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Basics ⬇

Basics

Definition

  • Traumatic-caused by external forces.
  • Non-traumatic-caused by non-violent forces (e.g., hypoxia, metabolic disorders, vascular disruption, infection, toxicity, neoplasia).
  • Primary-direct initial insult when tissue and vessels are stretched, compressed or torn.
  • Secondary-alterations of brain vasculature and tissue following primary injury.

Pathophysiology

  • Acceleration, deceleration, and rotational forces traumatize brain tissue.
  • High oxygen and glucose requirements put the brain at risk for hypoxia.
  • Oxygen delivery dependent on CBF and CPP (= MAP – ICP).
  • Intracranial bleeding, edema (vasogenic and cytotoxic), vasodilation, and/or vasospasms increase ICP, causing low CBF, ischemia, brain swelling, and herniation; slow, progressive increase in ICP better tolerated than small, acute rise.
  • Hypotension, hypoxia-major contributors to secondary injury.

Systems Affected

  • Nervous-altered mentation, cranial nerve deficits, seizures, twitching, postural changes.
  • Cardiovascular-arrhythmias.
  • Endocrine/Metabolic-alterations in ADH release and sodium concentration; central temperature dysregulation; insulin resistance; depletion of cortisol.
  • Ophthalmic-changes in eye position, eye movements, pupillary light reflexes, papilledema.
  • Respiratory-hyper- and hypocapnea; abnormal breathing patterns; neurogenic pulmonary edema.

Genetics

None

Incidence/Prevalence

  • Head and neck injuries found in up to 34% of dogs and cats suffering blunt force trauma.
  • Parenchymal and extradural hematomas found in 10% of dogs and cats with signs of mild head injury and in up to 80% with severe head injury.

Geographic Distribution

Widespread

Signalment

Species

Dog and cat

Signs

Historical Findings

  • Determine cause-trauma; cardiac arrest; heart failure; hypertension; toxins; coagulopathies; severe respiratory compromise; prolonged seizures; hypoglycemia.
  • Decline in neurologic condition-implies progression from intracranial bleeding, cerebral edema, ischemia.
  • Seizure activity-cerebral or diencephalon involvement.

Physical Examination Findings

  • Evidence of head trauma-open wounds, epistaxis, blood in the ear canals.
  • Cardiac or respiratory insufficiency-hypoxia, cyanosis, hypoventilation.
  • Poor perfusion-weak pulse, pale mucous membranes.
  • Skull palpation-fractures, open fontanelles.
  • Sustained bradycardia-midbrain, pontine, or medullary lesion.
  • Cushing's reflex-bradycardia and hypertension.
  • Ecchymosis, petechiae, retinal hemorrhages or distended vessels-hypertension, coagulopathy.
  • Papilledema-cerebral edema.
  • Retinal detachment-infectious, neoplastic, or hypertensive causes.

Neurologic Examination Findings

Mental Status

  • Level of consciousness and cranial nerve deficits-localize lesion to cerebral cortex (better prognosis), midbrain/brainstem, or multifocal.
  • Postural changes-decerebrate rigidity with midbrain lesion; decerebellate rigidity with cerebellar lesion.
  • Peracute focal deficits suggest vascular or neoplastic causes.

Pupillary Light Reflexes

  • Miotic responsive pupils-cerebral or diencephalic lesion (rule out traumatic uveitis, Horner's syndrome).
  • Pinpointed unresponsive pupils-diencephalic, pontine or medullary lesion.
  • Dilated unresponsive pupil(s) or midpoint fixed unresponsive pupils-midbrain lesion.

Cranial Nerves

  • Normal with altered mentation-cerebrum-diencephalon lesion.
  • CN II- Loss of menace and dazzle response with dilated unresponsive pupils-cranial forebrain.
  • Loss of physiologic nystagmus-brainstem lesion
  • CN III-midbrain lesion.
  • CN V–XII-pontine or medullary lesion.

Respiratory Patterns

  • Cheyne-Stokes-severe diffuse cerebral or diencephalon lesion
  • Hyperventilation-midbrain lesion
  • Ataxic or apneustic-pontine or medullary lesion

Causes

  • Trauma
  • Prolonged hypoxia or ischemia
  • Prolonged shock
  • Severe hypoglycemia
  • Prolonged seizures
  • Severe hyperthermia or hypothermia
  • Alterations in serum osmolality
  • Toxins
  • Neoplasia
  • Hypertension
  • Hemorrhage
  • Inflammatory, infectious, immune-mediated diseases
  • Thiamin deficiency
  • Hydrocephalus
  • Parasitic migration

Risk Factors

  • Free-roaming-trauma, toxins
  • Coexisting cardiac, respiratory, hemostatic, hepatic disease
  • Diabetes mellitus-insulin therapy

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

Systemic causes of altered states of consciousness or central vestibular signs-metabolic disease; toxins; drugs; infection.

