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Emergency Management of the Head Trauma Patient Adam Schneider, DVM Neurology and Neurosurgery Blue Pearl 9500 Marketplace Rd Fort Myers
Emergency Management of the Head Trauma Patient
Adam Schneider, DVMNeurology and Neurosurgery
Blue Pearl9500 Marketplace Rd
Fort Myers
Head trauma
• Common cause of morbidity and mortality
• 25% of blunt trauma injuries
• Dogs: 50% motor vehicle accidents
• Cats: 50% crush injuries
• May lead to traumatic brain injury (TBI)
Traumatic brain injury
”structural or physiologic disruption of the brain by external force”
Normal brain physiology
• Cerebral perfusion pressure (CPP)• CPP = MAP – ICP
• Cerebral blood flow (CBF)• CBF = CPP/CVR
• Cerebral vascular resistance (CVR)• CVR = L(n)/vessel diameter n = viscosity
• Autoregulation• Intrinsic ability of vasculature to maintain constant CBF and ICP over wide
range of pressure (50-150mmHg)
Autoregulation
• Pressure (sympathetic nervous system)
• Chemical (PaCO2)• Increased PaCO2 = vasodilation
• Example: hypoventilation
• Decreased PaCO2 = vasoconstriction• Example: hyperventilation
• Normal PaCO2 = 35-45 mmHg
Intracranial compliance
• Monro-Kellie hypothesis• ICP = Parenchymal volume + Blood volume + CSF volume
• Change in any one volume without compensatory decrease in others leads to increased ICP
• Head trauma• Adds hemorrhage and edema to the compartments
• Autoregulation lost
• Increase volume = increased ICP = decreased CPP(CBF) = ischemia and neuronal death 🙁
Primary brain injury
- Physical disruption of structures within skull at time of injury
- Beyond clinical control
Secondary injury
• Minutes to days
• All lead to increased ICP, decreased CBF, ischemia and neuronal death
Secondary injury
• Severely increased ICP leads to brainstem compression• Depressed mental, cardiac and respiratory function
• Brain herniation and death
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Cushing’s Reflex
• A.k.a cerebral ischemic response
• ↑ICP = ↓CBF and ↑CO2 -> systemic vasoconstriction (↑MAP) to maintain CPP
• Baroreceptors sense hypertension -> reflex bradycardia
• *Patients with decreased mentation, hypertension and bradycardia indicates increased ICP
• Time to treat!
Increased ICP
• Sudden decrease in mentation
• Pupillary light reflex/pupil size
• Decerebrate posture
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Modified Glasgow Coma Scale
• Validated in dogs
• 3 categories (score 1-6 each)• Motor activity
• Brainstem reflexes
• Level of consciousness
• Total score 18 (normal)
• MGCS of 8 w/in 48hrs = 50% chance survival
• *Designed for monitoring not predicting individual outcomes
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Imaging
• Extracranial
• Intracranial CT > MRI
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Fluid therapy
• ICP : MAP (when autoregulation lost)• Maintain systolic pressure >90mmHg
• Retrospective study (human): Single event of SBP <90mmHg = 150% increase in mortality
• Not exact science
• Pros/cons for all fluid types
• BBB not intact and brain is less tolerant of fluids
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Isotonic crystalloids (0.9%, P-lyte, LRS)
• Titrate to effect
• ¼ shock dose• 20ml/kg (dogs)
• 15ml/kg (cats)
• 0.9% NaCl (least amount of free water)
• Cons: • Acidifying (worsen acid-base status)
• Volume redistribution can worsen cerebral edema
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Colloids
• Supports plasma oncotic pressure to minimize extravasation
• Longer duration of action vs crystalloids
• Cons: • No clear benefit in major metaanalyses studies in people
• SAFE trial: 4% albumin significantly increased mortality vs 0.9% NaCl in TBI
• No studies with synthetic colloids (hetastarch) in TBI
• Some consider synthetic colloids fluid of choice in TBI
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Hyperosmolar Therapy: Hypertonic saline vs Mannitol
• Create osmotic gradient across the intact BBB
• Water shifts from interstitial space to intravascular space to decrease ICP
• Mannitol and Hypertonic saline routinely used
• Recent metaanalyses favors HTS, but controversy remains
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Hypertonic saline
• Several benefits• Rapidly expands intravascular space (patients in shock)
• Allows smaller volumes administered
• Reduces viscosity (CVR = L(n)/vessel diameter n = viscosity & CBF = CPP/CVR)
• Reduces endothelial swelling
• Modulation of neuroinflammatory pathways
• Duration: 75 minutes
• Cons:• Hypernatremic or hyponatremic patient
• Dose: 4ml/kg (7.5% NaCl); 5.4ml/kg (3% NaCl)
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Mannitol
• Sugar molecule• Acts as osmotic diuretic• Osmotic effect immediate
• Expands plasma volume and reduces viscosity, improving CBF• Persists 75 minutes
• Osmotic gradient crosses BBB in 15-30 mins, persists 2-5 hrs• Shifts fluid from brain to intravascular space
• Free radical scavenger• Cons:
• Diuretic effect: hypotensive patients and fluid correction must occur• Cannot use in hypovolemic patients
• Dose: 0.5-1g/kg over 20 mins (2 doses in 24 hours)
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Extravasation of Mannitol
• Concern for mannitol leaking into extravascular space • “reverse osmotic shift”
• Study: no difference found between patients with intracerebral hemorrhage that did or did not receive mannitol
