NURS 3101 COMPLETE SUMMARY SHOCK, SEPSIS, BURN INJURIES, TRAUMATIC, BRAIN INJURY, DROWNING, Exams of Nursing

Download NURS 3101 COMPLETE SUMMARY SHOCK, SEPSIS, BURN INJURIES, TRAUMATIC, BRAIN INJURY, DROWNING and more Exams Nursing in PDF only on Docsity! NURS 3101 COMPLETE SUMMARY SHOCK, SEPSIS, BURN INJURIES, TRAUMATIC, BRAIN INJURY, DROWNING, SPINAL CORD, INJURY FRACTURES, MASS DISASTER SHOCK What is MAP & SV & CO: • Mean arterial pressure (MAP) is an indication of the perfusion to the body’s vital organs and tissues in the patient’s arteries during one cardiac cycle. • MAP is also the pressure generated from the left ventricle and pumped into the arteries for the cardiac cycle. • Stroke volume (SV) is the volume of blood pumped from the left ventricle in one contraction. • Cardiac output (CO) is the amount of blood the heart is pumping through the circulatory system in one minute. How to calculate MAP & CO: MAP = SBP + 2 x (DBP) e.g. MAP for BP of 120/80 = 80 + 2 x (120) / 3 = 93 3 CO = SV x HR SV = EDV - ESV (Stroke volume = end diastolic volume – end systolic volume) Describe homeostatic – how compensation works when there is a decrease in MAP or CO: • When a decrease in pressure in the circulatory system is detected by baroreceptors, it stimulates cardio acceleratory centres, vasomotor centres and inhibits cardio inhibitory centres. Vasoconstriction then occurs and cardiac output is increased to compensate for the decrease in BP. As a result, BP rises. • NB: extensive bleeding causes a decrease in BP and BV. Short-term responses – Baroreceptors & Sympathetic Nervous System response: • Short-term responses are controlled by the nervous system. • The nervous system stimulates baroreceptors and, in conjunction with pain, fear and anxiety, activates cardiovascular centres and the sympathetic system. • The sympathetic system maintains CO by increasing the HR and causing vasoconstriction of the arterioles and peripheries which ultimately increasing BP. Long-term responses – RAA cascade response: • RAA = Renin-Angiotensin-Aldosterone. • The long-term response in homeostasis is directed by an endocrine response and focuses more on restoring blood volume to maintain MAP. • Renal blood pressure and volume is detected → renin is released to activate angiotensin I and is then converted in the lung capillaries to angiotensin II. 2. Progressive: – Where no intervention has occurred or has had no effect and the shock has progressed. – As BP drops, heart toxic substances are released from ischaemic tissues. – BP is so low that clots form in small vessels and vasodilation occurs due to reduced sympathetic stimulation and tissue ischemia. – Capillary permeability increases allowing fluid to leave the intravascular space and enter interstitial spaces. – Tissues deterioration intensifies due to inadequate blood flow. Signs and Symptoms: • Tachycardia • Weak, thready pulse • Listlessness, confusion, apathy, slow speech • Decreased BP • Moderate to severe orthostatic pressure • Chest pain • Metabolic acidosis (tissue hypoxia means cells must undergo anaerobic metabolism → produces lactic acid → pH drops) • Hyperventilation • Possible hypotension 3. Irreversible: – Decreasing function of the heart and progressive vasodilation in peripheral blood vessels lead to extensive tissue damage. – The damage to organs and tissues becomes so severe that it cannot be reversed and interventions have to be extraordinary to revive them. Signs and Symptoms: • Confusion, disorientation, slurred speech • Unconscious • Slow, irregular, thready pulse • Falling BP Shock: Initial Patient Assessment In trauma, consider the MOI of the patient’s presentation. Think about the 5 most common bleeding sites, using the acronym: PLACE Understand MIST in trauma call activation & who makes up the trauma team & what is their role. Understand the Primary survey (in trauma): • It is the initial assessment, resuscitation measures (priority interventions) & re- evaluation of the interventions A, B, C, D & E • Remember to re-evaluate an intervention. Re-assess your patient • Collect full PMHx using the acronym: SAMPLE Shock: Head-to-toe Patient Assessment In trauma, the Head-to-toe patient assessment is known as Secondary survey It is a detailed: A,B, C, D, E, F, G