CBC/Biochemistry/Urinalysis

  • Reflect systemic effects of neurologic signs
  • Alterations in serum sodium suggest central ADH abnormalities

Other Laboratory Tests

  • Arterial blood gas
  • Coagulation profile.
  • Infectious disease titers

Imaging

  • Skull radiographs-detect fractures.
  • CT-detects acute hemorrhage, infarcts, fractures, penetrating foreign bodies, hydrocephalus, herniation.
  • MRI-detects cerebral edema, hemorrhage, mass, hydrocephalus, infiltrative diseases, inflammation, herniation, fractures.
  • Ultrasound optic disk-if >3 mm diameter, may be associated with brain edema.

Diagnostic Procedures

  • ECG-detects arrhythmias
  • BP-determine perfusion
  • CSF analysis-if cause unknown and no contraindications

Pathologic Findings

  • Brain edema or inflammation
  • Herniation
  • Hemorrhage
  • Hydrocephalus
  • Infarct
  • Laceration, contusion
  • Hematomas
  • Skull fracture
  • Necrosis
  • Apoptosis

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Goals of therapy-maximize oxygenation and ventilation; support BP and CPP; decrease ICP; decrease cerebral metabolic rate.
  • Maintain systolic BP >90 mmHg and PCO2at 35–40 mm Hg; with suspected elevated ICP, hyperventilation to 32–35 mmHg.
  • Maintain PaO2 >60 mmHg, SaO2 >90%, SpO2 >94%.
  • Avoid cough or sneeze reflex during intubation or nasal oxygen supplementation; lidocaine (dogs: 1–2 mg/kg IV) before.
  • Do not compress jugular veins.
  • Orotracheal intubation if gag reflex lost.

Nursing Care

  • Aggressive therapy for midbrain/brainstem lesion or declining neurologic signs.
  • Overzealous fluid resuscitation can contribute to brain edema.
  • Small-volume fluid resuscitation techniques to maintain systolic BP >90 mmHg with normal heart rate.
  • Combination of isotonic crystalloids (10–20 mL/kg increments) with hydroxyethyl starch (5 mL/kg increments) over 5–8minutes.
  • Avoid hypertension.
  • Level head with body or elevate head and neck to a 20° angle.
  • Keep airway unobstructed; use suction and humidify if intubated; hyperoxygenate and consider IV lidocaine prior to suctioning.
  • Lubricate eye.
  • Reposition every 2–4hours to avoid hypostatic pulmonary congestion.
  • Prevent fecal/urine soiling.
  • Maintain normal core body temperature.
  • Maintain hydration with a balanced electrolyte crystalloid solution.
  • Rehabilitation exercises.

Activity

  • Restricted.
  • Consult rehabilitation specialist for appropriate exercises to maintain muscle tone.

Diet

Initiate trickle flow feeding to meet elevated metabolic demands.

Client Education

  • Neurologic signs may worsen before improving.
  • Neurologic recovery may not be evident for several days; possibly >6months for residual neurologic deficits.
  • Serious systemic abnormalities contribute to CNS instability.

Surgical Considerations

Depressed skull fracture, penetrating foreign body, uncontrollable ICP elevation (insufficient CSF drainage, hematoma/mass evacuation, herniation).

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Elevated ICP

  • Ensure systolic BP >90 mmHg. Lower ICP by hyperventilation, drug therapy, drainage of CSF from the ventricles, or surgical decompression.
  • 7% hypertonic saline-2–4 mL/kg IV; can reduce fluid volume needed to reach resuscitation endpoints; combine with colloid.
  • Furosemide-0.75 mg/kg IV; may decrease CSF production; used in patients with congestive heart failure, volume overload, hyperosmolar diseases, or anuric renal failure; use before mannitol.
  • Mannitol-0.1–0.5 g/kg IV bolus repeated at 2-hour intervals 3–4times in dogs, and 2–3three times in cats; repeated doses must be given on time; improves brain blood flow and lowers ICP; may exacerbate hemorrhage.
  • Glucocorticosteroids-no benefit in acute management and long-term outcome in humans; higher morbidity. Anti-inflammatory doses (prednisone 1 mg/kg/day) may be of benefit with brain edema related to intracranial neoplasia and infectious meningitis. Immunosuppressive doses (2 mg/kg/day) in combination with additional immunosuppressive drugs in immune-mediated meningitis.
  • Provide analgesia/sedatives (e.g., fentanyl 3–5 µg/kg IV then 3–5 µg/kg/h CRI ± lidocaine 3–5 mg/kg/h) as indicated. Avoid agents that can reduce CPP.
  • Thrashing, seizures, or uncontrolled motor activity-diazepam CRI (0.5–1 mg/kg/h), midazolam CRI (0.2–0.4 mg/kg IV), or propofol (3–6 mg/kg IV titrated to effect; 0.1–0.6 mg/kg/min CRI) monitor for hypotension; intubate if unable to protect airway.
  • Levetiracetam 20 mg/kg IV/IM/rectal q8h if seizure activity.

