ED Triage Past Paper PDF

LAST EXAM IN NURSING SCHOOL!!! ED triage Chapter 21 pp 385-392. Identify how to categorize emergency department clients according to the emergency severity index (ESI) ESI: emergency severity index ( incorporates concept of illness severity and resource use to de...

LAST EXAM IN NURSING SCHOOL!!! ED triage Chapter 21 pp 385-392. Identify how to categorize emergency department clients according to the emergency severity index (ESI) ESI: emergency severity index ( incorporates concept of illness severity and resource use to determine who we should treat first Triage system: most critically ill are treated first First asses for any threats to life, if have normal vital signs in ES3 ESI-1: unstable ABCs, obvious life/organ threat, risk of dying, high resource intensity with staff at bedside continuously Examples: cardiac arrest, intubated trauma patient, overdose with bradypnea, severe respiratory distress ESI-2: threatened ABCs, high-risk patient, should be seen within 10 minutes, high resource intensity with multiple often complex dx studies Examples: chest pain from ischemia, multiple trauma unless responsive ESI-3: stable ABCs, should be seen within 1 hour, medium to high resource intensity with multiple dx studies Examples: abdominal pain, gynecological disorders unless in severe distress, hip fracture in older patient ESI-4: stable ABCs, could be delayed being seen, need simple dx study or procedure, low resource intensity Examples: closed extremity trauma, simple laceration, cystitis ESI-5: stable ABCs, could be delayed being seen, need exam only Examples: cold symptoms, minor burn, prescription refill Determine how to triage emergency department clients based on primary and secondary surveys Primary Survey: ABCDEFG Asses ABC’s and assess for hemorrhage( if present address the hemorrhage before everything) apply direct pressure with sterile dressing 1) Alertness and Airway ○ stabilize cervical spine at same time as assessment of the airway is spinal cord injury ○ Airway management should be maintained from least to most invasive method i) Open airway using the jaw thrust maneuver( dont hyperextend the neck) ii) Suction foreign body (1) Airway obstruction: Cause of nearly all immediate trauma deaths (2) Sources: saliva, bloody secretions, vomitus, laryngeal trauma, dentures, facial trauma, fractures, and dentures (a) Signs of compromised airway (i) Dyspnea (ii) Inability to speak (iii) Gasping (agonal) breaths (iv) Foreign body in airway (v) Trauma to face or neck iii) Insert naso or oropharyngeal airway ( only in unconscious patients) + endotracheal intubation (1) If cant to intubation because of obstruction do a emergency cricothyroidotomy (2) Ventilate with 100 percent BVM before intubation 2) Breathing: just because there is airflow does not mean they are ventilated Asses for fractured ribs, pulmonary emboli, pneumothorax, asthma attacks etc. Give high flow with non-rebreather mask May need to do a bvm ventilation with 100 percent O2, needle decompression, intubation, and tx underlying cause 3) Circulation and control of hemorrhage ○ Asses for hemorrhagic shock ○ Check femoral or carotid pulse( peripheral pulses may be absent) ○ Asses skin for color, temperature and moisture (altered mental status and delayed cap refill sign of shock) i) Cold temperatures delayed capillary refill ○ Trx: 2 large bore IV catheters(14-16 gauge) + aggressive IV fluid trx with saline or lactated ringers, might need packed reg blood cells 4) Disability ○ Conduct neuro assessment with glascow coma scale i) Glascow not accurate for intubated or aphasic patients ii) Asses pupils for size shape equality and reactivity 5) Exposure and Environmental Control ○ Cut off clothing ○ Don't cut off anything that could be used for forensic evidence ○ Don't remove impaled objects ○ Prevent hypothermia by using warming objects etc. warming blankets, overhead warmers, warmed iv fluids to limit heat loss 6) Full set of vitals and family presence ○ Obtain full set of vitals ( obtain BP in both arms if chest trauma or if bp is abnormally high or low) ○ Helpful to have caregivers there during the assessments i) Assign a healthcare provider to be there with the family/friends to explain/answer questions 7) Get monitoring devices and give comfort ○ L-lab tests: cbc, blood alc, pregnancy etc. ○ M-monitor ecg ○ N-nasogastric tube- decompress and empty stomach (orogastric tube for someone with significant head trauma bc naso can enter the brain) ○ O-o2 and ventilation asses ○ P-pain assess Secondary Survey Brief survey that aims to address all injuries 1. History and Head to Toe assessment a. Listen to what caregivers provide b. MIST i. M-Mechanism of injury 1. Details of mechanism of injury help to provide understanding of injury ii. I-Injuries sustained iii. S-Signs and symptoms before arrival iv. T-Trx before arrival c. SAMPLE i. S-symptoms ii. A-allergies iii. M-medication history iv. P-past history v. L-last meal vi. E-events d. Full body asses abnormalities i. Head,neck and face 1. Check eyes for extraocular movements( could be sign of neurological damage) 2. Battle sign: bruising behind ears ( fracture of the skull ) 3. Racoon eyes: bruising around eyes ( fracture of skull ) 4. Check ears for fluid ( blood or CSF fluid) do not block clear drainage could increase ICP ii. Inspect Chest iii. Abdomen and Flanks 1. Don't remove impaled objects 2. If blunt trauma or intra abdominal hemorrhage, perform FAST assessment- helps to identify blood in the peritoneal space and assess cardiac function iv. Pelvis and peritoneum 1. Palpate the pelvis, do not rock the pelvis, pain may indicate a pelvis fracture 2. Asses for bladder distention, hematuria, dysuria, rectal exam v. Extremities  1. Asses lower and upper extremities for point tenderness crepitus and tenderness 2. Realign grossly deformed pulseless extremities before splinting 3. Immobilize and elevate injured extremities and apply ice packs 4. Asses extremities for compartment syndrome vi. Inspect posterior surfaces 1. Logroll trauma patients 2. Look at back of patient-often overlooked vii. Just Keep reevaluating 1. Keep assessing airway and breathing 2. Give prophylaxis tetanus 3. Asses LOC Pulmonary Chapter 27: Review of the Respiratory System need help with interpreting ABGS Chapter 28: Supporting Ventilation, pp 539-574, Artificial airways, Chest tubes ○ Ongoing crepitus at the chest tube site may indicate ongoing pneumothorax and pleural drainage, non-invasive and invasive ventilation (545-568)  Chapter 31: Obstructive Pulmonary Disease-Primary focus on Asthma, pp 638-656 Chapter 32: Acute Respiratory Failure and Acute Respiratory Distress Syndrome, pp 672-691 Select the appropriate indications for mechanical ventilation. ○ 1) ARF(acute respiratory failure) ○ 2) apnea ○ 3) inability to breath or protect the airway ○ 4)acute respiratory distress ○ 5)Severe hypoxemia and or hypercapnia ○ 6)Respiratory muscle fatigue Explain the difference between invasive vs non-invasive ventilation. Identify the purpose and frequently used equipment and explain the interprofessional care and nursing management for patients receiving noninvasive ventilation support and mechanical ventilation. ○ Non-invasive: uses a mask to ventilate patient instead of ET tube Typical patients for this is copd and heart failure Don't give to patients with an acute MI or GI bleed bad! Two common modes ○ CPAP: 1 level of pressure ex. Obstructive sleep apnea  ○ Bi-PAP: provides 2 level pressure support: inspiratory and expiratory positive pressure Patient must be awake and alert and able to breathe spontaneously +able to protest their airway ○ Invasive: ET, tracheostomy(via stoma in neck) Not adequately exchanging gases, airways compromised, guillain barre-progressive demyelination, trauma-facial Altered LOC, basically can’t breath on their own which sucks Select appropriate nursing interventions related to the care of an intubated patient. ○ Monitor LOC, hemodynamic stability, patient-ventilator interaction, patient tolerance to ET or tracheostomy. ○ Auscultate breath sounds and respiratory effort, assessing for decreased ventilation or adventitious sounds. ○ Monitor ventilator settings and alarms. ○ Monitor tube placement and cuff pressure. ○ Determine need for ET tube suctioning and suction patients as needed.  ○ Give sedatives, analgesics, and NMBA drugs as ordered. ○ Reposition and re-secure ET tube (per agency policy). ○ Provide ordered VTE and GI prophylaxis. ○ Develop plan for communication with the patient. ○ Monitor oxygenation level and signs of respiratory fatigue during weaning. ○ Teach patient and caregiver about mechanical ventilation and weaning. ○ Supervise assistive personnel Explain complications associated with mechanical ventilation and predict nursing interventions based on mechanical ventilator alarms. ○ Aspiration complication: treat by raising HOB 30 degrees, use Yankauer suction catheter or sterile use single catheter ○ Alterations in gastric mobility: start a bowel regimen ○ Ventilator disconnection and malfunction: teach patient not to touch tube or remove tube, check to make sure tubes are secure(obviously), put those alarms on! ○ Infection: complication, normal defences of the uper and lower respiratory systems are bypassed ○ Sodium and water imbalance: trx based on deficiencies ○ Alveolar hypotension: air leaking, not good settings on ET tube, sedation effects ○ barotrauma: to high air pressure ruptures the aveloi ○ Volutrauma: too large of volume causes rupture ○ Vent associated Pneumonia: ( bc no hand washing, contaminated equipment, adverse environment, or patient cant cough or clear secretions) How to avoid this? (1) minimizing sedation by doing daily spontaneous awakening trials or daily spontaneous breathing trials (2) early mobilization, (3) use of ET tubes with subglottic secretion drainage ports (4) elevating the head of the bed a minimum of 30 to 45 degrees unless contraindicated (5) oral care with chlorhexidine (6) no routine changes of the ventilator circuit tubing.  