Renal and Urologic Problems PDF

Renal and Urologic Problems Urinary Tract Infection - infection of the urinary tract - most common outpatiet infection - most common pathogen is E.coli - sometimes can be caused by fungal and parasitic - more common in immunsuppressed, diabetes kidney problems, or multiple rounds of...

Renal and Urologic Problems Urinary Tract Infection - infection of the urinary tract - most common outpatiet infection - most common pathogen is E.coli - sometimes can be caused by fungal and parasitic - more common in immunsuppressed, diabetes kidney problems, or multiple rounds of antibiotics - ex of parasitic is trichomoniasis Patho - urinary tract is sterile - defense mechanisms - voiding w/ complete bladder emptying - ureterovesical junction (UVJ) competence - ureteral peristatic activity that pushed urine to the bladder - slightly acidic pH (6.-7.5) - antimicrobial proteins and peptides that interfere with bacterial growth - most bacteria are introduced via ascending route - can result from a hematogenous transmission - where a blood borne pathogen invades the kidneys, urters or bladder from elsewhere in the body - i.e. obstructrion of the ureter, damage caused by stones, or renal scarring What puts people at risk for UTI? Gender: Women are more likely to get UTIs than men because their urethra is shorter and closer to the anus. Age: Both young children and older adults are more likely to get UTIs. Sexual activity: Recent sexual activity increases the risk of UTIs. Pregnancy: Pregnancy doesn't increase the risk of getting a UTI, but it can increase the risk of developing a serious infection. Urinary tract issues: Structural problems in the urinary tract, such as an enlarged prostate, can increase the risk of UTIs. Diabetes: Having diabetes increases the risk of UTIs. Menopause: The decrease in estrogen during menopause thins the lining of the urinary tract, making it more susceptible to bacterial infections. Other conditions: Conditions that affect personal care habits, such as Alzheimer's disease and delirium, can increase the risk of UTIs. Diet and lifestyle: An unhealthy diet and a sedentary lifestyle can increase the risk of UTIs. Classifications - can be upper or lower - different terms specify where the inflammation is occurring  - pyelonepritis (kidneys) - cystitis (bladder) - urethritis (urethra) - complicated - occurs in a patient with underlying disease or a structrual or functional problem in the urinary tract - uncomplicated - occurs in otherwise normal urinary tract Upper UTI- An infection of the kidneys or ureters, the tubes that connect the kidneys to the bladder. Lower UTI- An infection of the bladder (cystitis) or urethra, the tube that carries urine out of the body. Symptoms of upper UTIs are more severe than lower UTIs Pyelonephritis- kidney Cystitis- bladder Complicated UTI risks Anatomic abnormalities Functional abnormalities ○Bladder dysfunction: Conditions like overactive bladder and urinary incontinence can lead to recurrent UTIs. ○Poor bladder emptying: Conditions like pregnancy, uterine prolapse, and cystocele can impair bladder emptying. ○Neurogenic dysfunction: Can impair bladder emptying and lead to UTIs in older men. Recent GU instrumentation Foreign material, such as a ureteral stent Diabetes Immunocompromise Pregnancy Being male Clinical Manifestations General/Lower - dysuria - frequency - urgency - suprapubic discomfort - hematuria - sediment - cloudy appearance Upper - fever - chills - flank pain - fatigue - anorexia - confusion (older adults) Diagnostics - H&P - urinalysis (UA) - nitrate (+) - increased WBCs - leukocyte esterase - urine culture - clean catch specimen - straight cath specimen - foley cath specimen - ultrasound - pyelonephritis suspected - CT scan - obstruction suspected Treatment and Nursing Implications Treatment - antibiotics - trimethoprim/sulfamethoxazole (TMP/SMX) (bactrim and co-trimoxazole) - nitrofurantoin (macrobid) - cephalexin (keflex) - fosfomycin (monurol) - antifungal - fluconazole - urinary analgesic - phenazopyridine - excreted in urine - can cause urine to become orange/red Nursing Implications - education - empty bladder often and completely - evacuate bowel regularly - wipe perineal from front to back - drink adequate water - void