Other

  • Reducing cerebral metabolic rate with heavy sedation using dexmedetomidine or medically induced coma using pentobarbital (up to 10mg/kg IV over 30minutes then 1 mg/kg/h) or propofol (2–4 mg/kg IV then 0.1–0.4mg/kg/min); must intubate and support blood pressure, oxygenation, and ventilation.
  • Cooling the patient to 32–33°C (89–91°F) for 48h may provide cerebral protection when administered within 6hours of global ischemia or severe brain injury.
  • Glucose regulation.
  • Careful nasogastric tube feeding for early trickle flow feeding; cisapride (0.5 mg/kg PO q8–12h) and metoclopramide (1–2mg/kg/day) may promote GI motility.
  • Desmopressin for refractory hypernatremia. Emergency dosage not established for animals (dogs: 4 µg topical conjunctival q12h; cat: 5 µg SC q12h).

Contraindications

  • Drugs that cause hypertension, hypotension
  • Drugs that cause hyperexcitability or increase in metabolic rate

Precautions

  • Avoid hypotension, hypoxemia, hypertension, hyperglycemia, hypoglycemia, hypernatremia, hypovolemia, hypervolemia.
  • Keep head and neck above plane of body.
  • Do not compress jugular veins.
  • Furosemide, mannitol and hypertonic saline-can cause hypovolemia and hypotension.
  • Maintain PCO2 >32 mmHg; avoid hyperventilation in the first 24–8h and do not perform therapeutic hyperventilation (32–35 mmHg) for extended periods (>48h).

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Repeated neurologic examinations-deterioration warrants aggressive therapeutic intervention.
  • BP; maintain systolic BP >90mmHg.
  • Blood gases, pulse oximetry, end-tidal CO2-to assess need for oxygen supplementation or ventilation.
  • Blood glucose-avoid severe persistent hyperglycemia and hypoglycemia.
  • ECG-arrhythmias may affect perfusion, oxygenation, and CBF.
  • ICP-to detect elevations and monitor response to therapy.

Prevention/Avoidance

Keep pets in a confined area or leashed.

Possible Complications

  • Seizures
  • Brain herniation
  • Intracranial hemorrhage
  • Progression from cerebral cortical to midbrain signs
  • Malnutrition
  • Aspiration pneumonia
  • Hypostatic pulmonary congestion
  • Corneal desiccation
  • Urine scalding
  • Airway obstruction from mucus
  • Arrhythmias
  • Hypotension
  • Hypernatremia
  • Hypokalemia
  • Respiratory failure
  • Residual neurologic deficits
  • Death

Expected Course and Prognosis

  • Young animals, minimal primary brain injury, and secondary injury consisting of cerebral edema-best prognosis.
  • No deterioration of neurologic status for 48hours-better prognosis.
  • Rapid resuscitation of systolic BP to >90mmHg and avoiding hypoxemia-better neurologic outcome.
  • Glasgow Coma Score may offer prognostic insight.

Miscellaneous ⬆

Miscellaneous

Synonyms

  • Head trauma
  • Traumatic brain injury

Abbreviations

  • ADH = antidiuretic hormone
  • BP = blood pressure
  • CBF = cerebral blood flow
  • CN = cranial nerve
  • CNS = central nervous system
  • CPP = cerebral perfusion pressure
  • CSF = cerebrospinal fluid
  • CT = computed tomography
  • ECG = electrocardiogram
  • GI = gastrointestinal
  • ICP = intracranial pressure
  • MAP = mean arterial pressure
  • MRI = magnetic resonance imaging

Suggested Reading

Dewey CW, Fletcher DJ. Head trauma management. In: Dewey CW, ed. A Practical Guide to Canine and Feline Neurology. 2nd ed. Ames, IA: Wiley, 2008, pp. 221–235.

Fletcher D, Syring R. Traumatic brain injury. In: Silverstein D, Hopper K, eds. Small Animal Critical Care Medicine. St. Louis, MO: WB Saunders, 2009, pp. 658–662.

Freeman C, Platt SR. Head trauma, In: Platt SR, Garosi LS, eds. Small Animal Neurological Emergencies. London: Manson Publishing Ltd, 2012, pp. 363–382.

Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care 2010, 20:177–190.

Authors Rebecca Kirby and Elke Rudloff

Consulting Editor Joane M. Parent

Client Education Handout Available Online