherapy) Medicate prior to administering care

3) Management of Severe TBI In 1996, the Brain Trauma Foundation (BTF) published the first guidelines on the management of severe TBI. The second revised edition was published in 2000 with an update in 2003, and the 3rd edition was published in May 2007 in the Journal of Neurotrauma The same like moderate TBI plus 1) Intubation and ventilation 2) ICP monitoring :

3) Management of Severe TBI In 1996, the Brain Trauma Foundation (BTF) published the first guidelines on the management of severe TBI. The second revised edition was published in 2000 with an update in 2003, and the 3rd edition was published in May 2007 in the Journal of Neurotrauma The same like moderate TBI plus 1) Intubation and ventilation 2) ICP monitoring

Slide38:

3) Management of Severe TBI Bed rest Monitoring Analgesic Positioning Normalization Antiseizure prophylaxis Prophylactic antistress Prophylactic antibiotic Prophylaxis for DVT Treatment of associated complication Nutritional support Nursing Car e Intubation and ventilation ICP monitoring

Slide39:

Monitoring ECG, HR, RR Arterial oxygen saturation (SaO2), Capnography (end-tidal CO2, PetCO2), Arterial blood pressure (non invasive), Central venous pressure (CVP), Systemic temperature, Urine output, Arterial blood gases, Serum electrolytes and osmolality. Invasive arterial blood pressure & cardiac output monitoring may be required  

Intubation and ventilation Normocapnia and avoid routine hyperventilation. It is safer to keep the PaCO2 at 40–35 mmHg, thus avoiding the potential for cerebral ischemia. Positive end-expiratory pressure (PEEP) improves oxygenation without the need for a high inspired oxygen fraction (FiO2). It has been suggested that the higher of PEEP might raise venous pressure and hence ICP. However, studies in patients have suggested that ICP is not affected, even with intrathoracic pressures of up to 40 cmH2O. PEEP of 5 to 8 cm H2O that maintains adequate oxygenation and prevents end-expiratory collapse, should be used. Avoid muscle relaxant, ensure sedation and analgesia,:

Intubation and ventilation Normocapnia and avoid routine hyperventilation. It is safer to keep the P aCO2 at 40–35 mmHg, thus avoiding the potential for cerebral ischemia. Positive end-expiratory pressure (PEEP) improves oxygenation without the need for a high inspired oxygen fraction ( F iO 2 ). It has been suggested that the higher of PEEP might raise venous pressure and hence ICP. However, studies in patients have suggested that ICP is not affected, even with intrathoracic pressures of up to 40 cmH 2 O. PEEP of 5 to 8 cm H2O that maintains adequate oxygenation and prevents end-expiratory collapse, should be used. Avoid muscle relaxant, ensure sedation and analgesia ,

Slide41:

Propofol It is the hypnotic of choice in patients with an acute neurologic insult, as it is easily titratable and rapidly reversible once discontinued. These properties permit predictable sedation yet allow for periodic neurologic evaluation of the patient. However, propofol should be avoided in hypotensive or hypovolemic patients because of its deleterious hemodynamic effects. Moreover, propofol infusion syndrome (rhabdomyolysis, metabolic acidosis, renal failure, and bradycardia) is a potential complication of prolonged infusions or high doses.

Slide42:

Benzodiazepines Midazolam (Dormicum) and lorazepam (Ativan) are recommended as continuous infusion or intermittent boluses. In addition to sedation, they provide amnesia and anticonvulsive effect. Midazolam initial dose: 1-5 mg IV over 2-3 min, every 5-15 min to control acute agitation. Maintenance dose: 0.02 to 0.2 mg/kg/hour by continuous infusion. Risk factors for accumulation and oversedation : Prolonged infusion, High dose, Renal failure, Hepatic failure, and Old age

