Tirocinio 3 Infermieristica

Tirocinio 3

Polytraumatized patient

Polytrauma is characterized by the simultaneous occurrence of multiple injuries that can affect various body systems, often resulting from high-energy mechanisms such as motor vehicle accidents, falls, and explosions.

Trauma mortality disability, is one of the leading causes of and accounting for more than five million deaths per year, which is almost 9% of global mortality, eclipsing deaths from HIV/AIDS, malaria, and tuberculosis combined. The most common cause of traumatic death is motor vehicle crashes (MVC), followed by suicide, interpersonal violence.

Nurses are integral to the multidisciplinary team managing polytrauma patients. Their roles include:

• Assessment of injuries and vital signs.
• Intervention to stabilize the patient.
• Coordination with other healthcare professionals to ensure comprehensive care.
• Education to patients and families regarding injury management and recovery.

Initial assessment

The initial assessment of a polytrauma patient is crucial for identifying life-threatening conditions. The ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure) is a widely accepted framework for conducting rapid assessments.

• Airway: Ensure the airway is patent and clear of obstructions. Consider advanced airway management if necessary. Focus on securing the airway and protecting the cervical spine prior to further assessment. AVPU is useful for grading a patient’s level of consciousness, responsiveness, or mental status.
• Breathing: Assess respiratory rate, effort, and oxygen saturation. Administer supplemental oxygen as needed.
• Circulation: Monitor heart rate, blood pressure, and capillary refill. Establish intravenous access for fluid resuscitation.
• Disability: Evaluate neurological status using the Glasgow Coma Scale (GCS) to determine the level of consciousness.
• Exposure: Expose the patient to assess for hidden injuries while maintaining normothermia.

Airway management & cervical spine protection

Clinicians focus on securing the airway and protecting the cervical spine prior to further assessment of polytrauma patients. Responding to voice commands (AVPU) indicates the patient’s airway is patent, oxygenating, and perfusing the brain. AVPU is useful for grading a patient’s level of consciousness, responsiveness, or mental status. The basis of the AVPU scale is on the following criteria:

• Alert: The patient is aware of the examiner and can respond to the environment. The patient can follow commands, open their eyes, and track objects.
• Verbally responsive: Lack of spontaneous eye opening. The patient can respond to verbal stimuli.
• Painfully responsive: The patient’s eyes remain closed. The patient only responds to painful stimuli applied by an examiner. The patient may move, moan, or cry out in response to the painful stimuli.
• Unresponsive: The patient does not respond to verbal or painful stimuli.

If the patient is unable to respond, clinicians may use techniques such as the chin-tilt or jaw-thrust maneuver to open the airway. Because clinicians cannot rule out cervical spine injury in patients with head trauma, altered mental status, neck pain, or high-energy mechanisms, they treat the cervical spine as fractured until evaluation proves otherwise.

Strategies to manage the airway in a trauma patient range from basic mask ventilation with improved positioning to advanced techniques for securing the airway when standard methods are unachievable. Failed or unsuccessful oral intubation may require nasal intubation, laryngeal masks, alternative options, including fibreoptic bronchoscopy, surgical airways, or including cricothyrotomy. Upper airway obstruction or failed intubation necessitates a surgical airway. In emergency situations, clinicians prefer cricothyrotomy because it allows prompt airway access and requires less surgical skill.

When inspecting a trauma patient, it is crucial to remove their clothing to check for bruising, open wounds, and penetrating injuries. Thoracic injuries such as tension pneumothorax, massive hemothorax, flail chest, open chest wounds, and cardiac tamponade are dangerous and clinical conditions requiring immediate intervention.

A tension pneumothorax requires immediate intervention (needle decompression followed by tube thoracostomy) without diagnostic imaging tests to confirm the diagnosis. Both pneumothorax and hemothorax will require a chest tube. Pulse oximeters and bedside ultrasound can be helpful, but should not delay the start of treatment. Oxygenation may hide the initial signs of hypoventilation, making it even more important for clinical judgment in decision-making.

Circulation

Circulation and controlling bleeding are significant concerns in polytrauma patients, and hemorrhage is the leading cause of preventable death. Early warning signs of hypovolemic shock from bleeding include tachycardia, poor perfusion, and critical signs of shock, including cold hands and feet, narrow pulse pressure, fast breathing, and altered mental state. Hypotension often does not appear until one-quarter of blood volume is lost. The initial physiologic response to blood loss can be notable when a trauma patient experiences a hemorrhage.

• Class I hemorrhage: 15% blood loss. May present with normal vital signs, vital signs that can mask the beginning stages of a hemorrhage (29).
• Class II hemorrhage: 15 to 30% blood loss, early signs of compensation start to appear. Clinicians may notice tachycardia and tachypnea, and a narrowing of the pulse pressure (29).
• Class III hemorrhage: 30–40% loss of blood volume, compensatory mechanisms fail, and blood pressure drops, signaling significant hemorrhage (29).
• Class IV hemorrhage: 40% or greater blood loss, physiologic systems fail. Marked hypotension, a narrowed pulse pressure, and pronounced pallor indicate the severity of hemorrhage (29).