High pressure alarms: increased secretions are in the airway, wheezing or bronchospasm, et tube is displaced, ventilator tube is obstructed from water or kink in tubing, patient coughs or gags or bites on oral ett, patient is anxious or fights the vent Low pressure alarms: disconnection or leak in ventilator or in patient airway cuff/ patient stops spontaneous breathing Identify the pathophysiology, clinical manifestations, complications, interprofessional care, and nursing management of patients with an artificial or critical airway. Pg.558 Chapter 31: Obstructive Pulmonary Diseases: Primary Focus-Asthma Explain the difference between an acute asthma exacerbation and status asthmaticus.  Acute Asthma Status Asthmaticus 1) Alert and oriented but focused 1) Extreme acute asthma attack on breathing characterized by hypoxia, Frightened; agitated if hypercapnia, and acute hypoxemic respiratory failure; Tachycardia, tachypnea (>30 life-threatening(needs breaths/min) intubation) Accessory muscle use; sits 2) Altered LOC forward Wheezing 3) Like a state of shock Maybe blue-tinged (hypotension & bradycardia) can go into respiratory or cardiac 2) Give bronchodilators and oral arrest corticosteroids and antihistamines if allergic 4) Chest tightness, increased shortness of breath, and sudden inability to speak Most concern to nurse is being unable to speak and sweating 5) Minimal air movement in lungs profusely when auscultated 6) Medications dont work a) TRX: Oxygen, IV fluids, systemic bronchodilators, steroids b) Endotracheal intubation & mechanical ventilation may be needed, hemodynamic monitoring c) Silent chest(hear nothing when listening to chest)—immediately notify HCP Summarize clinical manifestations associated with severe asthma and propose pharmacologic and non-pharmacologic medical and nursing management. ○ Some sort of trigger- infection, allergen, exercise, irritant- leads to inflammatory mediators- massive vasodilation and cellular infiltration Symbicort drug of choice for everyday use (LABA/ICS inhaler) SABA and corticosteroid for rescue  Supplemental oxygen, need continuous pulse ox, normal PaO2— > or equal to 80% Drug therapy: Chapter 32: Acute respiratory Failure and Acute Respiratory Distress Syndrome Discuss the etiology, pathophysiology, and clinical manifestations of acute respiratory failure (ARF). ○ One or both of the gas exchange functions of the lungs are compromised ○ Not a disease but a symptom that reflects lung function ○ Life threatening disorder with a high mortality rate What are other causes of ARF?  Shunts: blood leaves the heart without gas exchange Diffusion limitation: gas exchanged across membrane is compromised Alveolar hypoventilation: decreased ventilation ○ Pathophys: mismatch between ventilation(V) and perfusion(Q) ○ Clinical manifestations: FIRST SIGN: mental status change! / late sign cyanosis(unreliable)/ PaO2 less than or equal to 45 mm Hg Describe the nursing and interprofessional management of hypoxemic or hypercapnic respiratory failure. Hypoxemic respiratory failure is defined as a PaO2 less than or equal to 60 mm Hg with normal or slightly suboptimal PaCO2 levels. Normal pa02 is 70-100 Common causes include pneumonia, pulmonary edema, pulmonary emboli, heart failure, and shock. Hypercapnic respiratory failure, the lungs are often normal, and the main problem is ventilatory failure (insufficient CO2 removal). Normal paCO2: 35-45 It is defined as a PaCO2 greater than 50 mm Hg, which may or may not be accompanied by hypoxemia and/or acidemia (arterial pH less than 7.35). Examples:sedative overdose, respiratory muscle paralysis, and flail chest  Treatment: treat underlying cause, assess ability to breath immediately/ oxygen therapy/ may need intubation and mechanical ventilation Medications: bronchodilators, corticosteroids, diuretics, iv antibiotics (reduce anxiety and pain- benzos and opioids) Nursing Management: maintain patent airway:suctioning, absence of dyspnea, ensure they can effectively cough and clear secretions:chest physiotherapy , keep abgs the same, may need non-invasive positive pressure ventilation, hydration(2-3 L a day) Discuss the pathophysiology and clinical manifestations of acute respiratory distress syndrome (ARDS). sudden, progressive form of ARF in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid, causing the alveoli to partially or completely fill with fluid Etiology: most common cause of ARDS is sepsis. It may develop because of multiple organ dysfunction syndrome (MODS). ○ Direct(pathogen in lungs,aspiration, virus,bacteria) or Drowning,aspiration, pneumonia  ○ indirect injury(sepsis or massive trauma)proliferate to lungs Sepsis, blood transfusion,pancreatitis Pathophysiology: injury or exudative phase, reparative or proliferative phase, fibrotic or fibroproliferative ARDS diagnostic criteria: development within 1 week of a known clinical insult or new or worsening respiratory symptoms, chest x-ray with new bilateral opacities, and a low PaO2/FIO2 (P/F) ratio: ○ Mild ARDS: P/F ratio < 300 with PEEP or CPAP > 5 cm H2O ○ Moderate ARDS: P/F ratio < 200 with PEEP or CPAP > 5 cm H2O ○ Severe ARDS: P/F ratio < 100 with PEEP or CPAP > 5 cm H2O Symptoms: initial presentation in first 24-72 hours( mild dyspnea, tacypnea, cough, restlessness) fine scatter crackles As ARDS worsens as fluid accumulates, changes in mental status, tachycardia, hypotension, and severe changes in oxygen, ventilation, and acid-base balance occur. Refractory hypoxemia and profound respiratory distress and/or failure require intubation and mechanical ventilation. Describe the nursing and interprofessional management of ARDS. Mechanical ventilation needed Antibiotics if caused by sepsis or organism Corticosteroids can help calm inflammation response Select measures to prevent and manage complications of ARF and ARDS.  Complications include changes in lung function, ventilator associated pneumonia, stress ulcers, VTE, acute kidney injury, and longer term problems with lung function and mental health issues. Infection control, managing secretions, keep well oxygenated Burns Chapter 14, pp. 230-235 Start with Human Leukocyte Antigen (HLA) System Chapter 26, pp. 495-511 Burns Chapter 14 - Organ Transplant & Graft-versus-host disease (GVHD) 1. Discuss the transplant process and management of clients receiving organ transplants. a. Some organs can be transplanted in parts or segments b. Common tissue transplants are corneas,skin, bone marrow, heart valves, bone and connective tissue i. Corneal transplants can prevent or correct blindness. Skin grafts are used in managing burn patients. Donated bone marrow can help patients with leukemias and other cancers. c. Organ donations come from deceased or living donors d. Just bc someone is an organ donor on their license does not mean they don't need family members consent to their organs( some places require consent from family) e. The Uniform Anatomical Gift Act regulates organ and tissue donations to allow for fair and consistent transplantation laws among all states. i. Patients are matched to available donors based on several factors: ABO blood and HLA typing, medical urgency, time on the waiting list, and geographic location. f. Tissue typing i. Recipient typically receives a transplant from an ABO blood group-compatible donor ( donor and recipient do not need to share the same rH factor) ii. Corneas are avascular so no antibodies can reach the cornea and cause rejection. In kidney and bone marrow transplantation, HLA matching is very important, since these transplants are at high risk for graft rejection. iii. Transporting and storing donated organs can take time. The “best” match may live many miles from the “ideal” recipient. The need to have the “best” matches must be balanced against the time it takes to obtain and transport a donated organ and then transplant it.  iv. A panel of reactive antibodies (PRA) shows the recipient’s sensitivity to various HLAs before receiving a transplant. PRA allows us to determine whether a recipient is of high or low reactivity to potential donors. 1. A high PRA means that the person has many cytotoxic antibodies and is highly sensitized. There will be a poor chance of finding a crossmatch-negative donor. ( basically high PRA- bad ) a. If have high PRA they can try various drugs to help lower the sensitively like plasmapheresis, IVIG v. A crossmatch is done to determine the existence of antibodies against the potential donor 1. The crossmatch can be used as a screening test when possible living donors are being considered or once a cadaver donor is chosen. a. You want a negative crossmatch- that means there are no antibodies present and a transplant can occur b. A positive crossmatch means that the recipient has cytotoxic anti- bodies to the donor. This is an absolute contraindication in living donor transplants. Live donor transplants may be done for patients with a positive crossmatch if no other live donors (with a negative crossmatch) exist. In this situation, plasmapheresis or IVIG can remove antibodies. c. A prospective crossmatch is especially important for kidney transplants. It is not an option for lung, liver, and heart transplants. 