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Makkah
protocol for the management of severe head injuries
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INTRODUCTION
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The management of patients with severe head injury remains controversial and the reported differences in the outcome are not precisely determined, whether due to differences in patient groups or more effective therapy. Our series includes only 50 patients, although not large, the suggested protocol is standard, applied to a selective group with Glasgow coma scale (GCS) 3-5 in a practical, easy and safe manner. It provides an adequate cerebral protection to interfere with mechanisms resulting in secondary damage and ensures reduction of cells; requirements to better tolerance to ischaemia and/or hypoxia would improve the functional outcome.
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MATERIALS
AND METHODS
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This series include 50 head injured patients with GCS 3-5 determined 6 hours after injury. Patients who fulfilled the criteria of brain death on arrival and gun shot injuries were excluded. Thirty-two patients were admitted directly from the scene of the accident and 18 were referred from other hospitals in the same city. All were seen by a neurosurgeon within 5 hours after injury. Mean age was 29 years with a range from 2-78 years. Forty-five (90%) were males (38 adults, 7 children) and 5 (10%) were females (one adult, 4 children). Forty-six cases (92%) were due to car accidents (8 pedestrians, 38 drivers) and 4 cases (8%) were due to fall from a height.
Following resuscitation including endotracheal intubation, all patients were started on mannitol, phenobarbitone, phenytoin and underwent com-puterised tomography (CT) scanning, which was repeated whenever indicated by the clinical situation. Patients with mass lesions were taken to theatre for evacuation and all patients were started on hypothermia in an intensive care unit.
Tracheostomy was performed when a prolonged need for endotracheal intubation was required. It was done within the first two days of injury with associated facial or chest injuries.8 Ventilation was assisted with PaCo2 around 4 KPa (30 mm Hg) and Pa02 around 9.3 KPa (70 mm Hg).4
Hypothermia around 340C was achieved using surface electric blankets, being easy, more controllable, slower and less shocking, and temperature was monitored using a rectal probe.14 Duration was 10 days then gradual rewarming within 4 days but shorter periods were used if patients showed shivering or started to have a GCS >5.
Barbiturates given were phenobarbitone 200 mg IM twice daily for adults or 6 mg/kg/day for children divided into two doses continued for 10 days, then gradually tapered over 4 days. Phenytion was given at a dose of 100 mg IV three times daily for adults or 5 mg/kg/day divided into 3 doses for children and continued for 3 months but longer if fits occurred.
A 20% solution of mannitol at a dose of 2 gm/kg/day divided into 4 doses was given for 5 days then gradually discontinued in 2 days with regular monitoring of serum electrolytes and osmolality was kept <320 m osmol. Studies of steroid use indicated no benefit in terms of mortality.3 They were used only for focal lesions and/or if there was a pulmonary complication in variable doses and durations.11 Antibiotics, chlorpromazine, muscle relaxants, sedatives and other medications were started as required.
Patients were classified into 3 groups:
| 1. | Reactive group with intact pupillary and occulocephalic reflexes. |
| 2. | Intermediate group if both were impaired or one is lost or very impaired and the second is normal. |
| 3. | Nonreactive group with absent pupillary and occulocephalic reflexes 6 hours after injury but not brain dead. |
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RESULTS
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Table 1 contains the data obtained at our centre and the data of the
seven centres as published by Gennarelli, et al., in 1982.6 The results
show marginal differences as the overall mortality rate in our series
is 42% versus 59%, vegetative state is 12% versus 6%, severely disabled
is 12% versus 13%, moderate disability is 12% versus 9% and good recovery
is 22% versus 12%.
Table 2 shows the outcome in relation to the response obtained from the
pupillary and occulocephalic reflexes. The outcome looks to be more reliably
determined using this method than using only GCS eg. while mortality was
100% in the nonreactive group, it was 77.8% in patients with GCS of 3
as seen in Table 3.
