**Intensive Care Management of the Traumatic Brain Injury**

Akarsu Ayazoglu Tülin1 and Özden Nihan2 *1Chief Asistant Kartal Kosuyolu Highly Specialized Education and Training Hospital İstanbul 2Göztepe Education and Training Hospital Istanbul Turkey* 

#### **1. Introduction**

Traumatic brain injury has been major cause of mortality and morbidity worldwide, especially in children and young adults and it has been continuing a difficult problem in intensive care units.

Brain trauma can be caused by a direct impact or by acceleration alone. In addition to the damage caused at the moment of injury, brain trauma causes secondary injury, a variety of events that take place in that minutes and/or days following the injury

Secondary brain injury is attributable to a decrease in cerebral oxygen delivery as a result of hypertension, hypoxia, cerebral oedema, intracranial hypertension or abnormalities in cerebral blood flow. Although the severity of primary brain injury cannot be reduced, secondary brain injury can be minimised if appropriate therapies are implemented in time.

The main aim in the traumatic brain injured patients must be to maintain a good result from primary injury caused by trauma and/or as a result of direct effect of trauma.

The second aim must be to prevent secondary brain injury caused by as results of the complications. The basic principle in the care and treatment of traumatic brain injury is to describe and begin the treatment these complications that worsen the primary injury and lead to secondary brain injury.

The main targets in these aims are:


The intensive care for traumatic brain injury should consist beside the control of ICP, respiratory system, central nervous system, and cirulatory system, it should also consist monitoring of metabolism especially glucose metabolism, temperature and electrolite balance in short intervals. With these invasive and noninvasive monitoring, all the precausions for the problems should be ready.

Intensive Care Management of the Traumatic Brain Injury 3

The patient who has an altered level of consciousness (GCS <8 ) and loss of gag/cough reflex often has deficits in a number of airway protection mechanisms or exhaustion need

The goals of mechanical ventilation of acute severely brain injured patients are to improve gas exchange, to minimize intrathoracic pressure, to reduce the work of breathing and to avoid complications. These patients are also in the risk of developing neurogenic pulmonary

Criteria for starting mechanical ventilation are difficult to define and the decision is made

edema, aspiration of oropharyngeal contents, pneumonia, and atelectasis.

clinically. It is decided according to respiratory status.

Altered level of consciousness (GCS <8 ) /airway protection.

Hypoxia - central cyanosis, SaO2 <90% on oxygen or PaO2 < 8kPa

None 1= Even to supra-orbital pressure To pain pressure 2=Pain from sternum/limb/supra-orbital To speech 3=Non-specific response, not necessarily to

Spontaneous 4=Eyes open, not necessarily aware

None 1=To any pain; limbs remain flaccid

Obeys commands 6=Follows simple commands

None 1=No verbalization of any type Incomprehensible 2=Moans/groans, no speech

Oriented 5=Converses and oriented

Inappropriate 3=Intelligible, no sustained sentences Confused 4=Converses but confused, disoriented

Flexor response 3=Withdrawal response or assumption of

Withdrawal 4=Arm withdraws to pain, shoulder abducts Localizes pain 5=Arm attempts to remove supra-orbital/chest

Extension 2=Shoulder adducted and shoulder and forearm

command

pressure

internally rotated

hemiplegic posture

ventilatory support.

**Neurologic indications** 

**Respiratory indications** 

**Eye Opening** 

**Motor Response** 

**Verbal Response** 

Table 1. Glascow Coma Scale.

Hypercarbia - PaCO2 > 8kPa

 Brainstem dysfunction. Intracranial hypertension.

Anticipated neurologic deterioration.

 Respiratory rate >35 or <5 breaths/ minute Exhaustion, with laboured pattern of breathing

Tidal volume < 5ml/kg or Vital capacity <15ml/kg

**Activity Score**

Beside heavy brain injury may result in a permanant neurologic sequale, it may also give a good results especially in young patients that aggresivelly lowered inreased ICP levels and optimized CPP and cerebral oxygenation by multidisiplinary approach with neurointensivist, neuroanesthesist and neurosurgeon.

In this chapter we will discuss the intensive care management of severe TBI with emphasis on the specific measures directed for prevention and/or treatment of secondary brain injury

### **2. Indication for admission to ICU**

The role of an intensive care unit is to maintain a patient's normal physiological homeostasis while actively treating the underlying cause of any physiological derangement. Discussion will be targeted towards a number of areas; respiratory system, cardiovascular system, alimentary system, nasocomial infection and infection surveillance, anticoagulation, patient comfort.

#### **Indication for admission to ICU include**


#### **Mechanical ventilation**

Most patients admitted to neuro-intensive care require respiratory support because of hypoxaemia, ventilatory failure or due to treatment modalities requiring respiratory support.

The support may range from oxygen therapy by face mask, through non-invasive techniques such as continuous positive airways pressure, to full ventilatory support with endotracheal intubation.

Oxygen is usually given by face mask, although nasal prongs or cannulas may be well tolerated.

If the patient remains hypoxaemic on high flow oxygen (15 l/min) continuous positive airways pressure (CPAP) may be used. The continuous positive airways pressure mask often becomes uncomfortable and gastric distension may occur. Patients must therefore be cooperative, able to protect their airway, and have the strength to breathe spontaneously and cough effectively.

In patients with acute brain lesions at risk for cerebral ischemia, maintenance of adequate cerebral perfusion pressure (CPP), artificial ventilation for prevention of hypercapnia and deep sedation are all major determinants for actual strategies of a cerebroprotective therapy (1).

The patient who has an altered level of consciousness (GCS <8 ) and loss of gag/cough reflex often has deficits in a number of airway protection mechanisms or exhaustion need ventilatory support.

The goals of mechanical ventilation of acute severely brain injured patients are to improve gas exchange, to minimize intrathoracic pressure, to reduce the work of breathing and to avoid complications. These patients are also in the risk of developing neurogenic pulmonary edema, aspiration of oropharyngeal contents, pneumonia, and atelectasis.

Criteria for starting mechanical ventilation are difficult to define and the decision is made clinically. It is decided according to respiratory status.

#### **Neurologic indications**

2 Emergency Medicine – An International Perspective

Beside heavy brain injury may result in a permanant neurologic sequale, it may also give a good results especially in young patients that aggresivelly lowered inreased ICP levels and optimized CPP and cerebral oxygenation by multidisiplinary approach with

In this chapter we will discuss the intensive care management of severe TBI with emphasis on the specific measures directed for prevention and/or treatment of secondary brain injury

The role of an intensive care unit is to maintain a patient's normal physiological homeostasis while actively treating the underlying cause of any physiological derangement. Discussion will be targeted towards a number of areas; respiratory system, cardiovascular system, alimentary system, nasocomial infection and infection surveillance, anticoagulation, patient comfort.

 Clinical or computed tomographic (CT) evidence of raised ICP caused by a space occupying lesion , cerebral edema or haemorrhagic conversion of a cerebral infarct. General medical complications (for example, hyper/hypotension, fluid and electrolyte disturbances, aspiration pneumonia,sepsis, cardiac arrhytmias, pulmonary embolism) Monitoring (for example level of conciousness, respiratory function, ICP continuous

Specific treatments(for example , neurosurgical intervention, intravenous or arterial

Most patients admitted to neuro-intensive care require respiratory support because of hypoxaemia, ventilatory failure or due to treatment modalities requiring respiratory support. The support may range from oxygen therapy by face mask, through non-invasive techniques such as continuous positive airways pressure, to full ventilatory support with

Oxygen is usually given by face mask, although nasal prongs or cannulas may be well

If the patient remains hypoxaemic on high flow oxygen (15 l/min) continuous positive airways pressure (CPAP) may be used. The continuous positive airways pressure mask often becomes uncomfortable and gastric distension may occur. Patients must therefore be cooperative, able to protect their airway, and have the strength to breathe spontaneously

In patients with acute brain lesions at risk for cerebral ischemia, maintenance of adequate cerebral perfusion pressure (CPP), artificial ventilation for prevention of hypercapnia and deep sedation are all major determinants for actual strategies of a cerebroprotective therapy (1).

Progressive respiratory impairment or the need for mechanical ventilation

neurointensivist, neuroanesthesist and neurosurgeon.

**2. Indication for admission to ICU** 

**Indication for admission to ICU include** 

 Impaired level of consciousness, Impaired airway protection

electroencephalography(EEG)

Seizures

trombolysis ) **Mechanical ventilation** 

endotracheal intubation.

and cough effectively.

tolerated.


#### **Respiratory indications**



Table 1. Glascow Coma Scale.

Intensive Care Management of the Traumatic Brain Injury 5

the cranium, therefore lesser effects on cerebral blood flow (CBF) and ICP. CPP may be indirectly affected by systemic effects of PEEP, but these effects still remain quantitatively modest. PEEP is therefore safe to apply as part of a ventilatory strategy

Alveolar overdistension should be avoided and stable haemodynamic parameters should be maintained. Head position also needs attention. At least 30º head elevation promotes intracranial venous drainage via anterior neck veins, as well as the vertebral venous system - which is not majorly affected by ITP. Jugular veins collapse and act as resistors to some of the ITP transmitted. Tight endotracheal tube ties around the neck and extremes of neck

Arterial CO2 tension is a powerful modulator of cerebral vascular calibre, CBF and ICP (12-15.) While the mechanisms are incompletely understood, CO2 relaxes pial arterioles by interactions between the endothelium, vascular smooth muscle, pericytes, adjacent neurons and glial cells. Studies supported that cerebral vessels are sensitive to changes in extracellular pH, rather than a direct response to CO2 or bicarbonate. In the limits of physiological PaCO2, 20-60 mmHg, the relationship between PaCO2 and CBF is linear. Therefore, increased PaCO2 results in vasodilation of cerebral vessels and this leads to increase CBF, increase CBV, decrease intracranial compliance and increase ICP. The reverse mechanism is also true for low CO2 tension. This has been the reason for inducing hyperventilation in the patients with intracranial hypertension, but there is a risk for cerebral vasoconstriction precipitating cerebral ischaemia because pericontusional areas are sensitive to hyperventilation-induced ischaemia. The Brain Trauma Foundation management guidelines do not recommend hyperventilation for initial management of raised ICP, unless ICP is unresponsive to first-line therapy or hyperventilation is for very

It is essential to monitor intracranial pressure, CPP, and brain oxygenation during ventilatory support in the patients with traumatic brain injury. Brain oxygenation monitoring technics are jugular venous saturation monitoring, near-infrared spectroscopy and microdialysis catheters. Availability and cost of these devices are limiting factors to their use. The studies on brain trauma patients shows that there is no proven mortality

There are some ventilatory strategies that may be used for proper patients. These are prone position, recruitment manouvres, high frequency oscillatory ventilation (HFOV) and newer technics like extracorporeal CO2 removal (ECCO2R), pumpless extracorporeal lung assist

brief periods of time. Maintaining normocarbia is recomended.

benefit in continuous ICP monitoring. **Non-conventional ventilatory strategies** 

 Recruitment of atelectatic lung units. Improved ventilation-perfusion matching.

(pECLA) and nitric oxide.

**Prone ventilation(15- 18)**

Benefits are:

**Role of brain monitoring during ventilatory support in brain injury** 

to improve oxygenation.

rotation should be avoided **The Role of PaCO2 control** 

#### **Intracranial physiology and mechanical ventilation**

The goals of positive-pressure ventilation (PPV) in patients with multitrauma with head trauma are improving oxygenation and controlling arterial CO2 tension to minimise intracranial hypertension. PPV increases functional residual capacity (FRC) by improving alveolar recruitment, thus optimising oxygenation.

On the other hand, increased intrathoracic pressure (ITP) increases intracranial pressure (ICP) by these mechanisms:


#### **Mechanical ventilatory strategies(2): conventional ventilation**

Current practice guidelines for ventilatory management advocate protective lung strategies to prevent volutrauma, barotrauma, atelectrauma and biotrauma (3-5). The principles are to use low tidal volumes (Vt) (5-6 ml/kg ideal body weight), maintenance of low mean airway pressures ≤ 30 cmH2O, judicious use of positive end-expiratory pressure (PEEP) with ∆ pressure ≤ 18 cmH2O, higher respiratory rates and permissive hypercapnia. This is in direct conflict with the previous "brain-directed" ventilatory strategies that used Vt of 10 ml/kg, high FiO2 and low PEEP or zero end-expiratory pressure. There is proven mortality benefit with the use of low Vt, but permissive hypercapnia may precipitate intracranial hypertension(3,6,7). Animal studies indicate a higher incidence of severe pulmonary oedema and haemorrhage after exposure to injurious ventilation in the presence of brain trauma. High Vt independently predicts ALI/ARDS and poor outcome in brain trauma patients(8). Haemodynamic fluctuations induced by mechanical ventilation may be detrimental in the brain with impaired autoregulation. That's why with starting mechanical ventilation, intravascular expansion and vasopressor may be necessary.

#### **The role of PEEP**

Lung protection strategy permising hypercapnia induces the development of cranial hyperemia and hypertension. On the other hand, "aggressive" ventilation with high tidal volume may aggravate lung injury and provoke ventilator-associated lung damage(9).

In mechanical ventilation treatment, PEEP improves oxygenation by recruitment of atelectatic alveolar units, improving FRC and preventing atelectrauma. Also it may have detrimental neurologic effects in certain clinical circumstances(10). In a recent study in patients with traumatic brain injury shows that increasing PEEP up to 15 cm H2O to optimize oxygenation has not been associated with reduced cerebral perfusion pressure or acute intracranial hypertension (11)

In normal pulmonary compliance, PEEP is associated with increased ITP, decreased right atrial volume, decreased MAP and thus compromised CPP. This situation is not similar to non-compliant lungs, where there is a comparatively low ITP transmission to the cranium, therefore lesser effects on cerebral blood flow (CBF) and ICP. CPP may be indirectly affected by systemic effects of PEEP, but these effects still remain quantitatively modest. PEEP is therefore safe to apply as part of a ventilatory strategy to improve oxygenation.

Alveolar overdistension should be avoided and stable haemodynamic parameters should be maintained. Head position also needs attention. At least 30º head elevation promotes intracranial venous drainage via anterior neck veins, as well as the vertebral venous system - which is not majorly affected by ITP. Jugular veins collapse and act as resistors to some of the ITP transmitted. Tight endotracheal tube ties around the neck and extremes of neck rotation should be avoided

#### **The Role of PaCO2 control**

4 Emergency Medicine – An International Perspective

The goals of positive-pressure ventilation (PPV) in patients with multitrauma with head trauma are improving oxygenation and controlling arterial CO2 tension to minimise intracranial hypertension. PPV increases functional residual capacity (FRC) by improving

On the other hand, increased intrathoracic pressure (ITP) increases intracranial pressure

Increased ITP decreases venous return to the right atrium, and increases jugular venous

 Decreased venous return decreases cardiac output and mean arterial pressure (MAP). This results in decreased cerebral perfusion pressure (CPP) leading to compensatory cerebral vasodilation, increased CBF and potentially increased ICP, if cerebral

Current practice guidelines for ventilatory management advocate protective lung strategies to prevent volutrauma, barotrauma, atelectrauma and biotrauma (3-5). The principles are to use low tidal volumes (Vt) (5-6 ml/kg ideal body weight), maintenance of low mean airway pressures ≤ 30 cmH2O, judicious use of positive end-expiratory pressure (PEEP) with ∆ pressure ≤ 18 cmH2O, higher respiratory rates and permissive hypercapnia. This is in direct conflict with the previous "brain-directed" ventilatory strategies that used Vt of 10 ml/kg, high FiO2 and low PEEP or zero end-expiratory pressure. There is proven mortality benefit with the use of low Vt, but permissive hypercapnia may precipitate intracranial hypertension(3,6,7). Animal studies indicate a higher incidence of severe pulmonary oedema and haemorrhage after exposure to injurious ventilation in the presence of brain trauma. High Vt independently predicts ALI/ARDS and poor outcome in brain trauma patients(8). Haemodynamic fluctuations induced by mechanical ventilation may be detrimental in the brain with impaired autoregulation. That's why with starting mechanical ventilation,

Lung protection strategy permising hypercapnia induces the development of cranial hyperemia and hypertension. On the other hand, "aggressive" ventilation with high tidal volume may aggravate lung injury and provoke ventilator-associated lung damage(9).

In mechanical ventilation treatment, PEEP improves oxygenation by recruitment of atelectatic alveolar units, improving FRC and preventing atelectrauma. Also it may have detrimental neurologic effects in certain clinical circumstances(10). In a recent study in patients with traumatic brain injury shows that increasing PEEP up to 15 cm H2O to optimize oxygenation has not been associated with reduced cerebral perfusion pressure or

In normal pulmonary compliance, PEEP is associated with increased ITP, decreased right atrial volume, decreased MAP and thus compromised CPP. This situation is not similar to non-compliant lungs, where there is a comparatively low ITP transmission to

**Intracranial physiology and mechanical ventilation** 

alveolar recruitment, thus optimising oxygenation.

Direct transmission of ITP to the intracranial cavity via the neck.

**Mechanical ventilatory strategies(2): conventional ventilation** 

intravascular expansion and vasopressor may be necessary.

pressure, thereby increasing cerebral blood volume (CBV) and ICP.

(ICP) by these mechanisms:

autoregulation is impaired.

**The role of PEEP** 

acute intracranial hypertension (11)

Arterial CO2 tension is a powerful modulator of cerebral vascular calibre, CBF and ICP (12-15.) While the mechanisms are incompletely understood, CO2 relaxes pial arterioles by interactions between the endothelium, vascular smooth muscle, pericytes, adjacent neurons and glial cells. Studies supported that cerebral vessels are sensitive to changes in extracellular pH, rather than a direct response to CO2 or bicarbonate. In the limits of physiological PaCO2, 20-60 mmHg, the relationship between PaCO2 and CBF is linear. Therefore, increased PaCO2 results in vasodilation of cerebral vessels and this leads to increase CBF, increase CBV, decrease intracranial compliance and increase ICP. The reverse mechanism is also true for low CO2 tension. This has been the reason for inducing hyperventilation in the patients with intracranial hypertension, but there is a risk for cerebral vasoconstriction precipitating cerebral ischaemia because pericontusional areas are sensitive to hyperventilation-induced ischaemia. The Brain Trauma Foundation management guidelines do not recommend hyperventilation for initial management of raised ICP, unless ICP is unresponsive to first-line therapy or hyperventilation is for very brief periods of time. Maintaining normocarbia is recomended.

#### **Role of brain monitoring during ventilatory support in brain injury**

It is essential to monitor intracranial pressure, CPP, and brain oxygenation during ventilatory support in the patients with traumatic brain injury. Brain oxygenation monitoring technics are jugular venous saturation monitoring, near-infrared spectroscopy and microdialysis catheters. Availability and cost of these devices are limiting factors to their use. The studies on brain trauma patients shows that there is no proven mortality benefit in continuous ICP monitoring.

#### **Non-conventional ventilatory strategies**

There are some ventilatory strategies that may be used for proper patients. These are prone position, recruitment manouvres, high frequency oscillatory ventilation (HFOV) and newer technics like extracorporeal CO2 removal (ECCO2R), pumpless extracorporeal lung assist (pECLA) and nitric oxide.

#### **Prone ventilation(15- 18)**

Benefits are:


Intensive Care Management of the Traumatic Brain Injury 7

to the duration and mode of ventilation. As possible as using assisted modes of ventilation and good nutritional support are essential to prevent atrophy of the respiratory muscles.

Critical illness polyneuropathy is seen in patients recovering from prolonged critical illness. In this condition, there is both respiratory and peripheral muscle weakness, with reduced tendon reflexes and sensory abnormalities. There is evidence that long-term administration of some aminosteroid muscle relaxants (such as vecuronium) may cause persisting

The plan for disengagement of the patient from mechanical ventilation should be made at initiation of ventilation therapy. The recognition of when mechanical ventilatory support should be reduced and ultimately discontinued is so important. Appropirate time for

Neurologic criteria. This includes stable neurological status, ICP ≤ 20 mmHg, CPP ≥ 60

Premature weaning and extubation may cause respiratory muscle fatigue, gas exchange

There is clear benefit to weaning according to protocol. There should be frequent assessment of ventilatory support requirement and re-evaluation of factors contributing to ventilator

Cardiovascular stability, optimal fluid balance and electrolyte replacement

Prior to trial of weaning, there should be no residual neuromuscular blockade and sedation should be stoped or decreased in appropirate level so that the patient must be awake, cooperative and in a semirecumbent position. Weaning is likely to fail if the patient is

paralysis. No absolute treatment is used for it except supportive therapy.

disengagement from ventilation has the following advantages:

 Decreased airway injury Decreased risk of VILI. Decreased risk of VAP.

Decreased delirium.

 Respiratory criteria. Haemodynamic criteria.

**Indications for weaning** 

Respiratory function:

mmHg.

Decreased sedation requirements.

 Shortened ICU length of stay. Assessment for extubation criteria:

failure and loss of airway protection.

Improving of underlying illness

Tidal volume > 5ml/kg Vital capacity > 10 ml/kg Minute volume < 10 l/min Absence of infection or fever

confused, agitated or unable to cough.

dependence before ventilation is discontinued.

Respiratory rate < 35 breaths/minute FiO2 < 0.5, SaO2 > 90%, PEEP <10 cmH2O


ICP and brain tissue oxygenation (PbtO2) monitoring are recomended. There are conflicting results on the effects of prone ventilation on ICP and CPP, but there are clear data on benefits for respiratory mechanics and oxygenation. Present studies shows that there is no mortality benefit to prone positioning.

#### **Recruitment manoeuvres**

In neurointensive patients with acute lung injury, achieving the goal of lung protection without threatening cerebral perfusion is very difficult. In patients with more refractory raised intracranial pressure, the optimal balance between brain and lung may not be well established. Multiple strategies are used to recruit atelectatic alveoli and improve oxygenation. Among them incremental levels of PEEP and high intermittent tidal volumes should require extend brain physiological monitoring.

#### **High frequency oscillatory ventilation (HFOV) (18,19)**

High frequency oscillatory ventilation (HFOV) forms high mean airway pressure with very small Vt of 1-5 ml/kg at a rapid rate. It's aim is to recruit alveoli, while preventing overdistension. Some studies have supported that HFOV is safe and effective in preventing ventilator-induced lung injury (VILI) and improving oxygenation in severe ARDS. There no sufficient studies supporting HFOV for the improvement of intracranial compliance.

#### **Extracorporeal CO2 removal (ECCO2R) (20)**

Extracorporeal membrane oxygenators have been attempted in brain-injured patients to improve oxygenation. By using ECMO increased intracranial pressure may decrease in a normal limits and CPP is maintained. But anticoagulation requirement in that technic increases the risk of intracranial bleeding.

#### **Pumpless extracorporeal lung assist (pECLA) (21)**

pECLA has recently been utilised in small case series with promising results. Protective respiratory care can be maintained while CO2 removal is optimised. Patients treated by pECLA must be hemodynamically stable. So cardiovascular instability and shock are contraindications for pECLA. Anticoagulation is as for thrombo prophylaxis in immobilised patients. The risk of the device clotting is not entirely eliminated by impregnation with anticoagulant in the filter. Vascular injury, exsanguination and limb ischaemia are some of the recognised complications.

