EXAM Prep Flashcards
Types of Traumatic Neurological Emergency Presentations:
Traumatic Brain Injury TBI: Concussions, Contusions, Skull Fractures, Traumatic Subdural/ Subarachnoid Haemorrhage
Symptoms of Traumatic Neurological Presentations
Headache
Confusion
Loss of Consciousness
Seizures
Focal Neurological deficits
Types of Non-Traumatic Neurological Presentations:
Stroke (Ischaemic or Haemorrhagic)
Seizures (Generalised or Focal)
Meningitis / Encephalitis
Brain Tumours
Pathophysiology of Ischaemic Stroke
Occlusion of a cerebral artery, leading to decreased blood flow and ischemia
Assessment of Ischaemic Stroke
Fast acronym (Face, Arms, Speech, Time)
CT scan to differentiate from Haemorrhagic Stroke
Neurological observations
Management of Ischaemic Stroke
Reperfusion
Thrombolytics (e.g. tPA) if within time window
Antiplatelet therapy and rehabilitation
Pathophysiology of Haemorrhagic Stroke
Rupture of a blood vessel in the brain, leading to increased intracranial pressure
Assessment of Haemorrhagic Stroke
Fast acronym (Face, Arms, Speech, Time)
CT scan to differentiate from ischaemic stroke
Neurological observations and Vital signs
Management of Haemorrhagic Stroke
Control of blood pressure (aim for less than 140mm Hg)
Surgical Intervention (e.g. Clipping or coiling of aneurysms)
Regular monitoring for complications
Thunderclap Headache is more likely to be symptom of what stroke
Haemorrhagic
What is autoregulation
The brain’s ability to maintain constant blood flow despite changes in perfusion pressure.
What is Cerebral Perfusion
CPP = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP). Normal CPP is crucial for adequate brain function. CPP should be maintained above 70-80mmHg
Nursing Care of The Patient Presenting with a Neurological Emergency
Management of Airway / breathing: Ensure airway is clear, administer oxygen as needed, intubation may be required.
Continuous monitoring of neurological status, vital signs
Administering medications
Interventions to Decrease ICP
Hyperventilate: Aim for 30 -35 CO2
Head up elevated 30 degrees
Use tape rather than tube ties if patient is intubated
Diabetes as a Co-morbidity to Neurological Presentations
Factor of atherosclerosis, significant impact on cardiovascular system, can compete with stroke management and recovery
Diabetes Management as a Co-morbidity to Neurological Emergencies
Maintain tight glycaemic control to reduce complications and improve outcomes
Monitor blood glucose levels regularly
Work with a diabetes educator or specialist when needed for comprehensive care.
Cushing’s Triad
Bradycardia
Widened pulse pressure
Irregular respirations
Pathophysiology of Haematology and Oncology Presentations
Nadir = Period after chemotherapy when blood counts are at their lowest (usually 7-14 days after chemotherapy)
Neutrophils are involved in the acute inflammatory response to infection and the removal of bacteria by phagocytosis.
Low levels of WBC make it harder for the body to fight infection making patients more susceptible to infection
Nursing and Medical Assessment, Interventions and Management for Febrile Neutropenia
Comprehensive patient assessments (history, physical exams, lab tests)
Aim to identify source (blood cultures, chest x-ray, specimens and swabs)
Administer broad spectrum intravenous antibiotics (IVABs) within 30 minutes of presentation (take blood cultures prior if able)
Collaborate with multidisciplinary teams (e.g. ICU, or med Onc) for holistic management
Complications of Chemotherapeutics
Febrile Neutropenia
Thrombocytopenia (bleeding risk)
Anaemia (hypoxia)
Common Side Effects of Chemotherapeutics
Nausea
Vomiting
Fatigue
Alopecia
Myelosuppression
Increased Infection Risk
Management Strategies for Complications and Side effects of Chemotherapeutics
Use of antiemetics
Growth factors
Pain management
Supportive care
Assessment of Dental Conditions
Monitor for oral mucositis, infections and dental cavities especially in immunocompromised patients
Assessment of ENT conditions
Assess for hoarseness, stridor, dysphagia and hearing loss
Also ask patient to open mouth properly. Look for swelling and how fast patient opened their mouth
Interventions for Dental and ENT Conditions
Drainage of the abscess
Referral to specialist teams
Management of pain
Treatment of Infection
Pathophysiology of Depression and Anxiety
Depletion of serotonin or dopamine, symptoms = low mood (depression), Anxiety = overwhelming feelings of worry, nervousness and fear, neurochemical dysregulation
Assessment of Depression and Anxiety
Use standardised tools
Clinical interviews
Be respectful
Establish a rapport
Speak calmly and in short sentences,
Assess suicide risk or harm to others
Management of Depression and Anxiety
Consider psychotherapy
Pharmacotherapy (SSRIs and SNRIs)
Referral to mental health team,
Encourage other supports
Support healthy coping mechanisms.