ICP monitoring There are four ways of monitoring intracranial pressure: 1) Intraventricular catheter (a catheter threaded into one of the lateral ventricles of the brain) 2) Parenchymal catheter tip pressure transducer 3) Subarachnoid screw or bolt (a screw or bolt placed just through the skull in the space between the arachnoid and cerebral cortex) 4) Epidural sensor (a sensor placed into the epidural space beneath the skull) Intraventricular and Parenchymal catheter are thought to be the most accurate. Subarachnoid bolt and epidural sensor are less accurate.:

ICP monitoring There are four ways of monitoring intracranial pressure: 1) Intraventricular catheter (a catheter threaded into one of the lateral ventricles of the brain) 2) Parenchymal catheter tip pressure transducer 3) Subarachnoid screw or bolt (a screw or bolt placed just through the skull in the space between the arachnoid and cerebral cortex) 4) Epidural sensor (a sensor placed into the epidural space beneath the skull) Intraventricular and Parenchymal catheter are thought to be the most accurate. Subarachnoid bolt and epidural sensor are less accurate.

Slide44:

ICP monitor is usually placed via the right side, since in approximately 80% of the populations the right hemisphere is the non-dominant, unless contraindicated. However, it might be placed on the side with maximal pathological features or swelling. Monitoring devices are usually continued for ≤1 week; with daily examination of the CSF for glucose, protein, cell count, Gram stain, and culture and sensitivity. Treatment for intracranial hypertension should be started with ICP thresholds above 20 mm Hg. Additional to ICP values, clinical and brain CT findings should be used to determine the need for treatment.

Benefits of ICP monitoring: 1) It helps in earlier detection of intracranial mass lesion 2) It can limit the use of therapies to control ICP which themselves can be potentially harmful 3) It can reduce ICP by CSF drainage 4) It helps in determining prognosis 5) It may improve outcome The risks are: 1) Infection 2) Bleeding 3) Brain damage with residual neurologic effects 4) Inability to locate ventricle (malposition) 5) Device malfunction:

Benefits of ICP monitoring: 1) It helps in earlier detection of intracranial mass lesion 2) It can limit the use of therapies to control ICP which themselves can be potentially harmful 3) It can reduce ICP by CSF drainage 4) It helps in determining prognosis 5) It may improve outcome The risks are: 1) I nfection 2) Bleeding 3) Brain damage with residual neurologic effects 4) Inability to locate ventricle (malposition) 5) Device malfunction

The indications for ICP monitoring There are insufficient data to support the usage of ICP monitoring as a standard. ICP should be monitored in all salvageable patients with a severe TBI : 1) with an abnormal CT 2) with normal CT and at least two adverse features a) age > 40 years; b) SBP < 90 mmHg after resuscitation c) Unilateral or bilateral motor posturing 3) Tight brain at operation following removal of a clot:

The indications for ICP monitoring There are insufficient data to support the usage of ICP monitoring as a standard. ICP should be monitored in all salvageable patients with a severe TBI : 1) with an abnormal CT 2) with normal CT and at least two adverse features a) age > 40 years; b) SBP < 90 mmHg after resuscitation c) Unilateral or bilateral motor posturing 3) Tight brain at operation following removal of a clot

CPP = MAP–ICP Normally, within a MAP range of 60–150 mmHg, CBF remains constant (cerebral autoregulation). However, in brain injury this autoregulation is altered making cerebral blood flow pressure dependent. Normal CPP is around 80 – 100 mmHg. While earlier studies suggested improved outcomes with a CPP of 70 -80 mmHg, three recent studies have shown that CPP > 70 mmHg may increase the incidence of ARDS. Additionally, some studies indicate that cerebral ischemia may occur in the head injury patient with CPP below 60 mmHg. Therefore, it would seem reasonable to try to maintain a CPP of 60 – 70 mmHg:

CPP = MAP–ICP Normally, within a MAP range of 60–150 mmHg, CBF remains constant (cerebral autoregulation). However, in brain injury this autoregulation is altered making cerebral blood flow pressure dependent. Normal CPP is around 80 – 100 mmHg. While earlier studies suggested improved outcomes with a CPP of 70 -80 mmHg, three recent studies have shown that CPP > 70 mmHg may increase the incidence of ARDS. Additionally, some studies indicate that cerebral ischemia may occur in the head injury patient with CPP below 60 mmHg. Therefore, it would seem reasonable to try to maintain a CPP of 60 – 70 mmHg

Slide48:

Clinical Indicators of Increased ICP = Pupil: unilateral or bilateral unreactive, dilated = Papilledema = Palsy: third and/or Sixth cranial nerve = Posturing: extensor (decerebrate) = Cushing’s Triad = GCS: <9 or 2 point decrease in GCS = Seizures

Treatment of raised ICP ICP may be increased by a number of extracranial factors, including nursing procedures such as endotracheal suction and physiotherapy. Before concluding that raised ICP is due to intracranial factors, a checklist should be considered: 1) Airway and head position: Ensure that there is no venous or airway obstruction. 2) Arterial blood gases: Ensure that PaCO2 is 40- 35mmHg, PaO2 >80 mmHg :

Treatment of raised ICP ICP may be increased by a number of extracranial factors, including nursing procedures such as endotracheal suction and physiotherapy. Before concluding that raised ICP is due to intracranial factors, a checklist should be considered: 1) Airway and head position: Ensure that there is no venous or airway obstruction. 2) Arterial blood gases: Ensure that P aCO2 is 40- 35mmHg, PaO2 >80 mmHg

3) Core temperature: A rise of 1°C can increase metabolic rate by 10%, thus increasing ICP by several millimeters of mercury. Core body temperature must be kept below 38°C. 4) Occult seizures: Anticonvulsants have been recommended in all ventilated patients with severe closed head injury because seizures occurring in heavily sedated and paralyzed patients are difficult to detect without EEG monitoring, yet they can lead to marked increases in CBF and ICP. 5) Sedation level: Consider whether the patient is becoming more conscious and ‘fighting the ventilator’.:

3) Core temperature: A rise of 1°C can increase metabolic rate by 10%, thus increasing ICP by several millimeters of mercury. Core body temperature must be kept below 38°C. 4) Occult seizures: Anticonvulsants have been recommended in all ventilated patients with severe closed head injury because seizures occurring in heavily sedated and paralyzed patients are difficult to detect without EEG monitoring, yet they can lead to marked increases in CBF and ICP. 5) Sedation level: Consider whether the patient is becoming more conscious and ‘ fighting the ventilator ’ .

Slide51:

Treatment of intracranial causes of raised ICP 1)Removing mass lesions 2)Reducing one of the other available intracranial fluid volumes : a) CSF by ventricular drainage; b) Brain tissue water content by diuresis; c) Cerebral blood volume by hyperventilation. d) Barbiturates e) Hypothermia f) Other agents 1)Hypertonic saline 2)Steroids

CSF drainage Total CSF production is approximately 20 mL/h or 500 mL/day Drainage of even small amounts of CSF produces an immediate fall in ICP and a rise in CPP. However if systolic BP has been increased by a Cushing response, then sudden release of ICP may precipitate a fall in BP and CPP. This can be minimized by i.v. fluid preloading. CSF drainage pressure should be set at about 20cmH2O since continuous drainage at a low pressure may lead to collapse of the ventricles and loss of this way for ICP control. :

CSF drainage Total CSF production is approximately 20 mL/h or 500 mL/day Drainage of even small amounts of CSF produces an immediate fall in ICP and a rise in CPP. However if systolic BP has been increased by a Cushing response, then sudden release of ICP may precipitate a fall in BP and CPP. This can be minimized by i.v. fluid preloading. CSF drainage pressure should be set at about 20cmH 2 O since continuous drainage at a low pressure may lead to collapse of the ventricles and loss of this way for ICP control.