#### **Nitric oxide**

Nitric oxide improves oxygenation in ALI/ARDS with no survival benefit. There is potential to cause harm. There is no data for its use in ARDS with the patients with brain taruma.

#### **Weaning (22-30)**

Without resolving underlying pathological condition, weaning must not be thought. With prolongation ventilatory support, the respiratory muscles become weaken and atrophy of this muscles is inevitable. As a consequence, the duration of weaning period is often related to the duration and mode of ventilation. As possible as using assisted modes of ventilation and good nutritional support are essential to prevent atrophy of the respiratory muscles.

Critical illness polyneuropathy is seen in patients recovering from prolonged critical illness. In this condition, there is both respiratory and peripheral muscle weakness, with reduced tendon reflexes and sensory abnormalities. There is evidence that long-term administration of some aminosteroid muscle relaxants (such as vecuronium) may cause persisting paralysis. No absolute treatment is used for it except supportive therapy.

The plan for disengagement of the patient from mechanical ventilation should be made at initiation of ventilation therapy. The recognition of when mechanical ventilatory support should be reduced and ultimately discontinued is so important. Appropirate time for disengagement from ventilation has the following advantages:


6 Emergency Medicine – An International Perspective

ICP and brain tissue oxygenation (PbtO2) monitoring are recomended. There are conflicting results on the effects of prone ventilation on ICP and CPP, but there are clear data on benefits for respiratory mechanics and oxygenation. Present studies shows that there is no

In neurointensive patients with acute lung injury, achieving the goal of lung protection without threatening cerebral perfusion is very difficult. In patients with more refractory raised intracranial pressure, the optimal balance between brain and lung may not be well established. Multiple strategies are used to recruit atelectatic alveoli and improve oxygenation. Among them incremental levels of PEEP and high intermittent tidal volumes

High frequency oscillatory ventilation (HFOV) forms high mean airway pressure with very small Vt of 1-5 ml/kg at a rapid rate. It's aim is to recruit alveoli, while preventing overdistension. Some studies have supported that HFOV is safe and effective in preventing ventilator-induced lung injury (VILI) and improving oxygenation in severe ARDS. There no

Extracorporeal membrane oxygenators have been attempted in brain-injured patients to improve oxygenation. By using ECMO increased intracranial pressure may decrease in a normal limits and CPP is maintained. But anticoagulation requirement in that technic

pECLA has recently been utilised in small case series with promising results. Protective respiratory care can be maintained while CO2 removal is optimised. Patients treated by pECLA must be hemodynamically stable. So cardiovascular instability and shock are contraindications for pECLA. Anticoagulation is as for thrombo prophylaxis in immobilised patients. The risk of the device clotting is not entirely eliminated by impregnation with anticoagulant in the filter. Vascular injury, exsanguination and limb ischaemia are some of

Nitric oxide improves oxygenation in ALI/ARDS with no survival benefit. There is potential to cause harm. There is no data for its use in ARDS with the patients with brain taruma.

Without resolving underlying pathological condition, weaning must not be thought. With prolongation ventilatory support, the respiratory muscles become weaken and atrophy of this muscles is inevitable. As a consequence, the duration of weaning period is often related

sufficient studies supporting HFOV for the improvement of intracranial compliance.

Improved drainage of secretions.

mortality benefit to prone positioning.

**Recruitment manoeuvres** 

Even distribution of mechanical ventilatory forces.

should require extend brain physiological monitoring. **High frequency oscillatory ventilation (HFOV) (18,19)**

**Extracorporeal CO2 removal (ECCO2R) (20)**

increases the risk of intracranial bleeding.

the recognised complications.

**Nitric oxide** 

**Weaning (22-30)**

**Pumpless extracorporeal lung assist (pECLA) (21)**


Premature weaning and extubation may cause respiratory muscle fatigue, gas exchange failure and loss of airway protection.

There is clear benefit to weaning according to protocol. There should be frequent assessment of ventilatory support requirement and re-evaluation of factors contributing to ventilator dependence before ventilation is discontinued.

#### **Indications for weaning**


Prior to trial of weaning, there should be no residual neuromuscular blockade and sedation should be stoped or decreased in appropirate level so that the patient must be awake, cooperative and in a semirecumbent position. Weaning is likely to fail if the patient is confused, agitated or unable to cough.

Intensive Care Management of the Traumatic Brain Injury 9

Sedation is the important factor in comfort of brain trauma patients. Insuffient sedation causes hypertension, tachycardia, hypoxia, hypercapnia and uncomfortable with ventilator. On the other hand excess sedation causes hypotansion, bradycardia, coma, respiratory

For the patients in the critical care unit firstly nonpharmacological method should be experinced for sedation. The patients should be frequently oriented. Sleep-awake cycling, proper enveriomental temperature, control of the noise aroused from alarms must be

Calling the family members, the relexing exercises, musical therapy, masaj and sitting

Safe and effective management of the pain and anxiety needs a delicate balance for

The weaning of patients from mechanical ventilation is often hampered by the sedation that they receive. Additionally, coordinated daily interruption of sedative infusions with objective re-titration in critically ill patients has been shown to decrease the durations of

Consequences of agitation include self-extubation, removal of IV catheters, dyssynchrony with mechanical ventilation, and, perhaps, a long-term risk of psychiatric problems, such as delirium and posttraumatic stress disorder can be prevented by a proper sedation. Prolonged and excessive sedation are problematic too, interfering with weaning from mechanical ventilation and leading to increased rates of nosocomial pneumonia, prolonged ICU stays, and difficulty identifying new problems, such as myocardial

Facilitates the cares like aspiration, invasive prosedures and dressing the wound

Brain protection (seizure control, decrease cerebral metabolism , control ICP)

Provide hemodynamic stability; protection against myocardial ischemia

depresion, ileus, renal insufficiency, veinous stasis and immunosupression.

exercises are important in control of anxiety and ajitation of patients.

analgesia and sedation protocols while managing delirium status.

mechanical ventilation and length of ICU stay.

**Sedation Indications in the Neuro-ICU** 

 Risk of self-injury or injury of others Withdrawal from alcohol or drugs

Risk of self-extubation or removal of invasive monitors

Reduce oxygen extraction/ utilization in ARDS and Sepsis

Increases the tolerance of ventilatory support

Decreases anxiety and agitation

Facilitate mechanical ventilation

Blunting adverse outcome

Suppreses stres response

**Sedation in the Neuro-ICU(34-67)**

arranged.

infarction or stroke.

Patient comfort

Control of pain

Relieve fear

#### **Modes of weaning**

There are several different approaches for the weaning that are not superior to others.


#### **Failure to wean**

During the weaning process, the patient should be observed for early indications of fatigue or failure to wean. These signs include distress, increasing respiratory rate, falling tidal volume and haemodynamic compromise, particularly tachycardia and hypertension. At this point it may be necessary to increase the level of respiratory support as, once exhausted, respiratory muscles may take many hours to recover.

It is sensible to start the weaning process in the morning to allow close monitoring of the patient throughout the day. In prolonged weaning, it is common practice to increase ventilatory support overnight to allow adequate rest for the patient.

#### **Tracheostomy in the intensive care unit (31-33)**

The commonest indication of tracheostomy in an ICU setting is to facilitate prolonged artificial ventilation and the subsequent weaning process. Tracheostomy allows a reduction in sedation and thus increased cooperation to the weaning process. It also allows effective tracheobronchial suction in patients who are unable to clear pulmonary secretions either due to excessive secretion production or due to weakness following critical illness. Tracheostomy can be performed as a formal surgical procedure in theatre or at the bedside in the intensive care unit using a percutaneous method. Tracheostomy placement leads to earlier liberation from mechanical ventilation, but without any mortality benefit or effect on pulmonary infection rates.

Other indications for tracheostomy are to bypass an upper airway obstruction, protect the lungs from soiling if the laryngopharygeal reflexes are depressed or as part of a surgical or anaesthetic technique eg larygectomy.

Advantages of tracheostomy is summerized as decreased risk of self-extubation; decreased sinusitis; decreased airway resistance, dead space and breathing work ;better tolerance; less sedative requirements; potentially-reduced duration of mechanical ventilation.

Risks of tracheostomy is summerized as surgical site infection, airway haemorrhage, pneumothorax, oesophageal perforation.

#### **Sedation in the Neuro-ICU(34-67)**

8 Emergency Medicine – An International Perspective

 Unsupported spontaneous breathing trials. The machine support is withdrawn and a T-Piece (or CPAP) circuit can be attached intermittently for increasing periods of time, thereby allowing the patient to gradually take over the work of breathing with

 Intermittent mandatory ventilation (IMV) weaning. The ventilator delivers a preset minimum minute volume which is gradually decreased as the patient takes over more of the respiratory workload. The decreasing ventilator breaths are synchronised to the

 Pressure support weaning. In this mode, the patient initiates all breaths and these are 'boosted' by the ventilator. This weaning method involves gradually reducing the level of pressure support, thus making the patient responsible for an increasing amount of ventilation. Once the level of pressure support is low (5-10 cmH2O above PEEP), a trial

During the weaning process, the patient should be observed for early indications of fatigue or failure to wean. These signs include distress, increasing respiratory rate, falling tidal volume and haemodynamic compromise, particularly tachycardia and hypertension. At this point it may be necessary to increase the level of respiratory support as, once exhausted,

It is sensible to start the weaning process in the morning to allow close monitoring of the patient throughout the day. In prolonged weaning, it is common practice to increase

The commonest indication of tracheostomy in an ICU setting is to facilitate prolonged artificial ventilation and the subsequent weaning process. Tracheostomy allows a reduction in sedation and thus increased cooperation to the weaning process. It also allows effective tracheobronchial suction in patients who are unable to clear pulmonary secretions either due to excessive secretion production or due to weakness following critical illness. Tracheostomy can be performed as a formal surgical procedure in theatre or at the bedside in the intensive care unit using a percutaneous method. Tracheostomy placement leads to earlier liberation from mechanical ventilation, but without any mortality benefit or effect on

Other indications for tracheostomy are to bypass an upper airway obstruction, protect the lungs from soiling if the laryngopharygeal reflexes are depressed or as part of a surgical or

Advantages of tracheostomy is summerized as decreased risk of self-extubation; decreased sinusitis; decreased airway resistance, dead space and breathing work ;better tolerance; less

Risks of tracheostomy is summerized as surgical site infection, airway haemorrhage,

sedative requirements; potentially-reduced duration of mechanical ventilation.

There are several different approaches for the weaning that are not superior to others.

shortening rest periods back on the ventilator.

of T-Piece or CPAP weaning should be commenced.

respiratory muscles may take many hours to recover.

**Tracheostomy in the intensive care unit (31-33)**

pulmonary infection rates.

anaesthetic technique eg larygectomy.

pneumothorax, oesophageal perforation.

ventilatory support overnight to allow adequate rest for the patient.

patient's own inspiratory efforts (SIMV).

**Modes of weaning** 

**Failure to wean** 

Sedation is the important factor in comfort of brain trauma patients. Insuffient sedation causes hypertension, tachycardia, hypoxia, hypercapnia and uncomfortable with ventilator. On the other hand excess sedation causes hypotansion, bradycardia, coma, respiratory depresion, ileus, renal insufficiency, veinous stasis and immunosupression.

For the patients in the critical care unit firstly nonpharmacological method should be experinced for sedation. The patients should be frequently oriented. Sleep-awake cycling, proper enveriomental temperature, control of the noise aroused from alarms must be arranged.

Calling the family members, the relexing exercises, musical therapy, masaj and sitting exercises are important in control of anxiety and ajitation of patients.

Safe and effective management of the pain and anxiety needs a delicate balance for analgesia and sedation protocols while managing delirium status.

The weaning of patients from mechanical ventilation is often hampered by the sedation that they receive. Additionally, coordinated daily interruption of sedative infusions with objective re-titration in critically ill patients has been shown to decrease the durations of mechanical ventilation and length of ICU stay.

Consequences of agitation include self-extubation, removal of IV catheters, dyssynchrony with mechanical ventilation, and, perhaps, a long-term risk of psychiatric problems, such as delirium and posttraumatic stress disorder can be prevented by a proper sedation. Prolonged and excessive sedation are problematic too, interfering with weaning from mechanical ventilation and leading to increased rates of nosocomial pneumonia, prolonged ICU stays, and difficulty identifying new problems, such as myocardial infarction or stroke.

#### **Sedation Indications in the Neuro-ICU**


Intensive Care Management of the Traumatic Brain Injury 11

1. Unarousable – Minimal or no response to noxious stimuli, does not communicate or

2. Very Sedated – Arouses to physical stimuli but does not communicate or follow

3. Sedated – Difficult to arouse, awakens to verbal stimuli or gently shaking, but drifts off

5. Agitated – Anxious or mildly agitated, attempting to sit up, calms down to verbal

6. Very Agitated – Does not calm despite frequent verbal reminding of limits, biting ET 7. Dangerous Agitation – Pulling ET, trying to remove catheters, climbing over bedrails,

1. Agitated patients are scored by their most severe degree of agitation, as described. 2. If patient is awake or awakens easily to voice ("awaken" means responds with voice or head shaking to a question or follows commands), that is a SAS 4 (same as calm and

3. If more stimuli such as shaking is required but patient eventually does awaken, that is

4. If patient arouses to stronger physical stimuli (may be noxious) but never awakens to

6. This helps separate sedated patients into those you can eventually awaken (SAS 3), those you can not awaken, but can arouse (SAS 2), and those you can not arouse (SAS 1).

4. Calm and Cooperative – Calm, awakens easily, follows commands

the point of responding yes/no or following commands, that is a SAS 2.

Table 2. Riker Sedation-Agitation Scale (SAS) (SAS Target Sedation = 3 to 4).

+4Combative Overtly combative, violent, immediate danger to staff +3 Very Agitated Pulls or removes tube(s) or catheter(s),aggressive +2 Agitated Frequent non-purposeful movement, fights ventilator +1 Restless Anxious but movements not aggressive vigorous

 -2 Light Sedation Briefly awakens with eye contact to voice (<10 seconds) -3 Moderate Sedation Movement or eye opening to voice (but no eye contact) -4 Deep Sedation No response to voice, but movement or eye opening to

 -1 Drowsy Not fully alert, but has sustained awakening (>10 seconds) (eye-opening/eye contact) to voice


5. Little or no response to noxious physical stimuli is a SAS

Score Term Descriptor

commands, may move spontaneously

striking at staff, thrashing side to side Guidelines for SAS Assessment

appropriate might even be napping).

again, follow simple commands

follow commands

stimuli

a SAS 3.

Score Description

0 Alert and Calm

physical stimulation


#### **Properties of an ideal agent for neurointensive care sedation:**


General expectational situations:


Sedation should be performed according to protocols standarized with scales. For this reason Ramsay Sedation Scale (RSS), Riker Sedation-Agitation Scale (SAS) and Richmond Agitation-Sedation Score (RASS) are used for planing treatment. For many years, the Ramsay Sedation Scale was the most commonly used tool to monitor sedation in the ICU. However, it cannot distinguish different levels of agitation, making it less useful than other available scales. Currently, two of the most commonly used techniques are the Riker Sedation-Agitation Scale (SAS) and the Richmond Agitation-Sedation Score (RASS).

Score Term Descriptor

10 Emergency Medicine – An International Perspective

To prevent movement (during imaging and transfering of the patient)

 Rapid onset and rapid recovery so that a neurologic evaluation can be conducted Predictable clearance independent of end-organ function, avoiding the problem of drug

Reduces intracranial pressure by cerebral blood volume reduction or cerebral

Reduces cerebral blood flow and cerebral metabolic rate of oxygen consumption,

Permits normal cerebral vascular reactivity to changes in arterial carbon dioxide tension

Rapid onset and rapid recovery so that a neurologic evaluation can be conducted

Respiratory depression, hypercarbia, and increased intracranial pressure (ICP)

Sedation-Agitation Scale (SAS) and the Richmond Agitation-Sedation Score (RASS).

Equipment and personnel to intubate and mechanically ventilate must be readily

Sedation should be performed according to protocols standarized with scales. For this reason Ramsay Sedation Scale (RSS), Riker Sedation-Agitation Scale (SAS) and Richmond Agitation-Sedation Score (RASS) are used for planing treatment. For many years, the Ramsay Sedation Scale was the most commonly used tool to monitor sedation in the ICU. However, it cannot distinguish different levels of agitation, making it less useful than other available scales. Currently, two of the most commonly used techniques are the Riker

**Properties of an ideal agent for neurointensive care sedation:** 

Easily titrated to achieve adequate levels of sedation

 Amnesia during paralysis with muscle relaxants During interventions (line insertion, tracheostomy)

Facilitate sleep

accumulation

vasoconstriction

Inexpensive

available

Facilitate nursing management

maintaining their coupling Maintains cerebral autoregulation

 Adapted with permission. Both sedative and analgesic Lack of respiratory depression

No tolerance over time

General expectational situations:

Poor airway protection

Hemodynamic instability

Impairment of neurological exam

 Inactive or non harmful metabolites No interactions with other ICU drug

Decreased level-of-consciousness or obtundation

 Minimal cardiovascular depressant effects Easy control respiratory side-effects

1. Unarousable – Minimal or no response to noxious stimuli, does not communicate or follow commands

2. Very Sedated – Arouses to physical stimuli but does not communicate or follow commands, may move spontaneously

3. Sedated – Difficult to arouse, awakens to verbal stimuli or gently shaking, but drifts off again, follow simple commands

4. Calm and Cooperative – Calm, awakens easily, follows commands

5. Agitated – Anxious or mildly agitated, attempting to sit up, calms down to verbal stimuli

6. Very Agitated – Does not calm despite frequent verbal reminding of limits, biting ET

7. Dangerous Agitation – Pulling ET, trying to remove catheters, climbing over bedrails, striking at staff, thrashing side to side

Guidelines for SAS Assessment

1. Agitated patients are scored by their most severe degree of agitation, as described.

2. If patient is awake or awakens easily to voice ("awaken" means responds with voice or head shaking to a question or follows commands), that is a SAS 4 (same as calm and appropriate might even be napping).

3. If more stimuli such as shaking is required but patient eventually does awaken, that is a SAS 3.

4. If patient arouses to stronger physical stimuli (may be noxious) but never awakens to the point of responding yes/no or following commands, that is a SAS 2.

5. Little or no response to noxious physical stimuli is a SAS

6. This helps separate sedated patients into those you can eventually awaken (SAS 3), those you can not awaken, but can arouse (SAS 2), and those you can not arouse (SAS 1).

Table 2. Riker Sedation-Agitation Scale (SAS) (SAS Target Sedation = 3 to 4).

Score Description

+4Combative Overtly combative, violent, immediate danger to staff

+3 Very Agitated Pulls or removes tube(s) or catheter(s),aggressive

+2 Agitated Frequent non-purposeful movement, fights ventilator

+1 Restless Anxious but movements not aggressive vigorous

0 Alert and Calm


(>10 seconds) (eye-opening/eye contact) to voice




physical stimulation


Intensive Care Management of the Traumatic Brain Injury 13

protect against seizures is less certain. Pharmacologic properties rapid onset and rapid recovery of hypnosis are the most important pharmacokinetic properties to consider when

Table 4. Pharmacokinetic parameters, dosing, and cost of sedative and analgesic agents.

↑, modest increase; ↑↑, pronounced increase; ↔, no clear effect; ↓, modest decrease; ↓↓, pronounced decrease; +++, very favorable; ++, favorable; +, not favorable; CBF, cerebral blood flow; CMRO2, cerebral metabolic rate of oxygen consumption; ICP, intracranial pressure; MAP, mean arterial

to a shorter acting agent such as Propofol for optimal weaning purposes.

Midazolam +++ ++ ++ ↓ ↓↓ ↓ ↓

Table 5. Cerebral and systemic characteristics of the available molecules.

Propofol +++ +++ +++ ↓↓ ↓↓ ↓↓ ↓↓

For patients that are mechanically ventilated for three days or less, short acting agents should be used such as Propofol or Midazolam. For longer periods of mechanical ventilation, longer acting agents such as Lorazepam should be used. Patients that have been ventilated for long periods using the long acting agent Lorazepam may need to be switched

> Lorazepam + + + ↓ ↓ ↓ ↓

Fentanyl +++ ++ ++ ↔/↓ ↔ ↓ ↓

Remifentanyl +++ +++ +++ ↔/↓ ↔ ↓ ↓↓

The drug used for sedation in intensive care summarized in table below.

comparing different hypnotic alternatives.

NR: Not recommended

Rapid onset Fast recovery Easily titrated ICP reduction CBF reduction CMRO2 reduction

MAP

pressure.

Procedure for RASS Assessment: The basis of the RASS assessment is to see what amount of stimulation is necessary to evoke a respons and evaluate sedation.


 When no response to verbal stimulation, physically stimulatepatient by shaking shoulder and/or rubbing sternum.


Table 3. Richmond Agitation Sedation Scale (RASS) ( RASS Target Sedation = 0 to -3).

Even if the sedative strategy in the NICU shares the same general aims as general intensive care, the characteristics of the patients in the NICU present other unique challenges and specific indications, including intracranial pressure control, cerebral oxygen consumption and seizure reduction . Analgesic and sedative agents are used both to prevent undesirable increases in intracranial pressure and to reduce cerebral metabolic requirements. Intracranial pressure control cerebral autoregulation may be impaired in the traumatic brain injury. Therefore, agitation and associated blood pressure elevations directly determine intracranial pressure surges. Moreover, severe agitation increases intrathoracic pressure, reducing jugular venous outflow and increases cerebral metabolism with concomitantly increased cerebral blood flow (CBF). These potentially deleterious phenomena can lead to increase in intracranial pressure. This can trigger an additional cerebral vasodilator cascade, as cerebral perfusion pressure (CPP) is reduced.

Sedatives decrease the cerebral metabolic rate of oxygen consumption (CMRO2), and because the coupling of CBF and CMRO2 is usually maintained with these agents, CBF is reduced by increasing cerebral vascular resistance. The reduction in CBF results in a reduction of cerebral blood volume and, consequently, a decrease in intracranial pressure. In order to maintain adequate oxygen availability and energy production at the cellular level, treatment is directed to increase oxygen delivery by optimizing systemic hemodynamics and reduce cerebral metabolic demand. Sedative drugs confer a protective effect by reducing oxygen demand and increasing oxygen delivery (through improvement of central perfusion pressure and by inhibiting deleterious pathologic intracellular processes). The pharmacologic reduction in CMRO2 depresses either the basal or the activation components of cerebral metabolism. The metabolic suppression is dose dependent until the electroencephalogram becomes isoelectric. Beyond this level, no further suppression of cerebral oxygen consumption or blood flow occurs because energy expenditure, associated with electrophysiologic activity, has been reduced to close to zero, and the minimal consumption for cellular homeostasis persists unchanged.

There is no appropirate ratio for seizure activity in patients with brain trauma, seizures are a frequent complication in the NICU. Sedation appears to be an attractive option in reducing seizures in the NICU. Benzodiazepines increase the seizure threshold and are useful anticonvulsants. There are conflicting data on propofol, and, consequently, its ability to protect against seizures is less certain. Pharmacologic properties rapid onset and rapid recovery of hypnosis are the most important pharmacokinetic properties to consider when comparing different hypnotic alternatives.