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Table
1 - Outcome in relation to the injury (%)
Table 2 - Outcome at 3 months in relation to pupillary and occulocephalic reflexes 6 hours after injury in very severely injured patients with GCS 3-5
Table 3 - Outcome at 3 months in relation to GCS 6 hours injury
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DISCUSSION
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The mortality rate among head injured patients with GCS 3-8 at 6 months is 40% and mortality among patients with GCS 3-5 is three times that of the group with scores 6-8.6 Accordingly, this group with GCS 3-5 has been considered in our study as very severe head injury and even sub-classified according to the responses obtained from the pupillary and oculocephalic reflexes into reactive, intermediate and non-reactive group.
Despite the use of Glasgow coma and outcome scales as an attempt at standardisation there is a wide variability of reported outcomes. The issue of comparability cannot be completely settled due to differences in age, pre-injury conditions, mechanism and nature of injury, intracranial mass lesions, secondary systemic insults and multiple trauma, intracranial hypertension and how rapid the treatment starts after injury.3,13 It is also difficult to establish the efficacy of treatment for severe head injury due to practical, ethical and statistical problems.
The use of hypothermia, barbiturates, mannitol and artificial ventilation for cerebral protection is not new. However, in Makkah protocol they have been employed in a new manner being a standard treatment for all cases and applied in an easy, practical and safe manner. This avoids techniques which are very demanding of personnel and facilities as intracranial pressure monitoring, profound hypothermia and barbiturate coma require these additional services.
Hypothermia: There is a re-awakening of interest in the role of “mild” hypothermia with central temperatures of 33-360C on the ischaemic process since there are suggestions in the literature of a protective effect of such small and easily achieved reductions in body temperature.10 When the body is cooled, metabolism decreases at about 8% per degree centigrade rendering the brain and other metabolically highly active organs less susceptible to periods of ischaemia or hypoxia.5,14 Hypothermia appears to depress not only metabolic rate devoted to function but metabolic rate required for structure integrity. Studies demonstrate preservation of high energy phosphates, pH and lactic acid levels in brain tissues which are cold as compared with normothermic brain tissue.14 Cerebral blood flow, metabolic demands for oxygen and glucose are reduced and there is leftward shift of the oxygen haemoglobin dissociation curve.14 A de-crease of 2.30C is usually tolerated but temperatures below 340C may lead to serious adverse consequences as cardiac arrythmias, decreased oxygen availability, slowing of metabolically dependent processes, decreased drug biotransformation and impaired renal transport processes.7 Hypothermia offers protection against the devastating effects of high fever or hyperthemia such as cerebral vasodilation, rise of intracranial pressure and increased rate of formation of vasogenic brain oedema. High fever is also associated with increased oxygen demand, respiratory and metabolic acidosis, increased ventilatory work, hypovolaemia due to evaporation and hypoglycemia.7
Barbiturates: Barbiturates produce a dose-dependent neuronal metabolic depression, reduction of cerebral blood flow and therefore reduction of intracranial pressure and brain oedema with an improvement in the cerebral perfusion.1 This reduction is about 25% in normal sleep dosages.9 Blood pressure and intracranial pressure tend to be more stable as barbiturates damp down cardiovascular responses. Together with phenytoin they provide protection on the basis of their anticonvulsant properties as seizures are associated with cerebral vasodilation and increased metabolism.10 Propylactic barbiturate coma was not applied, as two randomised controlled trials have shown no superior effectiveness over conventional therapy in the management of severe head injury.12,18 With low dose of phenobarbitone there were no episodes of arterial hypotension which is common with high doses.18
Intracranial pressure monitoring of patients with severe head injury is worthwhile.15 As we did not do it, we were committed to repeat a CT scan at regular intervals, treat empirically with hyperventilation and osmotherapy and avoid extra cranial factors that could increase intracranial pressure.15
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CONCLUSION
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Some of the mortality in severe head injury is inevitable and all the efforts are directed to increasing the proportion of avoidable fatality.
Makkah protocol is easy to apply and a safe method to minimise the metabolic demands and interfere with mechanisms (mainly hypoxia and/or ischaemia) resulting in secondary damage so may preserve cells that would otherwise die.
A series of 50 patients is insufficient to draw any conclusions, but hopefully, with larger series it might be proved as a beneficial regimen.
