Injuries are the leading cause of death in persons younger than 45 years old with approximately one-third of these deaths a result of head trauma. Traumatic brain injury (TBI) results from either direct or indirect forces to the brain matter. Annually, in the United States, there are approximately 1.7 million nonfatal TBIs, 275, 00 persons hospitalized as a result of a TBI, and 52,000 persons who die from TBI. (Faul M, 2010) The costs for treatment of both acute and chronic TBI are estimated to be $60 billion dollars in 2000. (Finkelstein E, 2006)
The primary injury occurs directly to the brain at the time of injury. The secondary injury, which in most case is the injury that results in the demise or permanent disability of the patient, begins hours after the initial injury. Secondary injury the brain begins to swell, and place pressure on the fluids within the skull, resulting in increased intracranial pressure (ICP). If we look back at our college neuroanatomy classes, and dust the cob webs from our text books we would find the “Monroe-Kellie Doctrine”. Which if you do not recall basically states that you head is a rigid box, and within that box there is brain, blood & cerebral spinal fluid (CSF). As one element increases, one or both of the remaining elements must decrease as the box (the skull) is rigid and will not expand.
As the brain swells it initially causes a decrease in CSF and then blood. When blood is decreased to the brain, oxygen and vital nutrients are also decreased, which leads to further injury. This new injury leads to more brain edema, and the cycle continues until the process is reversed of the patient dies.
It is important to note that research has shown that hypotension and hypoxia doubles the rate of death in the head injury patient. This makes complete sense. If the brain is being starved of oxygen the simple intervention is to provide more! Normally, the body provides a higher pressure (reflected as the cerebral perfusion pressure or CPP) to over come the ICP. The pressure gradient allows for blood to move freely into the brain. When there are signs and symptoms of increased ICP, and the body is suffering from hypotension the body is unable to overcome the pressure within the skull causing a decrease in blood flow.
We can see this in the following equation:
CPP (Normal 80mmHg) = MAP(Normal 70-110mmHg)-ICP(Normal 7-14mmHg)
NOTE: Minimum CPP is 70mmHg & Minimum MAP is 60-65mmHg.
I offer the following scenario for the purposes of this article:
EMS go to the scene of a motor vehicle crash. They obtain a patient and quickly bring him to your trauma room. You get the following verbal report:
This is John Doe. He is an approximately 40 year old male, who was riding his motor cycle down the highway and was struck by a SUV. Both the vehicles had an estimated speed of 65mph. Mr. Doe was ejected 20 feet striking the road. Mr Doe was not wearing a helmet and witnesses stated that he was unconscious and not moving for approximately 5 minutes. Vitals are: Pulse 112, agonal respirations of 7, blood pressure 70/38. There is blood from the right ear and nose, 6 inch laceration to the left head and visible deformity to the right femur. Two large bore IV’s have been established. C-spine precaution and spinal restriction in place. Hare traction applied. EBL 1000 to 1500mL and 800mL normal saline has been infused.
Lets pause and think for a moment. Is this patient hypoxic? Yep! It is a fairly safe assumption. The patient has lost 1.5 liters of blood and has poor ventilation's. (What type or types of hypoxia do you think he has?). So we intubate, because as we all know hypoxia kills brain tissue. So no the patient has an ETCO2 of 35 & a SpO2 of 100%. Well there is one problem solved. We now calculate the mean arterial pressure (MAP) and inject it into our CPP equation (we will assume that the patient has a normal, but high ICP).
CPP= 48 - 14
CPP=34 (OH CRAP!!!)
So now inevitably some one starts pouring in the saline or ringer’s, but is this the right treatment for the current dilemma? Absolutely not! It is here when we just go ahead and bust out the Massive Transfusion Protocol(PRBC,FFP, and Platelets). Mr. Doe requires and increase in oxygen carrying capacity and he needs to be volume expanded, both of which are not accomplished by crystalloid. To put is bluntly in Mr. Doe’s case if what you are administering does not address at least one component of the lethal triad it should not be given.
So you as the expert clinician gives 4 units of PRBC’s, 4 units of FFP, and 4 units of platelets (and you have pushed them in hard and fast!)
Now your blood pressure is 86/40 with a MAP of 62.
Again we play the numbers game.
