Purpose of Monitoring ICP: Elevated ICP is a critical concern because it can lead to secondary complications that worsen patient outcomes.
Normal Range of ICP: Generally accepted range is between 10-15 mmHg.
Interventions for High ICP: Start interventions when ICP exceeds 20 mmHg for 20 minutes or longer to avoid herniation, which is fatal.
Spikes vs. Sustained ICP: A brief spike in ICP (e.g., to 35 mmHg when rolling a patient) is less concerning than a sustained increase.
Early Manifestations (in Green):
Declining Level of Consciousness (LoC)
Restlessness
Irritability
Confusion
Headache
Unilateral weakness
Pupil changes
Late Manifestations (in Blue):
Severe headache
Deterioration of LOC to coma
Erratic respiratory rate (apnea or hyperventilation)
Tachycardia (rapid, thready pulse)
Hypotension
Hyperthermia
Projectile vomiting
Loss of corneal, cough, and gag reflexes
Posturing
Seizures
Fixed pupils (non-reactive)
Flaccidity
Cushing's Triad:
Hypertension with widened pulse pressure
Bradycardia
Bradypnea.
Cranial Volume: Fixed volume in the cranial cavity comprising brain, blood, and cerebrospinal fluid (CSF). An increase in any component requires a compensatory decrease in others to maintain balance.
Consequences of Imbalance: Increased blood volume (e.g., bleeding) leads to reduced space for brain and CSF, resulting in increased ICP.
Neuro Assessment: Regular neuro assessment, ICP monitoring, can include arterial lines for hemodynamic monitoring.
ICP Monitoring Methods: Common methods include a bolt or external ventricular drain (EDD).
Normal ICP Values: Remember, aim for ICP readings ideally below 20 mmHg.
CT/MRI
Craniotomy
Burr holes
Cranioplasty for edema
Cerebral Ventricular drains
Effects of Cerebral Edema: Increases capillary pressure and leakage contributing to elevated ICP. Increased pressure compresses blood vessels leading to ischemia, which prompts autoregulation (vasodilation) and further elevates ICP.
Role of CO2: High CO2 causes vasodilation (increased ICP) while low CO2 leads to vasoconstriction (decreased blood flow). Important to control CO2**
Cerebral perfusion pressure (CPP) Needs to be less than 70
MAP- ICP= CPP
Elevate head of the bed to 30 degrees for improved venous outflow.
Maintain midline positioning to prevent venous outflow obstruction.
Monitor and control patient temperature, as extremes can increase ICP.
Create a low-stimulation environment to reduce ICP.
Limit suctioning to 10 seconds to mitigate ICP spikes.
Mechanical ventilation to maintain CO2 (35-45) and paO2 (80-100)
Use Mannitol to draw fluid out of the brain for immediate ICP reduction and monitor urine output as it can also lead to hypotension.
Mannitol (Osmitrol): osmotic diuretic (Bolus ONLY!)
Reduces ICP through drawing water out of neurons and decreasing intracranial volume when bolused. Also increases cerebral blood flow/oxygen delivery
Continuous ICP monitoring, run through filter,
Monitor- UOP, hypovolemia, hypotension, tachycardia, watch electrolytes
May see MD order Furosemide (Lasix) as an adjunctive therapy to Mannitol
Succinylcholine (Anectine): fast acting paralytic. Mostly seen IVP
Intubation, decreases tissue oxygen demand, decreasing ICP.
Monitor-Apnea, hyperkalemia
Vecuronium (Norcuron): fast acting paralytic. IVP or as a drip
Intubation, decreases tissue oxygen demand, decreasing ICP
Monitor-Apnea, hyperkalemia
Classification of Spinal Cord Injuries:
Complete: No function below injury level.
Incomplete: Some function below injury level.
Causes of Injuries:
Examples include hyperflexion, hyperextension, axial loading, and penetrating injuries.
Secondary Injuries- worsen the primary injury (Hemorrhage, ischemia, shock, edema
Primary Assessments: Always assess the respiratory system, particularly in cervical injuries due to impacts on the phrenic nerve leading to respiratory failure.
Monitoring: Motor function, sensory function, bowel and bladder control, and vital signs. Perform ongoing neurological assessments including GCS.
Respiratory Management: Monitor respiratory function closely; intubation may be required. Prevent atelectasis through incentives and ventilation support.
DVT prophylaxis (TED hose, SED, Heparin, IVC filter)
incentive spirometry
Halo fixator to stabilize C-spine
If screw comes loose stabilize neck and call for help
MAP greater than 90 (it takes more to perfuse spinal cord
Methylprednisolone (Solu-Medrol): corticosteroid. Helps lessen secondary complications of SCI by reducing spinal edema. Scheduled blood sugar checks, avoid grapefruit (could increase med level), hyperglycemia
Neurogenic Shock: ANS imbalance (increased parasympathetic), common in those with injuries above T6 within first 24 hours
Can last weeks
Hypotension, bradycardia, peripheral vasodilation, decreased LOC/UOP (may have paralysis R/T injury)
Maintain airway, immobilize spine, fluids, vasopressors, control body temp
Can lead to organ failure/death—more serious
Autonomic Dysreflexia—ANS imbalance (increased sympathetic) caused by an irritant below the level of injury (injury above T6) (often constipation/bladder distention, constricted abdomen or extremity) p. 2078
Signs/Symptoms
Sudden, severe throbbing HA
Severe hypertension
Bradycardia
Nasal stuffiness, blurred vision, N/V
Flushing/sweating above injury
Pale, cool, goose bumps, no sweating below injury
Feeling of apprehension/sense of impending doom
Interventions
Sit in upright position
Call MD
Loosen tight clothing
Assess for and treat cause
Check catheter for kinks/obstructions—insert Cath if not in
Check for fecal impaction—disimpact
Make sure room temp isn’t too hot/cold
Give nitrates or nifedipine or hydralazine
Spinal Shock—complete loss of motor, sensory, and reflex function below the level of the injury (peripheral neurons become temporarily unresponsive to brain stimuli, connection between brain and body is messed up) Can happen in any location
Usually recover within 48 hours, can last weeks
Hypotension, bradycardia, flaccid paralysis
Maintain airway, immobilize spine, fluids, control body temp
Supportive care will usually bring patients to recover on their own