2. Prioritize the nursing care and treatment for clients receiving different types of organ transplants. a. Immunosuppression therapy, performing ABO and HLA matching, and ensuring that the crossmatch is negative reduces the risk for rejection b. Prevent infection! 3. Distinguish among the types of rejection after transplantation. a. Organ rejection occurs as a normal immune response to foreign tissue b. A perfect match is nearly impossible unless the tissue is from one’s self, an identical twin, or in some cases a sibling. c. Rejection can be hyperacute, acute, or chronic. i. Hyperacute 1. Occurs within 24 hours after transplantation 2. No treatment for this, must remove the transplanted organ unfortunately  3. 4. Usually rejection this quickly is rare ii. Acute: 1. Occurs within the first 6 months after transplantation 2. usually a cell-mediated immune response by the recipient’s lymphocytes, which are activated against the donated (foreign) tissue or organ 3. It is common to have at least one rejection episode especially with organs from deceased donors a. These are usually reversible with immunosuppressive drugs b. iii. Chronic: 1. Chronic rejection is a process that occurs over months or years. It is irreversible. 2. Chronic rejection results in fibrosis and scarring. In heart transplants it man ifests as accelerated coronary artery disease. In lung transplants it manifests as bronchiolitis obliterans. In liver transplants, we see a loss of bile ducts. In kidney transplants it manifests as fibrosis and glomerulopathy. 3. No definitive trx, just supportive measures d. Kidney transplant rejection main side effects: fever, oliguria, weight gain, Elevated BP i. Signs and symptoms of acute rejection of a transplanted kidney include pain at the graft site, decreased urine output, hypertension, elevated wbc, fever and increased creatinine level 4. Identify the types and side effects of immunosuppressive therapy. a. GO to TABLE 14.17 Drug Therapy b. (1) calcineurin inhibitors c. (2) corticosteroids (prednisone, methylpredniso- lone)  d. (3) purine synthesis antagonists, including mycopheno- late mofetil (CellCept, Myfortic) and azathioprine (Imuran)(4) sirolimus. e. IV Muromonab-CD3 and either horse anti- thymocyte globulin (Atgam) or rabbit antithymocyte globulin (ATG) are used for short periods to prevent early rejection or reverse acute rejection. f. Don't consume grapefruit juice with cyclosporine it inhibits the metabolism Antirejection therapy alter immune response causing bone marrow suppression Immunosuppressant medications are taken for life following transplant, these are needed to prevent rejection of the organ. Unfortunately, immunosuppressants increase the risk for infection, especially in the first few months after transplant when the immunosuppressive doses are highest. 5. Explain the assessment and treatment of Graft-versus-host disease (GVHD). a. Graft-versus-host disease (GVHD) occurs when an immunodeficient patient receives immunocompetent cells. b. However, in GVHD disease, the graft (donated tissue) rejects the host (recipient) tissue. A GVHD response is most common in hematopoietic stem cell transplants. i. The GVHD response may begin 7 to 30 days after transplantation. Once the reaction is started, little can be done to change its course ii. The target organs for the GVHD phenomenon are the skin, liver, and GI tract. The skin disease may be a maculopapular rash, which may be itchy or painful. It initially involves the palms and soles of the feet. It can progress to a generalized erythema with bullous formation and desquamation (shedding of the outer layer of skin). The liver disease may range from mild jaundice with high liver enzymes to hepatic coma. GI manifes- tations may include mild to severe diarrhea, severe abdominal pain, GI bleeding, and malabsorption. iii. TRX: corticosteroids, immunosuppressive agents, radiating blood products, Ibrutinib a kinase inhibitor used for leukemia and lymphoma Chapter 26 - Burns 1. Distinguish between partial-thickness and full-thickness burns. Pretty much full thickness is waxy dry leathery and partial is more vesicles and red Classification Appearance Possible Cause Structures Involved Partial-Thickness Skin Destruction Superficial Erythema, blanching on Quick heat flash Superficial epidermal (first-degree) burn pressure, pain and mild Superficial sunburn damage with swelling, no vesicles or hyperemia. Tactile and blisters (although after 24 pain sensation intact hr skin may blister and peel) Deep (second-degree) Fluid-filled vesicles that are Chemicals Epidermis and dermis burn red, shiny, wet (if vesicles Contact burns involved to varying have ruptured). Severe Electric current depths. Skin elements, pain caused by nerve Flame from which epithelial injury. Mild to moderate Flash regeneration occurs, edema Scald remain viable Tar, cement Full-Thickness Skin Destruction Third- and Dry, waxy white, leathery, Chemical All skin elements and fourth-degree burns or hard skin. Visible Electric current local nerve endings thrombosed vessels. Flame destroyed. Coagulation Insensitivity to pain Scald necrosis present. because of nerve Tar, cement Surgical intervention destruction. Possible required for healing involvement of muscles, tendons, and bones 2. Apply tools to determine the severity of burns. a. Rule of Nines…most common determination of TBSA burned, body parts broken down into multiples of 9% i. Whole head Head & neck = 9% Front of head and front neck 4.5% ii. Upper extremities = 9% each (whole arm) iii. Lower extremities = 18% each Front of one leg 9% iv. Front trunk = 18% v. Back trunk = 18% vi. Perineal area (adults) = 1% b.  1) Total body surface area (TBSA) percentage is essential to guiding adequate fluid resuscitation and treatment. Adult patients are resuscitated at injuries of 20% or greater TBSA. Extremes of age, including older adults and pediatric patients, are often resuscitated at 10% TBSA. 2) Rule of Palm. The size of the patient’s hand, including the fingers, accounts for approximately 1% TBSA. 3) Lund and Browder Classification. Measurements, which take into account surface area related to age, are assigned to each body part. Critical body areas are face, hands, feet, & perineum Severity factors: Inhalation injury, patient age, past medical history, and concomitant injury, with anatomical location of injury 3. Compare the pathophysiology, clinical manifestations, complications, and interprofessional care throughout the 3 burn phases. a. Types are Emergent, Acute, Rehabilitation i. Emergent: time required to resolve immediate problems resulting from injury 1. Up to 72 hours for burns extending over 20 percent of their bodies 2. Main concerns are hypovolemic shock and edema 3. Monitor for hypotension, tachycardia, and tachypnea. Report changes to the HCP. Patients can develop AKI and ultimately death if not resuscitated sufficiently. 4. Major electrolyte shifts of sodium and potassium occur during this phase. 5. Burn injury causes coagulation necrosis. 6. The inflammatory cytokine cascade, triggered by tissue damage, impairs the function of lymphocytes, monocytes, and neutrophils.( high infection risk) 7. Ends when fluid mobilization and diuresis begins 8. Manifestation/ TRX: Give the patient simple explanations of what to expect. Often patients will shiver from heat loss, anxiety, or  pain. Provide warm blankets and increase the room temperature or turn on heat lamps. a. Complications: 3 systems most susceptible to complications during the emergent phase of burn injury are the respiratory, cardiovascular, and renal systems. i. Respiratory: Inhalation injuries from breathing noxious chemicals or hot air will damage the respiratory tract. Examine sputum for carbon particles. Watch for signs of respiratory distress, such as increased agitation, anxiety, restlessness, or a change in the rate or character of breathing. ii. Cardiovascular: Deep circumferential burns and subsequent edema formation can impair blood flow to the extremities. If untreated, ischemia, paresthesia, and necrosis can occur. iii. Renal: The most common renal complication during the emergent phase is AKI. If the patient becomes hypovolemic, blood flow to the kidneys will decrease, causing renal ischemia. 9. Airway, Fluid and Wound Care are super important during this phase ii. Acute: begins with the mobilization of interstitial fluid and subsequent diuresis and continues until wounds are nearly healed. This may take weeks or months depending on the burn severity 1. patho:Vital signs are more stable. Wound healing begins as WBCs sur- round the burn wound and phagocytosis occurs. Necrotic tis- sue begins to slough. 