(b) Osmotic agents and diuretics A) Mannitol Mannitol is a powerful osmotic diuretic and draws fluid into the vascular compartment, thereby increasing circulating blood volume and reducing blood viscosity. It is not metabolized and the intact blood–brain barrier is relatively impermeable to it, although in high concentrations or after prolonged use the normal blood–brain barrier may open’, allowing it or other large molecules to enter the extra cellular space. :

(b) Osmotic agents and diuretics A) Mannitol Mannitol is a powerful osmotic diuretic and draws fluid into the vascular compartment, thereby increasing circulating blood volume and reducing blood viscosity. It is not metabolized and the intact blood–brain barrier is relatively impermeable to it, although in high concentrations or after prolonged use the normal blood–brain barrier may open’, allowing it or other large molecules to enter the extra cellular space.

The mechanism of action 1) Cerebral vasoconriction plasma expansion decreases blood viscosity which leads to constriction of the cerebral vasculature to maintain constant CBF. This rapid response is more likely with bolus injection rather than infusion. 2) The osmotic effect. 3) It may reduce CSF production. Other possible beneficial actions: 1) It may reduce red blood cell rigidity, thus allowing them to penetrate small vessels and makes marginal perfusion more easily. 2) It may scavenge O2 free radicals, which have been implicated in ischemic brain damage. :

The mechanism of action 1) Cerebral vasoconriction plasma expansion decreases blood viscosity which leads to constriction of the cerebral vasculature to maintain constant CBF. This rapid response is more likely with bolus injection rather than infusion. 2) The osmotic effect . 3) It may reduce CSF production . Other possible beneficial actions: 1) It may reduce red blood cell rigidity , thus allowing them to penetrate small vessels and makes marginal perfusion more easily. 2) It may scavenge O2 free radicals , which have been implicated in ischemic brain damage.

Mannitol is usually given in -20% solution in bolus doses, rather than as a continuous infusion. -Boluses of 0.25–1.0 g/kg (given over 10–20 min) repeated depending on the response. -ICP falls within 5–10 minutes. -The maximum effect occurs in about 60 minutes. -The total effect may last 4–6hours. -When used we must assure: a) serum osmolarity<320mOsm/l b) Euvolemia: fluid replacement with isotonic saline Indication for use of mannitol prior to ICP monitoring: 1) Signs of transtentorial herniation (by CT). 2) Progressive neurological deterioration not attributable to extracranial explanation.:

Mannitol is usually given in -20% solution in bolus doses, rather than as a continuous infusion. -Boluses of 0.25 – 1.0 g/kg (given over 10 – 20 min) repeated depending on the response. -ICP falls within 5 – 10 minutes. -The maximum effect occurs in about 60 minutes. -The total effect may last 4 – 6hours. -When used we must assure: a) serum osmolarity<320mOsm/l b) Euvolemia: fluid replacement with isotonic saline Indication for use of mannitol prior to ICP monitoring: 1) Signs of transtentorial herniation (by CT). 2) Progressive neurological deterioration not attributable to extracranial explanation.

Mannitol may become less effective with repeated doses because: 1) Hemoconcentration develops as a result of diuresis. 2) As osmolality rises, the increase in blood viscosity will lead to cerebral vasodilatation and hence to a rise in ICP. 3) Mannitol may enter the extra cellular space by opening the normal blood–brain barrier or where it is disrupted, taking fluid with it and cause a ‘rebound’ rise in ICP. :

Mannitol may become less effective with repeated doses because: 1) Hemoconcentration develops as a result of diuresis. 2) As osmolality rises, the increase in blood viscosity will lead to cerebral vasodilatation and hence to a rise in ICP. 3) Mannitol may enter the extra cellular space by opening the normal blood–brain barrier or where it is disrupted, taking fluid with it and cause a ‘ rebound ’ rise in ICP.