Pathophysiology of Hyperthermia and Heat Related Illness
Hyperthermia occurs when the body produces or absorbs more heat than it can dissipate
Mechanisms include:
- Impaired thermoregulation
- Excessive heat production
Assessment of Heat Exhaustion
A-E primary survey
Skin temperature and moisture
Mental status evaluation
Symptoms: Heavy sweating, weakness, dizziness, nausea, headache
Core temp <40 degrees Celsius
Assessment of Heat Stroke
Primary survey
Skin temperature and moisture
mental status evaluation
Symptoms: Altered mental status, cessation of sweating, rapid heart rate, hypotension, seizures, and hot and dry skin
Core temp >40
Management of Hyperthermia and Heat Related Illness
Supportive care and management of complications
Intubation + muscle relaxants to prevent shivering
Administer cool IV fluids
Remove clothing
Continuous assessment of vital signs and neurological status.
Assessment of Orthopaedic / Musculoskeletal Trauma
Initial Survey: A-E
History: Mechanism of injury, pain level and functional ability
Neurovascular observations
Physical Exam: Inspect for deformities, swelling, bruising and range of motion
5 Ps of the Neurovascular Assessment
Pallor
Pulselessness
Pain
Paraesthesia
Paralysis
Management Strategies for Orthopaedic / Musculoskeletal Trauma
Immobilisation: Use splints, casts, traction to stabilise fractures
Pain Management: Administer analgesics as needed
Surgical Intervention: May be necessary for severe fractures or dislocations
Procedural sedation: For painful relocation and casts.
Nursing Care for Orthopaedic / Musculoskeletal Trauma
Pain relief
Regular neurovascular assessments
Elevating effected limb
Assistance with ADLs
Complications for Orthopaedic / Musculoskeletal Trauma
Compartment syndrome
DVT
Non-union of fractures
Confounding Factors in Trauma Management
Age, pre-existing conditions and comorbidities
Medications and anticoagulants (can mask signs of shock, increased risk of injury)
Older age, paediatric patients, obesity.
Pathophysiology of Blunt Abdominal Trauma
Caused by non-penetrating forces (e.g. Motor vehicle accidents, falls). It may lead to organ laceration, contusion, or haemorrhage without disrupting the skin
Assessment of Blunt Abdominal Trauma
Mechanism of injury, associated symptoms (e.g. Pain, nausea), look for signs of internal bleeding (hypotension, tachycardia), tenderness, distension or rigidity, ultrasound (FAST), CT scan for abdominal injuries
Management of Blunt Abdominal Trauma
Stabilisation (IV fluids, blood products as needed), surgery may be required for significant haemorrhage or organ injury, monitoring for complications such as compartment syndrome or delayed haemorrhage.
Pathophysiology of Penetrating Abdominal Trauma
Involves an object piercing the abdomen (e.g. Stab wounds, gunshot wounds). The injury may directly damage organs or cause bleeding
Assessment of Penetrating Abdominal Trauma
History (type of weapon, depth of injury), Examine for entry and exit wounds, signs of peritonitis (rebound tenderness, guarding), CT scan or diagnostic peritoneal lavage may be used.
Management of Penetrating Abdominal Trauma
Immediate surgical intervention often needed for repair and to control bleeding, prophylaxis for infections and ongoing monitoring for sepsis
Assessment for Abdominal Trauma
Continuous monitoring of vital signs and signs of shock
Thorough abdominal assessment (inspection, palpation, percussion, auscultation)
Monitoring for changes in mental status indication potential hypovolemia or sepsis
Interventions for Abdominal Trauma
Administer IV fluids and blood products as ordered
Pain management
Prepare for possible surgical interventions
Educate the patient and family about the condition and treatment plan
Complications of Abdominal Trauma
Infection (peritonitis, abscess formation)
Organ failure (Kidney, liver)
Chronic pain or gastrointestinal dysfunction
Management of Abdominal Emergencies in the Elderly
Comorbidities: Elderly patients often have multiple health issues that complicate diagnosis and treatment (e.g. Diabetes, cardiovascular disease)
Atypical Presentations: Symptoms may be less pronounced (e.g. Altered mental status instead of pain)
Medication Effects: Increased sensitivity to medications and potential for adverse drug interactions
Surgical Risks: Higher operative risks and longer recovery times
ATOD Assessment
Determine the type and amount of alcohol, tobacco and other drugs used
Evaluate for withdrawal symptoms or overdose signs
ATOD Interventions
For alcohol withdrawal, consider medications like benzodiazepines and monitoring in a safe environment.