before and after intercourse - routine and thorough perineal hygiene - CAUTI prevention Acute Pyelonephritis Patho - inflammation of the renal parenchyma and collecting systems - starts in the renal medulla and spreads to the adjacent cortex - most common cause is bacterial infection - begins with colonization and infection of the lower urinary tract via the ascending ureteral tract - common bacteria: E.coli, Klebsiella, Enterobacter species - Preexisting factor: - vesicoureteral reflux - urine back up to urethra (spoiled milk) - dysfunction of the lower urinary tract - obstruction from BPH, structure or renal stones - pregnancy induced physiological changes Pregnancy Urinary Stasis and Dilation of the Urinary Tract: During pregnancy, the growing uterus presses on the bladder and ureters, which can slow or block the flow of urine. This causes urinary stasis (the retention of urine in the bladder or ureters), providing a favorable environment for bacterial growth. Hydronephrosis (dilation of the kidneys) and hydroureter (dilation of the ureters) are common in pregnancy due to hormonal changes and mechanical compression. This slows urine flow, allowing bacteria to ascend and multiply. Hormonal Changes: Progesterone levels rise significantly during pregnancy. Progesterone causes relaxation of smooth muscles, including those in the ureters and bladder. This results in decreased peristalsis of the ureters and reduced bladder tone, further contributing to urinary stasis and incomplete bladder emptying, which increase the risk of infection. Clinical Manifestations - fever/chills (CS) - N/V (CS) - Malaise (CS) - Flank pain (CS) - Dysuria - Urgency - Frequency - Costovertebral angle (CVA) tenderness - Urosepsis (can occur) Diagnostic Testing - H&P - CBC w/ differential - urinalysis - bacteriuria - hematuria - WBC casts - urine culture - blood culture (w/severe illness) - ultrasound - identify anatomic abnormalities, hydronephrosis, renal abscess, obstructing stones - CT (preferred) Treatment Mild Symptoms - adequate fluid intake - NSAIDS/antipyretic - follow up cultures and imaging - antibiotics - empirically broad spectrum - short IV antibiotic with culture results - can be treated outpatient antibiotics 5 to 14 days - improve or resolve within 24 to 72 hours Severe Symptoms - hospitalization - adequate fluid intake - NSAIDS/antipyretic - follow up cultures and imaging - antibiotics - IV antibiotics - swithc to oral antibiotics when patient tolerates PO Nursing Implications - emphasize taking all antibiotics as prescribed - need follow up culture - recognize signs of recurrence or relapse - adequate fluid intake - plenty of rest - relapse or reinfections may need long-term, low-dose antibiotics Urinary Diversons (DO NOT MEMORIZE) - incontinent urinary diverson - diversion to the skin, requiring a pouch - continent urinary diversion - an intraabdominal urinary reservoir that can be catheterized - essentially a pouch created that you straight cath - orthotopic bladder reconstruction - the construction of a new bladder unit the bladder’s normal anatomic position, with discharge of urine through the urethra Incontinent Urinary Diversion - colostomy for urine - most common is ileal conduit - a 4-6 inch segment of the ileum is converted into a conduit for urinary drainage - ureters are anastomosed into one end of the conduit - the other end is brought to the abdominal wall to form a stoma - the GI tract is then anastomosed together - no voluntary control, need a collection bag - can be hard to keep clean - need to have additional collection devices at all times - can fill easily, burst, etc. Continent Urinary Diversion - internal pouches - ex: kock, indiana, miami pouch - difference depends on which part of the bowel segment is used - created from the ileum, ileocecal segment of ascending colon - had a surgically created valve - need to self cath every 4-6 hrs - this is a clean cath and NOT sterile because the patient is doing it themselves Orthotopic Bladder Reconstruction - essentially a reconstructed fake bladder - neobladder is surgically shaped from intestinal segments to make a low pressure reservoir - isolated segment of the terminal ileum is usually used - the urethra and ureters are sutured to the neobladder - allows for natural