Complications of mannitol 1) Hyperosmotic prerenal renal failure. At serum osmolality of greater than 320 mosmol/l there is a risk of uremia and prerenal renal failure. 2) Hypokalemia usually occurs after a few days of treatment and requires potassium supplements. 3) Dehydration and hypotension. Reduced vascular volume leads to hypotension and the added risk of cerebral ischemia due to a fall in CPP. 4) Expansion of an intracranial hemorrhage. By shrinking the brain.:

Complications of mannitol 1) Hyperosmotic prerenal renal failure . At serum osmolality of greater than 320 mosmol/l there is a risk of uremia and prerenal renal failure. 2) Hypokalemia usually occurs after a few days of treatment and requires potassium supplements. 3) Dehydration and hypotension . Reduced vascular volume leads to hypotension and the added risk of cerebral ischemia due to a fall in CPP. 4) Expansion of an intracranial hemorrhage . By shrinking the brain.

B) Renal diuretics Lasix (frusemide) and other renal loop diuretics may reduce CSF formation directly, and decreases systemic and cerebral blood volume. Given alone, frusemide and other renal diuretics do not reliably reduce ICP. In combination with mannitol, frusemide produces a slightly greater reduction in ICP and increases the duration of its effect. When used it is important to avoid excessive dehydration and sodium loss. :

B) Renal diuretics Lasix (frusemide) and other renal loop diuretics may reduce CSF formation directly, and decreases systemic and cerebral blood volume. Given alone, frusemide and other renal diuretics do not reliably reduce ICP. In combination with mannitol, frusemide produces a slightly greater reduction in ICP and increases the duration of its effect. When used it is important to avoid excessive dehydration and sodium loss.

(c) Hyperventilation Hyperventilation will reduce ICP by cerebral vasoconstriction induced by alkalosis. Hypocapnia is capable of reducing cerebral blood flow 4% for each mm Hg change in PaCO2. Hyperventilation may have other beneficial effects: 1) Correct brain and CSF acidosis 2) It may restore pressure autoregulation and increase global O2 metabolism. 3) It may normalize cerebral glucose uptake. :

(c) Hyperventilation Hyperventilation will reduce ICP by cerebral vasoconstriction induced by alkalosis. Hypocapnia is capable of reducing cerebral blood flow 4% for each mm Hg change in PaCO2. Hyperventilation may have other beneficial effects : 1) Correct brain and CSF acidosis 2) It may restore pressure autoregulation and increase global O2 metabolism. 3) It may normalize cerebral glucose uptake.

Unfortunately, little objective evidence exists that treatment by hypocapnia has significantly improved mortality or survival. Mild hyperventilation (PaCO2 35-30 mmHg) should be used for short period (30 minutes) when acute neurological deterioration occurs. Mild hyperventilation is not recommended in the first 24h when CBF is critically reduced Aggressive hyperventilation (PaCO2 below 30 mmHg) is acceptable only as an emergency or when all other means of ICP control have failed (for less than 30 min). :

Unfortunately, little objective evidence exists that treatment by hypocapnia has significantly improved mortality or survival. Mild hyperventilation (PaCO2 35-30 mmHg) should be used for short period (30 minutes) when acute neurological deterioration occurs. Mild hyperventilation is not recommended in the first 24h when CBF is critically reduced Aggressive hyperventilation (PaCO2 below 30 mmHg) is acceptable only as an emergency or when all other means of ICP control have failed (for less than 30 min).

Slide61:

If aggressive hyperventilation is used, cerebral blood flow must be monitored using: 1) Jugular venous oxygen saturation (SjvO2) It measures global cerebral oxygenation The normal (SjvO2) is 62% with a range of 55% to 71%. A sustained (SjvO2) of < 50% is the threshold of cerebral ischemia and for treatment 2) Brain tissue oxygen tension (PbtO2) It is the most reliable monitor of focal cerebral oxygenation, The normal range between 35 mm Hg and 50 mm Hg, A value of a PbtO2 < 15 mm Hg is considered a threshold for focal cerebral ischemia and for treatment. PbtO2 monitoring is a promising, safe and clinically applicable method in severe TBI patients; however, it is neither widely used nor available.