which also includes assessing: ● Skin, colour, mucosa: head, neck, eyes and mouth, nose & ears ● Patient back: torso, legs, buttocks, perineal reflex ● Extremities for deformities that may indicate: fractures, congenital diseases ● 12 cranial nerves & full sensory and motor response ● Neurovascular – 5Ps ● Pelvis & abdominal: auscultation & palpation ● Wounds, lacerations & bruising ● Equipment attached: drains (volume of drainage & aspect) Interventions for Hypovolaemic shock caused by bleeding: Airway: • Cervical spine immobilisation if unsure of MOI • Suctioning, open airway manoeuvres , insertion of oropharyngeal airway (guedel). Breathing: • Consider intubation • Administer high flow oxygen via NRBM 15 L • Monitor RR and sats every 5 minutes Circulation • Establish IV access with two large bores • Place on cardiac monitoring and ECG record BP, HR and MAP every 20 min • Collect bloods ABGs, lactate, Hg • Consider insertion of arterial line • Consider blood transfusion Disability: • Analgesia • Consider sedation • GCS • AVPU Exposure: • Treat hypothermia: thermal blanket, warm fluids, heating light and pads, remove wet clothing • If bleeding, control haemorrhage by elevation, pressure or angiography or surgery Fluids: • Aggressive fluid therapy STAT bolus • Insert IDC and commence FBC and monitor UO for assessing the effectiveness of interventions Cite possible organisms that can cause sepsis and the most common sources of sepsis. • Common sources of sepsis include: - Wounds (e.g. abscesses, ulcers, sinuses) - Surgery (incisions, unsterile equipment, etc.) - Trauma - Devices e.g. IVCs, IDCs, central lines, IV drug users - Infection (e.g. kidney infection, lung infection (pneumonia), infected teeth, UTIs, etc.) • Often causative bacteria are nosocomial or opportunistic. Sepsis: Adult sepsis pathway – RECOGNISE phase and RESPOND & ESCALATE By consulting the pathway, list the main risk factors for sepsis: • Re-presentation within 48 hours • Recent surgery or wound • Indwelling medical device • Immunocompromised • Age >65 years • Fall Absence of risk factors does not exclude sepsis as a cause of deterioration! New onset signs and symptoms of infection: • Fever or rigors • Dysuria/frequency • Cough/sputum/breathlessness • Line associated with infection/redness/swelling/pain • Abdominal pain/distention/peritonism • Altered consciousness List the YELLOW ZONE observations: • Respirations <10 or >25 breaths/min • SpO2 <95% • SBP <100mmHg • HR <50 or >120 beats/min • Altered LOC or new onset of confusion • Temperature <35.5oC or >38.5oC • Lactate >2mmol/L (significant in sepsis) List the how to respond when you think patient may have SEPSIS • Call for a Clinical Review unless already made • Conduct targeted history and clinical examination • Obtain SENIOR CLINICAN review to confirm diagnosis and prioritise investions and management • DOES THE SENIOR CLINICAL CONSIDER THE PATIENT HAS SEPSIS? • IF YES: Commence treatment as per sepsis resuscitation guideline AND inform the Attending Medical Officer. Sepsis 6 Describe in your own words by consulting: HUBS, scientific literature, policies and guidelines the rationale of the SEPSIS 6 interventions AND how you know if the interventions have worked, or need to be repeated (Outcome) 1. Obtain a venous blood gas to check serum lactate > 2mmol/L is a red flag for patient with suspected sepsis → We do this to achieve a baseline or serum lactate and for an indication of how much the sepsis has progressed. 2. Collected blood cultures –Think about other cultures → Blood cultures are taken to identify the organism causing the infection. → Take two sets from two different sites 3. In ED insert cannulas and give IV fluid 20mls/kg bolus OR 250-500mls bolus and repeat if no response. Goal: MAP ≥ 65mmHg/ or SBP > 100mmHg is ideal (think about why) → We administer IV fluid therapy to prevent the patient from progressing further into shock. As fluids replace the fluid loss from fluid shift and leaky capillaries, fluid also improves cardiac output and ultimately improving perfusion to end tissues and organs. → We can measure the effectiveness of the fluid therapy by looking for an improvement in SBP to >100mmHg and maintaining the MAP at >65mmHg, and seeing an increase in urine output. 