2. manifest-Partial-thickness wounds begin to heal at the wound margins. Epithelial buds, from the hair follicles and glands in the dermal bed, eventually close the wound. Patients often have more pain during the acute phase due to repeated dressing changes, therapy exercises, opioid tolerance, fatigue, and reduced coping ability. a. Because the body is trying to reestablish fluid and electrolyte balance, it is important for you to follow the patient’s serum electrolyte levels closely, especially sodium and potassium levels 3. complications-wound infection progressing to sepsis because of manipulation (e.g., after showering and debridement) and prolonged presence of eschar. The same cardiovascular and  respiratory system complications seen in the emergent phase may continue/ Paralytic ileus if the patient becomes septic / Patients can become extremely agitated, withdrawn, or combative /As scar tissue forms, there may be the development of limited range of motion with contractures 4. Trx: The predominant therapeutic interventions in the acute phase are wound care, excision and grafting, pain management, physical and occupational therapy, nutrition therapy, and psychosocial care. a. goals of wound care are to prevent infection and promote wound re-epithelialization and/or successful skin grafting. Iii. Rehabilitation: begins when wounds have nearly healed, and the patient is able to take part in self-care activity. This may occur as early as 2 weeks or as long as 7 to 8 months after a major burn. b. Management includes positioning, splinting, and exercise to minimize skin and joint contractures. Continuous exercise and physical/occupational therapy cannot be overemphasized. 4. Compare the fluid and electrolyte shifts during the emergent and acute burn phases. a. Hyponatremia can develop from Excessive GI suction Diarrhea Water intoxication From excess water intake Offer juices, nutritional supplements B. Hypernatremia may occur after Successful fluid resuscitation Improper tube feedings Inappropriate fluid administration Restrict sodium in IVs, enteral or oral feedings Hyperkalemia may occur if patient has Renal failure  Adrenocortical insufficiency Massive deep muscle injury Large amounts of potassium are released from damaged cells Assess for manifestations of hyperkalemia Hypokalemia occurs with Vomiting, diarrhea Prolonged GI suction IV therapy without potassium supplementation Through burn wounds Assess for manifestations of hypokalemia Other Watch lactate levels 5. Outline the nutritional needs of the burn patient. a. The patient may benefit from an antioxidant protocol, which includes selenium, vitamin E, acetylcysteine, ascorbic acid, zinc, and a multivitamin. Meeting daily caloric requirements is crucial and should start within the first 1 to 2 days post-burn. The dieti- tian regularly calculates the daily caloric requirements and makes adjustments as the patient’s condition changes (e.g., wound heal- ing improves, sepsis develops). Monitor laboratory values (e.g., albumin, prealbumin, total protein, transferrin) as available. b. Encourage the patient to eat high-protein, high-carbohy- drate foods to meet caloric goals. Ask caregivers to bring in their favorite foods from home. Appetite is usually reduced. You will need to reinforce the steps being taken to achieve adequate intake. Ideally, weight loss should not be more than 10% of the pre-burn weight. Record the patient’s daily caloric intake using calorie count sheets. Review the sheets with the dietitian. Weigh the patient weekly to evaluate progress. c. Decreases complications and mortality/Optimizes burn wound healing/ Minimizes negative effects of hypermetabolism and catabolism  6. Prioritize nursing interventions in the management of the burn patient's physiologic and psychosocial needs. a. Don't give anything cool to the patient b. Use pulse ox to check oxygen level if patient is becoming agitated and restless from hypoxemia c. Coping d. Fluids and Electrolytes e. Infection f. Nutrition g. Pain h. Perfusion i. Tissue Integrity 7. Accurately calculate IV fluid replacement for burns using a fluid resuscitation formula (Parkland). A client (100kg) is admitted to the burn unit. Using the rule of nines, calculate % of burns. Burns to the anterior chest, right anterior and posterior arm, genital, and anterior right leg. Calculate the initial volume of fluid to infuse within the first 8 hours of resuscitation using the following parkland formula: 2mL/kg per %TBSA a. Total % = 37%, formula = 2mL x weight (100) x %burn (37) = 7400 → total volume to be infused b. We give half of the volume within the first 8 hours (3700) 8. Chapter 26 table 26.7 Medical Surgical Nursing Textbook Readings: Harding, M. M., Kwong, J., Roberts, D. Hagler, D. & Reinisch, C. (Eds.). (2023). Lewis’s medical surgical nursing: Assessment and management of clinical problems (12th Edition). St. Louis: Elsevier Chapter 60: Assessment Nervous System pp.1461-1481 (Review) Chapter 61: Acute Intracranial Problems; Increased Intracranial Pressure, Nursing Management, Head Injuries pp. 1483-1502; Cranial Surgery: 1506-1508 Chapter 62: Stroke pp. 1515-1536 Chapter 65: Spinal Cord and Peripheral Nerve Problems; Tetanus pp. 1594-1618 Chapter 60: Assessment Nervous System Discern normal from abnormal findings of a physical assessment of the nervous system. Normal Mental status: Alert and oriented, orderly thought processes, Appropriate mood and affect Cranial nerves: May be recorded as “CN I to XII intact”, Smell intact to soap or coffee, Visual fields full to confrontation, Intact extraocular movements, No nystagmus. PERRLA, Intact facial sensation to light touch and pinprick, Full facial movements, Hearing intact bilaterally, Intact gag and swallow reflexes. Symmetric smile., Midline protrusion of tongue. Full strength with head turning and shoulder shrugging Motor system: Normal gait and station. Normal tandem walk. Negative Romberg test, Normal and symmetric muscle bulk, tone, strength, Smooth performance of finger-nose, heel-shin movements Sensory system: intact sensation to light touch, position sense, pin- prick, heat, and cold Reflexes: Biceps, triceps, brachioradialis, patellar, and Achilles tendon reflexes 2/5 bilaterally, Toes pointed down with plantar stimulation Abnormal Dysphagia-difficulty swallowing Ophthalmoplegia-paralysis of eye muscles Anisocoria- inequality of pupil size Diplopia-double vision Homonymous hemianopsia-loss of vision in 1 side of visual field Papilledema-chocked disc Anosognosia- inability to recognize bodily defect or disease  apraxia-Inability to perform learned movements despite having desire and physical ability to perform them Ataxia-lack of coordination of movement Dyskinesia-impaired voluntary movement Hemiplegia-paralysis on 1 side Nystagmus-jerking or bobbing of eyes Analgesia-loss of pain Astereognosis-inability to recognize form of object by touch Aphasia- loss of impaired language faculty ] Dysarthria-lack of coordination in articulating speech paraplegia-paralysis of lower extremities Tetraplegia-paralysis of all extremities Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the nervous system. ○ Imaging Studies: MRI, CT scans, PET scans, and X-rays to visualize the structure of the brain and spinal cord. ○ Electrophysiological Tests: EEG, EMG, and nerve conduction studies to evaluate electrical activity and muscle function. ○ Cerebrospinal Fluid (CSF) Analysis: Lumbar puncture to analyze the composition of CSF for infections, bleeding, or other abnormalities. ○ Neuropsychological Testing: Assess cognitive function and behavioral changes. ○ Cerebral angiography ○ CT Scan ○ CTA ○ MRI ○ EEG ○ Xray ○ PET ○ Ultrasound  ○ Nerve conduction studies Chapter 61: Acute Intracranial Problems Describe the common etiologies, clinical manifestations, and interprofessional care of the patient with increased intracranial pressure./ Describe the nursing management of the patient with increased intracranial pressure. ○ 5-15 mm Hg = ICP ○ 60-100 mm Hg = CPP ○ 20-30 ml/hr = CSF ○ brain tissue(78 percent), blood(12 percent) and CSF(10 percent) must remain balanced= monro-kellie doctrine ○ Factors that influence ICP Arterial pressure, venous pressure, intra abdominal pressure, posture, temperature, blood gases (co2 levels) ○ Clinical manifestations LOC, vital signs, ocular signs, decreased motor function, headache, vomiting Cushing's triad( increased systolic, decreased pulse, decreased resp) ○ Management Increase HOB intubate/vent ICP monitor PbtO2, SjvO2 PaO2 greater than 100 mm Hg Fluid balance SBP between 100-160 mmHg CPP greater than 60 mmHg Decrease cerebral metabolism ○ Treatment Mannitol-IV Hypertonic saline-IV  Slowly Anti-Seizure meds- IV, PO Corticosteroids- IV, PO Histamine receptor antagonist- IV, PO Surgery- will be discussed shortly Compare types of head injury by mechanism of injury and clinical manifestations. Types of head injury: Scalp lacerations: usually see bleeding d/t the fact the scalp contains many blood vessels with poor restrictive abilities. Skull fractures Can be: (1) linear or depressed; (2) simple, comminuted, or compound; and (3) closed or open (Table 61.6) on page1496 goes over Types of skull fractures And manifestations are on Table 56.7 Location determines manifestation i.e. a basilar skull fx is specialized type of linear fracture involving the base of the skull. Manifestations are: Battle’s sign (post auricular bruising) and periorbital bruising or (raccoon eyes). This fracture is often associated with a tear in the dura and subsequent leakage of CSF. How do you test CSF leak? Glucose-send a specimen to the laboratory to determine the fluid type. If it’s snot, it’s not ○ Most common type of head injury are falls Young kids are more at risk for injury due to their nature ○ Scalp lacerations: external head trauma Blood loss and infection ○ Skull fracture Comminuted: multiple linear fractures with fragmentation of bone into many pieces. Cause: direct, high momentum impact. Compound: depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity. Cause: severe head injury. Depressed: inward indentation of skull. Cause: powerful blow. Linear: break in continuity of bone without change of relationship of parts.  