• Unlikely with appropriate dosing
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Furosemide
• Historically given with mannitol to:• Decrease CSF production
• Counteract initial plasma expansion
• Potentiate the osmotic gradient
• Unproven
• May increase risk of dehydration and hypovolemia
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Anesthetics, Analgesics and Sedatives
• Analgesia essential in head trauma
• Balanced approach reduces risks of side effects
• ICP increases with inhalant anesthesia (>1-1.5 MAC)• Hypoventilation and hypercapnia also raise ICP
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Inhalant anesthesia
• Isoflurane
• MAC > 1-1.5 increases ICP
• Lower concentrations cause vasodilation which may improve CPP
• Contraindicated if ICP already increased• Recommend total IV anesthesia (e.g. propofol)
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Total Intravenous anesthesia
• Required for MRI, mechanical ventilation or refractory seizures
• Propofol is ideal (1-6mg/kg IV to effect, then 100-400mcg/kg/min)
• Study: Improved CPP and maintain pressure autoregulation better than inhalants
• Also may be neuroprotective• Via modulation of GABA receptors and antioxidant effect
• Cons: hypotension and hypoventilation
• Careful titration, meticulous monitoring and supportive care essential!
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Analgesia
• Patient comfort helps prevent further increases in ICP
• Pain and anxiety shown to increase cerebral metabolic rate• Increases CBF, blood volume and ultimately ICP
• Opioids – ideal (full mu agonists best)• Cardiovascular sparing
• Easily reversible
• Cons: respiratory depression
• Minimized with titration
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Fentanyl
• Less emetogenic than hydromorphone
• Fast acting and quickly wears off
• Reversible (if necessary)
• Cons: • requires CRI
• Becoming difficult to come by
• Dose • 2-6 mcg/kg loading dose followed by 2-6mcg/kg/hr CRI (dogs)
• 1-3 mcg/kg, then 1-3 mcg/kg/hr (cats)
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Ketamine
• Analgesic and hypnotic effects
• NMDA receptor antagonist• Neuroprotective role?
• Minimal respiratory depression
• Stimulate cardiovascular system
• Historically thought to increase ICP• New studies do not support this claim
• TBI studies suggest ketamine improves CPP and lowers vasopressor requirements
• Dose: 0.1 -1 mg/kg IV followed by 2-10 mcg/kg/min
• Combine with opioid
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Alpha-2 agonists
• Demedetomidine
• Reversible
• Provides sedation, anxiolysis, and analgesia
• Controversial in TBI
• Only used when others unavailable or not enough
• Dose: 0.5-3 mcg/kg, then 0.5-1 mcg/kg/hr
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Anticonvulsants
• Established correlation between severity of TBI and post traumatic epilepsy (PTE) as well as development of epilepsy compared with general population• Human medicine and 1 paper in veterinary medicine
• Early and late seizure development post injury (<7 or >7 days)
• Cochrane review evaluated prophylactic antiepileptic medications for prevention of early and late seizures (humans)• No evidence to support prophylactic use in preventing seizures.
• No studies in veterinary medicine
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Anticonvulsants - Benzodiazepines
• Diazepam, midazolam• 0.5-1 mg/kg IV
• Repeat 3 times, if having to repeat every 15-30mins start CRI• 0.25-1 mg/kg/hr
• Lower dose in patients with hepatopathy
• Increase dose for patients on phenobarbital
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Anticonvulsants - Levetiracetam
• Fast acting
• Emergency and maintenance medication
• Few side effects (sedation)
• No monitoring required
• Emergency dose: 60mg/kg IV, then 20mg/kg IV q8hr
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Anticonvulsants - Phenobarbital
• For refractory seizures that are not responding to benzodiazepines
• Dose: 4mg/kg q6hrs x 4 doses, then 2-3 mg/kg q12hrs
• Cons:• Injections are expensive
• Heavily sedating/coma
• Hepatotoxicity if not monitored
• Requires routine monitoring
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Anticonvulsants - Propofol
• Alternative for refractory seizures
• Use same guidelines for monitoring as previously noted
• Same dose as for anesthetic plane
• Requires intubation and mechanical ventilation
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Corticosteroids
• Once part of routine therapy for TBI
• CRASH trial results• Increased risk of death at both 2 weeks and 6 months in people
• NOT recommended for TBI patients
• When are they recommended?• Solu medrol (methylprednisolone) ONLY
• Decrease lipid peroxidase (free radical production)
• Within first 8 hours of Spinal Cord Injury
• Falling out of favor here too
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Corticosteroids
• Cause hyperglycemia• Studies: Hyperglycemia associated with poorer outcomes in patients with TBI
• Side effects• Ulcerations
• Diarrhea – dehydration, hypovolemia
• That being said…• Some studies still support the use of Solu-medrol in TBI
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Gastric ulcer prophylaxis
• Studies: • Neurologically injured patients are increased risk of gastric ulceration and bleeding(69)