We should have a large bore venous line (18-gauge or larger, preferably 14–16 gauge) to obtain blood samples for laboratory testing and cross-matching in addition to ECG monitoring, pulse oximetry, and frequent vital signs. When noninvasive blood pressure monitoring is not possible, palpation of a peripheral pulse may be necessary. Palpation provides a quick, valid, and noninvasive method to estimate systolic blood pressure (SBP) when automated cuffs fail.

Initial resuscitation management begins with fluids to maintain organ perfusion and provide substrates, including oxygen and electrolytes. For patients who do not respond, clinicians may initiate transfusion. Prompt administration of tranexamic acid (TXA), given can also help reduce mortality via mechanisms that prevent the breakdown of blood clots (fibrinolysis) and reduce bleeding-related deaths.

The initial steps of fluid resuscitation include isotonic crystalloids. Lactated Ringer’s, with electrolyte and buffer composition of sodium, potassium, calcium, lactate, mirrors human plasma over 0.9% Normal Saline, chloride heavy, and yields lower rates of acute kidney injury (AKI) and hospital/intensive care unit length of stay.

For fluid resuscitation, the goals are clear: to control bleeding, replace lost blood volume, and restore target tissue perfusion and organ function. The target systolic blood pressure (SBP) in traumatic situations is 60-70 mmHg for penetrating injuries, 80-90 mmHg for blunt trauma without a traumatic brain injury, and 100-110 mmHg for blunt trauma cases that have suffered a head injury may require permissive hypotension, but clinical scenarios vary, and the guidelines adjust according to the situation.

Disability: neurologic assessment

Traumatic brain injury refers to brain damage from blunt, penetrating, or shockwave forces, and clinicians classify it as mild, moderate, or severe. Clinicians perform a thorough neurologic evaluation to establish a baseline and detect early deterioration when assessing a polytraumatized patient. This evaluation includes the Glasgow Coma Scale (GCS) score, pupil examination, and a detailed peripheral neurologic assessment. In trauma patients, toxic metabolic encephalopathy and hypoglycemia can mask underlying brain injury.

The severity of the injury can be measured by the Glasgow Coma Scale, where a score less than nine is classified as severe and is associated with a mortality rate of 40%, a score of nine to twelve falls into the moderate category and has a 10% mortality rate, and a score of thirteen to fifteen is classified as a mild or minor injury and has limited no mortality.

Exposure and environmental control

Clinicians undress the trauma patient to identify occult injuries while managing temperature with blankets, warming devices, and warmed fluids. After the initial assessment, the trauma verifies completion of all necessary interventions and reviews the patient’s physiologic status. The care team coordinates imaging coordination that they ensure the patient receives the care they need on time and achieves the best possible outcomes.

Continued resuscitation in the ICU

The ICU physician continues trauma, surgical management, and ongoing resuscitation, assessing the patient’s stability and the level of unresolved shock upon arrival. Conditions such as shock, in which the depth and duration of the shock are cumulative phenomena, in an integrative fashion, determine the total “dose,” and the timeliness of resuscitation can affect patient mortality.

Trauma patients require immediate physiologic support upon arrival in the ICU. Clinicians advocate low-dose vasopressin to correct relative vasopressin deficiency and reduce fluid requirements; however, its use remains controversial because it may impair microcirculatory flow and decrease splanchnic perfusion. Trauma patients with head injuries may require vasopressors to stop spinal shock or to perfuse the brain in cases of traumatic brain injury. Additional ICU considerations include tissue hypoperfusion, which causes harm. Respiratory acidosis superimposed on metabolic acidosis can be life-threatening, and the use of positive end-expiratory pressure and open-lung ventilation in a hypovolemic trauma patient can reduce venous return to the heart.

Trauma patients with multiple injuries come into the ICU; they may be suffering from profound metabolic acidosis and hypothermia, which limits the body’s ability to function. Clinicians must control hypothermia, and metabolic acidosis predicts increased mortality and the need for massive transfusion; restoring effective circulation provides the most effective treatment.

Controlling hemorrhage, whether in the emergency department or the ICU, is key to resuscitation. One of the biggest concerns is a condition known as life-threatening trauma-induced coagulopathy, when patients are in life-threatening shock due to a massive hemorrhage. Increased early transfusions, first 24 hours after trauma, can be an indicator of impending complications, including systemic inflammatory response syndrome (SIRS) and death.

Respiratory care is ongoing. Polytrauma patients are at risk of oxygen deprivation, acid–base disturbances, and ongoing respiratory problems, which cause severe cellular injury and increase mortality risk, and clinicians must address them within settings.

In the ICU, resuscitation goals after the initial hemorrhage have stopped are about preventing irreversible shock and managing homeostasis rather than. Once clinicians control bleeding and volume, they aim to achieve stable circulation, balanced acid–base status, adequate urine output, normothermia, and correction of coagulopathy.