urination; however, incontinence could be a problem or may require intermittent cath - ideal patients - normal liver and renal funciton - longer than 1-2 year life expectancy - adequate motor skills - no hx of inflammatory bowel disease or colon cancer - we don’t want to use a disease part of the body to reconstruct it Pre/Post Op Care Pre Op - may have anxiety that inhibits readiness to learn - explain procedure - involve care givers in education - incase patients can’t do it themselves - discuss the psychosocial aspects - clothing options - body image and sexuality - exercise - odor contol - bigger nighttime pouches or ones that drain Post Op - prevent surgical complications - atelectasis - incentive spirometer/deep breathing - infection - GI compliations - we worry about ielus, bleeding, rupture, obstruction, and decrease in peristalsis - NPO - Encourage PO intake - rehydrate - don’t eat heavy meals right after surgery - skin care around stoma - same as colostomy - educate on taking care of stoma - pink stoma - hand washing key Rhabdomyolysis Patho - a syndrome caused by the breakdown of skeletal muscle cells - breakdown causes myoglobin to enter the bloodstream - myoglobin is a big protein - myoglobin causes obstruction of renal tubules - can cause AKI Clinical Manifestaions - Triad - dark reddish-brown urine (tea color) - muscle pain - weakness - AKI symptoms Diagnostic Testing - H&P - trauma - old person on floor (ex: memaw broke her hip and was left on the floor for hours) - over workout - CK (lab) + increased lipase - UA - Myoglobinuria Treatment - IV fluids + rest - literally all we do, but we give liters of fluids Blood Cancers Leukemia Patho - cancer of the blood affecting blood, bone marrow, lymph system, and spleen - follows a progressive course that is fatal if untreated - there is no single cause - most result from a combination of genetic and environmental factors - increased risk facotrs: - chemical agents - chemotherapy - viruses - radiation + immuologic deficiencies - occrus most often with congenital or inherited anomalies (ex: down syndrome) Leukemia Classifications - four classifications - acute myeloid leukemia (AML) - acute lymphocytic leukemia (ALL) - chronic myelogenous leukemia (CML) - chronic lymphatic leukemia (CLL) General Clinical Manifestations - initially there is an increase in the # of WBC, but only a few # of them are working properly (they are immature cells) - anemia (predisposition) - thrombocytopenia - decreased number and functions of WBCs - as progresses - splenomegaly - hepatomegaly  - lymphadenopathy - bone pain - meningeal irritation (meningitis) - HA, photopbia, neck stiffness, seizures - oral lesions - solid masses may form (chloromas) Manifestations vary and are related to problems caused by the bone marrow. Failure of bone marrow is due to bone marrow overcrowding by malignant cells which results in a lack of blood platelet and regular WBC need to clot blood and fight infection. Leukemia patient will have elevated WBCs consisting primarily of immature and unhealthy WBC. Progression due to fewer and fewer normal blood cells are being produced. WBCs continue to accumulate because they no longer go through a normal cell cycle (so less cells die). This causes infiltrations to organs. Oral Lesions: Primary: direct infiltration or Secondary: underlying thrombocytopenia or neutropenia Diagnostic Studies - H&P - CBC - WBC count, neutrophils - peripheral blood smear - bone marrow aspiration/biopsy - cytochemistry (chemical components of a cell) - lumbar puncture - genetic/ chromosome testing - PET/CT scan Diagnosis is based on patient history and physical examination. The blood cell count demonstrating blast (immature white blood cells) cells greater than 20% and microscopic examination of blood cells is diagnostic. Peripheral Blood Smear: A visualization of the RBC, WBC, Platelets for count and morphology. Bone Marrow has a fluid portion and a spongy portion Cytochemistry: localizes the chemical components of cells LP: to see if it has spread to CSF Chromosome/Genetic: FISH: Fluorescence in situ hypbrization: detects chromosome changes in cancer cells. Done on tissued removed during bone marrow biopsy. PET/CT: Used to see if the leukemia cells have affect bones or organs. Acute Myeloid