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Cerebral Blood Flow

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When ICP is raised the following occurs: ã CSF moves into the spinal canal and there is increased reabsorption into the venous circulation ã Compensatory mechanisms are eventually overwhelmed so further small changes in volume lead to large changes in pressure (see Fig. 8.3) ã As ICP rises further, CPP and CBF decrease ã Eventually brainstem herniation (coning) occurs. The clinical features of acutely raised ICP are headache, nausea and vomiting, confusion, and a reduced conscious level. This can occur in traumatic brain injury, cerebral haemorrhage or infarction, meningitis/encephalitis, or quickly growing tumours. An estimate of ICP can be made in patients with brain injury who are not sedated:
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  Cerebral blood flow Cerebral blood flow (CBF) is around 15% of cardiac output and is affected by various factors. The mainones are as follows: ã PaCO2: A high PaCO2 causes vasodilatation of blood vessels and increases CBF. A low PaCO2 causesvasoconstriction. Reducing the PaCO2 from 5 to 4 kPa (38.5–30.5 mmHg) reduces CBF by almost 30%. ã Hypoxaemia: Below 6.7 kPa (51.5 mmHg) causes increasing CBF. ã Mean arterial pressure (MAP). ã Drugs.The relationship of CBF to PaCO2, PaO2 and MAP is shown in Fig. 8.1. Like the kidneys, the brainautoregulates blood flow so that it is constant between a MAP of 50 and 150 mmHg. CBF is regulated bychanges in the resistance of the cerebral arteries. Unlike the rest of the body, the larger arteries play amain role in this autoregulation. Local chemicals, endothelial mediators and neurogenic factors arethought to be responsible.CBF is controlled by alterations in cerebral perfusion pressure (CPP) and cerebral vascular resistance (R):CPP is the pressure gradient in the brain or the difference between the incoming arteries and the outgoingveins:CPP = MAP - Venous pressureVenous pressure is equal to intracranial pressure (ICP), so CPP is usually expressed as:CPP = MAP - ICP  Normal supine ICP is 7–17 mmHg and is frequently measured on neurointensive care units (ICUs). CPPcan then be calculated and manipulated. Intracranial pressure The skull is a rigid box and its contents are incompressible, therefore, ICP depends on the volume of intracranial contents: 5% blood, 10% cerebrospinal fluid (CSF) and 85% brain. The Monro–Kellie doctrine,named after two Scottish anatomists (see Fig. 8.2), states that as the cranial cavity is aclosed box, any change in intracranial blood volume is accompanied by an opposite change in CSF volume,if ICP is to be maintained.When ICP is raised the following occurs: ã CSF moves into the spinal canal and there is increased reabsorption into the venous circulation ã Compensatory mechanisms are eventually overwhelmed so further small changes in volume lead tolarge changes in pressure (see Fig. 8.3) ã As ICP rises further, CPP and CBF decrease ã Eventually brainstem herniation (coning) occurs. The clinical features of acutely raised ICP areheadache, nausea and vomiting, confusion, and a reduced conscious level. This can occur in traumaticbrain injury, cerebral haemorrhage or infarction, meningitis/encephalitis, or quickly growing tumours. Anestimate of ICP can be made in patients with brain injury who are not sedated: ã Drowsy and confused with Glasgow Coma Score (GCS) 13–15: ICP20mmHg ã GCS less than 8: ICP 30 mmHg. Primary and secondary brain injury Primary brain injury is the injury that has already occurred and has limited treatment. But the brain isuniquely vulnerable to secondary  insults and less capable of maintaining an adequate blood flow and  metabolic balance following injury. Research in the field of traumatic brain injury has shown thatpreventing secondary brain injury can improve outcome for the patient. Secondary brain injury is, bydefinition, delayed and therefore amenable to intervention. Examples of secondary brain injury include: ã Raised ICP ã Ischaemia ã Oedema ã Infection (e.g. in open fractures).Following brain injury, neurones are rendered dysfunctional although not mechanically destroyed. If thesubsequent environment is favourable, many of these cells can recover. Preventing raised ICP and savingthe penumbra (the area around the primary injury with its compromised microcirculation) is important. Anuncontrolled increase in ICP and brainstem herniation is the major cause of death after traumatic braininjury or intracerebral haemorrhage. In traumatic brain injury, the main precipitants of secondary injuryare hypotension and hypoxaemia. Hypoxaemia, as defined by oxygen saturations _93%, and hypotension,as defined by a systolic BP of less than 90 mmHg, are associated with a statistically significant worseoutcome and are common at the scene of injury [1]. Principles of brain protection Based on our knowledge of brain physiology and observations of traumatic brain injury, a set of measuresto protect the brain against secondary injury can be devised [2]. This can be applied to any kind of braininjury, for example, subarachnoid haemorrhage (SAH), meningitis or stroke.The aim of brain protection is to prevent: ã Raised ICP ã Cerebral ischaemia ã Cerebral oedema.In addition, fever has been observed to worsen outcome in patients with brain injury, probably becausethe cerebral metabolic rate for oxygen is increased and this exacerbates local ischaemia.Raised ICP is caused by an increase in the volume of blood, CSF or brain tissue, so treatment is aimed atreducing the volume of these three components and is summarised in Fig. 8.4.  Fig. 8.5 summarises these principles in an ABCDE format. Although most research has been done intraumatic brain injury, these principles have also been successfully applied to medical conditions such asmeningitis with raised ICP [3], and current research is focussing on prevention of secondary braininjury in stroke. Experimental methods of brain protection The cerebral metabolic rate for oxygen is reduced by hypothermia. Hypothermia has been used in the pastfor cerebral protection during complex cardiac and neurosurgery. Animal models demonstrate its benefitsbut actively cooling normothermic human subjects with brain injury has not yet been shown to improveoutcome [4]. However pyrexia is associated with an adverse outcome in brain injury [5] and thereforeshould be treated with paracetamol and active cooling.Hypertonic saline has been studied extensively in traumatic brain injury. The theory is that the hypertonicsolution will draw intracellular water into the intravascular space, reducing cerebral oedema andexpanding intravascular volume. The results of clinical trials have been mixed [6]. In patients with otherinjuries such as haemorrhage or burns, resuscitation with hypertonic saline has adverse effects, so its useis not recommended in the routine resuscitation of trauma victims. The unconscious patient A reduced conscious level is associated with potentially life-threatening complications (e.g. airwayobstruction and hypoxaemia, aspiration and immobilization injuries) which require urgent intervention.Unconsciousness, or coma, is present when the GCS is 8 or less (see Fig. 8.6). Comatose patients shouldbe referred to the ICU.The causes of non-traumatic coma (lasting more than 6 h) are [7]: ã Sedative overdose: 40% ã Hypoxic brain injury: 24% ã Cerebrovascular disease: 18% ã Metabolic coma (e.g. infection, diabetes, hepatic encephalopathy, hypothermia):15% ã Others: 3%.However, a slightly different pattern is observed in the elderly, who commonly become confused, drowsyor unresponsive due to a wide range of conditions, most commonly infection and dehydration.Seizures are an important, although less common, cause of coma, either because the patient is post-ictal(which can be prolonged in the elderly) or has non-convulsive status epilepticus [8]. A systematicapproach is required in the management of an unconscious patient. As usual, the ABCDE system is used: ã A: assess and treat airway  problems. ã B: assess and treat breathing problems. ã C: assess and treat circulation problems. ã D: assess disability  (pupil size and reactivity, capillary glucose and the simpleAlert, responds to Voice, responds to Pain, Unresponsive (AVPU) scale) and treat any problems. The GCSshould be recorded once A, B and C are stable so that any later changes can be documented precisely. ã E: includes a full neurological examination . Certain clusters of signs maypoint to a particular diagnosis (see Fig. 8.7).
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