• PPI and H2r antagonists effective in preventing GI bleeds in people
• No increase risk of nosocomial pneumonia (70)
• Proton pump inhibitors (PPI)*• Pantoprazole (injectable): 1mg/kg q24hrs
• Omeprazole (oral): <10kg = 10mg; >10kg = 20mg
• H2r antagonists• Famotidine: 0.5-1mg/kg PO or IV q12-24hrs
• *bonus effect: PPIs decrease CSF production (lower ICP)
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Oxygen and Ventilation
• Goals:• Sp02 > 94%
• Pa02 > 80mmHg
• Oxygen therapy• Individualized
• Nasal cannulas vs mask vs cage
• PaC02 most detrimental to CBF• Low C02 (<30mmHg)/hyperventilation = vasoconstriction = ischemia
• High C02 (>50mmHg)/hypoventilation/pulmonary contusion = vasodilation = increased ICP
• Prophylactic hyperventilation not recommended
• Normoventilation (PaCO2 35-40mmHg) ideal
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Nutrition
• Early support ideal
• Head trauma associated with hypermetabolic and hypercatabolic state
• Enteral nutrition• Supports GI integrity, immune function, decease stress
• Study: Retrospective found that nutritional support within 5 days reduced 2-week mortality and amount was inversely proportional to mortality
• Method of feeding dependent on patient mental status and ability to protect airway
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Head elevation
• Less than 30º ideal for reducing ICP, increasing CPP without affecting MAP
• Stiff board with towel underneath to avoid compressing jugulars and increasing ICP
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Therapeutic hypothermia
• Secondary brain injury inhibited by hypothermia (90 –93)ºF
• Standard of care in people for stroke, cardiac arrest, intracranial hypertension with status epilepticus
• Recent study showed no benefit for TBI with intracranial hypertension
• 1 case report in Veterinary medicine
• Current recommendation:• If head trauma patient is hypothermic, allow passive rewarming
• Do not actively cool
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Glycemic control
• Hyperglycemia leads to (humans):• increases in mortality and duration of hospitalization
• Worse neurological outcome
• Veterinary medicine, hyperglycemia is indication of severity• Not a prognostic indicator
• Insulin therapy not recommended
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Overview of head trauma stabilization
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Surgical treatment options - Case
• Chanel, 3yr FS Chihuahua
• Fell off stool
• Brought to family veterinarian for status epilepticus and dent in head since fall
• Family veterinarian called SVS for advice
• Not responding to valium
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Chanel
• Recommended propofol CRI and ambulance ride to SVS!
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Chanel
• Upon arrival Chanel intubated
• Phenobarbital load and levetiracetam
• Neurologic exam – limited!
• Next step…
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Chanel
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Decompressive craniectomy
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Post-operative
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Ideally…
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References• Platt S, Radaelli S, McDonnell J. The prognostic value of the Modified Glasgow Coma Scale in head trauma in dogs. J Vet Intern Med 2001;15(6):581–4.
• Dewey CW. Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract 2000;30(1):207–25.
• DiFazio J, Fletcher DJ. Updates in the management of the small animal patient with neurologic trauma. Vet Clin North Am Small Anim Pract 2013;43(4):915–40.
• Kuo K, Bacek L. Head Trauma. Vet Clin Small Anim 48 (2018) 111–128
• Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care (San Antonio) 2010;20(2):177–90.
• Sharma D, Holowaychuk M. Retrospective evaluation of prognostic indicators in dogs with head trauma: 72 cases (January–March 2011). J Vet Emerg Crit Care (San Antonio) 2015;25(5):631–9.
• Lagares A, Ramos A, Pe ́rez-Nun ̃ez A, et al. The role of MR imaging in assessing prognosis after severe and moderate head injury. Acta Neurochir 2009;151(4): 341–56.
• Beltran E, Platt SR, McConnell JF, et al. Prognostic value of early magnetic resonance imaging in dogs after traumatic brain injury: 50 cases. J Vet Intern Med 2014;28(4):1256–62.
• SAFE Study Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group, Australian Red Cross Blood Service, George Institute for In- ternational Health, Myburgh J, Cooper DJ, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med 2007; 357(9):874–84.
• Misra UK, Kalita J, Ranjan P, et al. Mannitol in intracerebral hemorrhage: a randomized controlled study. J Neurol Sci 2005;234(1–2):41–5.
• Roberts A, Pollay M, Engles C, et al. Effect on intracranial pressure of furosemide combined with varying doses and administration rates of mannitol. J Neurosurg 1987;66(3):440–6.
• McCulloch T, Visco E, Lam A. Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia. Anesthesiology 2000;93(5):1205.
• Zeiler FA, Teitelbaum J, West M, et al. The ketamine effect on ICP in traumatic brain injury. Neurocrit Care 2014;21(1):163–73.
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Questions?
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