Continuous monitoring of vital signs and neurological status is essential for detecting changes in the patient's condition. Nurses should employ standardized assessment tools, such as:

• Glasgow Coma Scale (GCS): To assess consciousness levels.
• Revised Trauma Score (RTS): To evaluate trauma severity.
• Pain assessment tools: To gauge pain levels and guide pain management strategies, both with pharmacological and non pharmacological interventions.

Trimodal pattern of trauma-related deaths

Over time, researchers have defined the trimodal pattern of trauma-related deaths: immediate, early, and late. Immediate deaths occur in minutes, from severe brain or cardiac injury; early deaths occur in hours, from hemorrhage or shock; and late deaths occur in days to weeks, from infection or organ failure. Immediate deaths occur at the scene or soon after, early deaths within hours, caused by head injuries or unstoppable bleeding, and delayed deaths days to weeks later, coming from sepsis or organ failure. Research indicates that 80% of these deaths occur within the first two categories, Immediate / Early.

Shock

Shock is a severe, life-threatening form of acute circulatory failure characterised by inadequate tissue perfusion resulting in systemic hypoxia and cellular dysfunction. It is a pathological state caused by the circulation being unable to deliver sufficient oxygen and nutrients to the tissues and cells.

Shock can result from traumatic injury or disease, creating a state of insufficient oxygenation and perfusion of vital organs throughout the body. The condition affects up to one in three patients in critical care environments. Once diagnosed, its treatment relies on the rapid initiation of fluid resuscitation and often includes the use of vasoactive medications to improve cardiac output and tissue perfusion status.

Shock is a condition that requires nurses to make timely, evidence-based decisions for their patients. It is therefore vital that nurses can recognise shock as it happens and assess and understand the signs and symptoms of its various causes in order to initiate individualised treatments and therapies. Patients can experience shock for a number of reasons, including physical trauma, blood loss, dehydration, or allergic reaction. Shock is used as an overarching term to describe a patient in a critical state of deterioration, so it is vital to first recognise and understand the type of shock being presented, which is typically categorised by causative factors.

Types of shock

There are four main types of shock: hypovolaemic, cardiogenic, obstructive and distributive. Distributive shock is classified according to its three main individual causes, which relate to sepsis, neurogenic disorder, or anaphylaxis. Each type can be categorised by its individual cause and sub-type.

Hypovolaemic shock

This is caused by a decrease in circulating blood volume. Considered to be the most common form of shock, hypovolaemic states are characterised by an inadequate intravascular volume caused by significant blood and/or fluid loss. Shock will occur when the circulating volume falls to a point at which the body's metabolic requirements cannot be met.

Hypovolaemic states can occur owing to visible haemorrhage outside the body and, less discernibly, that which occurs within the body. The circulating volume can also be altered by further causes of hypovolaemia, including plasma loss from extensive burns, fluid depletion because of dehydration, vomiting and diarrhoea, and internal fluid shifting such as occurs in peritonitis.

A significant decrease in circulatory volume leads to a lower volume of blood returning to the heart, decreasing cardiac output and reducing blood pressure.

Cardiogenic shock

This is caused by impaired cardiac function. Even if fluid volumes are adequate, poor cardiac output can result in tissue hypoxia in situations where the heart fails to pump blood effectively throughout the systemic circulation.

This type of shock can occur because of cardiac arrhythmias and myocardial impairment such as necrosis and heart valve dysfunction following myocardial ischaemia or infarction as a result of heart failure.

Obstructive shock

This is caused by obstruction to the circulating blood flow. Decreased cardiac output can have a physical obstructive cause that impedes blood flow and affects both the preload and afterload of the cardiac cycle. Such obstructions can be caused by numerous conditions, including cardiac tamponade, tension pneumothorax, pulmonary embolus, heart valve stenosis and certain anatomical defects that are more regularly observed in paediatric patients.

Distributive shock

This is caused by an altered distribution of circulating blood. It results from a number of conditions that cause blood vessels to lose their ability to maintain systemic vascular resistance and tone, which leads to a decrease in organ perfusion. Distributive shock has three main causes—septic shock, neurogenic shock and anaphylactic shock.

• Septic shock, its principle cause, is a result of a widespread dysregulated response to an infection or insult, typically associated with the systemic inflammatory response syndrome.
• Neurogenic shock is the loss of sympathetic nervous system activity, motor and sensory nerve impulses, because of brain or spinal cord injury, spinal anaesthesia and certain neuropathies including transverse myelitis and Guillain-Barré syndrome. While this condition creates a state of shock, it is vital that practitioners recognise that the usual stress response will not be observed.
• Anaphylactic shock is a severe, systemic hypersensitivity reaction to an allergen. Such allergic reactions can be caused by foods such as nuts, fish and dairy; drugs, including antibiotics and anaesthetics; and insect bites and stings.

Stages of shock

There are four stages of shock that occur sequentially as the patient's condition progresses and physiological changes begin to take place at a cellular level.

The first (initial), which has predominantly more acute clinical signs, and the second (compensatory) stages of shock are supported by the body's innate compensatory abilities to improve circulation and venous return to the heart. During the third (progressive) stage, symptoms worsen sign