The drug used for sedation in intensive care summarized in table below.


#### NR: Not recommended

12 Emergency Medicine – An International Perspective

Procedure for RASS Assessment: The basis of the RASS assessment is to see what amount

c. Patient awakens with eye opening and eye contact, but not sustained (Score –2) d. Patient has any movement in response to voice but no eye contact (Score –3) When no response to verbal stimulation, physically stimulatepatient by shaking

 If not alert, state patient's name and say "open eyes and look (speaker)." b. Patient awakens with sustained eye opening and eye contact (Score –1)

Table 3. Richmond Agitation Sedation Scale (RASS) ( RASS Target Sedation = 0 to -3).

Even if the sedative strategy in the NICU shares the same general aims as general intensive care, the characteristics of the patients in the NICU present other unique challenges and specific indications, including intracranial pressure control, cerebral oxygen consumption and seizure reduction . Analgesic and sedative agents are used both to prevent undesirable increases in intracranial pressure and to reduce cerebral metabolic requirements. Intracranial pressure control cerebral autoregulation may be impaired in the traumatic brain injury. Therefore, agitation and associated blood pressure elevations directly determine intracranial pressure surges. Moreover, severe agitation increases intrathoracic pressure, reducing jugular venous outflow and increases cerebral metabolism with concomitantly increased cerebral blood flow (CBF). These potentially deleterious phenomena can lead to increase in intracranial pressure. This can trigger an additional cerebral vasodilator cascade,

Sedatives decrease the cerebral metabolic rate of oxygen consumption (CMRO2), and because the coupling of CBF and CMRO2 is usually maintained with these agents, CBF is reduced by increasing cerebral vascular resistance. The reduction in CBF results in a reduction of cerebral blood volume and, consequently, a decrease in intracranial pressure. In order to maintain adequate oxygen availability and energy production at the cellular level, treatment is directed to increase oxygen delivery by optimizing systemic hemodynamics and reduce cerebral metabolic demand. Sedative drugs confer a protective effect by reducing oxygen demand and increasing oxygen delivery (through improvement of central perfusion pressure and by inhibiting deleterious pathologic intracellular processes). The pharmacologic reduction in CMRO2 depresses either the basal or the activation components of cerebral metabolism. The metabolic suppression is dose dependent until the electroencephalogram becomes isoelectric. Beyond this level, no further suppression of cerebral oxygen consumption or blood flow occurs because energy expenditure, associated with electrophysiologic activity, has been reduced to close to zero, and the minimal

There is no appropirate ratio for seizure activity in patients with brain trauma, seizures are a frequent complication in the NICU. Sedation appears to be an attractive option in reducing seizures in the NICU. Benzodiazepines increase the seizure threshold and are useful anticonvulsants. There are conflicting data on propofol, and, consequently, its ability to

of stimulation is necessary to evoke a respons and evaluate sedation.

e. Patient has any movement to physical stimulation (Score –4) f. Patient has no response to any stimulation (Score –5).

a. Patient is alert, restless, or agitated. (Score 0 to +4)

Observe patient.

shoulder and/or rubbing sternum.

as cerebral perfusion pressure (CPP) is reduced.

consumption for cellular homeostasis persists unchanged.

Table 4. Pharmacokinetic parameters, dosing, and cost of sedative and analgesic agents.

For patients that are mechanically ventilated for three days or less, short acting agents should be used such as Propofol or Midazolam. For longer periods of mechanical ventilation, longer acting agents such as Lorazepam should be used. Patients that have been ventilated for long periods using the long acting agent Lorazepam may need to be switched to a shorter acting agent such as Propofol for optimal weaning purposes.


decrease; +++, very favorable; ++, favorable; +, not favorable; CBF, cerebral blood flow; CMRO2, cerebral metabolic rate of oxygen consumption; ICP, intracranial pressure; MAP, mean arterial pressure.

Table 5. Cerebral and systemic characteristics of the available molecules.

Intensive Care Management of the Traumatic Brain Injury 15

intracranial pressure as a result of autoregulatory compensation (vasodilatory cascade) and consequently, can cause a reduction in CPP. The hemodynamic effects are usually dose dependent. Therefore, to avoid, or at least to limit, decreases in blood pressure, the patient should be euvolemic before the infusion is started, and slow boluses or continuous infusions

Because no single drug can achieve all of the requirements for sedation and analgesia in the ICU, use of a combination of drugs, each titrated to specific end points, is a more effective strategy. This allows lower doses of individual drugs and reduces the problems of drug accumulation. In the acute phase (ie, first 48–72 hours or when intracranial hypertension is not controlled), a continuous infusion of a combination of propofol (1.5–6 mg/kg/h) and

In the subacute phase (ie, after 72 hours or when intracranial pressure is normalized),

It is essential to contiue sedation until ventilatory support is required, and then sedation is stoped step by step to prevent withdrawal symptoms in 24 to 48 hours. No neuromuscular blocking drugs are routinely added, except in cases of severe, uncontrollable intracranial

The routine use of neuromuscular blockers varies between centres. The routine use of muscle relaxants should be avoided, they can be useful to prevent peaks in ICP induced by the patient coughing or "straining" or in the face of patient-ventilator dysynchrony. However, muscle paralysis makes it clinically impossible to recognise and treat seizures. Prolonged administration of neuromuscular blockers by continuous infusion can also lead to significant long-term problems, such as critical illness polyneuropathy

intermittent infusion of lorazepam (0.05 mg/kg every 2–6 h) should be initiated.

To eliminate spontaneous breathing and promote mechanical ventilation

 Severe pulmonary disease with inability to mechanically ventilated Cause a pharmacologic restraint so patients do not harm themselves

Transient increase in ICP with depolarizing blockade (succinylcholine)

Unexpected prolongation of neuromuscular blockade (e.g.,enzyme deficiencies, hepatic

To prevent movement (during imaging and to permit transfer of the patient)

are preferred.

hypertension.

and myopathy.

fentanyl (0.5–1.5 µg/kg/h) should be initiated.

**Neuromuscular blockers in the Neuro-ICU (68-71)**

**Neuromuscular blockers indications** 

Facilitate mechanical ventilation

During interventions (line insertion, tracheostomy)

Patient must be intubated for mechanically ventilated

Severe refractory intracranial hypertension

Complete loss of neurological examination

Facilitation of intubation

**General Precautions** 

or renal dysfunction)

Barbiturate, benzodiazepins, propofol and narcotics are all used as a sedative agent.

Propofol is very lipid soluble, has a large volume of distribution, and can be given for prolonged periods of time without significant changes in its pharmacokinetic profile. Because propofol has no active metabolites, the termination of its clinical effect is dependent solely on redistribution to peripheral fat tissue stores. When the infusion is discontinued, the fat tissue stores redistribute. Because of its pharmacokinetics and specific effects on cerebral hemodynamic variables, preserving autoregulation and vasoreactivity to carbon dioxide, propofol approximates the ideal sedative. Intravenous bolus administration produces a dose-dependent, coupled decrease in CBF and CMRO2 similar to that described after barbiturate administration. The effects on CBF are probably secondary to a reduction in CMRO2. A strong linear correlation between CBF and CMRO2 has been demonstrated. The major cardiovascular effect of propofol is a profound decrease in mean arterial pressure, resulting from a decrease in systemic vascular resistance, cardiac contractility, and preload. A bolus dose of 2 to 2.5 mg/kg propofol results in a 25 to 40% reduction in systolic blood pressure. This potent effect on mean arterial pressure may affect CPP by one of two mechanisms. If autoregulation is intact, a reduction in mean arterial pressure will produce reflex cerebral vasodilatation and a possible increase in intracranial pressure. Alternatively, if autoregulation is impaied hypotension may produce a critical decrease in CPP and CBF. The risk of hypotension is greatest in the presence of hypovolemia.

Evaluations of the effects of benzodiazepines on cerebral physiology have involved primarily diazepam and midazolam. Both cause dose-dependent decreases in CMRO2 and CBF, and by increasing cerebral vascular resistance, decreases in intracranial pressure have been observed. Usually CPP is not compromised. Moreover, a "ceiling effect" in CBF and CMRO2 reduction has been described, suggesting a saturation of the benzodiazepine receptors. It appears that benzodiazepines are safe to administer to patients with intracranial hypertension without respiratory depression and associated increases in arterial carbon dioxide tension.

The cerebral physiologic effects of opioids are controversial. Morphine-related increases in CBF, as described in early reports, were probably secondary to an increaseing arterial carbon dioxide tension resulting from respiratory depression. In general, opioids slightly reduce CMRO2, CBF, and intracranial pressure, as long as normocapnia is maintained by mechanical ventilation. Opioids can produce short-lasting, mild decreases in mean arterial pressure and then, subsequently, can produce decreases in CPP. Furthermore, remifentanyl may cause decreases in both cerebral metabolic rate and intracranial pressure, with minimal changes in CPP and cerebral blood flow. Opioids lead to dose-dependent, centrally mediated respiratory depression. The carbon dioxide response curve is shifted to the right, and the ventilatory response to hypoxia is obliterated. For this reason, in spontaneously ventilating NICU patients, if opioids are administered, strict end-tidal carbon dioxide monitoring or frequent blood gas analysis must be implemented to identify rapid onset of respiratory depression. When opioids and benzodiazepines are administered concomitantly, they may exhibit a synergistic effect on hemodynamics. The reasons for this synergy are not entirely clear.

Hypnotics can decrease mean arterial blood pressure by both cardiac depression and peripheral vasodilatation. The decrease in blood pressure can cause an increase in

Propofol is very lipid soluble, has a large volume of distribution, and can be given for prolonged periods of time without significant changes in its pharmacokinetic profile. Because propofol has no active metabolites, the termination of its clinical effect is dependent solely on redistribution to peripheral fat tissue stores. When the infusion is discontinued, the fat tissue stores redistribute. Because of its pharmacokinetics and specific effects on cerebral hemodynamic variables, preserving autoregulation and vasoreactivity to carbon dioxide, propofol approximates the ideal sedative. Intravenous bolus administration produces a dose-dependent, coupled decrease in CBF and CMRO2 similar to that described after barbiturate administration. The effects on CBF are probably secondary to a reduction in CMRO2. A strong linear correlation between CBF and CMRO2 has been demonstrated. The major cardiovascular effect of propofol is a profound decrease in mean arterial pressure, resulting from a decrease in systemic vascular resistance, cardiac contractility, and preload. A bolus dose of 2 to 2.5 mg/kg propofol results in a 25 to 40% reduction in systolic blood pressure. This potent effect on mean arterial pressure may affect CPP by one of two mechanisms. If autoregulation is intact, a reduction in mean arterial pressure will produce reflex cerebral vasodilatation and a possible increase in intracranial pressure. Alternatively, if autoregulation is impaied hypotension may produce a critical decrease in CPP and CBF.

Evaluations of the effects of benzodiazepines on cerebral physiology have involved primarily diazepam and midazolam. Both cause dose-dependent decreases in CMRO2 and CBF, and by increasing cerebral vascular resistance, decreases in intracranial pressure have been observed. Usually CPP is not compromised. Moreover, a "ceiling effect" in CBF and CMRO2 reduction has been described, suggesting a saturation of the benzodiazepine receptors. It appears that benzodiazepines are safe to administer to patients with intracranial hypertension without respiratory depression and associated increases in arterial carbon

The cerebral physiologic effects of opioids are controversial. Morphine-related increases in CBF, as described in early reports, were probably secondary to an increaseing arterial carbon dioxide tension resulting from respiratory depression. In general, opioids slightly reduce CMRO2, CBF, and intracranial pressure, as long as normocapnia is maintained by mechanical ventilation. Opioids can produce short-lasting, mild decreases in mean arterial pressure and then, subsequently, can produce decreases in CPP. Furthermore, remifentanyl may cause decreases in both cerebral metabolic rate and intracranial pressure, with minimal changes in CPP and cerebral blood flow. Opioids lead to dose-dependent, centrally mediated respiratory depression. The carbon dioxide response curve is shifted to the right, and the ventilatory response to hypoxia is obliterated. For this reason, in spontaneously ventilating NICU patients, if opioids are administered, strict end-tidal carbon dioxide monitoring or frequent blood gas analysis must be implemented to identify rapid onset of respiratory depression. When opioids and benzodiazepines are administered concomitantly, they may exhibit a synergistic effect on hemodynamics. The reasons for this synergy are not

Hypnotics can decrease mean arterial blood pressure by both cardiac depression and peripheral vasodilatation. The decrease in blood pressure can cause an increase in

Barbiturate, benzodiazepins, propofol and narcotics are all used as a sedative agent.

The risk of hypotension is greatest in the presence of hypovolemia.

dioxide tension.

entirely clear.

intracranial pressure as a result of autoregulatory compensation (vasodilatory cascade) and consequently, can cause a reduction in CPP. The hemodynamic effects are usually dose dependent. Therefore, to avoid, or at least to limit, decreases in blood pressure, the patient should be euvolemic before the infusion is started, and slow boluses or continuous infusions are preferred.

Because no single drug can achieve all of the requirements for sedation and analgesia in the ICU, use of a combination of drugs, each titrated to specific end points, is a more effective strategy. This allows lower doses of individual drugs and reduces the problems of drug accumulation. In the acute phase (ie, first 48–72 hours or when intracranial hypertension is not controlled), a continuous infusion of a combination of propofol (1.5–6 mg/kg/h) and fentanyl (0.5–1.5 µg/kg/h) should be initiated.

In the subacute phase (ie, after 72 hours or when intracranial pressure is normalized), intermittent infusion of lorazepam (0.05 mg/kg every 2–6 h) should be initiated.

It is essential to contiue sedation until ventilatory support is required, and then sedation is stoped step by step to prevent withdrawal symptoms in 24 to 48 hours. No neuromuscular blocking drugs are routinely added, except in cases of severe, uncontrollable intracranial hypertension.

#### **Neuromuscular blockers in the Neuro-ICU (68-71)**

The routine use of neuromuscular blockers varies between centres. The routine use of muscle relaxants should be avoided, they can be useful to prevent peaks in ICP induced by the patient coughing or "straining" or in the face of patient-ventilator dysynchrony. However, muscle paralysis makes it clinically impossible to recognise and treat seizures. Prolonged administration of neuromuscular blockers by continuous infusion can also lead to significant long-term problems, such as critical illness polyneuropathy and myopathy.

#### **Neuromuscular blockers indications**


#### **General Precautions**


Intensive Care Management of the Traumatic Brain Injury 17

Vecuronium: Initially 0.08 to 0.1 mg/kg IV bolus. (Higher initial doses-up to 0.3 mg/kg-may be used for rapid onset. Continuous infusion: 1 mcg/kg/min infusion, usual range: 0.8 to

Succinylcholine: Initially 0.3–1.1 mg/kg, bolus Infusion is 2.5–4.3 mg/min (cause refractory

Nutrition could also have an impact on the posttraumatic stress response, which is associated with adverse outcomes from TBI. The posttraumatic stress response is charaterized by increased blood levels of glucose, lactate, catecholamines, and cortisol. Nutrition support should be initiated as soon as possible following the head injury. Adequate nutrition is to provide the body healing. Early enteral nutrition (EN) support has been shown to attenuate the catabolic response and improve immune function and is associated with improved neurologic outcome(73,74) .If the digestive tract is functional, enteral nutrition, or nutrition given via a tube placed into the stomach, is the preferred route. Parenteral nutrition (PN) should be reserved for those patients with impaired gastrointestinal function or those who cannot meet their nutritional needs via EN alone.

The goal of nutritional support in patients who are critically ill is to provide protein and caloric replacement while attenuating a negative nitrogen balance. Incidence of malnutrition in hospitalized patients ranges between 30% to 55%. Delaying in the initiation of nutritional support may result in muscle and gastrointestinal atrophy, inability of weaning from ventilatory support, heart failure, impaired immunity, increase in the incidence of sepsis, length of hospital stay, morbidity and mortality and all of these resulte increase in costs (72). At the begining, all patients admitted to the critical care unit should be screened for risk or presence of malnutrition. Critically ill patients with neurologic impairment often require specialized nutrition support because of needing intubation, dysphagia, or altered mental

The provision of adequate nutritional support is an essential component of caring the critically ill patient. During starvation, homeostatic mechanisms are designed to burn fat rather than protein as an energy source until the fat stores are signicantly depleted. Especially in the begining of the infection, a catabolic state causing signicant protein loss progresses. Plasma and urine levels of catecholamines and cortisol are elevated. Hyperglycaemia is frequently seen and causes ketone production and lactic acid production leading acidosis in brain cells. The studies show that the severity and duration of

Enteral nutrition should be preferred in the critically ill patients(75,76). This can be achieved by either nasal tube feeding or via a percutaneous gastrostomy (PEG) if prolonged feeding is envisaged. Standard enteral feeding regiments aim to provide 1500–2500 kcal in 24 hours

A patient may require more calories for healing for the TBI. Patients with a GCS of 8 to 12 will require approximately 30 to 35 calories per kilogram of body weight per day. Patients

The main goal of nutrition should be preserve muscle mass, and provide adequate fluids

with a GCS of 6 to 7 require 40 to 50 calories per kilogram of body weight per day.

and strict electrolyte and glucose monitoring should be recommended.

hyperglycaemia following head injury correlate with longer term outcome.

with 70 g protein in a volume of 1.5–2 L.

intracranial hypertension Succinylcholine should be avoided due to increased ICP)

1.2 mcg/kg/min).

**Nutrition** 

status.


Agent Onset of action Duration of action ED90-95\* (mg/kg)

ED90-95 = Dose required to produce 90-95% suppression of muscle response

Table 6. Neuromuscular Blocking Agents.

Atracurium: initially 0.4 -0.5 mg/kg IV bolus, Maintenance infusion rates of 5 to 9 mcg/kg/min are usually adequate (Range:2 to 15mcg/kg/min). Toxic metabolite (laudanosine) may accumulate in renal failure

Doxacurium: initially, 0.05 mg/kg -0.08 mg/kg IV bolus, Maintenance, 0.005 mg/kg and 0.01 mg/kg IV to provide neuromuscular blockage for an average of 30 min and 45 min, respectively.

Rocuronium: initially, 0.6-1.2 mg/kg IV bolus. Maintenance, 0.1-0.2 mg/kg IV repeated as needed. Maintenance (continuous IV infusion): 0.01-0.012 mg/kg/minute.

Pancuronium: initially 0.1 to 0.2 mg/kg (usually 0.1) bolus, followed by 1 to 1.7 mcg/kg/min or 0.06 to 0.1 mg/kg/hr

Vecuronium: Initially 0.08 to 0.1 mg/kg IV bolus. (Higher initial doses-up to 0.3 mg/kg-may be used for rapid onset. Continuous infusion: 1 mcg/kg/min infusion, usual range: 0.8 to 1.2 mcg/kg/min).

Succinylcholine: Initially 0.3–1.1 mg/kg, bolus Infusion is 2.5–4.3 mg/min (cause refractory intracranial hypertension Succinylcholine should be avoided due to increased ICP)

#### **Nutrition**

16 Emergency Medicine – An International Perspective

2.5 min 15 - 20 min 0.07

Mean: 15 min

of action ED90-95\* (mg/kg)

(6 - 30 min) 1.03

(15 - 85 min) 0.3

(39 - 232) 0.025

(35 - 175) 0.07

Agent Onset of action Duration of action ED90-95\* (mg/kg)

Mivacurium (Mivacron)

Rapacuronium (Raplon)

Rocuronium

Atracurium

Cisatracurium

Pancuronium

Vecuronium

Doxacurium (Nuromax)

Pipecuronium

respectively.

Table 6. Neuromuscular Blocking Agents.

(laudanosine) may accumulate in renal failure

mcg/kg/min or 0.06 to 0.1 mg/kg/hr

Agent Onset of action Duration

Short Acting

Mean: 90 seconds (35 - 219 sec)

> 6 min (2.5 - 13)

ED90-95 = Dose required to produce 90-95% suppression of muscle response

needed. Maintenance (continuous IV infusion): 0.01-0.012 mg/kg/minute.

(Arduan) 2.5 - 5 min 75 min

Succinylcholine 30 - 60 seconds 5 - 8 min 0.3

(Tracrium) 2.5 - 5 min 20 - 45 min 0.2

(Nimbex) 2 - 3 min 30 - 40 min 0.05

(Pavulon) 2 - 3 min 60 - 90 min 0.06

(Norcuron) 2 - 3 min 25 - 40 min 0.05

Tubocurarine 3 - 5 min 70 - 90 min 0.05

Long Acting

Atracurium: initially 0.4 -0.5 mg/kg IV bolus, Maintenance infusion rates of 5 to 9 mcg/kg/min are usually adequate (Range:2 to 15mcg/kg/min). Toxic metabolite

Doxacurium: initially, 0.05 mg/kg -0.08 mg/kg IV bolus, Maintenance, 0.005 mg/kg and 0.01 mg/kg IV to provide neuromuscular blockage for an average of 30 min and 45 min,

Rocuronium: initially, 0.6-1.2 mg/kg IV bolus. Maintenance, 0.1-0.2 mg/kg IV repeated as

Pancuronium: initially 0.1 to 0.2 mg/kg (usually 0.1) bolus, followed by 1 to 1.7

100 min

Intermediate acting

(Zemeron) 1 - 3 min 31 min

Nutrition could also have an impact on the posttraumatic stress response, which is associated with adverse outcomes from TBI. The posttraumatic stress response is charaterized by increased blood levels of glucose, lactate, catecholamines, and cortisol. Nutrition support should be initiated as soon as possible following the head injury. Adequate nutrition is to provide the body healing. Early enteral nutrition (EN) support has been shown to attenuate the catabolic response and improve immune function and is associated with improved neurologic outcome(73,74) .If the digestive tract is functional, enteral nutrition, or nutrition given via a tube placed into the stomach, is the preferred route. Parenteral nutrition (PN) should be reserved for those patients with impaired gastrointestinal function or those who cannot meet their nutritional needs via EN alone.

The goal of nutritional support in patients who are critically ill is to provide protein and caloric replacement while attenuating a negative nitrogen balance. Incidence of malnutrition in hospitalized patients ranges between 30% to 55%. Delaying in the initiation of nutritional support may result in muscle and gastrointestinal atrophy, inability of weaning from ventilatory support, heart failure, impaired immunity, increase in the incidence of sepsis, length of hospital stay, morbidity and mortality and all of these resulte increase in costs (72).

At the begining, all patients admitted to the critical care unit should be screened for risk or presence of malnutrition. Critically ill patients with neurologic impairment often require specialized nutrition support because of needing intubation, dysphagia, or altered mental status.

The provision of adequate nutritional support is an essential component of caring the critically ill patient. During starvation, homeostatic mechanisms are designed to burn fat rather than protein as an energy source until the fat stores are signicantly depleted. Especially in the begining of the infection, a catabolic state causing signicant protein loss progresses. Plasma and urine levels of catecholamines and cortisol are elevated. Hyperglycaemia is frequently seen and causes ketone production and lactic acid production leading acidosis in brain cells. The studies show that the severity and duration of hyperglycaemia following head injury correlate with longer term outcome.