CPP=62-14
CPP=48 (Still not at 70!)
So what do you do now? If you said crystalloid walk yourself into the bathroom look in the mirror and slap yourself...hard! Repeat the blood transfusion! Do it again and again and again if you have to.
The avoidance of secondary injury is essential! A single episode of hypotension (systolic blood pressure of <90mmHg) has been shown to increase mortality in the adult population by 50%.
The role of the ER/Trauma clinician & prehospital provider is to not only stabilize the patient but it is prevent further injury. We must remember that simple interventions have profound effects. The prehospital provider giving 100% oxygen to prevent hypoxia, or the nurse keeping the patient warm in the trauma room to prevent the progression of the lethal triad, these simple interventions are imperative to decrease the morbidity and mortality of patients.
REFERENCES
1. Thurman DJ, Alverson C, Dunn KA, et al: Traumatic brain injury in the United States: A public health perspective. J Head Trauma Rehabil 14(6):602, 1999
2. Wax W, McKenzie EJ, Rice DP: Head injuries: Costs and consequences. J Head Trauma Rehabil 6:76, 1991.
3. Chestnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216, 1993.
4. Robinson N, Clancy M: In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J 18(6):453, 2001.
5. Albanese J: Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology 87(6):1328, 1997.
6. Modica PA: Intracranial pressure during induction of anaesthesia and tracheal intubation with etomidate-induced EEG burst suppression. Can J Anaesth 39(3):236, 1992.
7. Vassar MJ, Fischer, RP, O'Brien PE, et al: A multicenter trial for resuscitation of injured patients with 7.5 percent sodium chloride: The effect of added dextrose 70. Arch Surg 128:1003, 1993.
8. Servadei F, Teasdale G, Merry G, Neurotraumatology Committee of the World Federation of Neurosurgical Societies: Defining acute mild head injury in adults: A proposal based on prognostic factors, diagnosis, and management. J Neurotrauma 18(7):657, 2001.
9. Iverson GL, Lovell MR, Smith S, Franzen MD: Prevalence of abnormal CT scans following mild head injury. Brain Inj 14(12):1057, 2000.
10. Stein SC, Ross SE: Moderate head injury: A guide to initial management. J Neurosurg 77:562, 1992.
11. Snoey ER, Levitt MA: Delayed diagnosis of subdural hematoma following normal computed tomography scan. Ann Emerg Med 23:1127, 1994.
12. Arienta C, Caroli M, Balbi S: Management of head-injured patients in the emergency department: A practical protocol. Surg Neurol 48:213, 1997.
13. Bullock RM, et al: Management and prognosis of severe traumatic brain injury, part I, Guidelines for the management of severe traumatic brain injury. J Neurotrauma 17:451, 2000.
14. Friedman JA, Ebersold MJ, Quast LM: Post-traumatic cerebrospinal fluid leakage. World J Surg 25(8):1062, 2001.
15. Servadei F, Murray GD, Teasdale GM, et al: Traumatic subarachnoid hemorrhage: Demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery 50(2):261, 2002.
16. Harders A, Kakarieka A, Braakman R: Traumatic subarachnoid hemorrhage and its treatment with nimodipine. J Neurosurg 85:82, 1996.
17. Wiedemayer H, Triesch K, Schafer H, Stolke D: Early seizures following non-penetrating traumatic brain injury in adults: Risk factors and clinical significance. Brain Inj 16(4):323, 2002.
18. Schierhout G, Roberts I: Anti-epileptic drugs for preventing seizures following acute traumatic brain injury [review]. Cochrane Database Syst Rev (2):CD, 2003. http://www.update-software.com/abstracts/a6000173shtm. (Accessed May 30, 2003)
19. Wojtys EM, Hovda D, Landry G, et al: Concussion in sports. Am J Sports Med 27(5):676, 1999.
20. Alves W, Macciocchi S, Barth J: Postconcussive symptoms after uncomplicated mild head injury. J Head Trauma Rehabil 8:48, 1993.
21. Faul M, X. L. (2010). Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Centers for Disease Control and Prevention. Atlanta (GA): National Center for Injury Prevention and Control.
22. Finkelstein E, C. P. (2006). The Incidence and Economic Burden of Injuries in the United States. New York, NY, USA: Oxford University Press.
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