(d) Barbiturates High doses of barbiturates will frequently lower ICP even when osmolar therapy and hyperventilation have failed. Barbiturates and the other hypnotic drugs (such as etomidate and propofol), act by reducing cerebral metabolic rate for oxygen (CMRO2) and producing a coupled reduction in CBF. Barbiturates are used only in the following situations: 1) As part of a stepwise protocol for ICP control, once other medical management has failed. 2) For acute intraoperative brain swelling. Dose: Bolus 5mg/kg Maintenance 1-2mg/kg/h (for 48h):

(d) Barbiturates High doses of barbiturates will frequently lower ICP even when osmolar therapy and hyperventilation have failed. Barbiturates and the other hypnotic drugs (such as etomidate and propofol), act by reducing cerebral metabolic rate for oxygen (CMRO2) and producing a coupled reduction in CBF. Barbiturates are used only in the following situations: 1) As part of a stepwise protocol for ICP control, once other medical management has failed. 2) For acute intraoperative brain swelling. Dose: Bolus 5mg/kg Maintenance 1-2mg/kg/h (for 48h)

The actions of barbiturates include: 1) Decrease in metabolic rate with coupled reduction in CBF; 2) Free radical scavenging and reduction in lipid peroxidation; 3) Direct increase in vasomotor tone. Complications and contraindications 1) Hypotension 2) Hypothermia. 3) Gastric stasis. 4) Inability to diagnose brain death by clinical criteria for 24 hours or more after treatment has stopped.:

The actions of barbiturates include: 1) Decrease in metabolic rate with coupled reduction in CBF; 2) Free radical scavenging and reduction in lipid peroxidation; 3) Direct increase in vasomotor tone. Complications and contraindications 1) Hypotension 2) Hypothermia. 3) Gastric stasis. 4) Inability to diagnose brain death by clinical criteria for 24 hours or more after treatment has stopped.

(e) Hypothermia Hypothermia can reduce inflammatory process, reduce cerebral metabolism, limit secondary brain injury. The use of mild hypothermia involves decreasing the core temperature to 35°C for 24-48 hours and then slowly rewarming the patient over 2-3 days. Clinical Phase I and II studies have suggested that neurologic deficit and mortality are significantly reduced when prophylactic moderate hypothermia (32-34°C) was used following severe head injury (induced within 6-24 h and maintained for 24–48 hours). :

(e) Hypothermia Hypothermia can reduce inflammatory process, reduce cerebral metabolism, limit secondary brain injury. The use of mild hypothermia involves decreasing the core temperature to 35°C for 24-48 hours and then slowly rewarming the patient over 2-3 days. Clinical Phase I and II studies have suggested that neurologic deficit and mortality are significantly reduced when prophylactic moderate hypothermia (32-34°C) was used following severe head injury (induced within 6-24 h and maintained for 24–48 hours).

This promising phase-II-results were not confirmed by a prospective, randomized, controlled phase-III-investigation. Therefore, the trial did not confirm the utility of moderate hypothermia as a primary neuro-protective strategy in severe TBI patients. Moderate hypothermia may be used in refractory, uncontrolled ICP, when other medical management has failed (option). However, fever should be aggressively treated in patients with severe TBI. :

This promising phase-II-results were not confirmed by a prospective, randomized, controlled phase-III-investigation. Therefore, the trial did not confirm the utility of moderate hypothermia as a primary neuro-protective strategy in severe TBI patients. Moderate hypothermia may be used in refractory, uncontrolled ICP, when other medical management has failed (option). However, fever should be aggressively treated in patients with severe TBI.