Enteral nutrition should be preferred in the critically ill patients(75,76). This can be achieved by either nasal tube feeding or via a percutaneous gastrostomy (PEG) if prolonged feeding is envisaged. Standard enteral feeding regiments aim to provide 1500–2500 kcal in 24 hours with 70 g protein in a volume of 1.5–2 L.

A patient may require more calories for healing for the TBI. Patients with a GCS of 8 to 12 will require approximately 30 to 35 calories per kilogram of body weight per day. Patients with a GCS of 6 to 7 require 40 to 50 calories per kilogram of body weight per day.

The main goal of nutrition should be preserve muscle mass, and provide adequate fluids and strict electrolyte and glucose monitoring should be recommended.

Intensive Care Management of the Traumatic Brain Injury 19

The calorie:nitrogen ratio for TPN should be 150:1 and it must be contain lipid, carbonhyrates, amino acids, electrolytes, trace elements and vitamins as much as needed. Lipids are essential for cell wall integrity, prostaglandin synthesis and the action of fatsoluble vitamins, but should provide no more than 33% of the energy requirements. Intralipid, mixture of refined olive oil (approximately 80%) and refined soya oil (approximately 20%) ( which may rarely cause severe hypersensitivity reactions), is an isotonic emulsion of soyabean oil with egg phosphatides and lecithin. The particle size of the emulsion is similar to a chylomicron, and the lipidis handled in a similar manner. The energy yield from fat is 9 cal/g, but the presence of the egg phosphatides increase the caloric value of intralipid to 11 cal/g. The lipid load should be decreased in the presence of sedation with propofol, severe jaundice ,severe hypoxamia, thrombocytopaenia and

Carbohydrate should be consist of two-thirds of the energy requirement and is in the form of glucose having 4cal/g energy. An insulin sliding scale will frequently be required to

Protein is usually omitted from caloric calculations. A wide range of amino acids are supplied as the L-isomer in commercial preparations. Protein requirements increase in

Daily electrolyte requirements of sodium, potassium, calcium, phosphate, magnesium and chloride should be met by TPN. Trace elements essential for homeostasis include zinc, copper, manganese, iron, cobalt, chromium, selenium, molybdenum and iodine. Commercially prepared vitamin supplements contain most water-soluble and fat-soluble vitamins (A, D and E) with the exception of folic acid, vitamin B12 and vitamin K (fat-

> Electrolytes, BUN, Cr, Ca, Mg, PO4, glucose, liver function tests, triglycerides,

cholesterol, albumin

triglycerides

sepsis and burns and are 12–17 g nitrogen/day (1 g nitrogen=6.25 g protein).

Schedule Enteral Parenteral

then 1 to 2 times/week Ca, Mg, PO4 Ca, Mg, PO4

Weekly PT, prealbumin PT, prealbumin BUN, blood urea nitrogen; PT, prothrombin time; Cr, creatinine; PO4, phosphate Table 7. Recommended monitoring guidelines for enteral and parental nutrition.

PO4, glucose, albumin

Daily Intake and output, weight Intake and output, weight

times/week Electrolytes, BUN, Cr, glucose Electrolytes, BUN, Cr, glucose

Every 10-14 days Albumin Liver function tests, albumin,

Increasingly, hospital pharmacies are supplying pre-mixed 'big bag' TPN containing the

Baseline Electrolytes, BUN, Cr, Ca, Mg,

hypothermia .

soluble).

tightly control plasma glucose levels.

Daily until stable; then 2 to 3

Every other day until stable;

complete 24-hour nutritional requirements.

It is prudent to consider postpyloric feeding in patient with neurological catastrophies, because gastric atony increases the risk of aspiration. Enteral feeding should be preferably done by continuous infusion with a volumetric pump.

In the average patient in the intensive care unit who has no contraindications to EN or PN, the choice of route for nutritional support may be inuenced by several factors. Because EN and PN are associated with risks and benets(77,78)

#### **Advantages associated with enteral rather than parenteral nutrition include:**


Contraindications to enteral feeding are few, particularly in the patient with isolated intracranial pathology, but include abdominal sepsis, obstruction, acut malabsorption and inammatory syndromes and enteric stulae. Only a short segment of small intestine (30 cm) is required for adequate absorption since hypertrophy will occur in response to lumenal nutrients. Neither bowel sounds nor atus are required for successful enteral feeding. Enteral feeding should be started if gastric aspirates are less than 400 ml/day and there are no obvious contraindications. Commence with standard enteral feed at 25 ml/h, increasing the rate every 12 hours until 100 ml/h is achieved. Aspirate residual volume and rest for 1 hour in every 6 hours of feeding, and rest continuously for 8 hours overnight.

#### **Complications of enteral feeding (79).:**


Gastric atony and delayed emptying may be seen during enteral feeding. For treating this unwanted result pro-kinetic agents can be used. Also nasojejunal tube bypassing pylorus should be inserted. The passage of nasal feeding tubes should be avoided in patients with facial injuries and basal skull fracture. Instate oragastric replacement should be used. Diarrhoea also may be seen during enteral feeding and may resolve with using a different formula of feed. But persistent diarrhoea should be thought infection with Clostridium difcile , particularly in patients receiving multiple antibiotics. A specimen should always be sent for microbiological culture.

Total parenteral nutrision (TPN) is prefered especialy enteral nutrision is imposible(80). Protein calorie requirements are more easily met by parenteral nutrition comparing enteral nutrition. Excessive calorie intake, particularly consisting excessive carbohydrate increases oxygen consumption, carbon dioxide production, the respiratory quotient (RQ) and lipogenesis.

It is prudent to consider postpyloric feeding in patient with neurological catastrophies, because gastric atony increases the risk of aspiration. Enteral feeding should be preferably

In the average patient in the intensive care unit who has no contraindications to EN or PN, the choice of route for nutritional support may be inuenced by several factors. Because EN

Contraindications to enteral feeding are few, particularly in the patient with isolated intracranial pathology, but include abdominal sepsis, obstruction, acut malabsorption and inammatory syndromes and enteric stulae. Only a short segment of small intestine (30 cm) is required for adequate absorption since hypertrophy will occur in response to lumenal nutrients. Neither bowel sounds nor atus are required for successful enteral feeding. Enteral feeding should be started if gastric aspirates are less than 400 ml/day and there are no obvious contraindications. Commence with standard enteral feed at 25 ml/h, increasing the rate every 12 hours until 100 ml/h is achieved. Aspirate residual volume and rest for 1

Gastric atony and delayed emptying may be seen during enteral feeding. For treating this unwanted result pro-kinetic agents can be used. Also nasojejunal tube bypassing pylorus should be inserted. The passage of nasal feeding tubes should be avoided in patients with facial injuries and basal skull fracture. Instate oragastric replacement should be used. Diarrhoea also may be seen during enteral feeding and may resolve with using a different formula of feed. But persistent diarrhoea should be thought infection with Clostridium difcile , particularly in patients receiving multiple antibiotics. A specimen should always

Total parenteral nutrision (TPN) is prefered especialy enteral nutrision is imposible(80). Protein calorie requirements are more easily met by parenteral nutrition comparing enteral nutrition. Excessive calorie intake, particularly consisting excessive carbohydrate increases oxygen consumption, carbon dioxide production, the respiratory quotient (RQ) and

**Advantages associated with enteral rather than parenteral nutrition include:** 

hour in every 6 hours of feeding, and rest continuously for 8 hours overnight.

Maintenance of mucosal integrity and prevention of villous atrophy

done by continuous infusion with a volumetric pump.

and PN are associated with risks and benets(77,78)

Absence of requirement for central venous line

Better maintenance of uid balance

**Complications of enteral feeding (79).:**  Large residual gastric volumes. Regurgitation and aspiration.

Reduced infection rate

Reduced cost

Diarrhoea.

lipogenesis.

Ulceration of nares.

Contamination of feed (rare).

be sent for microbiological culture.

The calorie:nitrogen ratio for TPN should be 150:1 and it must be contain lipid, carbonhyrates, amino acids, electrolytes, trace elements and vitamins as much as needed.

Lipids are essential for cell wall integrity, prostaglandin synthesis and the action of fatsoluble vitamins, but should provide no more than 33% of the energy requirements. Intralipid, mixture of refined olive oil (approximately 80%) and refined soya oil (approximately 20%) ( which may rarely cause severe hypersensitivity reactions), is an isotonic emulsion of soyabean oil with egg phosphatides and lecithin. The particle size of the emulsion is similar to a chylomicron, and the lipidis handled in a similar manner. The energy yield from fat is 9 cal/g, but the presence of the egg phosphatides increase the caloric value of intralipid to 11 cal/g. The lipid load should be decreased in the presence of sedation with propofol, severe jaundice ,severe hypoxamia, thrombocytopaenia and hypothermia .

Carbohydrate should be consist of two-thirds of the energy requirement and is in the form of glucose having 4cal/g energy. An insulin sliding scale will frequently be required to tightly control plasma glucose levels.

Protein is usually omitted from caloric calculations. A wide range of amino acids are supplied as the L-isomer in commercial preparations. Protein requirements increase in sepsis and burns and are 12–17 g nitrogen/day (1 g nitrogen=6.25 g protein).

Daily electrolyte requirements of sodium, potassium, calcium, phosphate, magnesium and chloride should be met by TPN. Trace elements essential for homeostasis include zinc, copper, manganese, iron, cobalt, chromium, selenium, molybdenum and iodine. Commercially prepared vitamin supplements contain most water-soluble and fat-soluble vitamins (A, D and E) with the exception of folic acid, vitamin B12 and vitamin K (fatsoluble).


Table 7. Recommended monitoring guidelines for enteral and parental nutrition.

Increasingly, hospital pharmacies are supplying pre-mixed 'big bag' TPN containing the complete 24-hour nutritional requirements.

Intensive Care Management of the Traumatic Brain Injury 21

intracranial hypertension, systemic hypotension or relative hypotension (insufficient to maintain adequate CPP due to increased ICP) lead to poor cerebral perfusion and ischemic

Sustained intracranial hypertension has a negative effect on cerebral blood ow and cerebral perfusion pressure and can cause direct compression of vital cerebral structures and lead to herniation. Appropriate management of intracranial hypertension begins with stabilization of the patient and simultaneous assessment of the level of sensorium and the cause of it.

Stabilization is initiated with securing the airway, ventilation and circulation(87). The management of the patient involves the maintenance of an adequate CPP, prevention of intracranial hypertension and optimization of oxygen delivery. In patients with severe coma, signs of herniation or acutely elevated intracranial pressure, treatment should be

Indications for ICP monitoring, varing from unit to unit, may include traumatic brain injury, anoxic-ischaemic brain injury, intracerebral and subarachnoid haemorrhage, hydrocephalus, brain oedema after large strokes, hypoxic brain injury, central nervous system infections or

The primary goals of ICP monitoring are identification of intracranial pressure trends and evaluation of therapeutic interventions. Intracranial hypertension compromises the relationship between systemic blood pressure and the resistance that must be overcome to accomplish cerebral perfusion. When cerebral perfusion pressure (CPP) falls below 50 mm Hg, secondary brain ischemia, herniation, and, ultimately, brain death occur. ICP monitoring allows for early detection of intracranial hypertension and subsequent

ICP monitoring helps the earlier detection of intracranial mass lesions and can limit the indiscriminate use of therapies to control ICP which themselves can be potentially harmful. It can also reduce ICP by CSF drainage and thus improve cerebral perfusion and helps in

Currently, accurate monitoring requires invasive devices. Parenchymal pressure monitors (eg, Camino or Codman) measure ICP via a fiber-optic monitor placed in the subarachnoid space. Intraventricular catheters placed via ventriculostomy allow for both measurements of ICP and drainage of CSF. This device offers a therapeutic advantage over subarachnoid

Maintenance of adequate CPP(84,86, 89,90) is accomplished by reducing the ICP and ensuring

The first step typically includes the use of analgesia and sedation, elevation of head, airway and ventilatory management and preferably with concomitant monitoring of jugular venous saturation(86,88-90) Obtunded patients, especially those with a GCS ≤ 8 require intubation for airway protection. Mechanical ventilation will also facilitate deep sedation and hyperventilation. During mechanical ventilation hypercarbia should be avoided because it causes vasodilation and may further increase ICP. Therapeutic hyperventilation decreases ICP via vasoconstriction cerebral vessels. Also it must be thought that hyperventilation is rapidly effective but may lead to reduce CBF and may not be a reasonable long-term

adequate MAP. Adequate CPP and reducing ICP Interventions are used step by step.

insults and worse outcomes(81,85) and treatment is recommended (81,85,86) .

started prior to plan imaging technics or invasive monitoring.

monitors but carries a higher incidence of infection(83,85).

fulminant hepatic failure(83,85).

aggressive management.

determining prognosis.

While receiving enteral or parenteral nutrition, the patient must be monitored for changes in body composition, blood chemistry, blood glucose, triglycerides, and protein synthesis. Electrolytes (Na, K, Cl, Mg, Phosphate, and Ca) and markers of renal function (blood urea nitrogen and creatinine) should be monitored routinely. Daily weight and the total volume of the patient's intake and output need to be monitored in addition to assessing other markers of hydration and volume status.

#### **Management and treatment of intracranial hypertension**

The principle focus of critical care management for traumatic brain is to limit secondary brain injury (SBI). On admission to the NICU, all patients after trauma are at risk of increasing ICP, and standard systemic monitoring; pulse oximetry, invasive arterial blood pressure with regular analyses of arterial blood gases and blood glucose and central venous access with central venous pressure monitoring must be established. End-tidal carbon dioxide monitoring is invaluable in this group of patients because it enables early correction of hypercapnia-induced rises.

For the treatment and prevention of SBI, using a neuroprotective strategy to maintain cerebral perfusion and maintaining intracranial pressure within normal limits are important. Beside this optimizing oxygenation and blood pressure are needed and temperature, glucose, seizures, and other potential secondary brain insults management are essential.

If GCS of the patients equal and below the 8, there are clinical symptoms like unilateral or bilaterally fixed and dilated pupils suggesting possible impending herniation from elevated ICP and/or decorticate or decerebrate posturing, bradycardia, hypertension, and respiratory depression progress, the treatment of head elevation, hyperventilation, and osmotic therapy (mannitol 1 g/kg iv) is planed urgently. With the treatment neuroimaging and other assessments are organized. The evaluation and management of increased ICP are discussed in detail below.

In traumatic brain injury, ICP and low CPP cause mass effect in the brain and is associated with more severe symptoms and more abrupt onset and poor outcome. The increased ICP is caused by increases in tissue volume, cerebral blood volume, or cerebrospinal uid (CSF) volume. The pathophysiology and management of increased ICP is based on the Monro-Kellie doctrine.

Cerebral blood flow is maintained through adequate CPP, which is determined by the mean systemic arterial pressure minus intracranial pressure (CPP = MAP – ICP). Normal CPP values 80 mm Hg for adults, CPP > 50–60 mm Hg for children and CPP > 40–50 mm Hg for infants/toddlers.

If the CPP reduces below the value of 70 mmHg, it assosiated with high mortality and poor outcome(81-83) Especially the value reduces to less than 50 mmHg, metabolic evidence of ischaemia, reduced electrical activity and, ultimately, brain death are expected.

Normal values of ICP are within the range of 10 to 15 mm Hg for adults and older children, 3 to 7 mm Hg for young children, and 1.5 to 6 mm Hg for term infants( 84). Intracranial hypertension (ICH) is dened when the ICP values ebow 20 mm Hg. The values greater than 20 to 25 mm Hg require treatment in most circumstances. Sustained values of greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension(76). During

While receiving enteral or parenteral nutrition, the patient must be monitored for changes in body composition, blood chemistry, blood glucose, triglycerides, and protein synthesis. Electrolytes (Na, K, Cl, Mg, Phosphate, and Ca) and markers of renal function (blood urea nitrogen and creatinine) should be monitored routinely. Daily weight and the total volume of the patient's intake and output need to be monitored in addition to assessing other

The principle focus of critical care management for traumatic brain is to limit secondary brain injury (SBI). On admission to the NICU, all patients after trauma are at risk of increasing ICP, and standard systemic monitoring; pulse oximetry, invasive arterial blood pressure with regular analyses of arterial blood gases and blood glucose and central venous access with central venous pressure monitoring must be established. End-tidal carbon dioxide monitoring is invaluable in this group of patients because it enables early correction

For the treatment and prevention of SBI, using a neuroprotective strategy to maintain cerebral perfusion and maintaining intracranial pressure within normal limits are important. Beside this optimizing oxygenation and blood pressure are needed and temperature, glucose, seizures, and other potential secondary brain insults management are essential.

If GCS of the patients equal and below the 8, there are clinical symptoms like unilateral or bilaterally fixed and dilated pupils suggesting possible impending herniation from elevated ICP and/or decorticate or decerebrate posturing, bradycardia, hypertension, and respiratory depression progress, the treatment of head elevation, hyperventilation, and osmotic therapy (mannitol 1 g/kg iv) is planed urgently. With the treatment neuroimaging and other assessments are organized. The evaluation and management of increased ICP are discussed

In traumatic brain injury, ICP and low CPP cause mass effect in the brain and is associated with more severe symptoms and more abrupt onset and poor outcome. The increased ICP is caused by increases in tissue volume, cerebral blood volume, or cerebrospinal uid (CSF) volume. The pathophysiology and management of increased ICP is based on the Monro-

Cerebral blood flow is maintained through adequate CPP, which is determined by the mean systemic arterial pressure minus intracranial pressure (CPP = MAP – ICP). Normal CPP values 80 mm Hg for adults, CPP > 50–60 mm Hg for children and CPP > 40–50 mm Hg for

If the CPP reduces below the value of 70 mmHg, it assosiated with high mortality and poor outcome(81-83) Especially the value reduces to less than 50 mmHg, metabolic evidence of

Normal values of ICP are within the range of 10 to 15 mm Hg for adults and older children, 3 to 7 mm Hg for young children, and 1.5 to 6 mm Hg for term infants( 84). Intracranial hypertension (ICH) is dened when the ICP values ebow 20 mm Hg. The values greater than 20 to 25 mm Hg require treatment in most circumstances. Sustained values of greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension(76). During

ischaemia, reduced electrical activity and, ultimately, brain death are expected.

markers of hydration and volume status.

of hypercapnia-induced rises.

in detail below.

Kellie doctrine.

infants/toddlers.

**Management and treatment of intracranial hypertension** 

intracranial hypertension, systemic hypotension or relative hypotension (insufficient to maintain adequate CPP due to increased ICP) lead to poor cerebral perfusion and ischemic insults and worse outcomes(81,85) and treatment is recommended (81,85,86) .

Sustained intracranial hypertension has a negative effect on cerebral blood ow and cerebral perfusion pressure and can cause direct compression of vital cerebral structures and lead to herniation. Appropriate management of intracranial hypertension begins with stabilization of the patient and simultaneous assessment of the level of sensorium and the cause of it.

Stabilization is initiated with securing the airway, ventilation and circulation(87). The management of the patient involves the maintenance of an adequate CPP, prevention of intracranial hypertension and optimization of oxygen delivery. In patients with severe coma, signs of herniation or acutely elevated intracranial pressure, treatment should be started prior to plan imaging technics or invasive monitoring.

Indications for ICP monitoring, varing from unit to unit, may include traumatic brain injury, anoxic-ischaemic brain injury, intracerebral and subarachnoid haemorrhage, hydrocephalus, brain oedema after large strokes, hypoxic brain injury, central nervous system infections or fulminant hepatic failure(83,85).

The primary goals of ICP monitoring are identification of intracranial pressure trends and evaluation of therapeutic interventions. Intracranial hypertension compromises the relationship between systemic blood pressure and the resistance that must be overcome to accomplish cerebral perfusion. When cerebral perfusion pressure (CPP) falls below 50 mm Hg, secondary brain ischemia, herniation, and, ultimately, brain death occur. ICP monitoring allows for early detection of intracranial hypertension and subsequent aggressive management.

ICP monitoring helps the earlier detection of intracranial mass lesions and can limit the indiscriminate use of therapies to control ICP which themselves can be potentially harmful. It can also reduce ICP by CSF drainage and thus improve cerebral perfusion and helps in determining prognosis.

Currently, accurate monitoring requires invasive devices. Parenchymal pressure monitors (eg, Camino or Codman) measure ICP via a fiber-optic monitor placed in the subarachnoid space. Intraventricular catheters placed via ventriculostomy allow for both measurements of ICP and drainage of CSF. This device offers a therapeutic advantage over subarachnoid monitors but carries a higher incidence of infection(83,85).

Maintenance of adequate CPP(84,86, 89,90) is accomplished by reducing the ICP and ensuring adequate MAP. Adequate CPP and reducing ICP Interventions are used step by step.

The first step typically includes the use of analgesia and sedation, elevation of head, airway and ventilatory management and preferably with concomitant monitoring of jugular venous saturation(86,88-90) Obtunded patients, especially those with a GCS ≤ 8 require intubation for airway protection. Mechanical ventilation will also facilitate deep sedation and hyperventilation. During mechanical ventilation hypercarbia should be avoided because it causes vasodilation and may further increase ICP. Therapeutic hyperventilation decreases ICP via vasoconstriction cerebral vessels. Also it must be thought that hyperventilation is rapidly effective but may lead to reduce CBF and may not be a reasonable long-term

Intensive Care Management of the Traumatic Brain Injury 23

diuresis. The altered osmolar gradient facilitates fluid shifts and reduces cerebral edema. Similarly, furosamide increases intravascular oncotic pressure via hypoosmolar diuresis, which reduces cerebral edema and CSF production and is synergistic with mannitol. These agents should be used with caution because hypovolemia and hypotension may result, further impairing CPP(84,91,92). Urine output should be matched with crystalloid replacement

Attention has to be paid to the fluid balance so as to avoid hypovolemia and shock. There is also a concern of possible leakage of mannitol into the damaged brain tissue potentially leading to "rebound" rises in ICP (93). For this reason, when it is time to stop mannitol, it should be tapered and its use should be limited to 48 to 72 h. Mannitol can also lead to

Hypertonic saline has an obvious advantage over mannitol in children who are hypovolemic or hypotensive. These may be preferred are renal failure or serum osmolality >320 mosmol/Kg too. It has been found effective in patients with serum osmolality of up to 360 mosmol/Kg(94). The expected complications with the use of hypertonic saline are bleeding, rebound rise in ICP, hyperchloremic acidosis and hypokalemia, central pontine myelinolysis, acute volume overload, renal failure, cardiac failure or pulmonary edema (95- 97). In different studies the concentration of hypertonic saline used has varied from 1.7% to 30% (98). There are also a variety of application method and evidence-based recommendations are difficult. It would be reasonable to administer hypertonic saline as a continuous infusion at 0.1 to 1.0 mL/kg/hr, to target a serum sodium level of 145–155 meq/L (99,100) Serum sodium level and neurological status should be closely monitored during treatment. While finishing hypertonic saline treatment, serum sodium should be slowly returned to normal values (hourly decline in serum sodium of not more than 0.5 meq/L) to avoid complications related to fluid shifts(101). Monitoring of serum sodium and serum osmolality should be done every 2–4h till target level is reached and then followed up with 12 hourly estimations. Under careful monitoring, hypertonic saline has been used for

Agitation and the painful stimuli may significantly increase ICP in traumatic brain injury patients, and therefore, the use of sedative agents is important in ICP management. A variety of pharmacological agents have been suggested to treat agitation. But no optimal

Sedatives, analgesics, and neuromuscular blocking agents are commonly used in the management of traumativ brain injury. This agents are used for two purposes, emergency intubation and management including control of ICP in the intensive care unit (ICU).