4. Administer oxygen to maintain spO2 ≥ 95% (88-92% COPD patients) → Commencing oxygen therapy allows for better oxygen delivery and improves perfusion to the organs, in sepsis induced hypoperfusion patients. → We can measure this via the sats probe to see an improvement in saturation levels and work of breathing in the patient. 5. Administer IV broad-spectrum antibiotic within 60 minutes of sepsis recognition → Once the patient has a confirmed diagnosis of sepsis, we follow the sepsis resuscitation guidelines. These guidelines state that we MUST commence antibiotic therapy within 60 minutes of sepsis recognition to prevent the patient from progressing into irreversible stages of shock. As literature indicates that any delay in antimicrobial therapy increases mortality. → Broad spectrum antibiotics are also used when the cause of the infection is unknown and time is a critical component in the patients survival. As literature indicates that delays in treatment, worsen the infection and increase morality. → After administering IV antibiotics, I expect to see an improvement in the patients GCS within 6 hours and improved serum lactate levels of <2mmol in 24 hours – can be measured by collecting bloods. I also expect to see nil signs of infection within 3-7 days, this can be measured by a midstream urine sample, an afebrile temperature of <37.0C, complete absence of chills, normal respiratory rate between 12-20, a stable heart rate below 100bpm and nil reports of fatigue. 6. Monitor at least every 30 minutes RR/WOB, sats, BP, HR, capillary refill, Temp, and Urine output → Regular observations of patient’s with sepsis are critical, as sepsis is a MEDICAL EMERGENCY. Vital signs are crucial for identifying patient deterioration. → Monitoring every 30 minutes allows for HCPs to see the effectiveness of team interventions. Septic shock – ICU presentation Understand the indication of escalating oxygen treatment to high flow nasal prongs and/or invasive mechanical ventilation: Understand the role of vasopressors and the need of central venous access for this treatment: • Vasopressors constrict the blood vessels → this increases cardiac output, maintains a sufficient MAP of greater than 65mmHg and increases overall blood pressure. BURN INJURIES • Burns: an injury resulting from exposure to heat, chemicals, radiation, cold injuries or electrical current. The transfer of energy from the sources leads to the destruction of tissue. • Types of burns: → Thermal burns (e.g. flames, steam, hot liquids) → Chemical burns (e.g. acids, alkalis, organic chemicals) → Electric burns (e.g. contact with electrical current) → Radiation burns (e.g. sunburn, cancer radiation, X-ray) → Cold burns (e.g. exposure to cold environments; frostbite) → Friction burns (carpet burns, road rash) List the 5-depth classification of burns and key clinical characteristics of each classification: • Epidermal: - Skin intact, dry, red, blanches, localised oedema. - Heals within 3-7 days with moisturiser or protective dressing. • Superficial dermal: - Painful, red or pink, oedema, blisters may appear. - Should heal within 7-10 days with minimal dressing requirements. • Mid-dermal: - Painful, often blistered, dark pink, moist, blanches, sluggish CRT (capillary refill time). - Should heal within 14 days. - Deeper areas or over a joint may require surgical intervention and referral. • Deep-dermal: - May blister, mottled, blotchy red/white, fairly dry, discomfort rather than pain, slow to no CRT. - Generally needs surgical intervention e.g. skin grafting. - Refer to specialist burns unit. • Full thickness: - Damage to all layers of skin, nerves and muscles, non-blanchable, oedema, leathery, waxy, white brown or black skin, no CRT. - Surgical intervention and long-term scar management required. - Refer to specialist burns unit. Identify the 3 zones of a burn injury: I. Zone of coagulation: the first area is the most central area of damage. Where necrosis occurs. Necrosis is permanent and irreversible here. Cell death. II. Zone of stasis: AKA zone of ischaemia. Is reversible if perfusion is restored. Oedema occurs. III. Zone of hyperaemia: area of increased blood flow and tissue perfusion. List the Referral criteria to a burns unit: • Mid to deep dermal burns in adults >10% TBSA (total body surface area) • Full thickness burns in adults >5% TBSA • Mid-dermal, deep dermal or full thickness burns in children >5% TBSA • Burns to face, hands, feet, genitalia, perineum and major joints • Chemical burns • Electrical burns including lightning injuries • Burns with concomitant trauma • Burns with associated inhalation injury • Circumferential burns of the limbs or chest • Burns in patients with pre-existing medical conditions that could aversely affect patient care and outcome • Suspected non-accidental injury including children, assault or self-inflicted • Pregnancy with cutaneous burns • Burns at the extremes of age – infancy and frail elderly Explain when to consider major fluid resuscitation for Adult and Children • Major fluid resuscitation should occur if >10% in children and >20% for adults. Understand the rule of nines & palmer method to calculate TBSA% • Estimate from fingers positioned together as above. Utilize the patient’s palm size, not your own. • The Palmer Method of estimating total body surface area (TBSA) is an easy way to get a rough burn size estimate that can be used when calculating a patient’s fluid resuscitation needs. • The patient’s palmer surface including their fingers = 1% TBSA. KEY PRIORITY INTERVENTIONS Airway - Spinal precautions - If facial, neck and chest burns → intubation due to swelling of airway Breathing - Oxygen therapy → highflow humidified oxygen at 100% with NRBM Circulation - Fluid resuscitation: using parklands formula 3ml x weight (kg) x TBSA % - NB: fluid resus must be given as Hartmanns solution within 24 hrs from the time of injury. Half of the fluid in the first 8 hours and the second half over 16 hrs. Disability - Analgesia ➔ pain management. STAT IV morphine 2mg. max = 0.2mg/kg every 5 min PRN Exposure - Wound care management: HH and aseptic technique clean and irrigate wound with saline. Choose appropriate dressing that will maintain moisture, manage exudate and protect the wound. Then apply the dressing with pressure. - Prevent hypothermia: apply emergency thermal blanket, warm fluids, heating light, remove any wet clothing Fluids - Insert IDC and catheterise the patient if burns are >10% - And monitor urine output hourly via FBC List and understand the complications of major burn injuries, such as: acute renal failure; circumferential burns complications, altered thermoregulation and excessive pain. • Acute renal failure: due to reduced cardiac output which is a result of extreme fluid loss is. Reduced urine output despite fluid loss is a sign of AKI • Circumferential burn complications: burns around chest restrict expansion and breathing. Skin loses its elasticity. Also reported loss of pulse in burned limbs • Altered thermoregulation: skin is compromised in burns and the body cannot maintain homeostasis effectively without skin and fluid. • Excessive pain Understanding the inhalation burn injury pathophysiology of the upper and lower airway and its consequences such as development of ARDS. • CO poisoning – systemic toxinity • Thermal injury to airways • Smoke inhalation Describe what is systemic intoxication, signs and symptoms • Closed space injury that involves CO and hydrogen cyanide • It displaces O2 from Hb • Symptoms include headache, dyspnoea, irritability, confusion, coma • Usually combined with hypoxia Secondary brain injury occurs after the initial trauma and are a consequence of the primary injury. → Includes cerebral oedema/swelling, cell death, increased ICP, hypoxia, intracranial haemorrhage, infection and decrease in cerebral perfusion and O2. Definition of closed head Injury severity A close head injury in which the skull and dura remain intact. It is a result of a sudden violent motion that causes the brain to knock against the skull. No penetration of the skull or dura. How to calculate Cerebral perfusion pressure (CPP) Normal CPP 70-90mmHg for ADULT Anything >60mmHg is adequate for perfusion CPP = MAP -ICP Normal values for Intracranial pressure (ICP) Normal ICP for ADULTS is 5-15mmHg Severe is anything >20mmHg AS ICP RISES THE CPP WILL FALL = FATAL! Cushing triad signs of increased ICP 1. Bradycardia 2. Widening pulse pressure (SBP up and DBP down) 3. Irregular resp rate Signs and symptoms of raised ICP Early