(f) Other agents 1)Hypertonic saline Intravenous hypertonic saline (HTS) may produce a prolonged reduction in ICP by osmosis without diuresis and improve renal function in dehydrated patients. Currently hypertonic saline represents an option rather than a standard in the treatment of elevated ICP due to lack of convincing clinical data. Hypertonic saline has more recently been found to be useful in patients who no longer respond to mannitol, hypotensive and are developing uremia. :

(f) Other agents 1)Hypertonic saline Intravenous hypertonic saline (HTS) may produce a prolonged reduction in ICP by osmosis without diuresis and improve renal function in dehydrated patients. Currently hypertonic saline represents an option rather than a standard in the treatment of elevated ICP due to lack of convincing clinical data. Hypertonic saline has more recently been found to be useful in patients who no longer respond to mannitol , hypotensive and are developing uremia.

Slide67:

Dose : over 15min 3% NaCl (513 mmol/L) bolus 150 ml 7.5% NaCl (1283 mmol/L) bolus 70 ml Maintaining serum sodium levels of 145–155 mmol/L is likely to achieve this goal. HTS can be repeated if Na<160 and Cl<120 Contraindicated if patient is hyponatremic. Monitoring : serum Na & Cl, and urinary output.

2)Steroids Because of their effectiveness in treating the brain swelling associated with brain tumors and abscesses, steroids were at one time widely used in traumatic brain swelling. However, several trials, some using very high-dose steroid regimes, have failed to identify a benefit. Steroids probably have no place in the routine management of closed head injury. However a non-glucosteroid, the 17 amino steroid (tirilazad), has shown promise in experimental head injury. :

2)Steroids Because of their effectiveness in treating the brain swelling associated with brain tumors and abscesses, steroids were at one time widely used in traumatic brain swelling. However, several trials, some using very high-dose steroid regimes, have failed to identify a benefit. Steroids probably have no place in the routine management of closed head injury. However a non-glucosteroid, the 17 amino steroid (tirilazad), has shown promise in experimental head injury.

Slide69:

Phase-III-clinical trials in patients with acute stroke, subarachnoid hemorrhage, and head injury failed to confirm the experimental neuroprotective evidence. In general, glucocorticoids have no significant positive or negative effect in patients with head injury or acute stroke. High-dose methylprednisolone slightly improves sensory and motor function following spinal cord injury.

Previous strategies Current strategies Reduce ICP Maintain CPP Elective dehydration Euvolemia Routine osmotherapy Selective osmotherapy (< 300 mosmol/l) Routine hyperventilation Normocapnia (PaCO2 < 30mmHg) Hyperventilation only to control rises in ICP Maintain SjvO2 above 55% Routine barbiturates Limited barbiturates :

Previous strategies Current strategies Reduce ICP Maintain CPP Elective dehydration Euvolemia Routine osmotherapy Selective osmotherapy (< 300 mosmol/l) Routine hyperventilation Normocapnia ( P aCO2 < 30mmHg) Hyperventilation only to control rises in ICP Maintain S jvO2 above 55% Routine barbiturates Limited barbiturates

Previous strategies Current strategies Routine corticosteroids No corticosteroids Avoid sedation, use muscle Avoid muscle relaxants, relaxants ensure sedation and analgesia Avoid PEEP Use PEEP to maintain PaO2 ICP monitoring – ICP monitoring – intraventricular or subdural intraventricular or fluid-filled catheters intraparenchymal solid state systems:

Previous strategies Current strategies Routine corticosteroids No corticosteroids Avoid sedation, use muscle Avoid muscle relaxants, relaxants ensure sedation and analgesia Avoid PEEP Use PEEP to maintain P aO2 ICP monitoring – ICP monitoring – intraventricular or subdural intraventricular or fluid-filled catheters intraparenchymal solid state systems

THANK YOU :

THANK YOU

authorStream Live Help