Pain and agitation produce sympathetic hyperactivity, resulting in an increase in heart rate, stroke volume, myocardial oxygen consumption and ICP and should be avoided. Analgesia and sedation reduce the neuro-endocrine response to stress by resulting an increase in adrenocorticotrophic hormone (ACTH), cortisol, antidiuretic hormone (ADH), growth hormone (GH) and glucagon. The stress response reduces insulin uptake, causing hyperglycaemia, relative glucose intolerance and insulin resistance, and promotes

to maintain intravascular volume.

**Hypertonic Saline** 

up to 7 days (102).

hypokalemia, hemolysis and renal failure.

**Sedatives, analgesics, and neuromuscular blocking agents** 

sedative regimen has been exactly identified.

strategy. Therefore, it is recommended that maintaining the PaCO2 at the low end of normal level is more definitive strategies for reducing ICP.

The second step includes using mannitol or hypertonic saline infusions for refractory intracranial hypertension. In the third step rescue therapies such as high-dose barbiturate infusions and possibly decompressive craniectomy or hypothermia may be needed. Thus, interventions are traditionally chosen in the order of an increasing risk of complications. The goal for patients presenting with raised ICP is reduce ICP immediately ( Table 8).


Table 8. Treatment to reduce intracranial pressure.

#### **Osmotic Diuresis**

#### **Mannitol**

The optimal dosing of mannitol is not known. Mannitol is used as a rapid and effective method for reducing ICP. It is given as a 0.5- to 1g/kg bolus and repeat every 6-8 hours to maintain serum osmolarity ebow the value of 310 mOsm/L. Mannitol results osmotic diuresis. The altered osmolar gradient facilitates fluid shifts and reduces cerebral edema. Similarly, furosamide increases intravascular oncotic pressure via hypoosmolar diuresis, which reduces cerebral edema and CSF production and is synergistic with mannitol. These agents should be used with caution because hypovolemia and hypotension may result, further impairing CPP(84,91,92). Urine output should be matched with crystalloid replacement to maintain intravascular volume.

Attention has to be paid to the fluid balance so as to avoid hypovolemia and shock. There is also a concern of possible leakage of mannitol into the damaged brain tissue potentially leading to "rebound" rises in ICP (93). For this reason, when it is time to stop mannitol, it should be tapered and its use should be limited to 48 to 72 h. Mannitol can also lead to hypokalemia, hemolysis and renal failure.

#### **Hypertonic Saline**

22 Emergency Medicine – An International Perspective

strategy. Therefore, it is recommended that maintaining the PaCO2 at the low end of normal

The second step includes using mannitol or hypertonic saline infusions for refractory intracranial hypertension. In the third step rescue therapies such as high-dose barbiturate infusions and possibly decompressive craniectomy or hypothermia may be needed. Thus, interventions are traditionally chosen in the order of an increasing risk of complications. The

2. Early intubation if; GCS <8, evidence of herniation, apnea, inability to maintain

4. Hyperventilation: Target PaCO2:30–35 mm Hg (suited for acute, sharp increases in

5. Mannitol: Initial bolus: 0.25–1 g/kg, then 0.25–0.5g/kg,q 2–6 has per requirement, up

6. Hypertonic Saline: Preferable in presence of hypotension, hypovolemia, serum osmolality >320 mOsm/kg, renal failure, dose: 0.1–1 ml/kg/hr infusion, target Na+

7. Steroids: Intracranial tumors with perilesional edema, neurocysticerocosis with high

9. Prevention and treatment of seizures: use lorazepam or midazolam followed by

10. Avoid noxious stimuli: use lignocaine prior to ET suctioning [nebulized (4% lidocaine mixed in 0.9% saline) or intravenous (1–2 mg/kg as 1% solution) given 90 sec prior to

12. Maintenance IV Fluids: Only isotonic or hypertonic fluids (Ringer lactate, 0.9% Saline,

The optimal dosing of mannitol is not known. Mannitol is used as a rapid and effective method for reducing ICP. It is given as a 0.5- to 1g/kg bolus and repeat every 6-8 hours to maintain serum osmolarity ebow the value of 310 mOsm/L. Mannitol results osmotic

goal for patients presenting with raised ICP is reduce ICP immediately ( Table 8).

1. Assessment and management of ABC's (airway, breathing, circulation)

3. Mild head elevation of 15–30° (Ensure that the patient is euvolemic)

level is more definitive strategies for reducing ICP.

ICP or signs of impending herniation)

lesion load, pyomeningitis, abscess 8. Adequate sedation and analgesia

11. Control fever: antipyretics, cooling measures

5% D in 0.9% NS), No Hypotonic fluids 13. Maintain blood sugar: 80–120 mg/dL

Table 8. Treatment to reduce intracranial pressure.

phenytoin as initial choice.

airway

to 48 h

145–155 meq/L.

suctioning]

14. Refractory raised ICP:

 Barbiturate coma Hypothermia

**Osmotic Diuresis** 

**Mannitol** 

Heavy sedation and paralysis

Decompressive craniectomy

Hypertonic saline has an obvious advantage over mannitol in children who are hypovolemic or hypotensive. These may be preferred are renal failure or serum osmolality >320 mosmol/Kg too. It has been found effective in patients with serum osmolality of up to 360 mosmol/Kg(94). The expected complications with the use of hypertonic saline are bleeding, rebound rise in ICP, hyperchloremic acidosis and hypokalemia, central pontine myelinolysis, acute volume overload, renal failure, cardiac failure or pulmonary edema (95- 97). In different studies the concentration of hypertonic saline used has varied from 1.7% to 30% (98). There are also a variety of application method and evidence-based recommendations are difficult. It would be reasonable to administer hypertonic saline as a continuous infusion at 0.1 to 1.0 mL/kg/hr, to target a serum sodium level of 145–155 meq/L (99,100) Serum sodium level and neurological status should be closely monitored during treatment. While finishing hypertonic saline treatment, serum sodium should be slowly returned to normal values (hourly decline in serum sodium of not more than 0.5 meq/L) to avoid complications related to fluid shifts(101). Monitoring of serum sodium and serum osmolality should be done every 2–4h till target level is reached and then followed up with 12 hourly estimations. Under careful monitoring, hypertonic saline has been used for up to 7 days (102).

#### **Sedatives, analgesics, and neuromuscular blocking agents**

Agitation and the painful stimuli may significantly increase ICP in traumatic brain injury patients, and therefore, the use of sedative agents is important in ICP management. A variety of pharmacological agents have been suggested to treat agitation. But no optimal sedative regimen has been exactly identified.

Sedatives, analgesics, and neuromuscular blocking agents are commonly used in the management of traumativ brain injury. This agents are used for two purposes, emergency intubation and management including control of ICP in the intensive care unit (ICU).

Pain and agitation produce sympathetic hyperactivity, resulting in an increase in heart rate, stroke volume, myocardial oxygen consumption and ICP and should be avoided. Analgesia and sedation reduce the neuro-endocrine response to stress by resulting an increase in adrenocorticotrophic hormone (ACTH), cortisol, antidiuretic hormone (ADH), growth hormone (GH) and glucagon. The stress response reduces insulin uptake, causing hyperglycaemia, relative glucose intolerance and insulin resistance, and promotes

Intensive Care Management of the Traumatic Brain Injury 25

CPP(95). Propofol has also neurovascular, neuroprotective, and electroencephalographical effects that are salutory in the patient in neurocritical care. The short half-life of propofol facilitates serial neurologic exams and is the prefered agent. However, excessive sedation and analgesia may mask examination findings and prolong the course of mechanical

Propofol will be initiated at 25 mcg/kg/min and titrated to achieve an ICP < 20 mm Hg (up to a maximum of 75 mcg/kg/min). Propofol will be continued for up to 48 h or until

Propofol is employed as a first-line sedative agent in neurosurgecal patients due to its favorable pharmacokinetic profile (105) . However, some patients require prolonged infusions and high rates of propofol. This has been shown increase their risk for development of a severe propofol-related infusion syndrome, which can be fatal. Propofol infusion syndrome is expected in ebow 5 mg/kg/hr infusion more than 48 hours. Its clinical features consist of cardiomyopathy with acute cardiac failure, myopathy, metabolic acidosis, hiperkalemia and hepatomegaly. Mechanism of this syndrome is by though inhibition of free faty acids entry into mitochondria and failure of its metabolism. Both barbiturates and propofol have favorable effects on cerebral oxygen balance, but propofol is more potent in this regard. Benzodiazepines and propofol have the added benefit of increasing the seizure threshold. Barbiturates act on the GABA receptors and its mechenism of action in zero order kinetics. It provides a cerebral protection effect and uses in neurointensive care units in patients with

Barbiturates are less effective than mannitol for lowering ICP. Thiopentone can be used for this purpose and the dosing of the drug is adjusted to a target ICP as monitored on an ICP monitor. The drug is titrated to a 90% burst suppression (2–6 bursts per minute) using an EEG monitor. Monitoring in barbiturate coma should include EEG, ICP monitoring, invasive hemodynamic monitoring (arterial blood pressure, central venous pressure, SjvO2) and frequent assessment of oxygenation status. The complication rate of barbiturate therapy is high and includes hypotension, hypokalemia, respiratory complications, infections,

Morphine, fentanyl and remifentanil can be used not only pain management but also sedation effect. Morphine and fentanyl are the two most commonly used opioids for the analgesia of critically ill patients(107,108). They are routinely used in patients with severe head injury as part of the management of increased intracranial pressure (ICP). However, the cerebrovascular effects of such drugs remain controversial. Studies in laboratory animals and humans have shown increases, decreases or no change in ICP after opioid administration(109-120). Most of these studies find a concomitant decrease in systemic arterial pressure and, recently, it has been suggested that reduced MAP could in fact be responsible for the increases in ICP observed after the administration of potent opioids such as sufentanil(107). In patients with low intracranial compliance and intact autoregulation, reduced MAP would be expected to result in vasodilation, increased blood volume, and

Remifentanil is a selective mu-opioid agonist with a context-sensitive half-time of 3 to 5 minutes, independent of dose or administration duration of. Its metabolism by nonspecific

removal of the ICP or when mechanical ventilation is discontinued.

ventilation(82,88,104).

high ICP and status epilepticus.

**Opiods:** 

thus increased ICP.

hepatic dysfunction and renal dysfunction (106).

catabolism of proteins and lipids and a decrease in gastrointestinal motility and urine output.

#### **Benzodiazepines**

The benzodiazepines are the favoured group of drugs for sedation and are divided into short-acting, intermediate-acting and long-acting drugs. Among them midazolam, lorazepam and diazepam are mostly used.

Midazolam (Dormicum) is short-acting benzodiazepine and 2-3 times more potent than diazepam, and is available in three strengths. Midazolam is well known for its idiosyncratic effects. It has active metabolites, and can accumulate. Its duration of action is approximately 45 minutes. The adult loading dose is 2 mg intravenously over 30 seconds. The maximum effect is in 3 minutes. After 3 minutes, increments of 1 mg can be given every 3 minutes until the desired effect is achieved. Midazolam may cause respiratory depression. Elderly patients should be given half of the above recommended dosage. Midazolam can be used orally, rectally, intranasally, or intravenously in children. The recommended paediatric doses are as follows: intranasal 0.4 mg/kg, oral/rectal 0.5 mg/kg, intravenous 0.1 mg/kg.

Lorazepam (Ativan) is an intermediate-acting benzodiazepine which has no metabolites. It is useful in acute anxiety, acute phsychosis and status epilepticus. The maximum safe adult dosage is 4 mg and the minimum effective dose should be titrated to the individual patient's needs. The intravenous dose for children is 0.1 mg/kg.

Diazepam (Valium) is a long-acting benzodiazepine which is less potent than the previous two. It has active metabolites, and a sclerosing effect on veins. The intravenous dosage of 0.1 mg/kg applies to both adults and children, and the rectal dosage is 0.5 mg/kg.

#### **α-2 receptors agonists**

Sedative and hypnotic effects of these drugs are due to the action on α2-receptors in the locus ceruleus. Analgesic effect is maintened by an action on α2-receptors within the locus ceruleus and the spinal cord. These are dextmedetomidine and clonidine.

Dexmedetomidine (Precedex) is a new selective α-2 adrenoreceptor agonist drug. It has both anxiolytic and analgesic properties. It does not cause respiratory depression, and patients maintain cognitive function and are easily rousable. The bradycardia and hypotension may be seen as side effects. There is no effect on ICP, but CPP may decrease by virtue of decreasing MAP.

#### **Anaesthetics**

Propofol and thiopentone are used for sedation and lowering ICP in traumatic brain injuried patients.

#### Propofol


Propofol is widely used in the ICU to sedate intubated neurolojic patients with increased ICP(94). Propofol has been shown to maintain or reduce ICP while maintaining an adequate CPP(95). Propofol has also neurovascular, neuroprotective, and electroencephalographical effects that are salutory in the patient in neurocritical care. The short half-life of propofol facilitates serial neurologic exams and is the prefered agent. However, excessive sedation and analgesia may mask examination findings and prolong the course of mechanical ventilation(82,88,104).

Propofol will be initiated at 25 mcg/kg/min and titrated to achieve an ICP < 20 mm Hg (up to a maximum of 75 mcg/kg/min). Propofol will be continued for up to 48 h or until removal of the ICP or when mechanical ventilation is discontinued.

Propofol is employed as a first-line sedative agent in neurosurgecal patients due to its favorable pharmacokinetic profile (105) . However, some patients require prolonged infusions and high rates of propofol. This has been shown increase their risk for development of a severe propofol-related infusion syndrome, which can be fatal. Propofol infusion syndrome is expected in ebow 5 mg/kg/hr infusion more than 48 hours. Its clinical features consist of cardiomyopathy with acute cardiac failure, myopathy, metabolic acidosis, hiperkalemia and hepatomegaly. Mechanism of this syndrome is by though inhibition of free faty acids entry into mitochondria and failure of its metabolism. Both barbiturates and propofol have favorable effects on cerebral oxygen balance, but propofol is more potent in this regard. Benzodiazepines and propofol have the added benefit of increasing the seizure threshold.

Barbiturates act on the GABA receptors and its mechenism of action in zero order kinetics. It provides a cerebral protection effect and uses in neurointensive care units in patients with high ICP and status epilepticus.

Barbiturates are less effective than mannitol for lowering ICP. Thiopentone can be used for this purpose and the dosing of the drug is adjusted to a target ICP as monitored on an ICP monitor. The drug is titrated to a 90% burst suppression (2–6 bursts per minute) using an EEG monitor. Monitoring in barbiturate coma should include EEG, ICP monitoring, invasive hemodynamic monitoring (arterial blood pressure, central venous pressure, SjvO2) and frequent assessment of oxygenation status. The complication rate of barbiturate therapy is high and includes hypotension, hypokalemia, respiratory complications, infections, hepatic dysfunction and renal dysfunction (106).

#### **Opiods:**

24 Emergency Medicine – An International Perspective

catabolism of proteins and lipids and a decrease in gastrointestinal motility and urine

The benzodiazepines are the favoured group of drugs for sedation and are divided into short-acting, intermediate-acting and long-acting drugs. Among them midazolam,

Midazolam (Dormicum) is short-acting benzodiazepine and 2-3 times more potent than diazepam, and is available in three strengths. Midazolam is well known for its idiosyncratic effects. It has active metabolites, and can accumulate. Its duration of action is approximately 45 minutes. The adult loading dose is 2 mg intravenously over 30 seconds. The maximum effect is in 3 minutes. After 3 minutes, increments of 1 mg can be given every 3 minutes until the desired effect is achieved. Midazolam may cause respiratory depression. Elderly patients should be given half of the above recommended dosage. Midazolam can be used orally, rectally, intranasally, or intravenously in children. The recommended paediatric doses are as

Lorazepam (Ativan) is an intermediate-acting benzodiazepine which has no metabolites. It is useful in acute anxiety, acute phsychosis and status epilepticus. The maximum safe adult dosage is 4 mg and the minimum effective dose should be titrated to the individual patient's

Diazepam (Valium) is a long-acting benzodiazepine which is less potent than the previous two. It has active metabolites, and a sclerosing effect on veins. The intravenous dosage of 0.1

Sedative and hypnotic effects of these drugs are due to the action on α2-receptors in the locus ceruleus. Analgesic effect is maintened by an action on α2-receptors within the locus

Dexmedetomidine (Precedex) is a new selective α-2 adrenoreceptor agonist drug. It has both anxiolytic and analgesic properties. It does not cause respiratory depression, and patients maintain cognitive function and are easily rousable. The bradycardia and hypotension may be seen as side effects. There is no effect on ICP, but CPP may decrease by virtue of

Propofol and thiopentone are used for sedation and lowering ICP in traumatic brain injuried

Propofol is widely used in the ICU to sedate intubated neurolojic patients with increased ICP(94). Propofol has been shown to maintain or reduce ICP while maintaining an adequate

follows: intranasal 0.4 mg/kg, oral/rectal 0.5 mg/kg, intravenous 0.1 mg/kg.

mg/kg applies to both adults and children, and the rectal dosage is 0.5 mg/kg.

ceruleus and the spinal cord. These are dextmedetomidine and clonidine.

needs. The intravenous dose for children is 0.1 mg/kg.

output.

**Benzodiazepines** 

**α-2 receptors agonists** 

decreasing MAP.





**Anaesthetics** 

patients. Propofol

lorazepam and diazepam are mostly used.

Morphine, fentanyl and remifentanil can be used not only pain management but also sedation effect. Morphine and fentanyl are the two most commonly used opioids for the analgesia of critically ill patients(107,108). They are routinely used in patients with severe head injury as part of the management of increased intracranial pressure (ICP). However, the cerebrovascular effects of such drugs remain controversial. Studies in laboratory animals and humans have shown increases, decreases or no change in ICP after opioid administration(109-120). Most of these studies find a concomitant decrease in systemic arterial pressure and, recently, it has been suggested that reduced MAP could in fact be responsible for the increases in ICP observed after the administration of potent opioids such as sufentanil(107). In patients with low intracranial compliance and intact autoregulation, reduced MAP would be expected to result in vasodilation, increased blood volume, and thus increased ICP.

Remifentanil is a selective mu-opioid agonist with a context-sensitive half-time of 3 to 5 minutes, independent of dose or administration duration of. Its metabolism by nonspecific

Intensive Care Management of the Traumatic Brain Injury 27

According to American Thoracic Society (ATS) guidelines, nosocomial pneumonia (also known as hospital-acquired pneumonia or health care–associated pneumonia) is defined as pneumonia that occurs more than 48 hours after hospital admission but that was not

Ventilator-associated pneumonia (VAP) is becoming common nosocomial infection in hospitals with devolopment of intensive care units(129). VAP is defined as pneumonia that develops in 48 hours mechanicaly ventilated patients. The mechanism of VAP progresion is retrograde colonisation of the oropharynx caused by gastro-oesophageal reux and possibly also cross colonisation from contaminated hospital personnel or equipment. In addition many mechanically ventilated patients are immobile and cannot expand the distal airways with sighs, deep breaths, and coughs. The main pathogens of VAP are Pseudomonas aeruginosa, Enterobacteriaceae, and other Gram-negative bacilli, Streptococcus faecalis, Staphylococcus aureus, Candida sp, Aspergillus sp, and episodes of polymicrobial pneumonia etc. Mortality rates, morbidity, and costs are all increased in the patient with VAP because the treatment of it is difficult and expensive. Early-onset VAP has almost no risk for having multidrug-resistant (MDR) pathogens. Currently recommended initial empiric antibiotics include ceftriaxone, fluoroquinolones, ampicillin-sulbactam or ertapenem. Late-onset VAP has a risk of having MDR pathogens. Their initial antibiotherapy may consist antipseudomonal cephalosporins (eg, cefepime, ceftazidime), antipseudomonal carbapenems (imipenem or meropenem), beta-lactam/beta-lactamase inhibitors (piperacillin-tazobactam) with an antipseudomonal fluoroquinolone (ciprofloxacin) or aminoglycoside plus linezolid or vancomycin (if risk factors for methicillin-resistant Staphylococcus aureus are present). If infection with Legionella pneumophila is suspected, the regimen should include a macrolide or fluoroquinolone rather than an aminoglycoside. Early administration of appropriate antibiotic regimens and with adequate dosing of antibiotics improve outcomes after VAP. Antibiotics should be further adjusted on the basis of culture results. The first antibiotic regimen must be optimized, because inappropriate initial therapy is associated with worsened outcomes, even if the regimen is subsequently changed on the basis of the microbiologic results.

Aspiration pneumonia is usually caused by colonisation of aerobic bacteria from gastric and oesophageal flora because of repeated small volume aspiration during sleep, especially with impaired pharyngeal reex (130). It usually develops subclinically and fulminant aspiration syndrome is rare. There may be no symptoms before the development of transient hypoxaemia or inltrates on x-ray. Increasing pulmonary artery pressure because of hypoxaemic vasoconstriction and pulmonary oedema developing secondary to acid induced lung damage. Chest X-Ray usually shows right lower lobe inltration, atelectasis, and sometimes shows air bronchogram with bilateral, diffuse inltrates. Treatment must be

ARDS is a severe lung disease caused by a variety of directly and indirectly pertaining the lungs. It is characterized by inflammation of the lung paranchyme leading to impaired gas

planed on the base of antibiograme results of tracheal and blood culture.

**Nosocomial pneumonia** 

**Aspiration pneumonia** 

**Adult respiratory distress syndrome** 

incubating at the time of admission. **Ventilator-associated pneumonia** 

esterases results in rapid and uniform clearance leading to highly predictable onset and offset of action. Other desirable effects include decreased cerebral metabolism and decrease intracranial pressure (ICP) with minimal cerebral perfusion pressure changes .

#### **Neuromuscular blockade**

Neuromuscular blocking agents can facilitate mechanical ventilation and management of raised ICP, but their use should be reserved for specific indications. The depth and duration of neuromuscular blockade should be monitored and optimized, respectively. Although therapeutic paralysis may in a fall in ICP and prevents shivering if induced hypothermia is attempted. However, it may mask seizure activity, negates the physical exam potentially delaying early signs for deterioration, prolongs ventilation, and increases the risk for pressure ulcers and venothromboemboli (121). Deep sedation may be safer while providing similar benefits(122).

#### **Hypothermia**

Hyperthermia increases ICP and should be prevented. Moderate hypothermia can help to control critically elevated ICP values in severe space-occupying edema.

The basic mechanisms through which hypothermia protects the brain are clearly multifactorial and include at least the following: reduction in brain metabolic rate, effects on cerebral blood flow, reduction of the critical threshold for oxygen delivery, blockade of excitotoxic mechanisms, calcium antagonism, preservation of protein synthesis, reduction of brain thermopooling, a decrease in edema formation, modulation of the inflammatory response, neuroprotection of the white matter and modulation of apoptotic cell death (123).

Hypotermia have some risks include coagulopathy and electrolyte abnormalities. Shivering may occur, which will increase ICP(88,124).

