Refresher Course HEAD INJURED PATIENTS AND MECHANICAL VENTILATION 7 RC 2. European Society of Anaesthesiologists INTRODUCTION

Size: px

Start display at page:

Download "Refresher Course HEAD INJURED PATIENTS AND MECHANICAL VENTILATION 7 RC 2. European Society of Anaesthesiologists INTRODUCTION"

Reynold Harvey
5 years ago
Views:

1 European Society of Anaesthesiologists Refresher Course HEAD INJURED PATIENTS AND MECHANICAL VENTILATION 7 RC 2 P. PELOSI, D. D ONOFRIO, D. CHIUMELLO* Dipartimento di Scienze Cliniche e Biologiche, Università degli Studi dell Insubria, Varese, Italy; *Istituto di Anestesia e Rianimazione, Universita degli Studi di Milano, Ospedale Policlinico-IRCCS, Milano, Italy Sunday June 1, 2003 Euroanaesthesia Glasgow INTRODUCTION It is common knowledge that in head injured patients the principal morbidity and mortality is frequently caused by the primary disease, i.e. cerebral nervous system injury and its neurological consequences [1,2]. However, it has been recognized that neurological outcome may also depend on the prevention of the secondary brain injury due to the negative effects on cerebral parenchyma of increased intracranial pressure (ICP) and/or altered cerebral volemia [3]. Moreover, extracerebral organ dysfunctions are also frequent in head injured patients influencing morbidity and mortality [4,5]. Ventilatory management can markedly affect the regulation of cerebral volemia, intracranial pressure control and lung function. The aim of this review is to discuss the ventilatory management and its pathophysiological rationale: 1) in the early phase after head injury; 2) in the stable phase (1 week after head injury). VENTILATION IN THE EARLY PHASE AFTER HEAD INJURY CEREBRAL ISCHEMIA VERSUS HYPERPERFUSION Normal neurological aerobic metabolism, combined oxygen and glucose consumption lead to normal CO 2 production which in turn, mediates the normal microcirculatory diameter. Since cerebral blood flow and oxygen consumption are normally coupled, cerebral extraction of oxygen remains in the normal range. After severe head injury the cerebral consumption of oxygen is decreased due to the trauma by itself and sedatives. Accordingly, a decreased neuronal aerobic metabolism and CO 2 production lead to a physiologic and proportional decrease in cerebral blood flow ( intact metabolic autoregulation ), and therefore the cerebral extraction of oxygen remains normal, indicating a good balance between blood flow and oxygen consumption. If cerebral blood flow is low relative to a decreased oxygen consumption, cerebral extraction of oxygen increases to compensate for the excessive decrease in cerebral blood flow ( oligemic cerebral hypoxia ). Conversely, if cerebral blood flow is high relative to decreased oxygen consumption ( defective metabolic autoregulation ), cerebral oxygen extraction decreases ( relative cerebral hyperperfusion or luxury perfusion )[6]. Studies evaluating cerebral blood flow alone have overemphasized the occurrence of regional or global brain ischemia [7,8]. This is because true ischemic metabolites can not be evaluated by any standard technique for measuring cerebral blood flow alone (e.g., stable xenon computerized tomography cerebral blood flow measurements, or single photon emission computerized tomography). Bouma et al. reported that 33% of severe head injured patients presented an early ischemia [9]. However, reduced flow levels were not associated with increased oxygen extraction, indicating an adequate coupling between reduced blood flow and pathologically decreased oxygen consumption. On the contrary, Jaggi et al. have shown that cerebral oxygen consumption is approximately 50% below normal in brains with a high probability of favorable clinical recovery [10]. Thus, ischemic thresholds for cerebral blood flow in humans in recoverable coma would be expectedly 50% less than the levels normally reported in animal studies [11]. CLINICAL STUDIES ON HYPERVENTILATION The theoretical advantages of hyperventilation as cerebral vasoconstriction for intracranial pressure control and reversal of brain and cerebrospinal fluid acidosis, can be balanced by a cerebral vasoconstriction to such an extent that cerebral ischemia ensues with a minimum effect on acid-base homeostasis in the cerebrospinal fluid. In 1991, Muizelaar et al. found that prophylactic profound hyperventilation induced a slowness in neurological recovery with increased severe disability or vegetative state at 6 months, in patients with less severe motor scores (4-5) at moment of injury without significant outcome differences in relation to moderate hyperventilated patients at one year post injury [12]. Unexpectedly, the clinical application of this study was that profound hyperventilation was no more suggested as first intervention line in the ICP management, independently of the severity of head injury. 125