Cause: low-velocity injuries Simple: linear or depressed skull fracture without fragmentation or communicating lacerations. Cause: low to moderate impact. Manifestations of skull fractures Basilar:CSF or brain otorrhea,bulging of tympanic membrane caused by blood or CSF, battle sign, tinnitus, or hearing difficulty, rhinorrhea, facial paralysis, conjugate deviation of gaze, vertigo. Frontal:Exposure of brain to contaminants through frontal air sinus,possible association with air in forehead tissue, CSF rhinorrhea, pneumocranium. Orbital:Periorbital bruising(racoon eyes),optic nerve injury. Parietal:Deafness,CSF or brain otorrhea,bulging of tympanic membrane caused by blood or CSF, facial paralysis, loss of taste, battle sign. Posterior fossa:Occipital bruising resulting in cortical blindness,visual field defects, rare appearance of ataxia or other cerebellar signs. Temporal:Boggy temporal muscle because of extravasation of blood, oval-shaped bruise behind the ear in mastoid region (Battle Sign), CSF otorrhea, middle meningeal artery disruption, epidural hematoma. Rhinorrhea or otorrhea can confirm that a fracture has traversed the dura. Rhinorrhea may also manifest as post nasal sinus drainage, often overlooked unless we assess this finding. Head Trauma Brain injuries are categorized as diffuse (generalized) or focal (localized). In a diffuse injury (e.g., concussion, diffuse axonal injury), damage to the brain is not localized to one area. In a focal injury (e.g., contusion, hematoma), damage is localized to a specific area of the brain. Brain injury can be classified as minor (GCS 13 to 15), moderate (GCS 9 to 12), or severe (GCS 3 to 8). P 1312 Contusions involve-bruising of the brain tissue within a focal area. It is usually associated with a closed head injury and often occurs at a fracture site. A contusion may have areas of hemorrhage, infarction, necrosis, and edema. Complications are: Concussion- a sudden transient mechanical head injury with disruption of neural activity and a change in the LOC, is considered a minor diffuse head injury. The patient may or may not lose total consciousness with this injury. Diffuse axonal injury (DAI) is widespread axonal damage occurring after a mild, moderate, or severe TBI. The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem. The clinical signs of DAI vary. They may include a decreased LOC, increased ICP, decortication or decerebration, and global cerebral edema. About 90% of patients with DAI stay in a persistent vegetative state. Focal Injuries can be minor to severe and localized to an area of injury. Focal injury consists of lacerations, contusions, hematomas, and cranial nerve injuries. Lacerations involve tearing of the brain tissue epidural hematoma which occurs when blood collects in the potential space between the skull and the dura mater. This is a neurologic emergency r/t a tear in the dura, opening a venous or arterial bleed. Hemorrhage occurs into the epidural space, which lies between the dura and inner surface of the skull. Classic signs of an epidural hematoma include an initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC. Other manifestations may be a headache, nausea and vomiting, or focal findings. Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation, along with medical management for increasing ICP, dramatically improves outcomes. Great pic of this on pg 1314 subdural hematoma refers to bleeding between the dura mater and arachnoid layer of the meninges which is most often caused by venous bleeding but can involve arterial disruption. Subdural hematomas may be acute, subacute, or chronic (Table 56.8). An acute subdural hematoma manifests within 24 to 48 hours of the injury. Intracerebral Hematoma: Intracerebral hematoma occurs from bleeding within the brain tissue. It occurs in about 16% of head injuries. It usually happens in the frontal and temporal lobes, possibly from rupture of intracerebral vessels at the time of injury. The size and location of the hematoma are key in determining the patient’s outcome. Describe the interprofessional and nursing management of the patient with a head injury. Test for fluid leaking 1. Dextrostix 2. Tes-Tape strip CSF gives a positive reading for glucose, if blood is present in the fluid, testing for glucose is unreliable because blood also contains glucose. In this event, look for the halo or ring sign, allow the leaking fluid to drip onto a white gauze pad or towel, and then observe the drainage. Within a few minutes, the blood coalesces into the center, and a yellowish ring encircles the blood if CSF is present. Note the color, appearance, and amount of leaking fluid because both tests can give false positives. Management In general, the diagnostic studies are similar to those used for a patient with increased ICP (pg 1499). CT scan is the best diagnostic test to evaluate for head trauma. Emergency management of the patient with a head injury is outlined in Table 61.9 pg. 1500. The principal treatment of head injuries is prompt diagnosis and surgery (if needed), In addition, we institute measures to prevent secondary injury by treating cerebral edema and managing increased ICP. For the patient with concussion and contusion, observation and management of increased ICP are the main management strategies. The choice of type of ICP monitoring is typically related to the type of injury as well as whether there is disruption of the skull. Transcranial Doppler studies may also be used to indirectly measure cerebral blood flow and are often used to determine cerebral blood cessation in severe head injuries. Laboratory analysis includes baseline serum electrolytes, complete blood cell count, and coagulation studies.  Surgical management- Craniotomy to remove loose fragments and elevate the bone, if large amounts of bone are removed craniectomy, a cranioplasty will be performed at a later date to restore shape of skull. In cases where extreme swelling is expected or cases of large acute subdural and epidural hematomas, blood must be removed through surgical evacuation. A craniotomy is generally done to see and allow control of the bleeding vessels. Burr-hole openings may be used in an extreme emergency for a more rapid decompression, followed by a craniotomy. Describe the nursing management of the patient undergoing cranial surgery. Primary goal of care after cranial surgery is prevention of increased ICP, frequent neurologic status, close monitoring of fluid and electrolyte levels and serum osmolality to detect changes in sodium regulation, onset of diabetes insipidus, or severe hypovolemia. Maintain patent airway. Turning and positioning patient will depend on site of operation. Control pain with short-acting opioids, Nausea and vomiting are common post surgery and are treated with antiemetic drugs. GCS is a quick way to assess LOC, test pupillary reaction with a penlight. Brains heal best in a calm, quiet, and dark environment. Chapter 62: Stroke Compare and contrast the etiology and pathophysiology of ischemic and hemorrhagic strokes. Ischemic =Clot However, in an embolic stroke, the blood clot forms somewhere else in the body. It then travels through the bloodstream to the brain artery. The blood clot usually comes from the heart. Hemorrhagic=Bleed (either around or into brain) This bleeding can occur either within the brain or between the brain and the skull. Hemorrhagic strokes account for about 20% of all strokes, and are divided into categories depending on the site and cause of the bleeding.  Correlate the clinical manifestations of stroke with the underlying pathophysiology. Ischemic to Hemorrhagic transformation can be life threatening Cytotoxic edema Weakness or paralysis of the extremities Disorders of speech Due to facial muscle or cranial nerve weakness Apraxia Depression Identify diagnostic studies done for patients with strokes. ○ Screening includes a noncontrast CT scan or MRI to rule out hemorrhagic stroke; blood tests for coagulation disorders; screening for recent history of gastrointestinal (GI) bleeding, stroke, or head trauma within the past 3 months; major surgery within 14 days; or recent active internal bleeding within 22 days. Distinguish the interprofessional care, drug therapy, and surgical therapy for patients with ischemic strokes and hemorrhagic strokes. Describe the acute nursing management of a patient with a stroke. Early treatment is best remember Time is Brain IV-tPA is Clot buster that re-opens arteries tPA must be given within 3 to 4½ hours of the onset of signs of ischemic stroke-earlier is better. Patients are screened carefully before tPA can be given. Screening includes a noncontrast CT scan or MRI to rule out hemorrhagic stroke; blood tests for coagulation disorders; screening for recent history of gastrointestinal (GI) bleeding, stroke, or head trauma within the past 3 months; major surgery within 14 days; or recent active internal bleeding within 22 days. Chapter 65: Spinal Cord and Peripheral Nerve Problems Describe the clinical manifestations and management of clients with Spinal Cord Injuries (SCI). Relate the clinical manifestations of spinal cord injury to the level of disruption and rehabilitation potential. Explain the types, clinical manifestations, and interprofessional and nursing management of disorders associated with SCI such as spinal shock, neurogenic shock and autonomic dysreflexia. Discuss etiology and manifestations of tetanus and botulism ○ Tetanus is a severe infection of the nervous system caused by anaerobic bacillus clostridium tetani Spores are present in soil incubation period 4 to 14 days. The shorter the period, the more severe the symptoms. Could be caused by IV drug use on injection sites, human and animal bites, cuts from stepping on nails, gardening injuries, burns, frostbite, open fractures and GSW Manifestations: stiffness in the jaw (trismus) and neck and signs of infection such as fever. As the disease progresses the neck muscles, back abdomen and extremities become progressively rigid. In severe forms, continuous tonic seizures may occur with extreme arching of the back and retraction of the head (opisthotonos). Laryngeal and respiratory spasms cause apnea and anoxia. The slightest noise, jarring motion or bright light can cause a seizure (agonizingly painful). Mortality rate is almost 100% in the severe form.  