**Glycemic control**; Hyperglycemia has an adverse effect on outcomes in neurointensive patients and should be aggressively treated(125).

**CSF drainage**: The role of CSF drainage is to reduce intracranial fluid volume and thereby lower ICP. Removal of CSF through an intraventricular catheter reduces ICP. Drainage should be continued to maintained the ICP between 5 mm Hg and 15 mm Hg(126,127).

**Craniectomy**: Although drastic, bone and potentially brain removal are extremely effective in reducing ICP. Craniectomy greatly facilitates ICP management and may improve outcomes and is recommended if other therapies are not effective (128).

#### **Intensive Care Unit Complications**

Intensive care unit complications are very various because the illnesses affecting the various organ systems and the interventions put in the practise on the patients as a means of getting health. The patients being in neurointensive care unit would be expected more diferent diversty complications.

#### **Pulmonary Complications**

Pulmonary complications like nasocomial pneumonia, ARDS progressed in mechanicaly ventilated patients, neurogenic pulmonary oedema, pulmonary embolism are discussed below.

#### **Nosocomial pneumonia**

26 Emergency Medicine – An International Perspective

esterases results in rapid and uniform clearance leading to highly predictable onset and offset of action. Other desirable effects include decreased cerebral metabolism and decrease

Neuromuscular blocking agents can facilitate mechanical ventilation and management of raised ICP, but their use should be reserved for specific indications. The depth and duration of neuromuscular blockade should be monitored and optimized, respectively. Although therapeutic paralysis may in a fall in ICP and prevents shivering if induced hypothermia is attempted. However, it may mask seizure activity, negates the physical exam potentially delaying early signs for deterioration, prolongs ventilation, and increases the risk for pressure ulcers and venothromboemboli (121). Deep sedation may be safer while providing

Hyperthermia increases ICP and should be prevented. Moderate hypothermia can help to

The basic mechanisms through which hypothermia protects the brain are clearly multifactorial and include at least the following: reduction in brain metabolic rate, effects on cerebral blood flow, reduction of the critical threshold for oxygen delivery, blockade of excitotoxic mechanisms, calcium antagonism, preservation of protein synthesis, reduction of brain thermopooling, a decrease in edema formation, modulation of the inflammatory response, neuroprotection of the white matter and modulation of apoptotic cell death (123).

Hypotermia have some risks include coagulopathy and electrolyte abnormalities. Shivering

**Glycemic control**; Hyperglycemia has an adverse effect on outcomes in neurointensive

**CSF drainage**: The role of CSF drainage is to reduce intracranial fluid volume and thereby lower ICP. Removal of CSF through an intraventricular catheter reduces ICP. Drainage

**Craniectomy**: Although drastic, bone and potentially brain removal are extremely effective in reducing ICP. Craniectomy greatly facilitates ICP management and may improve

Intensive care unit complications are very various because the illnesses affecting the various organ systems and the interventions put in the practise on the patients as a means of getting health. The patients being in neurointensive care unit would be expected more diferent

Pulmonary complications like nasocomial pneumonia, ARDS progressed in mechanicaly ventilated patients, neurogenic pulmonary oedema, pulmonary embolism are discussed

should be continued to maintained the ICP between 5 mm Hg and 15 mm Hg(126,127).

outcomes and is recommended if other therapies are not effective (128).

control critically elevated ICP values in severe space-occupying edema.

intracranial pressure (ICP) with minimal cerebral perfusion pressure changes .

**Neuromuscular blockade** 

similar benefits(122).

may occur, which will increase ICP(88,124).

**Intensive Care Unit Complications** 

diversty complications.

below.

**Pulmonary Complications** 

patients and should be aggressively treated(125).

**Hypothermia** 

According to American Thoracic Society (ATS) guidelines, nosocomial pneumonia (also known as hospital-acquired pneumonia or health care–associated pneumonia) is defined as pneumonia that occurs more than 48 hours after hospital admission but that was not incubating at the time of admission.

#### **Ventilator-associated pneumonia**

Ventilator-associated pneumonia (VAP) is becoming common nosocomial infection in hospitals with devolopment of intensive care units(129). VAP is defined as pneumonia that develops in 48 hours mechanicaly ventilated patients. The mechanism of VAP progresion is retrograde colonisation of the oropharynx caused by gastro-oesophageal reux and possibly also cross colonisation from contaminated hospital personnel or equipment. In addition many mechanically ventilated patients are immobile and cannot expand the distal airways with sighs, deep breaths, and coughs. The main pathogens of VAP are Pseudomonas aeruginosa, Enterobacteriaceae, and other Gram-negative bacilli, Streptococcus faecalis, Staphylococcus aureus, Candida sp, Aspergillus sp, and episodes of polymicrobial pneumonia etc. Mortality rates, morbidity, and costs are all increased in the patient with VAP because the treatment of it is difficult and expensive. Early-onset VAP has almost no risk for having multidrug-resistant (MDR) pathogens. Currently recommended initial empiric antibiotics include ceftriaxone, fluoroquinolones, ampicillin-sulbactam or ertapenem. Late-onset VAP has a risk of having MDR pathogens. Their initial antibiotherapy may consist antipseudomonal cephalosporins (eg, cefepime, ceftazidime), antipseudomonal carbapenems (imipenem or meropenem), beta-lactam/beta-lactamase inhibitors (piperacillin-tazobactam) with an antipseudomonal fluoroquinolone (ciprofloxacin) or aminoglycoside plus linezolid or vancomycin (if risk factors for methicillin-resistant Staphylococcus aureus are present). If infection with Legionella pneumophila is suspected, the regimen should include a macrolide or fluoroquinolone rather than an aminoglycoside. Early administration of appropriate antibiotic regimens and with adequate dosing of antibiotics improve outcomes after VAP. Antibiotics should be further adjusted on the basis of culture results. The first antibiotic regimen must be optimized, because inappropriate initial therapy is associated with worsened outcomes, even if the regimen is subsequently changed on the basis of the microbiologic results.

#### **Aspiration pneumonia**

Aspiration pneumonia is usually caused by colonisation of aerobic bacteria from gastric and oesophageal flora because of repeated small volume aspiration during sleep, especially with impaired pharyngeal reex (130). It usually develops subclinically and fulminant aspiration syndrome is rare. There may be no symptoms before the development of transient hypoxaemia or inltrates on x-ray. Increasing pulmonary artery pressure because of hypoxaemic vasoconstriction and pulmonary oedema developing secondary to acid induced lung damage. Chest X-Ray usually shows right lower lobe inltration, atelectasis, and sometimes shows air bronchogram with bilateral, diffuse inltrates. Treatment must be planed on the base of antibiograme results of tracheal and blood culture.

#### **Adult respiratory distress syndrome**

ARDS is a severe lung disease caused by a variety of directly and indirectly pertaining the lungs. It is characterized by inflammation of the lung paranchyme leading to impaired gas

Intensive Care Management of the Traumatic Brain Injury 29

pulmonary diseases. Because treatment of NPE is different. Pharmacological agents are not used routinely in the treatment of neurogenic pulmonary edema. Several agents, such as alpha-adrenergic antagonists, beta-adrenergic blockers, dobutamine, and chlorpromazine, are advocated by some authors, but assessment of their effectiveness is difficult because neurogenic pulmonary edema is usually a self-limited condition that resolves

Patients with neurological disease are susceptible to deep vein thrombosis (DVT) and pulmonary embolism (PE) particularly if they are immobilised or paralysied. PE and DVT are two clinical presentations of venous thromboembolism (VTE) and share the same predisposing factors. In most cases PE is a consequence of DVT. PE is a relatively common cardiovascular emergency and a difficult diagnosis that may be missed because of nonspecific clinical presentation(136). Smaller emboli may cause few haemodynamic effects or may result in infarction of a section of lung tissue if collateral blood ow is inadequate. Large and/or multiple emboli might abruptly increase pulmonary vascular resistance to a level of afterload which cannot be matched by the right ventricle (RV) and right heart failure identified acute cor pulmonale may develope. Sudden death may occur, usually in the form

The treatment of pulmonary embolism depends upon its size. Cardiopulmonary resuscitation may be necessary following a massive embolus with the patient in shock from acute cor pulmonale, justifying aggressive treatment with thrombolysis. Supportive treatment includes correcting hypoxaemia, intravenous uid replacement, inotropic drugs, and analgesia. Mechanical ventilation may be necessary if the patient cannot maintain adequate oxygenation. Anticoagulation is usually begun with unfractionated heparin, the dose being titrated against the activated partial thromboplastin time. In ischaemic stroke, dosage should not be adjusted to lower levels for fear of haemorrhagic conversion as an inadequate dose increases mortality from pulmonary emboli. Warfarin administration should begin 48 hours after the start of heparin and continue for six

Hypovolaemia often accompanies traumatic brain injury due to decreased intake and increased loss (vomiting, sweating). Fluid should be restricted to those who are in various grade of coma and central venous pressure can be measured to guide fluid therapy. Full maintenance of sodium should be given as hyponatraemia impairs cerebrovascular

The choice of uid replacement depends on a number of factors. If the patient is anaemic (haemoglobin < 8 g/dl), transfusion of red cells should be considered, especially if the patient has a history of ischaemic heart disease. If the patient's haemoglobin is above this value, blood volume may be increased by the use of colloids or crystalloid solutions. Colloids are expensive, carry the risk of anaphylaxis, and the absence of clotting factors may precipitate a coagulopathy. Generally, in neurointensive care practice, 0.9% sodium chloride solution is favoured over glucose or lactate containing solutions which have the potential to increase intracellular glucose concentrations and thus increase the risk of ischaemic damage.

reactivity and serum sodium level should be maintained above 140mmol/l.

spontaneously.

**Pulmonary embolism** 

months thereafter.

**Hypovolaemia** 

of electromechanical dissociation(137).

exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia and frequently resulting in multiple organ failure. This condition is often fatal, usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form of this fulminanat lung disease is called acut lung injury (ALI). Before thinking ARDS any cardiogenic cause of pulmonary edema should be excluded(131). ARDS is a form of non-cardiogenic pulmonary oedema characterised by reduced respiratory compliance and increased work of breathing and V/Qmismatch, leading to an increased shunt and hypoxaemia. The definition of ARDS is based on the table below.


Table 9. ARDS criteria.

ARDS may follow any major illness, sepsis or surgery but is common following aspiration or septicaemia. Multiorgan failure may occur and is a common cause of death. The treatment of ARDS consist of apropirate managment of ventilatory support. Ventilatory support is arraenged for adequate oxygenation with different strategies. As saying baby lung ventilation with low tidal volumes between 5 and 6 mL/kg or predicted body weight are used. The aim this is to save the healty lung reagions from excessively high inflation pressures. The management depends on the recruitment of collapsed alveoli with PEEP to correct the pronounced ventilation–perfusion mismatch and to prevent compression atalectasis. The peak inspiratory (plateau) pressure should be kept below 30-35 cm water, and as possible as eucapnia should be maintained to avoid further increases in intracranial pressure. High levels of PEEP may be required to treat severe hypoxemia. Caution is advised, however, because PEEP can inhibit cerebral venous return and increase intracranial hypertension.

#### **Neurogenic pulmonary oedema**

Neurogenic pulmonary edema (NPE) is defined as an increase in pulmonary interstitial and alveolar fluid (132-135)developing after an acute injury to the brain or brainstem in patients with intracranial pathology, including subarachnoid haemorrhage, cerebral emboli, cerebral tumours, status epilepticus, and raised intracranial pressure (ICP). The increased intracranial pressure is thought to precipitate an increased central sympathetic nerve activity transmitted via peripheral alpha and beta-adrenergic receptors. Neurogenic pulmonary edema results from a predominant alpha-receptor stimulation with a significant increase in the preload and afterload. The patient may present with excessive sweating, hypertension, tachypnoea, and frothy sputum. Chest X-Ray shows diffuse pulmonary inltrates, but the diagnosis depends on showing hypoxaemic respiratory failure with a normal pulmonary artery wedge pressure in the absence of a cardiac cause. Supplemental oxygen is required in most patients to correct hypoxemia. Mechanical Ventilation may be necessary, either noninvasive with a face mask or via an endotracheal tube. Neurogenic pulmonary oedema should be distinguished from aspiration pnomonia, ARDS, and other pulmonary diseases. Because treatment of NPE is different. Pharmacological agents are not used routinely in the treatment of neurogenic pulmonary edema. Several agents, such as alpha-adrenergic antagonists, beta-adrenergic blockers, dobutamine, and chlorpromazine, are advocated by some authors, but assessment of their effectiveness is difficult because neurogenic pulmonary edema is usually a self-limited condition that resolves spontaneously.

#### **Pulmonary embolism**

28 Emergency Medicine – An International Perspective

exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia and frequently resulting in multiple organ failure. This condition is often fatal, usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form of this fulminanat lung disease is called acut lung injury (ALI). Before thinking ARDS any cardiogenic cause of pulmonary edema should be excluded(131). ARDS is a form of non-cardiogenic pulmonary oedema characterised by reduced respiratory compliance and increased work of breathing and V/Qmismatch, leading to an increased

Pulmonary artery wedge pressure ≤18 mmHg or absence of clinical evidence of left

ARDS may follow any major illness, sepsis or surgery but is common following aspiration or septicaemia. Multiorgan failure may occur and is a common cause of death. The treatment of ARDS consist of apropirate managment of ventilatory support. Ventilatory support is arraenged for adequate oxygenation with different strategies. As saying baby lung ventilation with low tidal volumes between 5 and 6 mL/kg or predicted body weight are used. The aim this is to save the healty lung reagions from excessively high inflation pressures. The management depends on the recruitment of collapsed alveoli with PEEP to correct the pronounced ventilation–perfusion mismatch and to prevent compression atalectasis. The peak inspiratory (plateau) pressure should be kept below 30-35 cm water, and as possible as eucapnia should be maintained to avoid further increases in intracranial pressure. High levels of PEEP may be required to treat severe hypoxemia. Caution is advised, however, because PEEP can inhibit cerebral venous return and increase intracranial

Neurogenic pulmonary edema (NPE) is defined as an increase in pulmonary interstitial and alveolar fluid (132-135)developing after an acute injury to the brain or brainstem in patients with intracranial pathology, including subarachnoid haemorrhage, cerebral emboli, cerebral tumours, status epilepticus, and raised intracranial pressure (ICP). The increased intracranial pressure is thought to precipitate an increased central sympathetic nerve activity transmitted via peripheral alpha and beta-adrenergic receptors. Neurogenic pulmonary edema results from a predominant alpha-receptor stimulation with a significant increase in the preload and afterload. The patient may present with excessive sweating, hypertension, tachypnoea, and frothy sputum. Chest X-Ray shows diffuse pulmonary inltrates, but the diagnosis depends on showing hypoxaemic respiratory failure with a normal pulmonary artery wedge pressure in the absence of a cardiac cause. Supplemental oxygen is required in most patients to correct hypoxemia. Mechanical Ventilation may be necessary, either noninvasive with a face mask or via an endotracheal tube. Neurogenic pulmonary oedema should be distinguished from aspiration pnomonia, ARDS, and other

shunt and hypoxaemia. The definition of ARDS is based on the table below.

Acute respiratory distress syndrome is present if Pao2/Fio2 ratio ≤ 200

Acute lung injury (ALI) is present if Pao2/Fio2 ratio is≤ 300

Acute onset

atrial hypertension

Table 9. ARDS criteria.

hypertension.

**Neurogenic pulmonary oedema** 

Bilateral infiltrates on chest radiography

Patients with neurological disease are susceptible to deep vein thrombosis (DVT) and pulmonary embolism (PE) particularly if they are immobilised or paralysied. PE and DVT are two clinical presentations of venous thromboembolism (VTE) and share the same predisposing factors. In most cases PE is a consequence of DVT. PE is a relatively common cardiovascular emergency and a difficult diagnosis that may be missed because of nonspecific clinical presentation(136). Smaller emboli may cause few haemodynamic effects or may result in infarction of a section of lung tissue if collateral blood ow is inadequate. Large and/or multiple emboli might abruptly increase pulmonary vascular resistance to a level of afterload which cannot be matched by the right ventricle (RV) and right heart failure identified acute cor pulmonale may develope. Sudden death may occur, usually in the form of electromechanical dissociation(137).

The treatment of pulmonary embolism depends upon its size. Cardiopulmonary resuscitation may be necessary following a massive embolus with the patient in shock from acute cor pulmonale, justifying aggressive treatment with thrombolysis. Supportive treatment includes correcting hypoxaemia, intravenous uid replacement, inotropic drugs, and analgesia. Mechanical ventilation may be necessary if the patient cannot maintain adequate oxygenation. Anticoagulation is usually begun with unfractionated heparin, the dose being titrated against the activated partial thromboplastin time. In ischaemic stroke, dosage should not be adjusted to lower levels for fear of haemorrhagic conversion as an inadequate dose increases mortality from pulmonary emboli. Warfarin administration should begin 48 hours after the start of heparin and continue for six months thereafter.

#### **Hypovolaemia**

Hypovolaemia often accompanies traumatic brain injury due to decreased intake and increased loss (vomiting, sweating). Fluid should be restricted to those who are in various grade of coma and central venous pressure can be measured to guide fluid therapy. Full maintenance of sodium should be given as hyponatraemia impairs cerebrovascular reactivity and serum sodium level should be maintained above 140mmol/l.

The choice of uid replacement depends on a number of factors. If the patient is anaemic (haemoglobin < 8 g/dl), transfusion of red cells should be considered, especially if the patient has a history of ischaemic heart disease. If the patient's haemoglobin is above this value, blood volume may be increased by the use of colloids or crystalloid solutions. Colloids are expensive, carry the risk of anaphylaxis, and the absence of clotting factors may precipitate a coagulopathy. Generally, in neurointensive care practice, 0.9% sodium chloride solution is favoured over glucose or lactate containing solutions which have the potential to increase intracellular glucose concentrations and thus increase the risk of ischaemic damage.

Intensive Care Management of the Traumatic Brain Injury 31

Seizures are a common complication of traumatic brain injury, and can occur immediately following the injury, or may develop later.The risk of post-traumatic seizure is generally

Hypo/hypernatremia, hypo/hyperglycemia, hypocalcemia, hypomagnesemia, hyperosmolarity, hypoxia and uremia can also lead to seizures. Many antibiotics often used in co-existant infections such as quinolones, third or fourth generation cephalosporins and

Subclinical seizures or status epilepticus were associated with episodic clinically relevant increases in ICP. Often, subclinical status epilepticus is neither diagnosed nor treated in the ICU, and may be a target in neurointensive care for improving patient outcomes. Use of

As a complication of infection(150-154)seizure may seen only one single attact or may become a chronic epilepsy. Seizures may arise as an acute, subacute, or long- term consequence of an

The patients with fever and having alteration in sensory status may be associated with focal neurological signs and seizures. Febrile seizures occur with a prodromal fever. A simple febrile seizure occurs as a brief generalized tonic clonic seizure occurring after the onset of fever. A complicated febrile seizure is occure with prolonged seizure activity or focal seizure

The use of antiepileptic drugs to arrest the seizures and other general measures including the use of antibiotic and antiviral drugs, electrolyte and fluid management, blood pressure monitoring, respiratory monitoring and other aspects of intensive care are equally

The clinician should rst search for underlying etiologies producing the seizures and treat it (hypoglycemia, hypocalcemia, sepsis). There are many different types of seizure medication used to treat many different types of seizures(155). Examples of first -line medications are carbamazepine (Tegregol, Carbatrol), valproate (Depakote), phenytoin (Dilantin) and ethosuximide (Zarontin). Additional medications known as add-on medications or second-

**Seizures** 

infectious state.

activity.

important. .

**Management and goals of seizures** 





Treatment of a patients with seizures requires:


Following protocols for management is vital.



The initial treatment is directed towards:

related to the severity of the injury.

meropenem may presipitate or aggrevate seizures.

continuous EEG monitoring represents an important research priority.

#### **Hypo/Hypertension(138-149)**

For ensuring adequate organ perfusion, monitoring and maintenance of arterial blood pressure and blood volume in normal limits are essential. Arterial catheterization is indicated in ICU setting when abnormal blood pressure threatens to compromise blood flow to the brain, exacerbate high intracranial pressure. During hypotension, arterial and jugular venous oxygen contents significant decrease. Also hypotension causes inadequate blood flow to the brain, especially if intracranial pressure is already elevated. CVP monitoring, pulmonary pulmonary artery catheterisation and devices using Doppler principles are used to help untangle the explanation of hypotension and allow appropriate treatment.

Hypertension cause elevation of intracranial pressure and/or increase bleeding into the brain and surrounding compartments. Hypertension is a common sequelae of acute neurological events. When cerebral autoregulation is disturbed or its limits are exceeded, blood flow passively increases with increasing blood pressure. This in turn can increase intracranial pressure or cause breakdown of the blood–brain barrier with resultant transudation of intravascular fluid. Acute hypertension may also increase morbidity and mortality by exacerbating cerebral edema, raising intracranial pressure and bleeding. Treatment of hypertension requires carefull consideration. Causes of hypertension pertaning with acute neurological events are summerised at the below.

#### **Causes of hypertension**

Neurological disorders

	- Brain tumours
	- Encephalitis/encephalomyelitis
	- Respiratory acidosis
	- Psychogenic hyperventilation
	- After resuscitation
	- Hypoglycaemia
	- Hypoksemia
	- Ephedrine
	- Phenylephrine
	- Pseudoephedrine
	- β-agonist bronchodilators
	- Glucocorticoids

On the other hand patients with raised ICP require an elevated MAP to maintain an adequate cerebral perfusion pressure, and any fall in cerebral blood ow may lead to global ischaemia. So treatment of hypertension must be planed according the situation of brain. Pharmacotherapy used to treat acute situation may have undesirable effects on cerebral perfusion pressure (CPP). Intravenous labetalol, hydralazine, and sodium nitroprusside are commonly used drugs. Longer term treatment includes oral β adrenergic receptor antagonists, angiotensin converting enzyme inhibitors, and calcium channel antagonists. Treatments are indicated if the mean arterial blood pressure is higher than 130 mm Hg or cerebral perfusion pressure is higher than 85 mm Hg.

#### **Seizures**

30 Emergency Medicine – An International Perspective

For ensuring adequate organ perfusion, monitoring and maintenance of arterial blood pressure and blood volume in normal limits are essential. Arterial catheterization is indicated in ICU setting when abnormal blood pressure threatens to compromise blood flow to the brain, exacerbate high intracranial pressure. During hypotension, arterial and jugular venous oxygen contents significant decrease. Also hypotension causes inadequate blood flow to the brain, especially if intracranial pressure is already elevated. CVP monitoring, pulmonary pulmonary artery catheterisation and devices using Doppler principles are used

Hypertension cause elevation of intracranial pressure and/or increase bleeding into the brain and surrounding compartments. Hypertension is a common sequelae of acute neurological events. When cerebral autoregulation is disturbed or its limits are exceeded, blood flow passively increases with increasing blood pressure. This in turn can increase intracranial pressure or cause breakdown of the blood–brain barrier with resultant transudation of intravascular fluid. Acute hypertension may also increase morbidity and mortality by exacerbating cerebral edema, raising intracranial pressure and bleeding. Treatment of hypertension requires carefull consideration. Causes of hypertension

On the other hand patients with raised ICP require an elevated MAP to maintain an adequate cerebral perfusion pressure, and any fall in cerebral blood ow may lead to global ischaemia. So treatment of hypertension must be planed according the situation of brain. Pharmacotherapy used to treat acute situation may have undesirable effects on cerebral perfusion pressure (CPP). Intravenous labetalol, hydralazine, and sodium nitroprusside are commonly used drugs. Longer term treatment includes oral β adrenergic receptor antagonists, angiotensin converting enzyme inhibitors, and calcium channel antagonists. Treatments are indicated if the mean arterial blood pressure is higher than 130 mm Hg or

to help untangle the explanation of hypotension and allow appropriate treatment.

pertaning with acute neurological events are summerised at the below.