2 Other non randomized studies investigated the role of hyperventilation in head injured patients. Gordon et al. have long reported a substantial mortality reduction in a retrospective analysis of severely brain injured patients subjected to semi-empirical (not optimized) hyperventilation [13]. Finally a recent European- American survey on a large population of head injury patients reported that, among other therapeutic maneuvers profound hyperventilation could be associated with a better outcome [14]. Based upon these findings and differently from common clinical application, even not optimized profound hyperventilation in the early phases after severe head injury seems to be effective to reduce mortality, without affecting neurological outcome, at least in more severe patients. VENTILATORY MANAGEMENT IN THE STABLE PHASE (1 WEEK AFTER HEAD INJURY) Recently, it has been emphasized that the outcome in head injured patients is more frequently the result of a progressive dysfunction of organ systems remote from the site of the primary disease process, i.e. multiple organ dysfunction process [15]. In table 1 is summarized the average prevalence of extracerebral complications (partitioned into overall and severe) in head injured patients, as reported by the most recent literature. The pulmonary alterations accounted up to 50% of the deaths after head injury [4]. We can identify three major causes of pulmonary complications in head injured patients: 1) neurogenic pulmonary edema; 2) abnormalities in ventilation perfusion mismatch; 3) structural parenchymal abnormalities, which likely play the most relevant role. TABLE 1. PREVALENCE OF EXTRACEREBRAL ORGAN DYSFUNCTIONS IN HEAD INJURED PATIENTS Total Severe Pulmonary pneumonia 40 % 25 % embolism < 1 % 100 % Gut 40 % 5 % Cardiac arrhythmia 30 % 5 % cardiac failure 5 % 1 % Metabolic electrolytes disorders 30 % 2 % diabetes insipidus 7 % 7 % Hepatic 25 % 4% Hematologic 20 % 6 % Renal 10 % 15 % STRUCTURAL PARENCHYMAL ABNORMALITIES We can mainly identify several causes of structural parenchymal alterations in head injured patients, among them: 1) abnormal breathing pattern; 2) release of inflammatory mediators; 3) release of catecholamines («sympathetic storm»); 4) pulmonary infectious processes. Abnormal breathing pattern Abnormal breathing patterns are commonly seen after head injury. In particular, both hyperventilation and hypoventilation have been described. Hyperventilation is usually associated with periods of hypoventilation which can induce, together with a reduction in cough reflexes and impaired airway patency from inspissated secretions, alveolar atelectasis and consolidations [16]. Release of inflammatory mediators Head injury causes a marked release in the brain and in the systemic circulation of pro and con inflammatory agents which can lead to peripheral organ dysfunction, prevalently of the lung and to a moderatesevere immunodepression [17]. 126

3 Thus, the release of these inflammatory mediators can lead to multiple organ failure where the lung parenchyma appears to be a preferential and more susceptible target. Release of catecholamines Head injury is followed by prolonged sympathetic hyperactivity, which may lead to hypertension and/or tachycardia. This circulatory hyperactivity induces an increase in cerebral blood volume, and/or cerebral blood flow and hence ICP increase [18]. Moreover the outcome after head injury appears to be related to the intensity of the plasma catecholamines [19]. Pulmonary infectious processes Head injured patients are characterized by an increased risk to develop ventilator associated pneumonia (VAP)[20]. Its incidence is estimated in a range between 30-50% of the head injured patients, being extremely severe in only 20-25% of the cases. In table 2 are shown the independent risk factors for VAP in head injured patients. TABLE 2. THE INDEPENDENT RISK FACTORS FOR VENTILATOR ASSOCIATED PNEUMONIA (VAP) IN HEAD INJURED PATIENTS Risk Risk factors related to brain injury Altered coscience 6.6 Risk factors associated to the treatment of brain injury Aspiration 7.0 Emergency intubation 6.4 Mechanical ventilation > 3 die 2.3 Risk factors associated to the treatment of a general population of critically ill patients Reintubation 5.4 Age > 60 years 5.3 Supine position 4.8 Previous disease 3.6 Prior antibiotics 2.9 PREVENTION AND OF PULMONARY INFECTIOUS PROCESS Since VAP plays a relevant role in the outcome of head injured patients, it is extremely important to prevent it. Unfortunately, very few studies investigated the efficacy of specific protocols to prevent VAP. We believe that the main goals should be: 1) to prevent lung infection. 2) to prevent lung collapse and/or consolidation; Prevention of lung infection 1) Antibiotic prophylaxis with a cephalosporin of second generation (cefuroxime or cefoxitin) or ampycillin-sulbactam can be useful to prevent early pneumonia. 2) Selective digestive decontamination (SDD) has been proposed to reduce the microbiological load in the oropharynx and in the stomach. Recently, a large metaanalysis, reported that SDD can be effective to reduce ICU stay and mortality when associated with i.v. prophylaxis [21]. 127