Treatment: Adults should receive tetanus and diphtheria toxoid booster every 10 years. Teach patients the importance of immediate, thorough cleansing of all wounds with soap and water. Open wound occurrence with tetanus booster if pt. not immunized within the past 5 years. ○ Botulism is a rare but serious type of food poisoning Gi absorption of Clostridium botulinum Spores found in soil Hard to destroy spores Grows on any food contaminated with spores Improper home canning is often the cause Etiology: The neurotoxin destroys or inhibits the neurotransmission of acetylcholine at the myoneural junction, resulting in disturbed muscle innervation. Neurologic manifestations can develop rapidly or evolve over several days. They include a descending paralysis with muscle incoordination and weakness, difficulty swallowing, and seizures. Manifestations: neurologic, paralysis, muscle incoordination and weakness, difficulty swallowing and seizures Trx:Supportive nursing interventions include rest, activities to maintain respiratory function, adequate nutrition, and preventing loss of muscle mass. GI Chapter 43: Assessment Gastrointestinal System (Review the chapter) Describe the structures and functions of the organs of the gastrointestinal tract gallbladder, biliary tract and pancreas Distinguish normal from abnormal findings of a physical assessment of the gastrointestinal system. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the gastrointestinal system. Chapter 46: Upper Gastrointestinal Problems. Describe the etiology, complications, interprofessional and nursing management of nausea and vomiting ★ Nausea and vomiting are symptoms rather than diseases and can be caused by various factors: ○ Gastrointestinal disorders:gastroenteritis, gastritis, peptic ulcer disease, and irritable bowel syndrome. ○ Central nervous system disorders: Including migraines, brain tumors, and meningitis.  ○ Cardiovascular problems: MI & HF ○ Pregnancy: Particularly in the first trimester. ○ Endocrine/Metabolic disorders: Including diabetic ketoacidosis, Addison's disease, and uremia. ○ Side effects of medications: Including chemotherapy, anesthesia, and certain antibiotics. ○ Psychological factors: Such as stress, anxiety, and fear. ○ Motion sickness: Triggered by certain types of movement. ★ Complications of Nausea and Vomiting ○ Dehydration: Due to loss of fluids ○ Electrolyte imbalances: Such as hypokalemia and hyponatremia. ○ Aspiration pneumonia: Caused by inhaling vomit into the lungs. ○ Malnutrition: Resulting from prolonged inability to eat. ○ Esophageal tears: Such as Mallory-Weiss syndrome, due to forceful vomiting. ★ Interprofessional Management of Nausea and Vomiting ○ Identify and treat the underlying cause: Diagnostic evaluations include a thorough history, physical examination, and appropriate laboratory and imaging studies. ○ Symptom relief→Medications Antiemetics: Such as ondansetron, promethazine, and metoclopramide. Prokinetic agents: Such as erythromycin to enhance gastric motility. ○ Nutritional therapy: Start with clear liquids and progress to bland foods. Small, frequent meals. Avoid strong odors and foods that may trigger nausea. ○ Hydration: IV fluids if oral intake is not tolerated. Electrolyte replacement as needed. ★ Nursing Management of Nausea and Vomiting ○ Assessment: Gather subjective data including the patient's history of nausea/vomiting, potential triggers, and associated symptoms. Assess objective data such as vital signs, skin turgor, and mucous membranes to identify dehydration. Monitor laboratory values for electrolyte imbalances and renal function. ○ Nursing Interventions: Maintain a NPO status: Initially for patients with severe vomiting. Administer prescribed medications: Ensure antiemetics are given as ordered. Hydration and electrolyte management:  Monitor and maintain fluid and electrolyte balance through IV fluids and oral rehydration as appropriate. Dietary adjustments: Begin with clear liquids, advancing to more solid foods as tolerated. Encourage small, frequent meals. Environmental modifications: Provide a quiet, odor-free environment. Encourage rest and relaxation techniques. Patient and caregiver education: Teach strategies to manage nausea and vomiting. Discuss the importance of maintaining hydration and nutrition. Educate on when to seek medical help, especially if symptoms worsen or new symptoms develop. Monitoring and Evaluation: Regularly assess the patient's response to treatment. Monitor for signs of complications such as dehydration or electrolyte imbalances. Describe the etiology of peptic ulcer disease (PUD), clinical manifestations, complications, and interprofessional and nursing management of PUD ★ Peptic Ulcer Disease (PUD) ○ involves the erosion of the gastrointestinal mucosa due to the digestive action of hydrochloric acid (HCl) and pepsin. ○ The primary factors contributing to the development of PUD include: Helicobacter pylori (H. pylori) Infection: Prevalence: Major cause of PUD, present in 80% of gastric and 90% of duodenal ulcers. Mechanism: H. pylori bacteria produce urease, which neutralizes stomach acid and damages the mucosal lining. ○ Medications: Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): These inhibit prostaglandin synthesis, leading to decreased mucus and bicarbonate production, making the mucosa more susceptible to damage. ○ Other Medications: Corticosteroids and anticoagulants, especially when combined with NSAIDs, increase the risk of ulcer development. ○ Lifestyle Factors: Smoking: Increases gastric acid secretion and reduces bicarbonate production. Alcohol Consumption: Irritates and erodes the mucosal lining. Caffeine:Increases gastric acid secretion. Psychological Stress: Stress-related mucosal damage can contribute to PUD.  ○ Medical Conditions: Zollinger-Ellison Syndrome: Characterized by excessive gastric acid production due to a gastrin-secreting tumor. Chronic Diseases: Conditions such as COPD, cirrhosis, chronic renal failure, and hyperparathyroidism are associated with higher risk. ★ Clinical Manifestations of PUD ○ The symptoms of PUD can vary depending on the ulcer's location and severity: Gastric Ulcers: epigastric pain, discomfort or burning sensation 1-2 hours after meals. Often described as burning or gaseous. Eating may worsen the pain. Other Symptoms: Bloating, nausea, vomiting, early satiety, weight loss. In some cases, the first symptom may be a complication like perforation. Duodenal Ulcers: epigastric pain, burning or cramp-like pain 2-5 hours after meals, often relieved by eating or antacids. Pain at Night: Commonly wakes patients at night. Other Symptoms: Bloating, nausea, vomiting, and early satiety. Symptoms may be cyclical, occurring, disappearing, and recurring over time. Silent ulcer: Most common in elderly and when taking NSAIDS ★ Diagnostics/labs ○ GOLD STANDARD to rule out H.pylori is BIOPSY of the antral mucosa w/ urease testing (urea breath and stool test) ○ Barium contrast study to diagnose gastric outlet obstruction or for ulcer detection for those contraindicated for endoscopy. ○ Labs: CBC shows anemia, d/t ulcer bleeding Liver enzyme help detect cirrhosis Serum amylase evaluate pancreatic function for posterior duodenal ulcer penetration Stool examination tested for blood ★ Complications of PUD ○ Hemorrhage: Most Common Complication Due to ulcer erosion into a blood vessel. Symptoms: Hematemesis (vomiting blood), melena (black, tarry stools), anemia. ○ Perforation: Most Lethal Complication Ulcer penetrates the full thickness of the stomach or duodenum, spilling contents into the peritoneal cavity.  