**Hypo/Hypertension(138-149)**

**Causes of hypertension**  Neurological disorders

Acute stress,

 Increased intracranial pressure Brain tumours

Respiratory acidosis

 After resuscitation Hypoglycaemia Hypoksemia

Vasoconstrictors/Medications

β-agonist bronchodilators

cerebral perfusion pressure is higher than 85 mm Hg.

 Ephedrine Phenylephrine Pseudoephedrine

Glucocorticoids

Encephalitis/encephalomyelitis

Psychogenic hyperventilation

Seizures are a common complication of traumatic brain injury, and can occur immediately following the injury, or may develop later.The risk of post-traumatic seizure is generally related to the severity of the injury.

Hypo/hypernatremia, hypo/hyperglycemia, hypocalcemia, hypomagnesemia, hyperosmolarity, hypoxia and uremia can also lead to seizures. Many antibiotics often used in co-existant infections such as quinolones, third or fourth generation cephalosporins and meropenem may presipitate or aggrevate seizures.

Subclinical seizures or status epilepticus were associated with episodic clinically relevant increases in ICP. Often, subclinical status epilepticus is neither diagnosed nor treated in the ICU, and may be a target in neurointensive care for improving patient outcomes. Use of continuous EEG monitoring represents an important research priority.

As a complication of infection(150-154)seizure may seen only one single attact or may become a chronic epilepsy. Seizures may arise as an acute, subacute, or long- term consequence of an infectious state.

The patients with fever and having alteration in sensory status may be associated with focal neurological signs and seizures. Febrile seizures occur with a prodromal fever. A simple febrile seizure occurs as a brief generalized tonic clonic seizure occurring after the onset of fever. A complicated febrile seizure is occure with prolonged seizure activity or focal seizure activity.

The use of antiepileptic drugs to arrest the seizures and other general measures including the use of antibiotic and antiviral drugs, electrolyte and fluid management, blood pressure monitoring, respiratory monitoring and other aspects of intensive care are equally important. .

#### **Management and goals of seizures**

Treatment of a patients with seizures requires:


Following protocols for management is vital.

The initial treatment is directed towards:


The clinician should rst search for underlying etiologies producing the seizures and treat it (hypoglycemia, hypocalcemia, sepsis). There are many different types of seizure medication used to treat many different types of seizures(155). Examples of first -line medications are carbamazepine (Tegregol, Carbatrol), valproate (Depakote), phenytoin (Dilantin) and ethosuximide (Zarontin). Additional medications known as add-on medications or second-

Intensive Care Management of the Traumatic Brain Injury 33

Traumatic Brain İnjury can be fatal if it is not diagnosed and treated promptly; even with treatment, some patients have CNS damage and serious permanent neurologic problems at

The critical-care nurse must be alert with the potential problems encountering the brain-

Managing a patient with TBI requires a well-defined plan, plenty of resources, and an organized team to prevent secondary injuries. Nursing interventions for TBI are performing frequent vital signs and neurologic assessments for signs of disease progression, such as decreased level of consciousness and assessing mental status, muscle strength, headache severity, and pupillary reactions. An important nursing care for TBI is raising the head of the bed 30 degrees, these intervention promote cerebral venous drainage and to prevent increased ICP. Routine caring like maintaining a patent airway, suctioning the patient as needed and positioning him to encourage drainage of oral and nasal secretions is also essential. Monitorizing oxygenation, administering supplemental oxygen if indicated and monitorizing arterial blood gas analysis results is needed for planing of treatment. Reducing stimuli around the patient, and avoiding Valsalva maneuver, i.e., coughing, sneezing and straining during bowel movements are important intervention in progression of TBI . Keeping the patient's room quiet and darkened can make more comfortable and reduce agitation. An indwelling urinary catheter for accurate intake and output monitoring should

Patients with TBI frequently have hyperthermia, or fever. Nursing interventions includes reducing fever, not only for a patient's discomfort, but because fever causes increase in intracranial pressure. Nursing care plans that for reducing hyperthermia in TBI patients should include monitoring body temperature every four hours, administering antipyretics and cooling baths as ordered by the physician, and monitoring the patient for signs of dehydration. TBI can cause severe headaches and nursing interventions must be planed as completly pain-free. Positioning (if it is not contraindicated by ICP) and administering mild analgesics to combat discomfort are that can be doing for pain management. It may be helpful to cover the patient's eyes with a cool cloth because this will reduce unnecessary

 Many patients may need mechanical ventilation and endotracheal tube/suctioning can increase ICP so that the use of lidocaine IV %2 1.5 – 2 mg/kg iv prior to endotracheal

Traumatic brain injury is a serious public health problem all over the world. Each year, traumatic brain injuries contribute to a substantial number of deaths and cases of permanent disability. Management of TBI in intensive care is very difficult. Management is becoming more difficult when the pulmonary complications and organ dysfunctions added. Disease spesific applications are needed in treatment of mechanical ventilation. The aim of mechanic ventilation is to maintain adaquate oxgenation and ventilation without increasing ICP. Nurition strategy in these patients must be planned to support immune system without

injured patient, who has the risk of sudden deterioration at any time.

**Intensive Care Nursing** 

the end of disease.

be performed.

stimuli and photophobia.

**3. Conclusions** 

loading CO2.

suctioning to attenuate the ICP response.

line therapy may be required in addition to first -line medications. Examples of second-line seizure drugs include gababentin (Neurontin), lamotrigine (Lamictal) and topiramate (Topamax). Loss of cerebral autoregulation and neuronal damage begin after 30 minutes of continuous seizure activity. Lorazepam is better than diazepam or phenytoin alone for cessation of seizures and carries a lower risk of continuation of status epilepticus requiring a different drug or general anaesthesia.

#### **Fever (156-162)**

Fever is among the most frequently detected abnormal physical signs in critically ill patients and may arise due to infectious or noninfectious etiologies. Fever is a complex adaptive response involving elaborate interactions between the immune and nervous systems. High temperatures inhibit growth of microorganisms, may reduce the expression of virulence factors, increase susceptibility to anti-microbials and enhance host immune responses. At the same time fever can worsen primary brain damage. Because increase in cerebral oxygen consumption may leads to increase in blood flow and accordingly in blood volume. This increase potentiates neurologic injury and causes brain edema. Fever is deleterious in patient with low cerebral compliance and generate dangerous intracranial pressure rises accelerating the terminal stages of fulminant infections (through cytokine-induced tissue injury).

Non-infectious causes of fever are common in the ICU. Transfusion reactions and drug hypersensitivity, in particular to anti-microbial agents, are frequent causes. Deep vein thrombosis, pulmonary embolus/infarct, myocardial infarction and acute haemorrhage may also cause fever. Neurogenic fever usually is caused by damage to the hypothalamus from CNS trauma, intracerebral bleeding, or an increase in intracranial pressure. Neurogenic fevers are characterized by a high temperature that's resistant to antipyretic therapy and isn't associated with sweating.

Fever treatment methods may include direct cooling and anti-pyretic medications such as acetylsalicylic acid, non-steroidal anti-inflammatory agents and acetaminophen. An alternative method for temperature management may be an intravascular approach.

Direct cooling is done by many methods for example reducing the ambient room temperature, application of cool external substances such as mist, ice packs, wet sponges and cooling blankets, and administration of cooled intravenous fluids(161,162). A number of newer techniques have evolved including cooling jackets and intravascular catheter-based heat exchange systems. Convective cooling (ie, blowing cold air) is thought to be more effective than cooling blanket for decreasing body temperature and is also thought to be more comfortable for patients. Administration of ice cold intravenous fluid also directly cools core tissues and has been used for his purpose in physiologic studies. The method is obviously restricted by the volume that can be administered without overloaing the cardiovascular system.

Aggressive fever treatment strategy ; Acetaminophen ( Adults 0.5-1 gm, every 4-6 hours upto a maximum of 4 gms. Children 10 mg/kg, every 4-6 hours) for fever >38.5°C and a cooling blanket added if >39.5°C) .Routes of Administration Oral, Parenteral (I.M.). Never IV use with great caution in patients with hepatic dysfunction and in alcoholics.

#### **Intensive Care Nursing**

32 Emergency Medicine – An International Perspective

line therapy may be required in addition to first -line medications. Examples of second-line seizure drugs include gababentin (Neurontin), lamotrigine (Lamictal) and topiramate (Topamax). Loss of cerebral autoregulation and neuronal damage begin after 30 minutes of continuous seizure activity. Lorazepam is better than diazepam or phenytoin alone for cessation of seizures and carries a lower risk of continuation of status epilepticus requiring a

Fever is among the most frequently detected abnormal physical signs in critically ill patients and may arise due to infectious or noninfectious etiologies. Fever is a complex adaptive response involving elaborate interactions between the immune and nervous systems. High temperatures inhibit growth of microorganisms, may reduce the expression of virulence factors, increase susceptibility to anti-microbials and enhance host immune responses. At the same time fever can worsen primary brain damage. Because increase in cerebral oxygen consumption may leads to increase in blood flow and accordingly in blood volume. This increase potentiates neurologic injury and causes brain edema. Fever is deleterious in patient with low cerebral compliance and generate dangerous intracranial pressure rises accelerating the terminal stages of fulminant infections (through cytokine-induced tissue

Non-infectious causes of fever are common in the ICU. Transfusion reactions and drug hypersensitivity, in particular to anti-microbial agents, are frequent causes. Deep vein thrombosis, pulmonary embolus/infarct, myocardial infarction and acute haemorrhage may also cause fever. Neurogenic fever usually is caused by damage to the hypothalamus from CNS trauma, intracerebral bleeding, or an increase in intracranial pressure. Neurogenic fevers are characterized by a high temperature that's resistant to antipyretic therapy and

Fever treatment methods may include direct cooling and anti-pyretic medications such as acetylsalicylic acid, non-steroidal anti-inflammatory agents and acetaminophen. An

Direct cooling is done by many methods for example reducing the ambient room temperature, application of cool external substances such as mist, ice packs, wet sponges and cooling blankets, and administration of cooled intravenous fluids(161,162). A number of newer techniques have evolved including cooling jackets and intravascular catheter-based heat exchange systems. Convective cooling (ie, blowing cold air) is thought to be more effective than cooling blanket for decreasing body temperature and is also thought to be more comfortable for patients. Administration of ice cold intravenous fluid also directly cools core tissues and has been used for his purpose in physiologic studies. The method is obviously restricted by the volume that can be administered without overloaing the

Aggressive fever treatment strategy ; Acetaminophen ( Adults 0.5-1 gm, every 4-6 hours upto a maximum of 4 gms. Children 10 mg/kg, every 4-6 hours) for fever >38.5°C and a cooling blanket added if >39.5°C) .Routes of Administration Oral, Parenteral (I.M.). Never

IV use with great caution in patients with hepatic dysfunction and in alcoholics.

alternative method for temperature management may be an intravascular approach.

different drug or general anaesthesia.

isn't associated with sweating.

cardiovascular system.

**Fever (156-162)**

injury).

Traumatic Brain İnjury can be fatal if it is not diagnosed and treated promptly; even with treatment, some patients have CNS damage and serious permanent neurologic problems at the end of disease.

The critical-care nurse must be alert with the potential problems encountering the braininjured patient, who has the risk of sudden deterioration at any time.

Managing a patient with TBI requires a well-defined plan, plenty of resources, and an organized team to prevent secondary injuries. Nursing interventions for TBI are performing frequent vital signs and neurologic assessments for signs of disease progression, such as decreased level of consciousness and assessing mental status, muscle strength, headache severity, and pupillary reactions. An important nursing care for TBI is raising the head of the bed 30 degrees, these intervention promote cerebral venous drainage and to prevent increased ICP. Routine caring like maintaining a patent airway, suctioning the patient as needed and positioning him to encourage drainage of oral and nasal secretions is also essential. Monitorizing oxygenation, administering supplemental oxygen if indicated and monitorizing arterial blood gas analysis results is needed for planing of treatment. Reducing stimuli around the patient, and avoiding Valsalva maneuver, i.e., coughing, sneezing and straining during bowel movements are important intervention in progression of TBI . Keeping the patient's room quiet and darkened can make more comfortable and reduce agitation. An indwelling urinary catheter for accurate intake and output monitoring should be performed.

Patients with TBI frequently have hyperthermia, or fever. Nursing interventions includes reducing fever, not only for a patient's discomfort, but because fever causes increase in intracranial pressure. Nursing care plans that for reducing hyperthermia in TBI patients should include monitoring body temperature every four hours, administering antipyretics and cooling baths as ordered by the physician, and monitoring the patient for signs of dehydration. TBI can cause severe headaches and nursing interventions must be planed as completly pain-free. Positioning (if it is not contraindicated by ICP) and administering mild analgesics to combat discomfort are that can be doing for pain management. It may be helpful to cover the patient's eyes with a cool cloth because this will reduce unnecessary stimuli and photophobia.

 Many patients may need mechanical ventilation and endotracheal tube/suctioning can increase ICP so that the use of lidocaine IV %2 1.5 – 2 mg/kg iv prior to endotracheal suctioning to attenuate the ICP response.

#### **3. Conclusions**

Traumatic brain injury is a serious public health problem all over the world. Each year, traumatic brain injuries contribute to a substantial number of deaths and cases of permanent disability. Management of TBI in intensive care is very difficult. Management is becoming more difficult when the pulmonary complications and organ dysfunctions added. Disease spesific applications are needed in treatment of mechanical ventilation. The aim of mechanic ventilation is to maintain adaquate oxgenation and ventilation without increasing ICP. Nurition strategy in these patients must be planned to support immune system without loading CO2.

Intensive Care Management of the Traumatic Brain Injury 35

[14] Lee SW, Hong YS, Han C, et al. Concordance of end-tidal carbon dioxide and arterial

[15] Pelosi P, Brazzi L and Gattinoni L. Prone position in acute respiratory distress

[16] Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of

[17] Reinprecht A, Greher M, Wolfsberger S, et al. Prone position in subarachnoid

[18] Lo TM, Jones PA, Freeman JA, McFazcan and Minns RA. The role of high frequency

[19] Salim A, Miller K, Dangleben D, Cipolle M and Pasquale M. High-frequency

[21] Reng M, Philipp A, Kaiser M, Pfeifer M, Gruene S, Schoelmerich J. Pumpless

[22] Ngubane T. Mechanical ventilation and the injured brain. South Afr J Anaesth Analg.

[23] Feeley TW, Saumarez R, Klick JM, McNabb TG, Skillman JJ. Positive end-expiratory

[24] Ely EW, Baker AM, Dunagan DP, et al. Effect on the duration of mechanical ventilation

[25] Kollef MH, Shapiro SD, Silver P, et al. A randomized,controlled trial of protocol-

[26] Esteban A, Anzueto A, Frutos F, et al. Mechanical Ventilation International Study

[28] Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning

[29] Vallverdu I, Calaf N, Subirana M, Net A, Benito S, Mancebo J. Clinical characteristics,

ventilation: a 28-day international study. JAMA 2002; 287:345–355.

[27] Tobin MJ. Mechanical ventilation. N Engl J Med 1994; 330:1056–1061

injury.Journal of Trauma. 2005 ; 58(6):124-127.

randomised trial. Lancet 1975; 2: 725–729.

syndrome. European Respiratory Journal. 2002; 20(4):1017-1028.

530.

345(8):568-573.

31(6):1831-1838.

2000;356:219–220.

2011;17(1) 76-80.

1864–1869.

Med 1997; 25: 567–574.

Engl J Med 1995; 332: 345–350.

158: 1855–1862.

9(5): 38-42.

carbon dioxide in severe traumatic brain injury. Journal of Trauma. 2009; 67(3):526-

patients with acute respiratory failure. New England Journal of Medicine. 2001;

haemorrhage patients with acute respiratory distress syndrome: effects on cerebral tissue oxygenation and intracranial pressure. Critical Care Medicine. 2003;

oscillatory ventilation in the management of children with severe traumatic brain injury and concomitant lung pathology. Paediatric Critical Care Medicine. 2008;

percussive ventilation: an alternative mode of ventilation for head-injured patients with adult respiratory distress syndrome. Journal of Trauma. 2004; 57:542-546. [20] Bein T, Scherer MN, Philipp A, Weber F and Woertgen C. Pumpless extracorporeal

lung assist in patients with acute respiratory distress syndrome and severe brain

extracorporeal lung assist and adult respiratory distress syndrome. Lancet.

pressure in weaning patients from controlled ventilation. A prospective

of identifying patients capable of breathing spontaneously. N Engl J Med 1996;335:

directed versus physician-directed weaning from mechanical ventilation. Crit Care

Group. Characteristics and outcomes in adult patients receiving mechanical

patients from mechanical ventilation. Spanish Lung Failure Collaborative Group. N

respiratory functional parameters, and outcome of a two-hour T-piece trial inpatients weaning from mechanical ventilation. Am J Respir Crit Care Med 1998;

In conclusion, with the proper support therapy and close management, the mortality and morbidity of TBI patients can be decreased.

#### **4. Abbreviations**

TBI: traumatic brain injury; PaO2: arterial partial pressure of oxygen; PEEP: positive endexpiratory pressure; PbtO2; brain tissue oxygenation, VILI: ventilator-induced lung injury; ICP:intracranial pressure; CBP:cerebral blood flow; CPP: cerebral perfusion pressure; MAP: mean arterial pressure; GCS; Glascow coma scale; PECLA:Pumpless extracorporeal lung asist; VAP:Ventilatory Associated Pneumonia; ITP: intrathoracic pressure; IV:intravenous; ALI:Acute lung injury; ARDS: Acute respiratory distress syndrome; PaO2 : partial pressure of arterial oxygen; FiO2:percentage of inspired oxygen; SBI: secondary brain injury; CMRO2: cerebral metabolic rate of oxygen consumption; PbtO2:brain tissue oxygenation; TPN: Total parenteral nutrition; EN:Enteral nutrition, PN: Parenteral nutrition , MDR:multidrugresistant , DVT: Deep vein thrombosis, PE: Pulmonary embolism

#### **5. References**


In conclusion, with the proper support therapy and close management, the mortality and

TBI: traumatic brain injury; PaO2: arterial partial pressure of oxygen; PEEP: positive endexpiratory pressure; PbtO2; brain tissue oxygenation, VILI: ventilator-induced lung injury; ICP:intracranial pressure; CBP:cerebral blood flow; CPP: cerebral perfusion pressure; MAP: mean arterial pressure; GCS; Glascow coma scale; PECLA:Pumpless extracorporeal lung asist; VAP:Ventilatory Associated Pneumonia; ITP: intrathoracic pressure; IV:intravenous; ALI:Acute lung injury; ARDS: Acute respiratory distress syndrome; PaO2 : partial pressure of arterial oxygen; FiO2:percentage of inspired oxygen; SBI: secondary brain injury; CMRO2: cerebral metabolic rate of oxygen consumption; PbtO2:brain tissue oxygenation; TPN: Total parenteral nutrition; EN:Enteral nutrition, PN: Parenteral nutrition , MDR:multidrug-

[1] Pelosi P, Severgnini P and Chiaranda M. An integrated approach to prevent and treat

[2] Refresher Course: Mechanical ventilation and the injured brain. South Afr J Anaesth

[3] Stevens RD, Lazaridis C and Chalela JA. The role of mechanical ventilation in acute

[4] Mascia L. Acute Lung Injury in Patients with Severe Brain Injury: A Double Hit Model.

[5] Nyquist P, Stevens RD and Mirski MA. Neurologic injury and mechanical ventilation.

[6] Bratton SL, Chestnut RM, Ghajar J, et al. Hyperventilation. Journal of Neurotrauma.

[7] Lapinsky SE, Posadas-Colleja JG and McCullagh I. Clinical review: ventilatory strategies for obstetric, brain-injured and obese patients. Critical Care. 2009; 13(2):206-213. [8] Bratton SL and Davis RL. Acute lung injury in isolated traumatic brain injury.

[9] Ricard JD, Dreyfuss D, Saumon G. Ventilator-induced lung injury.Current Opinion in

[10] Huyn T, Messer M, Sing RF, Miles W, Jacobs DG, Thomason MH. Positive end-

[11] Davis DP. Early ventilation in traumatic brain injury. Resuscitation. 2008; 76:333-340. [12] Gelb AW and Chan MTV. Hyperventilation -an ill wind that sometimes blows good.

[13] Warner KJ, Cuschieri J, Copass MK, Jurkovich GJ and Bulger EM. Emergency

traumatic brain injury. The Journal of Trauma. 2002;53:488–493.

Canadian Journal of Anaesthesia. 2008; 55(11):735-738.

expiratory pressure alters intracranial and cerebral perfusion pressure in severe

department ventilation effects outcome in severe traumatic brain injury. Journal of

respiratory failure in brain injured patients. Current Opinion in Critical Care. 2005;

morbidity of TBI patients can be decreased.

resistant , DVT: Deep vein thrombosis, PE: Pulmonary embolism

brain injury. Neurologic Clinics. 2008; 26:543-563.

**4. Abbreviations** 

**5. References** 

11:37-42.

Analg 2011;17(1): 76-80

2007; 24 (1):87-90.

Neurocrit Care. 2009; 11:3, 417-426

Neurocritical Care. 2008; 9:400-408.

Neurosurgery. 1997; 40:707-712.

Critical Care. 2002;8:12–20.

Trauma. 2008; 64(2):341-347.


Intensive Care Management of the Traumatic Brain Injury 37

[49] Ostermann ME, Keenan SP, Seiferling RA, et al.: Sedation in the intensive care unit: a

[50] Mirski MA, Muffelman B, Ulatowski JA, et al.: Sedation for the critically ill neurologic

[51] Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation-Sedation Scale:

[52] Riker RR, Picard JT, Fraser GL. Prospective evaluation of the Sedation-Agitation Scale

[53] Ely EW, Truman B, Shintani A, et al. Monitoring sedation status over time in ICU

[54] Simmons LE, Riker RR, Prato BS, et al. Assessing sedation during intensive care unit

[55] Devlin JW, Boleski G, Miynarek M, et al. Motor activity assessment scale: a valid and

[56] Lemos de.J , Tweeddale M, Chittock D. Measuring quality of sedation in adult

[57] Detriche O, Berre J, Massaut J, et al. The Brussels sedation scale: use of a simple clinical

[59] Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines for the sustained use

[60] Oertel M, Kelly DF, Lee JH, et al.: Metabolic suppressive therapy as a treatment for

[61] Robertson CS, Cormio M: Cerebral metabolic management. New Horiz. 1995, 3:410–

[62] Clausen T, Bullock R: Medical treatment and neuroprotection in traumatic brain injury.