Provide counselling and support for cessation
Refer to addiction services if needed
Nursing and Medical Care for Patients With ATOD Dependence
Monitor for complications of ATOD use (e.g. Liver disease from alcohol, respiratory issues from tobacco)
Provide education on the risks of continued use and benefits of cessation
Implement harm reduction strategies as appropriate.
ETOH or other withdrawal scores
Pathophysiology of DKA
Occurs due to absolute insulin deficiency. Lack of insulin leads to increased lipolysis, producing free fatty acids that are converted to ketones, causing metabolic acidosis. More commonly found in T1DM.
Pathophysiology of Hyperglycaemic Hyperosmolar State (HHS):
Characterised by severe hyperglycaemia, significant dehydration, and high serum osmolality without significant ketoacidosis. Insulin levels are of sufficient to prevent ketogenesis but inadequate to control blood sugar levels. More commonly found in T2DM.
Fluid and Electrolytes in DKA
DKA typically involves dehydration, electrolyte imbalances (especially potassium) and acidosis due to ketone accumulation.
Presentation of DKA
Rapid onset (hours to days), polyuria, polydipsia, weight loss, abdominal pain, vomiting, fruity breath (due to acetone), altered mental status
Presentation of HHS
Presentation: Gradual onset (days to weeks), polyuria, polydipsia, confusion, lethargy, severe dehydration, hypotension, and elevated serum osmolality.
Medical Management of Diabetes
Insulin Therapy: Initiated in both DKA and HHS to lower blood glucose
Fluid Resuscitation: Isotonic saline in DKA; may start with normal saline in HHS, transitioning to 0.45% if hypernatremia is present.
Electrolyte Management: Monitoring and replacement of potassium, magnesium and phosphate as needed.
Laboratory Values: Blood glucose, electrolytes, ketones and regular venous blood gases.
Nursing Management of Diabetes
Monitoring: Vital signs, neurological status, fluid intake/output.
Education: Importance of adherence to medication, dietary management, recognising symptoms of hypo/hyperglycaemia and when to seek help
Support: Emotional and psychological support, especially for patients experiencing severe illness.
Microvascular Complications with Diabetes
Retinopathy: Damage to retinal blood vessels, leading to vision loss
Nephropathy: Kidney damage due to chronic hyperglycaemia, leading to end-stage renal disease
Neuropathy: Nerve damage causing pain, tingling or loss of sensation.
Macrovascular Complications with Diabetes
Increased risk of cardiovascular diseases (CVD) due to atherosclerosis, leading to heart attack and stroke.
Pathophysiological Changes With Diabetes
Persistent hyperglycaemia leads to glycation of proteins, resulting in vascular and nerve damage
Inflammation and oxidative stress contribute to complications, exacerbated by metabolic syndrome.
Fluid and Electrolytes in HHS
HHS involves profound dehydration and hypernatremia, with potential electrolyte imbalances but typically less severe than in DKA.
Core temp > 41 degrees increasingly leads to what?
Protein denaturing
Loss of energy producing processes
Loss of cell membrane function
Management of HHS
Fluid replacement (more aggressive than in DKA), insulin therapy (often less intensive) and careful monitoring of electrolytes.
Management of DKA
Immediate insulin therapy, fluid replacement (with isotonic fluids) electrolyte monitoring (especially potassium) and treatment of acidosis.
Cushing’s Triad: Widening pulse pressure
As ICP becomes higher than MAP, CPP decreases. CNS is activated in response causing vasoconstriction to increase MAP to maintain CPP resulting in widening pulse pressures.
Cushing’s Triad: Bradycardia
The baroreceptors at the aortic arch and carotid sinuses sense the increased BP and stimulate the vagus nerve in response slowing down the heart rate.
Cushing’s Triad: Irregular breathing
Increased ICP compresses the brainstem particularly the medulla and pons which regulate breathing leading to abnormal breathing patterns and Cheyne-stokes
Monro Kellie Doctrine
Within a fixed volume an increase in one component will show reciprocal decrease in the other remaining 1 or 2
Increased ICP results in decreased CSF and blood flow
Special court in abdo traumas
Kids: Blood loss differs, soft bones / less abdo protection
Elderly: comorbidities, poly pharmacy, less physiological reserve
Obstetrics: Placental abruption, Uterine rupture, feto-maternal haemorrhage
GCS and head injury characterisation
GCS 14-15 - mild head injury
GCS 9-13 - Moderate head injury
GCS 3-8 - Severe Head Injury