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ACKNOWLEDGEMENT
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This work was carried out at Al Noor Specialist Hospital, Makkah, Saudi Arabia during the period from September 1989 until January 1992.
I acknowledge with great appreciation the co-operation of Dr. A Barakat, Consultant Anaesthetist and Chief of the Intensive Care Unit, Residents and Nursing staff of the Neurosurgical and Intensive Care Units.
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REFERENCES
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| 1. | Albin MS: Neuroanaestheisa in: Youman YR (Ed) Neurological Surgery, 3rd Ed, Vol 2, WB Saunders, Philadelphia 1990, 903-921 |
| 2. | Aitkenhead A: Cerebral protection. Br J Hospital Med 1986, 290-299 |
| 3. | Becker DP, Gade GF, Miller JD: Prognosis after head injury. In Youman JR (Ed) Neurological Surgery, 3rd Ed, Vol 3, WB Saunders, Philadelphia 1990, 2194-2229 |
| 4. | Campkin TV, Turner JM, Beasley J: The care of the head injured patient. In: Campkin TV, Turner JM. (Ed) Neurosurgical Anaesthesia and Intensive Care – 2nd Ed. Boston Butterworths, London 1986, 291-312 |
| 5. | Carlsson C, Hagerdal M, Siesio BK: Protective effect of hypothermia in cerebral oxygen deficiency caused by arterial hypoxia. Anesthesiology 1976, 44: 27 |
| 6. | Gennarelli TA: Spielman GM, Langfit TW, et al: Influence of the type of intracranial lesion on outcome from severe head injury. A multicentre study using a new classified system. J Neurosurg 1982, 56:32 |
| 7. | Hug JR, Carl C: Preparation of the patient/use of anaesthetic agents: Intra operative monitoring. In: Miller RD (Ed), Anaesthesia 2nd Ed, Vol. 1, Churchill Livingstone, Edinburgh, London, Melbourne 1986, 411-464 |
| 8. | Jennet B, Teasdale G, Fry J, et al: Treatment of severe head injury. J Neurol Neurosurg Psychiat 1980, 43: 289-295 |
| 9. | Loh L: Anaesthesia and the maintenance of brain function: In: Crockard A, Hayward R, Hoff JT. (Ed) Neurosurgery, the scientific basis of clinical practice. Blackwell Scientific Publications, Oxford: 1985, 297-309 |
| 10. | McDowal DG: Brain Ischaemia – its prevention and treatment: Br J Anaest 1985, 57: 1-2 |
| 11. | Miller JD: Normal and increased intracranial pressure. In: Miller JD (Ed) Northfield’s Surgery of the central nervous system. 2nd Ed. Blackwell, Edinburgh, Oxford, London 1987, 7-57 |
| 12. | Miller JD: Head injury: In Miller JD (Ed) Northfield’s Surgery of the central nervous system, 2nd Ed. Blackwell, Edinburgh, Oxford, London 1987, 795-870 |
| 13. | Miller JD, Butterworth JF, Gudeman SK, et al: Further experience in the management of severe head injury. J Neurosurg 1981, 54: 289-299 |
| 14. | Rupp SM, Severinghans JW: Hypothermia. In: Miller RD (Ed). Anaesthesia 2nd Ed. Vol. 3, New York, Edinburgh, London, Melbourne, 1986, 1995-2022 |
| 15. | Saul T: Is intracranial pressure monitoring worthwile. In: Proceeding of the Congress of Neurological Surgeons. Clinical Neurosurgery. Williams & Wilkins, Baltimore 1986, 560-571 |
| 16. | Shapiro HM: Barbiturates in brain ischaemia: Br J Anaesth 1985, 57: 82-95 |
| 17. | Thomas D, Crockard A: Cerebral metabolism and blood flow. In: Crockard A, Hayward R, Hoff TT. (Ed) Neurosurgery, the scientific basis of clinical practice, Blackwell Scientific Publications, Oxford 1985, 223-239 |
| 18. | Ward JD: Decker DP, Miller JD, et al: Failure of prophylactic barbiturate coma in the treatment of severe head injury: J Neurosurg 1985, 62: 383-388 |
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