NRS 215 Term 4 Notes - Spinal Cord Injury

Spinal Cord Injury ================== Any injury or trauma to the spinal cord and vertebrae that causes temporary or permanent changes in its function. Associated with MVA, falls from heights, sporting accidents and direct blows to the back and vertebrae. **Risk factors:** - [Age]: more than 50...

Spinal Cord Injury ================== Any injury or trauma to the spinal cord and vertebrae that causes temporary or permanent changes in its function. Associated with MVA, falls from heights, sporting accidents and direct blows to the back and vertebrae. **Risk factors:** - [Age]: more than 50% of SCI occur in age group 16-30 y/o, older people experience the most fall related injuries. - [Gender]: males are 4x more affected than females - [Alcohol use]: a factor in many MVA resulting in SCI, as well as diving or violent trauma. **Classification and level of injury** The part of the spinal cord that was damaged corresponds to spinal nerves at that level and below. Injuries can be cervical (C1-C8), thoracic (T1-T12), lumbar (L1-L5) or sacral (S1-S5). *Paraplegia* results is thoracic or lumbar cord is damaged. [Complete], with total loss of sensation and muscle function at lower sacral segments [Incomplete], involving preservation of motor or sensory function below the level of injury in the spinal cord. *Sensory impairment*: based on neurological responses, touch and pinprick sensations and strength of the muscles that control key motions on both sides of the body. *Motor impairment*: [muscle strength] is scored on a scale of 0-5 and sensation is graded on a scale of 0-2 (0 is no sensation). 1. No muscle contraction 2. Muscle flickers 3. Full ROM, gravity eliminated 4. Full ROM, against gravity 5. Full ROM, against resistance 6. Normal strength **\ ** **Major mechanisms of injury** - [Hyperextension:] excessive posterior movement of the head, e.g. rear end collisions or falls on the chin - [Hyperflexion]: head and neck forcibly hyper-flex and the snapped backward into forced hyperextension, e.g. sudden deceleration as a head-on collision causing whiplash - [Compression movement]: extreme vertical movement, causing vertebrae to shatter/burst, e.g. dive into shallow water, fall greater than 10 to 20 feet on legs - [Rotational movement]: caused by extreme lateral flexion or twisting of the head and neck, e.g. rollover MVC or motorcycle accident - [Distraction]: excessive force of column and cord, e.g. child inappropriately wear shoulder belt around the neck - [Penetrating injury]: caused by direct contact with the spinal cord by knife or bullet **Pathophysiology** The pathophysiology of spinal cord injury (SCI) progresses in several stages: - [Shortly after the injury]: Petechial haemorrhages are observed in the central grey matter of the spinal cord. - [1 to 2 hours post-injury]: red blood cells, fluid, and polymorphonuclear leukocytes infiltrate the grey matter, leading to vascular stasis and endothelial damage. Haemorrhage, oedema, and metabolic changes cause ischemia, leading to necrosis. Hypoxia worsens, as oxygen levels drop below what the spinal cord requires, resulting in increased lactate and toxic levels of norepinephrine. Norepinephrine causes vasospasm, furthering hypoxia and necrosis. - [4 hours post-injury]: Coagulation necrosis affects up to 40% of the grey matter and adjacent white matter. - [24 hours post-injury]: The spinal cord becomes mostly necrotic tissue, with aggregated red blood cells and minimal recognizable white matter. Oedema spreads above and below the injury site, increasing ischemic damage, and the outcome mimics mechanical severance of the cord. - [48 hours post-injury]: Haemorrhagic necrosis completes the lesion, and nerve function at the level of the injury is irreversibly lost. **[Spinal Shock]:** **Clinical manifestations** - Flaccid paralysis or weakness of all the muscles below the level of injury - Loss of spinal reflex and absence of somatic or visceral sensation below the level of injury - Spinal shock (temp loss of motor, sensory and reflex function below the level of injury - Bowel and bladder dysfunction - Severe tenderness or pain on the neck and back - Spasms of the neck and back muscles, respiratory irregularities and impaired thermoregulation **Emergency management** - Open and maintain airway using jaw thrust method. - Ensure minimal movement and immobilisation by instructing pt not to move neck or head and stabilise the head with a neck collar. - Apply a back splint by strapping the pt onto a stretcher/special spinal board. - Assess motor and sensory function - Administer prescribed sedatives or analgesics - Observe for changes in level of consciousness, such as drowsiness. **Complications** - Pneumonia, other pulmonary complications (hypoventilation, ineffective breathing patterns) - DVT (look out for skin discoloration, warmth, swelling) - Autonomic hyperreflexia (med emergency, may result in stoke, blindness or death) - Altered thermoregulation - Orthostatic hypotension - GIT problems, urinary (UTI, renal calculi) and musculoskeletal complication (spasticity, osteoporosis) - Anxiety and depression Burns and Shock =============== **Understand Burns** Burns are any injuries to