Symptoms: Sudden, severe abdominal pain radiating to the back, rigid abdomen, absent bowel sounds, nausea, vomiting, shallow respirations, tachycardia, hypotension. **Urgency:** Medical emergency requiring immediate surgical intervention. ○ Gastric Outlet Obstruction: Cause: Edema, inflammation, or scar tissue obstructing the pylorus or duodenum. Symptoms: Epigastric fullness, early satiety, bloating, nausea, vomiting of undigested food, weight loss. Management: NG tube decompression, IV fluids, correction of electrolyte imbalances, possible surgery. ★ Interprofessional and Nursing Management of PUD ○ Assessment: Subjective Data: Detailed health history, including symptom description, medication use, dietary habits, lifestyle factors, and psychological stress. Objective Data: Physical examination focusing on abdominal tenderness, presence of melena, hematemesis, and signs of complications. Laboratory tests and diagnostic studies (endoscopy, H. pylori tests). ○ Interprofessional Management: Medications: Proton Pump Inhibitors (PPIs): Reduce gastric acid secretion. (pantoprazole aka protonix) or (omeprazole) H2 Receptor Blockers: Decrease acid production. (famotidine) Antibiotics: Eradicate H. pylori infection. (amoxicillin) Antacids: Neutralize stomach acid. (think tums) Cytoprotective Agents: Protect the mucosal lining. (misoprostol sucralfate) Endoscopic Therapy:Direct visualization, biopsy, and treatment of ulcers. Surgical Intervention:Reserved for complications like perforation, hemorrhage, or obstruction. ★ Nursing Management: ○ Acute Care: Monitor Vital Signs: Observe for signs of hemorrhage or perforation. NPO Status: Until symptoms improve. IV Fluid Administration: Maintain hydration and electrolyte balance. Pain Management: Administer medications and provide comfort measures. NG Tube Management: For decompression in cases of obstruction. Patient Education: Explain disease process, treatment plan, and lifestyle modifications. ○ Ambulatory Care:  Medication Adherence: Ensure patients understand the importance of taking prescribed medications. Lifestyle Modifications: Educate patients on the importance of quitting smoking, reducing alcohol intake, avoiding NSAIDs, and managing stress. Dietary Changes: Advise on eating small, frequent meals and avoiding foods that irritate the stomach. Follow-up Care: Schedule regular follow-ups to monitor progress and detect any recurrence early. ○ Health Promotion: Prevention: Educate at-risk populations on avoiding known risk factors, such as NSAIDs and smoking. Screening: Encourage screening for H. pylori in symptomatic patients and those with a family history of PUD. Compare and contrast gastric and duodenal ulcers, (etiology, pathophysiology, clinical manifestations, complications and interprofessional and nursing management) ★ Comparison of Gastric and Duodenal Ulcers ○ Etiology Gastric Ulcers: Helicobacter pylori Infection: Present in about 80% of cases. NSAID Use: Significant risk factor due to its inhibition of prostaglandin synthesis. Bile Reflux: Contributes to the breakdown of the gastric mucosal barrier. Other Factors:Smoking, alcohol use, stress, and chronic diseases such as cirrhosis. ○ Etiology Duodenal Ulcers: Helicobacter pylori Infection: Present in about 90% of cases. Increased Gastric Acid Secretion:Commonly associated with Zollinger-Ellison syndrome. NSAID Use: Also a significant risk factor. Other Factors: Smoking, alcohol use, and chronic diseases such as COPD and chronic renal failure. ○ Pathophys Gastric Ulcers: Location: Usually occurs in the antrum of the stomach. Mechanism: The presence of H. pylori and NSAIDs leads to the breakdown of the mucosal barrier, allowing acid to damage the gastric lining. Bile reflux further contributes to mucosal damage. Acid Production: Often normal or decreased. ○ Pathophys Duodenal Ulcers: Location:Typically found in the first portion of the duodenum. Mechanism: Excessive gastric acid secretion overwhelms the protective mechanisms of the duodenal mucosa, leading to ulceration. H. pylori infection increases acid secretion and decreases mucosal resistance. Acid Production: Increased acid production is a common feature. Compare and contrast presentations of GI bleeding Gastrointestinal (GI) bleeding ○ can present in various forms, depending on the location and severity of the bleed. ○ can be categorized into upper GI bleeding and lower GI bleeding. Upper GI Bleeding ○ Cause: Peptic ulcers (gastric and duodenal) Esophageal varices Mallory-Weiss tears Gastritis Esophagitis Gastric cancer Presentations ○ Hematemesis: Vomiting of blood Bright red (indicating active bleeding). Coffee-ground appearance (indicating older, digested blood). Etiology: Often associated with bleeding from the esophagus, stomach, or duodenum. ○ Melena: Black, tarry stools with a distinctive foul odor, indicating the presence of digested blood. Etiology:Typically associated with bleeding from the upper GI tract, such as from peptic ulcers or esophageal varices. ○ Occult GI Bleeding: Hidden blood in the stool, not visible to the naked eye but detectable with fecal occult blood tests (FOBT). Etiology: Can be caused by slow, chronic bleeding from peptic ulcers, gastritis, or malignancies. ○ Symptoms of Blood Loss or Anemia: fatigue, pallor, shortness of breath, and tachycardia, indicating chronic blood loss leading to anemia. Etiology:Often due to slow, chronic bleeding from peptic ulcers or gastric cancer. Lower GI Bleeding ○ Cause: Diverticulosis Angiodysplasia Colorectal cancer Inflammatory bowel disease (ulcerative colitis, Crohn's disease) Hemorrhoids Anal fissures Presentations: ○ Hematochezia:Passage of fresh, bright red blood per rectum, often mixed with stool.  Etiology: Usually indicates bleeding from the lower GI tract, such as from diverticulosis, hemorrhoids, or colorectal cancer. However, it can also result from a massive upper GI bleed with rapid transit through the intestines. ○ Occult GI Bleeding: Hidden blood in the stool, detectable with FOBT. Etiology: Chronic bleeding from colorectal cancer, angiodysplasia, or inflammatory bowel disease. Describe the pathophysiology, clinical manifestations, complications, and interprofessional management of esophageal cancer Esophageal Cancer ○ Pathophysiology: arises from the lining of the esophagus, typically progressing from the mucosa through the submucosa and muscularis layers. The development of esophageal cancer involves genetic mutations and alterations in oncogenes and tumor suppressor genes, leading to uncontrolled cell proliferation, resistance to apoptosis, and invasion of surrounding tissues. ○ The two main types of esophageal cancer are: Squamous Cell Carcinoma: Originates from the squamous cells lining the upper and middle parts of the esophagus. Risk factors include smoking, alcohol consumption, achalasia, and consumption of hot liquids. Adenocarcinoma: Originates from glandular cells, typically in the lower esophagus, often associated with Barrett's esophagus. Risk factors include gastroesophageal reflux disease (GERD), Barrett's esophagus, obesity, and smoking. ○ Clinical Manifestations Esophageal cancer is often asymptomatic in its early stages. As the disease progresses, symptoms become more pronounced and may include: Dysphagia (Difficulty swallowing) initially with solid foods and later with liquids. Most common and often the first symptom. Odynophagia: (Painful swallowing) Weight Loss: Unintentional weight loss due to difficulty eating and decreased caloric intake. Chest Pain: Pain or discomfort in the chest or back, often worsening with swallowing. Hoarseness: Due to recurrent laryngeal nerve involvement. Cough and Aspiration: Due to esophageal obstruction and possible tracheoesophageal fistula. Regurgitation and Vomiting: From obstruction or esophageal narrowing.  Hematemesis or Melena: Vomiting blood or black, tarry stools from tumor bleeding. ○ Complications Obstruction: Tumor growth can block the esophagus, making it difficult or impossible to swallow. Perforation: Tumor invasion can lead to esophageal wall perforation, causing severe chest pain and potential mediastinitis. Fistula Formation: Development of abnormal connections between the esophagus and trachea or bronchus, leading to aspiration and recurrent pneumonia. Metastasis: Spread to lymph nodes, liver, lungs, and other organs, leading to systemic symptoms and organ dysfunction. ○ Interprofessional Management Diagnosis:Endoscopy with Biopsy: Definitive diagnosis through direct visualization and tissue sampling. Barium Swallow: Identifies strictures and filling defects. Endoscopic Ultrasound (EUS): Assesses tumor depth and regional lymph node involvement. CT and PET Scans: Evaluate for metastatic disease. ○ Treatment: Surgical Resection: Esophagectomy for localized tumors, often with reconstruction using stomach or colon. Chemotherapy and Radiation: Used for locally advanced or metastatic disease, either as neoadjuvant (preoperative) therapy or definitive treatment. Targeted Therapy and Immunotherapy: For specific molecular targets and immune checkpoint inhibitors. Palliative Care: Focuses on symptom management and quality of life for advanced disease, including stent placement for obstruction and pain management. ○ Nursing Management: Preoperative Care: Nutritional support, including enteral or parenteral nutrition if necessary.  