signs: - Change in mental status; confusion, lethargy, agitated, restlessness and disorientation - Some muscle weakness - Mild pupillary dilation and decreased pupillary responses - Nausea and vomiting - Headache Late signs: - Unequal pupils - Posturing - seizures Duty of care & Mental Health act Management of Acute behavioural disturbance Goals and Aims of TBI treatment is to prevent Secondary injury - Prevent hypoxia - Maintain CPP at 60mmHg or above - Prevent ICP from increasing to 20mmHg - Avoid or correct hypotension - Maintain normal Co2 levels - Reverse hypothermia TBI INTERVENTIONS Airway - Spinal precautions - Early intubation Breathing - Administer high flow oxygen and mechanical ventilation on low PEEP. Circulation - IV access - Strictly monitor BP, MAP and HR every 5 minutes if patient is showing signs of deterioration - CPR if required Disability - GCS & pupillary reaction. - Analgesia and sedation infusions - External ventricular drain - Monitor ICP - Sit head up 30-35 degrees - Consider mannitol Exposure - Thermal blanket - Warm fluids - Heating light and pads Fluids - Insert IDC - Maintain strict and accurate FBC Glucose - Monitor glucose levels SPINAL CORD INJURY Understand the pathophysiology of spinal injury, classification and the difference between neurogenic shock and spinal shock & the MOI in SCI • Pathophysiology: • MOI: includes direct impact or compression of the SC, or flexion, contusion, rotation, penetration • Classifications of the SCI include: cervical, thoracic, lumbar and sacral. Consists of 33 vertebrae, 31 nerves • Spinal shock: is the disruption of ion concentrations across the neurone membrane. It is NOT physical damage. Once the ion concentrations resolve after swelling, then normal functions will restore. Can last from hours to weeks. Autonomic control is lost. • Neurogenic shock: A form of distributive shock – interruption of normal sympathetic nervous system via injury. PT will present with low BP and bradycardia. SPINAL TRACTS: Spinothalamic tract - Sensory information - ascending - Pain and temperature information Dorsal tract - Sensory information - ascending - Touch and proprioception (awareness of the body’s position and movement) - White Spinocerebellar tract - Sensory information - ascending - Balance, posture and coordination Corticospinal tract - Motor - “pyramidal” - Descending tract - Voluntary movement - Conscious movement - Afferent: sensory information coming into the brain. - Efferent: motor information sent from the brain to muscles and brain Describe the management/interventions for patients with suspected spinal cord injury with focus on: prevention of secondary SCI Secondary SCI is a series of changes that occurs from the initial structural injury Implement spinal precautions: • Maintain neck in a neutral position by immobilising with a hard cervical collar • Maintain spine alignment using log roll with adequate staff • Early surgical intervention • Treat hypotension to prevent hypo perfusion of the spinal cord. Identify the diagnostic studies performed in a patient with suspected spinal injury • MRI, CT scan, x-ray • Reflex testing • Motor and sensory nerve testing Outline spinal precautions • AKA complete spinal, neck and head immobilisation and is done to prevent further injury/damage to the spinal cord. • It involves placing: - Cervical collars (hard and soft) - Log rolling to maintain spine alignment - Maintaining spine in a neutral alignment = bed flat - Using head foam blocks with straps - Immobilising the entire body as any movement can cause damage to the SC Understand the definition of autonomic Dysreflexia → Autonomic Dysreflexia is a MEDICAL EMERGENCY that develops in individuals with spinal cord injuries T6 or above → resulting in acute uncontrolled hypertension. → A.D is where the autonomic nervous system has excessive responses to noxious stimuli below the level of injury List the key interventions/management strategies to treat A.D • We can manage AD by removing as much of the noxious stimuli as possible: - Remove clothing that may be tight, compression stockings - Catheterise the patient to assist with bladder emptying and control and do regular bladder scans - Look for pressure areas and evidence of fractures - Monitor BP and HR regularly (5 min) - Administer antihypertensive if above interventions are not successful What are the signs and symptoms of A.D • Hypertension • Bradycardia • Vasodilation above the level of injury or sweating • Vasoconstriction below the level of injury • Nausea and nasal congestion • Anxiety • Pupillary dilation SCI INTERVENTIONS Airway & Breathing • Spinal precautions: immobilise neck, spine and head using cervical collar, firm mattress, head foam block and any other strapping support. • Remove spinal board using LOG ROLL with adequate amount of staff. • Airway clear of obstructions, look, listen and feel • C4 injuries and above require mechanical ventilation through NRBM (airway support) • High flow oxygen • Closely monitor spO2%, RR, WOB and auscultation Circulation • Establish an ABG baseline and take other bloods • Gain IV access with large gauge for fluid resus • Place on cardiac monitoring for BP, HR and attach ECG • Vasopressors for perfusion? Disability • GCS score • Monitor pupils • Analgesia for pain management • Neurovascular observations • NB: Assess motor (limbs strength) and sensory response (Dermatomes), and once patients are stabilised (during head-to-toe assessment) a more thorough neuro assessment of SCI should be done including: classification: ASIA tool & log roll assessment of the entire spinal column Exposure • Injuries T6 and above cannot regulate body temperature → initiate warming using heating lights and pads, warm fluids, and thermal blanket Fluids • Insert an IDC and strictly monitor FBC • Fluid resuscitation carefully, as an overload may worsen swelling on spinal cord injury. MASS DISASTER What is disaster triage - describe the difference between sieve and sort? • Sieve is used to initially triage and prioritise patient movement and treatment from the impact area to the casualty clearing post. • Once at the clearing post, the Triage Trauma score then validates the casualty’s priority for transport. SORT uses the pt’s GCS, RR and SBP. What is the Australian Triage System (ATS) – categories and time to be seen? What does MIST represent? - Mechanism of injury - Injuries found - Signs and symptoms - Treatment Steps of how to manage Acute Behavioural Disturbance in the ED and in the wards 1. Assessment of the patient in a safe environment: - what is the cause of agitation (mental health, intoxication, other general medical condition) - risk of injury and violence - psychiatric assessment (once pt is calm) 2. De-escalation techniques: - be empathetic, non-judgemental and respectful. Listen to their concerns. - introduce yourself, your role and the purpose of the discussion - approach in a calm, non-threatening and non-aggressive way - use short clear statements - encourage trusted family members and friends to help - offer water, tea, coffee, etc - try to identify the patient’s unmet needs - emphasise your desire to help 3. Sedation 4. Post sedation care: - observations and documentation 5. Disposition decisions and transport of the patient from the ED to the most appropriate area for continuation of their care. Understand what Post traumatic disorder (PTSD) – what are the signs and when can it occur • Post-traumatic stress disorder (PTSD) is a mental health condition that's triggered by a terrifying event — either experiencing it or witnessing. • PTSD symptoms may start within one month of a traumatic event, but sometimes symptoms may not appear until years after the even. • Signs of PTSD include: - Intrusive memories (recurrent, unwanted distressing memories, flashbacks, upsetting dreams/nightmares, sever emotional distress/physical reaction to reminders of the traumatic event) - Avoidance (avoiding thinking/talking about the traumatic event, avoiding places/people/activities that remind you of the traumatic event) - Negative changes in thinking and mood (negative thoughts about yourself/others/the world, hopelessness about the future, memory problems, difficulty maintain close relationships, detachment, lack of interest, difficulty experiencing positive emotions, numbness) - Changes in physical and emotional reactions (being easily startled/frightened, always on guard for danger, self-destructive behaviour, difficulty sleeping and/or concentrating, aggression, angry outbursts, guilt, shame)