body tissues caused by heat, electricity, chemicals or gases The depth of a burn injury depends on the [intensity] (temp\ 12 years or taller than 150cm) and one for children \< 12 years or less than 150cm. - Both SATS charts consists of a flow diagram, sections for Emergency (red), Very urgent (orange) and Urgent (yellow) signs, a section for calculating TEWS based on vital signs and a section for additional observations. - TEWS is not calculated if a patient presents with any emergency signs; these patients are automatically categorized as RED and taken to the resuscitation area immediately. **Principles of triage in a trauma unit** - Triage involves sorting patients based on injury severity and making management decisions for patients with multiple traumas in an emergency. - The primary goal of triage is to prioritize patients based on medical urgency when patient load exceeds available resources. - SATS priority levels are characterized by colour and target time for treatment: - [Red]: emergency signs\* or TEWS of 7 or more -- immediate treatment in resus area - Not breathing, current seizures, cardiac arrest, hypoglycaemia (less than 3mmol/L) or burns (facial/inhalation); TEWS do NOT need to be calculated - [Orange]: very urgent signs\* or TEWS of 5/6 -- treat within 10 minutes - High speed injuries, e.g. MVA, PVA, fall from roof or high velocity GSW - Reduced level of consciousness, patient not fully alert (confused, only responds to verbal/painful stimuli or unresponsive) - Patient presents with painful, pale, pulseless, weak, numb limb - [Yellow]: urgent signs\* or TEWS of 3 or 4 - treat within 1 hour - Controlled haemorrhage -- patient presents with active bleed, apply direct pressure with dry dressing; dislocated finger/toe - Abdominal pain, pregnancy + trauma/PV bleed, closed fracture, diabetic, glucose over 17mmol/L with no ketonuria - [Green]: no emergency, very urgent or urgent signs and TEWS of less than 3 -- treat within 4 hours **Primary and secondary survey in emergency care** - Changed from ABC to CAB; CAB prioritizes chest compressions over airway and breathing in adults and children. ([Primary survey]) - [Circulation]: check responsiveness, call for help if unresponsive and not breathing and begin chest compressions immediately - [Airway]: establish patient airway using the head tilt-chin method unless head or neck injury is suspected. Protect cervical spine in case of injury - [Breathing]: give two rescue breaths or use an ambu bag, allowing chest rise and fall between breaths, continue compressions afterwards. - [Disability]: determine neurological status using Glasgow Coma Scale. - Once respiration and heartbeat are re-established, control bleeding if present and treat for shock. - [Secondary survey] involves a complete history, head-to-toe assessment, diagnostic and lab tests, monitoring device insertion, splinting suspected fractures, wound cleansing, closure, dressing and other interventions based on the patient\'s condition. **Types of fractures** - Closed fracture: broken bone has not pierced the skin - Open fracture: broken bone cuts through the skin, or wound leads to fracture site - Greenstick fracture: small, slender crack in the bone Asthma and COPD --------------- **Definition and triggers** Asthma is defined as a chronic inflammatory condition of the airways which is usually allergic in origin. This chronic inflammation makes the airways hyper-responsive, leading to obstruction from increased inflammation, bronchoconstriction and mucus plugs. Asthma attacks can be triggered by extrinsic and/or intrinsic factors. One specific factor is **Exercise-Induced Asthma (EIA)**, which is characterized by a narrowing of the airways that occurs 5-20 minutes after activity. Breathing in cool, dry unfiltered air through the mouth during exercise is the main reason behind the narrowing of the airways. Constricted airways reduce airflow, making it harder to breathe, leading to coughing, wheezing and difficulty breathing. Symptoms usually worsen 5-20 minutes after stopping activity, with some people experiencing a less severe "late-phase reaction" 4-12 hours later. **Pathophysiology** Characterized by hyper-responsiveness and narrowing of bronchi due to: - [Swelling of mucosa]: this swelling increases the production of sticky mucus or secretions lying in the airways, signifying inflammation. - [Muscle spasms around the bronchi]: these spasms are directly related to inflammation and contribute to airway narrowing. - [Bronchial narrowing or obstruction]: when the bronchi become too narrow or partially obstructed due to inflammation and spasm, the classic symptoms of asthma arise. **Clinical manifestations** Symptoms commonly include coughing, wheezing, tight chest and shortness of breath, which are typically worse at night and after activity or exercise. **Diagnostic Tests** - History and clinical manifestations - [Peak expiratory flow rate]: assess lung function with a typical value around 600L/min. - [Forced expiratory volume]: lung function test that measures the amount of air forcefully exhaled in one second - [FeNO test]: measures nitric oxide levels in your breath, which indicates inflammation in the lungs - [Spirometry]: measures how fast