Respiratory exercises and pulmonary hygiene to prepare for surgery. Patient education about the procedure and postoperative expectations. Postoperative Care: Monitoring for complications such as anastomotic leak, infection, and respiratory issues. Pain management and early mobilization. Nutritional management, including gradual reintroduction of oral intake and monitoring for aspiration. Emotional support and counseling for the patient and family. Chapter 47: Lower Gastrointestinal Problems Describe the clinical manifestations and interprofessional and nursing management of colorectal cancer. Colorectal Cancer ○ Can present with a variety of symptoms depending on the tumor's location, size, and whether it has spread. ○ The symptoms can be subtle and often resemble other gastrointestinal disorders, making early diagnosis challenging. Key clinical manifestations include: Changes in Bowel Habits: Diarrhea, constipation, or a change in stool consistency lasting more than a few weeks. Narrow stools (pencil-thin): which might indicate a narrowing in the colon. Rectal Bleeding or Blood in Stool: Bright red or very dark blood in the stool, which may be a sign of a tumor in the lower colon or rectum. Can also appear as occult blood (hidden blood) detected through a fecal occult blood test (FOBT). Persistent Abdominal Discomfort: Cramping, gas, pain, or feeling of fullness. Feeling of Incomplete Evacuation: Sensation of not being able to completely empty the bowel Weakness or Fatigue: Can result from anemia due to chronic blood loss from the tumor. Unexplained Weight Loss: Significant weight loss without trying, which can be due to metabolic changes associated with cancer. Symptoms Specific to Location: Right-sided (ascending colon): ○ May cause iron-deficiency anemia due to occult bleeding, weakness, and fatigue. Left-sided (descending colon):  ○ Often leads to changes in bowel habits and obstruction symptoms such as cramps and rectal bleeding. Rectal Cancer: Typically presents with rectal bleeding, tenesmus (feeling of incomplete evacuation), and pain during defecation. Interprofessional and Nursing Management ○ Diagnosis: Screening Tests Colonoscopy: Gold standard for diagnosis, allowing for direct visualization, biopsy, and polyp removal. Flexible Sigmoidoscopy: Examine the lower part of the colon. Fecal Occult Blood Test (FOBT) and Fecal Immunochemical Test (FIT): Detect hidden blood in stool. Stool DNA Test:Detects genetic mutations associated with cancer. ○ Imaging Studies: CT Colonography (Virtual Colonoscopy): Non-invasive imaging to visualize the colon. CT or MRI Scan: Evaluate the extent of the disease and detect metastasis. ○ Treatment: Surgical Resection: Polypectomy:Removal of polyps during colonoscopy. Colectomy: Partial or total removal of the colon, often with reanastomosis or creation of a stoma (colostomy or ileostomy). Radiation Therapy: Often used preoperatively to shrink tumors or postoperatively to prevent recurrence, particularly in rectal cancer. Chemotherapy: Used as adjuvant therapy to reduce the risk of recurrence or as palliative treatment for advanced cancer. Common drugs include fluorouracil (5-FU), oxaliplatin, and irinotecan. Targeted Therapy: Monoclonal antibodies and other agents targeting specific molecular pathways, such as bevacizumab (anti-VEGF) and cetuximab (anti-EGFR). ○ Ongoing Monitoring and Follow-up: Regular follow-up appointments to monitor for recurrence. Surveillance colonoscopies. Blood tests, including carcinoembryonic antigen (CEA) levels, to detect recurrence. Nursing Management: ○ Preoperative Care:Patient Education: Provide information about the surgical procedure, potential outcomes, and recovery process. ○ Bowel Preparation:  Ensure the patient follows a prescribed bowel prep regimen. ○ Nutritional Support: Assess and address nutritional needs, including possible preoperative enteral or parenteral nutrition. ○ Postoperative Care: ○ Pain Management: Administer analgesics and monitor pain levels. ○ Wound Care: Monitor surgical site for signs of infection and promote healing. ○ Ostomy Care: Provide education and support for patients with new stomas, including appliance management, skin care, and dietary modifications. ○ Early Ambulation: Encourage mobility to prevent complications such as deep vein thrombosis (DVT) and pneumonia. ○ Fluid and Electrolyte Balance: Monitor intake and output, and administer IV fluids as needed. ○ Discharge Planning and Education: Signs of Complications: Educate patients on recognizing signs of infection, obstruction, and other complications. Follow-up Care: Stress the importance of follow-up appointments and ongoing monitoring. Lifestyle Modifications: Provide guidance on dietary changes, smoking cessation, and physical activity to support overall health and recovery. Emotional Support: Offer resources for psychological support, including counseling and support groups for patients and their families. ○ Palliative Care: Symptom Management: Focus on relieving symptoms such as pain, nausea, and constipation in advanced disease. Quality of Life: Provide holistic care aimed at improving the patient's quality of life. End-of-Life Care: Support patients and families through end-of-life decisions and provide compassionate care. Select nursing interventions to manage the care of the patient after bowel resection and ostomy surgery Nursing Interventions to Manage Care After Bowel Resection and Ostomy Surgery Immediate Postoperative Care ○ Monitor BP, HR, RR, TEMP ○ Observe for signs of infection (fever, increased WBC count, bleeding, shock) ○ Pain Management: admin pain meds methods of non pharmacological relief such as positioning, heat/cold therapy, relaxation techniques. ○ Respiratory Care: Deep breathing USE IP Monitor oxygen saturation and provide supplemental oxygen if needed. ○ Fluid and Electrolyte Management: Carefully monitor I & O’s,including urine output, NG tube drainage, and wound drainage. Administer IV fluids and electrolytes as ordered to maintain fluid balance and prevent dehydration. ○ Early Ambulation: Encourage the patient to mobilize as early as possible to prevent complications such as deep vein thrombosis (DVT) and pulmonary embolism. Assist with ambulation and provide support to prevent falls. ○ Wound and Ostomy Care: Inspect the surgical incision and ostomy site regularly for signs of infection, bleeding, or other complications. Keep the surgical site clean and dry, changing dressings as needed. Educate the patient on proper wound and ostomy care techniques. Ostomy-Specific Care ○ Ostomy Assessment: Check the stoma for color, swelling, and output. A healthy stoma should be pink or red and moist. Monitor for signs of complications such as ischemia (dark or black stoma), excessive bleeding, or retraction. ○ Ostomy Appliance Management: Assist the patient in selecting and applying an appropriate ostomy appliance to ensure a secure fit and prevent leakage. Teach the patient how to empty and change the ostomy pouch, emphasizing the importance of skin care around the stoma. ○ Skin Care: Protect the skin around the stoma from irritation and breakdown caused by stoma output. Use skin barriers, creams, and powders as recommended to maintain skin integrity. ○ Nutritional Management  Dietary Adjustments: Start with a clear liquid diet and gradually advance to a low-residue diet as tolerated. Educate the patient on foods that may cause gas, odor, or blockages (e.g., high-fiber foods, nuts, seeds, and certain vegetables). Hydration: Encourage adequate fluid intake to prevent dehydration, especially if the patient has an ileostomy, which can lead to increased fluid loss. Nutritional Supplements: Provide nutritional supplements if needed to ensure adequate calorie and nutrient intake during recovery. ○ Patient and Family Education Ostomy Care Education: Teach the patient and family members how to care for the ostomy, including changing the appliance, managing output, and maintaining skin integrity. Provide written instructions and resources for home care. Lifestyle Modifications: Discuss adjustments in daily activities, including clothing choices, exercise, and travel, to accommodate the ostomy. Encourage participation in support groups or counseling to address emotional and psychological concerns. Signs of Complications: Educate the patient on recognizing signs of complications such as infection, stoma blockage, and dehydration. Instruct the patient to seek medical attention if they experience symptoms like persistent abdominal pain, fever, or changes in stoma appearance. ○ Psychological Support Emotional Support: Provide a supportive environment where the patient can express their feelings and concerns about the surgery and ostomy. Offer reassurance and positive reinforcement to boost the patient's confidence in managing their ostomy. Support Groups: Encourage participation in ostomy support groups where patients can share experiences and gain support from others who have undergone similar procedures. Explain the difference between blunt force and penetrating abdominal trauma, abdominal compartment syndrome Blunt Force vs. Penetrating Abdominal Trauma Blunt Force Abdominal Trauma ○ Caused by non-penetrating impacts such as motor vehicle accidents (MVAs), falls, direct blows, or sports injuries. ○ The impact can result in compression, shearing, or deceleration forces on the abdominal organs. ○ Common Injuries: Solid Organs: Liver and spleen are the most frequently injured, leading to lacerations, contusions, and hematomas. Hollow Organs: Less commonly injured, but can include the stomach, intestines, and bladder, which may suffer from contusions or ruptures due to pressure and compression. ○ Clinical Presentation: Abdominal pain,distention, tenderness, and bruising. Signs: Hemodynamic instability, signs of internal bleeding (e.g., Cullen's sign, Grey Turner's sign), and shock. ○ Diagnosis and Management: Imaging: Ultrasound (FAST scan) CT scan Diagnostic peritoneal lavage (DPL) to identify internal injuries. ○ Treatment: Stabilization, IV fluids, blood transfusion, and potentially surgical intervention if there is significant bleeding or organ damage.