[63] Grasshoff C, Gillessen T: The effect of propofol on increased superoxide concentration

[64] Starbuck VN, Kay GG, Platenberg RC, et al.: Functional magnetic resonance imaging

[65] Hanley DF, Pozo M: Treatment of status epilepticus with midazolam in the critical care

[66] Magarey JM: Propofol or midazolam–which is best for the sedation of adult ventilated

[67] Cremer OL, Moons KG, Bouman EA, et al.: Long-term propofol infusion and cardiac

failure in adult head-injured patients. Lancet 2001, 357:117–118

ventilation in the intensive care unit. Br J Anaesth 1999; 83:698-701 [58] Ramsay MA, Savege TM, Simpson BR, et al. Controlled sedation with alphaxalone-

for adult critically ill patients. Crit Care Med 1999; 27:1325-29

surgical intensive care unit. Crit Care Med 1999; 27:1271-1275

Calmness Scale. J Clin Epidemiol 2000; 53:908-919

alphadolone. Br Med J 1974; 2:656-659

Curr Pharm Des 2001, 7:1517–1532.

receptors. Anesth Analg 2002, 95:920–922.

setting. Int J Clin Pract 2000, 54:30–35.

2002, 81:69–70.

15:613–618.

154.

422.

validity and reliability in adult intensive care unit patients. Am J Respir Crit Care

patients-reliability and validity of the Richmond Agitation-Sedation Scale (RASS).

mechanical ventilation with Bispectral Index and the Sedation-Agitation Scale. Crit

reliable sedation scale for use with mechanically ventilated patients in an adult

mechanically ventilated critically ill patients: the Vancouver Interaction and

sedation scale can avoid excessive sedation in patients undergoing mechanical

of sedatives and analgesics in the critically ill adult. Crit Care Med 2002; 30:119-141

intracranial hypertension—why it works and when it fails. Acta Neurochir Suppl

in cultured rat cerebrocortical neurons after stimulationof N-methyl-D-aspartate

reflects changes in brain functioning with sedation. Hum Psychopharmacol 2000,

patients in intensive care units? A systematic review. Aust.CritCare 2001, 14:147–

systematic review. JAMA 2000, 283:1451–1459.

patient. Crit Care Med 1995, 23:2038–2053.

Med 2002; 166:1338-1344

JAMA 2003; 289:2983-91.

Care Med 1999; 27:1499-1504


[30] Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual

[31] Scales DC, Thiruchelvam D, Kiss A and Redelmeier DA. The effect of tracheostomy

[32] Combes A, Luyt CE, Nieszkowska A, Trouillet JL, Gibert C and Chastre J. Is

[34] Ostermann ME, Keenan AP, Seiferling RA, Sibbald WJ. Sedation in the intensive care

[35] Rotondi AJ, Chelluri L, Sirio C, et al. Patients' recollections of stressful experiences

[36] Soltész S, Biedler A, Silomon M, Schöpflin I, Molter GP. Recovery after remifentanil

[37] Park G. Improving sedation and analgesia in the critically ill. Minerva Anestesiol 2002;

[38] Muellejans B, Lopez A, Cross MH, et al. Remifentanil versus fentanyl for analgesia

[39] Schelling G, Richter M, Roozendaal B, et al. Exposure to high stress in the intensive

[40] Devlin JW, Fraser GL, Kanji S, Riker RR. Sedation assessment in critically ill adults.

[41] Akçabay M. Yoğun bakm ünitesinde sedasyon ağr kontrolü ve paralitik ilaç kontrolü.

[42] Baillaard C, Cohen Y, Toumelin PL, et al. Remifentanil-Midazolam compared to

[43] Cohen IL, Abraham E, Dasta JF, et al.: Management of the agitated intensive care unit

[44] Blanchard AR: Sedation and analgesia in intensive care. Medications attenuate stress response in critical illness. PostgradMed 2002, 111:59–60, 63–4,67–70 passim. [45] Gemma M, Tommasino C, Cerri M, et al.: Intracranial effects of endotracheal

[46] Hurford WE: Sedation and paralysis during mechanical ventilation. RespirCare 2002,

[47] Gehlbach BK, Kress JP: Sedation in the intensive care unit. Curr Opin Crit Care 2002,

[48] Kress JP, Pohlman AS, Hall JB: Sedation and analgesia in the intensive care unit. Am J

trauma or major surgery. Brit J Anaesth 2001; 86:763-768.

double blind controlled trial. Crit Care 2004; 8(1) 1-11.

cardiac surgery. Crit Care Med 2003; 31:1071-1079.

Ann Pharmacother 2001; 35:1624-1632.

Yoğun Bakm Dergisi 2002; 2:151-161.

´sie et de Re ´animation 2005; 24: 480–486.

patient. Crit Care Med 2002, 30:116–117.

Respir Crit Care Med 2002, 166:1024–1028.

mechanical ventilation? Critical Care Medicine. 2007; 35(3): 802-807. [33] Clec'h C, Alberti C, Vincent F, et al. Tracheostomy does not improve the outcome of

Am J Respir Crit Care Med 1994; 150: 896–903.

Critical Care Medicine. 2007; 35(1):132-138.

unit. JAMA 2000; 283:1451-1459.

Care Med 2002; 30:746-752.

68:505-512.

54.

47:334–346.

8:290–298.

36(9):2547-2557.

withdrawal from ventilatory support during weaning from mechanical ventilation.

timing during critical illness on long-term survival. Critical Care Medicine. 2008;

tracheostomy associated with better outcomes for patients requiring long-term

patients requiring prolonged mechanical ventilation: A propensity analysis.

while receiving prolonged mechanical ventilation in an intensive care unit. Crit

and sufentanil for analgesia and sedation of mechanically ventilated patients after

based sedation to provide patient comfort in the intensive care unit: a randomized,

care unit may have negative effects on health related quality of life outcomes after

sufentanil-midazolam for ICU long term sedation. Annales Franc ¸aises d'Anesthe

suctioning in the acute phase of head injury. J Neurosurg Anesthesiol 2002,14:50–


Intensive Care Management of the Traumatic Brain Injury 39

[88] Guha A. Management of traumatic brain injury: some current evidence and

[89] Signorini DF, Andrews PJ, Jones PA, et al. Adding insult to injury: the prognostic value

[90] Skippen P, Seear M, Poskitt K, et al. Effect of hyperventilation on regional cerebral blood flow in head-injured children. Crit Care Med. 1997;25:1402-409. [91] Mendelow AD, Teasdale GM, Russell T, et al. Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury. J Neurosurg. 1985;63:43-48.

[92] Muizelaar JP, Lutz HA, Becker DP, et al. Effect of mannitol on ICP and CBF and

[93] Kaufmann AM, Cardoso ER. Aggravation of vasogenic edema by multiple –dose

[94] Ziai WC, Toung TJ, Bhardwaj A. Hypertonic saline: first-line therapy for cerebral

[95] Doyle JA, Davis DP, Hoyt DB. The use of hypertonic saline in the treatment of

[96] Himmelseher S. Hypertonic saline solutions for treatment of intracranial hypertension.

[97] Suarez JI. Hypertonic saline for cerebral edema and elevated intracranial pressure.

[98] Strandvik GF. Hypertonic saline in critical care: a review of the literature and

[99] Larive LL, Rhoney DH, Parker D, Coplin WM, Carhuapoma JR. Introducing hypertonic saline for cerebral edema. Neurocrit Care.2004;1:435–440. [100] Qureshi A, Suarez J, Bhardwaj A, et al. Use of hypertonic saline/ acetate infusion in the

[101] Peterson B, Khanna S, Fischer B, Marshall L. Prolonged hypernatremia controls

[102] Marcoux KK. Management of increased intracranial pressure in critically ill child with

[103] Kelly DF, Goodale DB, Williams J, et al. Propofol in the treatment of moderate and

[104] McKeage K, Perry CM. Propofol: a review of its use in intensive care sedation of

[105] Johnston AJ, Steiner LA, Chatfield DA, et al. Effects of propofol on cerebral oxygenation and metabolism after head injury. Br J Anaesth. 2003;91:781-786. [106] Shapiro BA, Warren J, Egol AB, Greenbaum DM, Jacobi J, Nasraway SA, Schein RM,

[107] Hans P, Martin C: La sédation du traumatisé crânien. Cahiers d'Anesthesiologie 1994;

displacement of the brain. Crit Care Med. 1998;26:440–446.

acute neurological injury. AACN Clin Issues. 2005;16:212–231.

guidelines for use in hypotensive states and raised intracranial pressure.

treatment of cerebral edema: effect on intracranial pressure and lateral

elevated intracranial pressure in head injured pediatric patients. Crit Care Med.

severe head injury: a randomized, prospective double-blinded pilot trial. J

Spevetz A, Stone JR: Practice parameters for intravenous analgesia and sedation for adult patients in the intensive care unit: An executive summary. Crit Care Med

of early secondary insults for survival after traumatic brain injury. J Neurol

correlation with pressure autoregulation in severely head injured patients. J

applications. Postgrad Med J. 2004;80:650-653.

Neurosurg Psychiatry. 1999;66:26-31.

mannitol. J Neurosurg. 1992;77:584–589.

edema? J Neurol Sci. 2007;261:157–166.

Curr Opin Anaesthesiol. 2007;20:414–26.

Cleve Clin J Med. 2004;71:9–13.

Anaesthesia. 2009;64:990–1003.

Neurosurg 1999; 90: 1042–1052.

adults. CNS drugs 2003; 17: 235–272.

2000;28:1136–1143.

1995; 23:1596-1600

42:521-24

traumatic brain injury. J Trauma. 2001;50:367–383.

Neurosurg. 1984;61:700-706.


[68] Prielipp RC, Coursin DB. Sedative and neuromuscular blocking drug use in critically

[69] Lowson SM, Sawh S. Adjuncts to analgesia: sedation and neuromuscular blockade.

[70] Coursin DB, Prielipp RC. Use of neuromuscular blocking drugs in the critically ill

[71] Hsiang JK, Chesnut RM, Crisp CB, Klauber MR, Blunt BA, Marshall LF. Early, routine

[72] Riley KO, May AK, Hadley MN: Neurological injury and nutritional support. In: Batjer

[73] Roger Härtl, ,Lnda M. Gerber, ,Quanhong N, Jamshd Ghajar, Effect of early nutrition on deaths due to severe traumatic brain injury J Neurosurg . 2008;109:50-56 [74] Marik PE, Zaloga GP: Early enteral nutrition in acutely ill patients: a systematic

[75] K.G. Kreymanna, M.M. Berger, N.E.P. Deutz, M. Hiesmayr, P. Jolliet G. Kazandjiev, G.

[76] Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, compared with

[77] Adams S, Dellinger EP, Wertz MJ, Oreskovich MR, Simonowitz D, Johansen K. Enteral

[78] Braunschweig CL, Levy P, Sheean PM, Wang X. Enteral compared with parenteral

[80] Andre ´ Van Gossuma, Eduard Cabre, Xavier He ´buterne , Palle Jeppesen , Zeljko

[81] McGraw C P. "A cerebral perfusion pressure greater than 80 mmHg is more

[82] Rosner M J, Rosner S D & Johnson A H. "Cerebral perfusion: management protocol and

[84] Castillo LR, Gopinath S, Robertson CS. Management of intracranial hypertension.

[85] Juul N, Morris GF, Marshall SB, Marshall LF. Intracranial hypertension and cerebral

[86] Lane PL, Skoretz TG, Doig G, et al. Intracranial pressure monitoring and outcomes

[87] Vincent JL, Berre J. Primer on medical management of severe brain injury. Crit Care

randomized prospective trial. J Trauma 1986;26:882–891

clinical results." J.Neurosurgery 1985; 83: 949-962.

[83] Welch K. The intracranial pressure in infants. J Neurosurg.1980;52:693–699.

after traumatic brain injury. Can J Surg. 2000;43:442-448.

nutrition: a meta-analysis. Am J Clin Nutr 2001;74:534–542 [79] MD Bastow. Complications of enteral feeding Gut. 1986 ; 27(1): 51–55.

paralysis for intracranial pressure control in severe head injry: is it necessary? Crit

HH and Loftus CM (eds) Textbook of Neurological Surgery, Lippincott Williams &

Nitenbergg, G.et al. ESPEN Guidelines on Enteral Nutrition:Intensive care Clinical

parenteral, reduces postoperative septic complications. The results of a meta-

versus parenteral nutritional support following laparotomy for trauma: a

Krznaric ,Bernard Messing , Jeremy Powell-Tuck , Michael Staun , Jeremy Nightingale ESPEN Guidelines on Parenteral Nutrition: Gastroenterology Clinical

beneficial." Intracranial Pressure VII. Edits. Hoff J T & Betz A L. 1989; 839-41.

perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. J

ill patients with head injuries. New Horizons. 1995;3(3):456–468

Crit Care Clin. 1999;15:119–141

Care Med. 1994;22:1471–476

Nutrition :2006; 25: 210–223

Nutrition 2009;28 415–27

Springer-Verlag, Berlin.

Neurosurg. 2000;92:1-6.

Med 2005; 33:1392–1399

Neurol Clin. 2008;26:521–541.

patient. Crit Care Clin. 1995;11:957–981

Wilkins, Philadelphia, PA. In press, 2001.

review. Crit Care Med 2001; 29:2264–70

analysis. Ann Surg 1992;216:172–183.


Intensive Care Management of the Traumatic Brain Injury 41

[125] Vogelzang M, Nijboer JM, van der Horst IC, et al. Hyperglycemia has a stronger

[126] Mokri B. The Monro-Kellie hypothesis: applications in CSF volume depletion.

[127] Polin RS, Shaffrey ME, Bogaev CA, et al. Decompressive bifrontal craniectomy in the

[129] Fagon JY, Chastre J, Hance A, et al. Nosocomial pneumonia in ventilated patients: a

[130] Bernard GR, Artigas A, Brigham KL, et al. The American-European consensus

[133] Rogers FB, Shackfor SR, Trevisani GT, et al. Neurogenic pulmonary edema in fatal and

[134] Baumann A, Audibert G, McDonnell J, Mertes PM Neurogenic pulmonary edema.

[135] Fletcher SJ, Atkinson JD. Use of prone ventilation in neurogenic pulmonary oedema.

[136] Carson JL, Kelley MA, Duff A, et al. The clinical course of pulmonary embolism. N

[137] Morpurgo M, Marzagalli M. Death in pulmonary embolism. In: Morpurgo M, editor.

[140] Robertson CS, Clifton GL, Taylor AA, et al. Treatment of hypertension associated with

[141] Heyka RJ. Evaluation and management of hypertension in the intensive care unit. In:

[142] Alexander SC, Lassen NA: Cerebral circulatory response to acute brain disease: Implications for anesthetic practice. A nesthesiology 1970; 32 (1):60–68 [143] Fieschi C, Agnoli A, Battistini N, Bozzao L, Prencipe M: Derangement of regional

[144] Skinhoj E, Strandgaard S: Pathogenesis of hypertensive encephalopathy. Lancet 1973;

[145] Strandgaard S, MacKenzie ET, Sengupta D, Rowan JO, Lassen NA, Harper AM: Upper

Irwin RS, Rippe JM (eds). Irwin and Rippe's Intensive Care Medicine. 6th ed.

cerebral blood flow and of its regulatory mechanisms in acute cerebrovascular

limit of autoregulation of cerebral blood flow in the baboon. Circ Res 1974; 34

Pulmonary Embolism. New York: Marcel Dekker; 1994. p. 107-114. [138] Hravnak M, Boujoukos A. Hypotension. Am Assoc Crit Care Nur 1997;8:303-318 [139] Jones AE, Aborn LS, Kline JA. Severity of emergency department hypotension predicts

Philadelphia: Lippincott Williams and Wilkins, 2008:391-98.

[128] Vincent JL Ventilator-associated pneumonia . J Hosp Infect. 2004; 57(4):272-280.

trials co-ordination. Am J Respir Care Med1994;149:818–824. [131] Chang CH, Smith CA. Postictal pulmonary edema.Radiology 1967; 89:1087-1089. [132] Lagerkranser M, Pehrsson K, Sylven C. Neurogenic pulmonary oedema, a review of

non fatal head injuries. J Trauma 1995;39:860–866.

adverse hospital outcome. Shock 2004;22:410-414.

head injury. J Neurosurg 1983;59:455–460.

lesions. Neurology 1968; 18 (12):1166–1179

1(801):461–462

(4):435–440

Acta Anaesthesiol Scand. 2007;51(4):447 -455

Br J Anaesth. Feb 2003;90(2):238-240

Engl J Med 1992;326:1240–1245

Trauma. 2006;60:873-877.

1997;41:84-92.

1993;94:281–288.

1982; 212:267-270.

Neurology. 2001;56:1746-1748

relation with outcome in trauma patients than in other critically ill patients. J

treatment of severe refractory posttraumatic cerebral edema. Neurosurgery.

cohort study evaluating attributable mortality and hospital stay.Am J Med

conference on ARDS. Definitions, mechanisms, relevantoutcomes, and clinical

the pathophysiology with clinical and therapeutic implications. Acta Med Scand


[108] Sperry RJ, Bailey PL, Reichman MV, Peterson JC, Petersen PB, Pace NL: Fentanyl and

[109] Trindle MR, Dodson BA, Rampil IJ: Effects of fentanyl versus sufentanil in

[110] Albanèse J, Durbec O, Viviand X, Potie F, Alliez B, Martin C: Sufentanil increases intracranial pressure in patients with head trauma. Anesth. 1993; 79:493-497 [111] Werner C, Kochs E, Bause H, Hoffman WE, Schulte am Esch J: Effects of sufentanil on

[112] Mayberg TS, Lam AM, Eng CC, Laohaprasit V, Winn R: The effect of alfentanil on

[113] Scholz J, Bause H, Schulz M, Klotz U, Krishna DR, Pohl S, Schulte am Esch J:

[114] Jamali S, Ravussin P, Archer D, Goutallier D, Parker F, Ecoffey C: The effects of bolus

[115] Warner DS, Hindman BJ, Todd MM, Sawin PD, Kircner J, Roland CL, Jamerson BD:

[117] Moss E, Powell D, Gibson RM, McDowall DG: Effects of fentanyl on intracranial

[118] Moss E: Alfentanil increases intracranial pressure when intracranial compliance is low.

[119] Albanèse J, Viviand X, Potie F, Rey F, Alliez B, Martin C: Sufentanil, fentanyl, and

[120] Tipps LB, Coplin WM, Murry KR, Rhoney DH. Safety and feasibility of continuous

[121] Prough DS, Joshi S. Does neuromuscular blockade contribute to adverse outcome in

[122] Hsiang JK, Chesnut RM, Crisp CB, et al. Early, routine paralysis for intracranial

[123] Ahuquillo J, Vilalta A. Cooling the injured brain: how does moderate hypothermia

[124] Jiang JY, Xu W, Li WP, et al. Effect of long-term mild hypothermia or short-term mild

oxide anesthesia in humans. Anesth. 1993; 78:288-294

supratentorial lesions. Anesth Analg 1996; 82:600-606

patients. Br J Clin Pharmac 1994; 38:369-372

77:416-420

78:454-460

50:779-784

1476.

Anaesthesia 1992; 47:134-136

2000 ;46(3):596-601; discussion 601-602.

Blood Flow Metab. 2006;26:771-776.

head-injured patients? J Neurosurg Anes. 1994;5:135

Med 1999; 27:407-411

2007;13(22):2310-2322

Anesth. 1995; 83:721-726

sufentanil increase intracranial pressure in head trauma patients. Anesth.1992;

equianesthetic doses on middle cerebral artery blood flow velocity. Anesth. 1993;

cerebral hemodynamics and intracranial pressure in patients with brain injury.

cerebral blood flow velocity and intracranial pressure during isofluorane-nitrous

Pharmacokinetics and effects on intracranial pressure of sufentanil in head trauma

administration of opioids on cerebrospinal fluid pressure in patients with

Intracranial pressure and hemodynamic effects of remifentanil versus alfentanil in patients undergoing supratentorial craniotomy. Anesth Analg 1996; 83:348-353 [116] Herrick IA, Gelb AW, Manninen PH, Reichman H, Lownie S: Effects of fentanyl,

sufentanil and alfentanil on brain retractor pressure. Anesth Analg 1991; 72:359-363

pressure and cerebral perfusion pressure during hypocapnia. Br J Anaesth 1978;

alfentanil in head trauma patients: A study on cerebral hemodynamics. Crit Care

infusion of remifentanil in the neurosurgical intensive care unit. Neurosurgery

pressure control in severe head injury: is it necessary? Crit Care Med. 1994;22:1471-

influence the pathophysiology of traumatic brain injury. Curr Pharm Des

hypothermia on outcome of patients with severe traumatic brain injury. J Cereb


**2** 

*Iran* 

**Lumbar Puncture: Techniques,** 

*University of Medical Sciences, Zahedan,* 

**Complications and CSF Analyses** 

Ali Moghtaderi1, Roya Alavi-Naini2 and Saleheh Sanatinia2 *1Neurology Department, Zahedan University of Medical Sciences 2Research Center for Infectious Diseases and Tropical Medicine,* 

Lumbar puncture (LP) is one of the well-known ancillary procedures in clinical neurology performed for a variety of functions such as spinal anesthesia, intrathecal administration of drugs, myelography, obtaining cerebrospinal fluid (CSF) samples and measuring pressure since more than 100 years ago. The question that who was really the discoverer of LP is still under debate. Most authors assume that it was Heinrich Irenaeus Quincke (1842-1922) a German internist who was introduced the procedure to medicine in 1891, however, some authors mentioned the American neurologist James Leonard Corning (1855-1923) as the first one who performed LP using birds quills in 1885 (Frederiks et al., 1997; Dakka et al., 2011). The technique was passed on through generations of physicians to the next but the rules are the same. Quincke's aim on performing LP was to treat patients with hydrocephalus. In 1898 August Bear's assistant attempted to administer a spinal anesthetic to Dr. Bear which was never completed because the syringe did not fit the already implanted spinal needle. However, continued CSF leakage through the dural puncture site was the cause of post lumbar puncture headache (PLPH), discussed later in this monograph (Raskin, 1990).

Before performing LP it is important to think cautiously about the indications and the required diagnostic studies. Patient should be examined especially for papilledema; and cranial CT scans or MRI should be reviewed carefully. Obtaining a cranial CT scan before performing LP in all patients if possible is mandatory especially in patients with papilledema, loss of consciousness, focal neurologic deficit, new seizure onset, and inability

In adults with suspected meningitis, clinical features can be used to differentiate between patients with abnormal findings in their CT scans of the head. Clinical features at baseline that are associated with an abnormal findings in CT scans of the brain were an age of at least 60 years, immunocompromised patients and a history of CNS disease (Hasbun et al., 2001). A cranial MRI is an important diagnostic procedure when patient had symptoms and signs of a lesion in posterior fossa. Both CT scan and MRI should be reviewed especially for

**1. Introduction** 

**2. Before beginning the procedure** 

to visualize optic fundi (Kastenbauer et al., 2002; Roos, 2003).