you can breathe out and the amount of air your lungs can hold - [Chest X-ray and allergy test]: performed after an asthma diagnosis to identify potential triggers like allergies **Management** [Preventative/Prophylactic Measures]: aim to reduce and prevent airway inflammation; do NOT provide immediate symptom relief - Inhaled corticosteroids, e.g. Budesonide (Pulmicort) and Beclomethasone (Becotide) - Cromolyn's, e.g. sodium cromoglycate (Lomudal) and ketotifen [Relievers (Short-acting bronchodilators)]: provide immediate relief from bronchospasm by relaxing the muscles surrounding the bronchial tubes - Beta-2-agonists, e.g. Salbutamol, Ventolin, Breatheze, etc. - Theophyllines, e.g. Alcophyllin [Controllers (Long-acting bronchodilators)]: provide sustained bronchodilation and protection against bronchoconstriction, e.g. long-acting Beta-2-agonists like Salmeterol and Theophyllines/Aminophylline, anticholinergics and combination drugs. **A**drenergic (Beta 2 Agonists -- Albuterol) **S**teroids **T**heophylline **H**ydration (IV) **M**ask O~2~ **A**nticholinergics **Promotive measures**: encourage patients to avoid asthma triggers and regular medication adherence, even in absence of symptoms. **Rehabilitative measures**: with the appropriate treatment, most asthmatics can lead normal lives, although asthma cannot be completely cured. **Complications** - Poorly controlled asthma can negatively impact quality of life, leading to: - Fatigue or exhaustion; limited ability to exercise - Poor sleep and mental health - Decreased lung function and reduced productivity at work Epilepsy ======== Epilepsy is a neurological condition characterized by unusual electrical activity in the brain causing unprovoked seizures. **Aetiology** Specific causes of convulsions include brain damage from prenatal/perinatal causes (loss of O~2~ or trauma during birth), congenital abnormalities or genetic conditions associated with brain malformations; inborn errors of metabolism; brain tumours; hyperpyrexia; acidosis, hypoxia or alcohol/ drug abuse. **Pathophysiology** Decreased inhibitory neurotransmitter (INT) activity/Inactivation of INT activity leads to excitatory neurotransmitter (ENT) activity. This causes rhythmic repetitive hyper synchronous discharge of neurons which leads to seizure focus and seizures. This eventually leads to repetitive seizures, resulting in epilepsy. **Clinical Manifestations** - Characteristics of seizures may vary and depend on where in the brain the disturbance first starts and how far it spreads. - Temporary symptoms occur such as loss of awareness/consciousness and disturbance of movement, sensation, mood or other cognitive functions. **Classification of seizures** - [Partial (Focal) Seizures]: originate in a specific brain region and symptoms may very depending on the affected area. - [Focal/Simple Partial]: awareness is preserved during the seizure; symptoms involve sensory disturbances, motor actions, psychic experiences or autonomic changes. - [Complex Partial]: altered awareness characterizes these seizures; individuals may appear dazed, confused or display unusual behaviours - [Generalized Seizures:] affect both brain hemispheres, typically causing LoC and occur without warning. - [Tonic-Clonic] (Grand Mal): characterized by 2 phases- a tonic phase with muscle stiffening and LoC, followed by a clonic phase with rhythmic jerking movements. - [Absence] (Petit Mal): brief episodes of starting, often lasting less than 10 seconds, with impaired awareness. - [Myoclonic:] sudden, brief muscle jerks that may involve a limb or the entire body - [Atonic:] sudden loss of muscle tone leading to falls, dropping objects or head nodding. **Diagnostic Tests** Utilize diagnostic tools like EEG (Electroencephalogram), CT scans, MRIs, blood tests, PET and SPECT scans to confirm seizure activity, classify seizure types and rule out other potential causes. **Pharmacological Management** Anticonvulsants act in one of two ways: suppression of dysfunctional neuronal discharge or prevention of seizure discharge spread - [Sodium channel blockers] (e.g. Phenytoin): stabilize neuronal cell membranes, preventing seizure impulse propagation - [GABAergic meds] (e.g. Barbituates, Valproic Acid): enhance inhibitory effects of GABA, reducing neuronal excitability - Other mechanisms (e.g. Succinimides, Benzodiazepines): target specific pathways to suppress seizure activity **Patient Management** - Medication adherence: emphasize importance of lifelong treatment adherence to prescribed anticonvulsant meds. - Medic-alert disc: to inform others in case of seizure - Sedative effects: educate on potential sedative effects of meds and increased sedation when combined with alcohol - **Lifestyle modifications:** advise against engaging in activities like horse riding and swimming alone; promote a balanced lifestyle (moderate exercise, rest, etc.) - **Injury prevention:** provide guidance on seizure first-aid measures, such as protecting the individual from harm by clearing the surrounding area, cushioning their head, loosening tight clothing, not restricting movement or putting anything in their mouth, and assisting with breathing by positioning them on their side after the seizure subsides.