4 3) Upright position has been suggested to reduce VAP and ICU stay in a general population of critically ill patients. Anyway, upright position is usually adopted in head injured patients to reduce intracranial pressure, when necessary [22]. 4) Continuous oropharyngeal aspiration has been found to reduce the oropharyngeal contamination and the occurrence of VAP [23]. 5) Correct use of antiacid drugs: the routine use of antiacid drugs seems to be reasonable, because head injured patients are at increased risk of gastric hemorrhage. Recent randomized trial suggest that the use of H2 antagonist reduce the incidence of clinically important gastric bleeding, with no increase in VAP [24]. 6) Nutrition is important to positively affect outcome in head injured patients, but it is not clear the respective role of enteral and parenteral nutrition [25]. 7) Protocols to regulate hygiene of the physicians and nurses are warranted. In particular, a careful handwashing policy seems to reduce the incidence of infections and improve patient s outcome [26]. Prevention of lung collapse and/or consolidation 1) The use of fibroscopy to clear secretions should be very important to reduce the formation of micromacro atelectasis, consolidations and lobar infections. 2) Fluid balance: it is not clear if head injured patients should be maintained more hypervolemic or hypovolemic. It is possible that excessive overfluid treatment can increase interstitial lung edema and favor lung collapse. On the other hand hypervolemia has been advocated for the treatment of these patients [27]. 3) Mechanical ventilation is also likely important to avoid progressive collapse and consolidation of the lung. However, many aspects in the ventilatory management are not clear: - the superiority of controlled or assisted ventilation; - the use of preventive recruitment manoeuvres and PEEP (applied before lobar consolidation occurrence); - the routine use of prone position or kinetic therapy. Among all these different maneuvers to prevent and treat respiratory failure due to VAP in head injured patients, prone position is gaining more and more attention. Beuret et al. investigated in a small prospective randomized trial if a daily prone position compared with staying in supine position in comatose patients requiring mechanical ventilation; reduced the incidence of lung worsening and VAP [28]. The patients were proned for at least 4 hours a day, in horizontal position, head out of bed, with respect of the axis head-neck-trunk to avoid any obstacle to cerebral venous return. They found that preventive prone positioning effectively reduced the lung worsening from 55% to 10% at 28 days and the incidence of VAP, approximately halfed from 44.2/1000 days of intubation to 22/1000 days of intubation. Moreover, the favorable neurological outcome and survival were increased in the prone group (from 46% to 60%and from 54% to 72%, respectively). Thus, we believe that prone positioning can be useful to prevent and treat respiratory failure due to traumatic or non traumatic respiratory failure in head injured patients, but under strict clinical, intracranial pressure and cerebral oxygen extraction monitoring. CONCLUSIONS Ventilatory management plays a relevant role in the management of head injured patients in the different phases of the disease. In the early phases (within the first week after head injury), profound hyperventilation physiologically targeted on cerebral oxygen extraction is likely to reduce mortality and improve neurological outcome. However, a randomized prospective control trial is warranted to better define the relative importance of hyperventilation by itself and cerebral oxygen extraction monitoring. During the stable phase (1 week after head injury) prone positioning seems to be useful to prevent and treat ventilator associated pneumonia and associated respiratory failure. Whether different protocols combining respiratory parameters with neurological measures lead to superior outcomes in this population requires further investigation. 128

5 REFERENCES 1. Kassell NF, Torner JC, Haley EC et al. The international cooperative study on the timing of aneurysm surgery. Part 1: overall management results. J Neurosurg 1990; 73: Kassell NF, Torner JC, Jane JA et al. The international cooperative study on the timing of aneurysm surgery. Part 2: Surgical results. J Neurosurg 1990; 73: Robertons CS, Valadka AB, Hannay HJ et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med 1999; 27: Solenski N, Haley C, Kassell NF et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Crit Care Med 1995; 23: Clifton GC, Miller ER, Choi SC et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 2000; 344: Cruz J. The first decade of continuous monitoring of jugular bulb oxyhemoglobin saturation: management strategies and clinical outcome. Crit Care Med 1998; 26: Marion DW, Darby J, Yonas H. Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 1991; 74: Ritter AH, Muizelaar JP, Barnes T et al. Brain stem blood flow, papillary response and outcome in patients with severe head injuries. Neurosurgery 1999; 44: Bouma GJ, Muizelaar JP, Choi SC et al. Cerebral circulation and metabolism after severe traumatic brain injury. The elusive role of ischemia. J Neurosurg 1991; 75: Jaggi JL, Obrist WD, Gennarelli JA et al. Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. J Neurosurg 1990; 72: Jones TH, Morazetz RB, Crowell RM et al. Threshold of focal cerebral ischemia in awake monkeys. J Neurosurg 1981; 54: Muizelaar JP, Marmarou A, Ward JD et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991; 75: Gordon E, Rossanda M. Further studies on cerebrospinal fluid acid base status in patients with brain lesions. Acta Anaestesiol Scan 1970; 14: Hukkelhoven CW, Steyerberg EW, Forace E, Habbema JD, Marshall LF, Maas AI. Regional differences in patients characteristics case management and outcomes in traumatic brain injury: experience from the tirilazad trials. J Neurosurg 2002; 97: Knaus WA, Draper EA, Wagner DP et al. Prognosis in acute organ-system failure. Ann Surg 1985; 202: North J, Jennett S. Abnormal breathing patterns associated with acute brain damage. Arch Neurol 1974; 31: Nieto-Sampedro M, Berman MA. Interleukin-1 like activity in rat brain: sources, targets, and effect of injury. J Neuro Res 1987; 17: Rosner MJ, Nesome HH, Becker DP et al. Mechanical brain injury: the sympathoadrenal response. J Neurosurg 1984; 61: Woolf PD, Hamill RW, Lee LA et al. The predictive value of catecholamines in assessing outcome in traumatic brain injury. J Neurosurg 1987; 66: Hsieh AH, Bishop MJ, Kubilis PS et al. Pneumonia following closed head injury. Am Rev Respir Dis 1992; 146: D Amico R, Pifferi S, Leonetti C et al. Effectiveness of antibiotic prophylaxis in critically ill adult patients: systematic review of randomized controlled trials. BMJ 1998; 316: Drakulovic MB, Torres A, Bauer TT et al. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomized trial. Lancet 1999; 354: Shorr AF, O Malley PG. Continuous subglottic suctioning for the prevention of ventilator associated pneumonia: potential economic implications. Chest 2001; 119: Cook D, Guyatt G, Marshall J. A comparison of Sucralfate and Ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation N Engl J Med 1998; 338: Taylor SJ, Fettes SB, Jewkes C et al. Prospective, randomized, controlled trial to determine the effect of early enhanced enteral nutrition clinical outcome in mechanically ventilated patients suffering head injury. Crit Care Med 1999; 27: Bischoff WE, Reynolds TM, Sessler CN, et al. Handwashing compliance by health care workers: the impact of introducing an accessible, alcohol-based hand antiseptic. Arch Intern Med 2000; 160: York J, Arrillaga A, Graham R et al. Fluid resuscitation of patients with multiple injuries and severe closed head injury: experience with an aggressive fluid resuscitation strategy. J Trauma 2000; 48: Beuret P, Carton MJ, Nourdine K, Kaaki M, Tramoni G, Ducreux JC. Prone position as prevention of lung injury in comatose patients: a prospective randomized controlled study. Intensive Care Med 2002; 28:

Head injuries. Severity of head injuries

Head injuries. Severity of head injuries Head injuries ED Teaching day 23 rd October Severity of head injuries Minor GCS 14-15 Must not have any of the following: Amnesia 10min Neurological sign or symptom Skull fracture (clinically or radiologically)