Leukemia (AML) - acute is symptoms that occur for acute -> treated -> stable - no symptoms in early disease - clinical manifestations - fatigue - weakness - fever - night sweats  - sternal tenderness - weight loss - joint pain - bone pain - splenomegaly - philadelphia chromosome (CML) - present in about 98% of patients - HOWEVER, also found in ALL and sometimes in AML Chronic Lymphatic Leukemia (CLL) - there is production of and accumulation on long lived mature appearing lymphocytes - lymphocytes infiltrate the liver, spleen, and bone marrow - most common leukemia in adults - increases incidence after 72 years of age and predominance in males - clinical manifestation - frequently no symptoms - when symptoms present: - chronic fatigue - anorexia - splenomegaly - lymphadenopathy - hepatomegaly - progressive symptoms - fever - night sweats - weight loss - fatigue - frequent infections Treatment Optins - Chemotherapy - chemotherapy (3 stages) - Induction therapy (happens once) - aggressive treatment to destroy leukemic cells in the tissues, peripheral blood, and bone marrow - bone marrow is severely depressed, so may become critically ill - pt is very neutropenic - after 1 course of induction therapy approx. 70% achieve complete remission - Postinduction/Postremission therapy - Intesification therapy (postinduction): high dose therapy may start immeditely after induction therapy and last for several months - Consolidation therapy (postremission): started after remission is achieved - consists of 1 or 2 more courses of same drugs as induction therapy  - purpose is to eliminate remaining leukemic cells that may not be clinically evident - Maintenance Therapy - goal is to keep the body free of leukocytic cells - maybe used for acute leukemia depending on specific cytogenic markers - combination drug therapy is the standard for leukemia - Three purposes - decrease drug resistance - minimize drug toxicity - interrupt cell growth at multiple points in the cell cycle - Other therapies - corticosteroids - radiation - used a lot during stem cell transplant - immunotherapy - hematopoietic stem cell transplant (HSCT) - we radiate entire body beforehand - complications: graft vs. host disease, relapse, infection, sepsis Whole body radiation gets body ready for bone marrow transplants Radiation can be on specific areas such as spleen and liver. Immunotherapy: for certain types of leukemia Stem Cell Transplant: Goal to eliminate all leukemic cells from the body using combination chemo with or without radiation. It eradicates the hematopoietic stem cells which are replaced with a matching donor. Nursing Implications - clinical probelms - anemia - this is because not as many RBC being produced; the cancer cells are taking over the bone marrow - discuss iron rich diets, or iron supplements - thrombocytopenia - neutropenia - neutropenic patients should not eat raw fruit and veggies - psychosocial problems - quality of life - family stress - family needs - education - treatment plan - side effects - we educate on the more significant ones because there is a lot (ex: hair loss, N/V, fatigue)  - resources available - we can reach out to case management for assistance Hodgkin Lymphoma - cause is unknown - starts in a single location and then spreads - originates either above OR below the diaphragm - above: stays confined to lymph nodes for a period of time - below: speads to extralyphoid sights, such as liver - a proliferation of Reed-Sternberg cells - abnormal giant, multinucleated cells - Hodgkin Cells - mononucleated that proliferate in the lymph nodes - 10% of all lymphomas Etiology - Etiology - Epstein-Barr virus (EBV) - Genetic predisposition - exposure to environmental toxins - HIV - occurs in people 15 to 30 years of age or over 55 years of age - males affected twice as much - approx 85% are cured Clinical Manifestations - Initial - Enlargement of the cervical (most common), axillary or inguinal lymph nodes - nodes movable and nontender - weight loss - fatigue - chills - tachycardia - B symptoms - weight loss - fever - night sweats - Advanced - hepatomegaly - splenomegaly - anemia - Specific Sites - Liver - pain w/alcohol intake, jaundice  - Mediastinal nodes - cough, dyspnea, stridor, dysphagia Diagnostics - peripheral blood analysis - lymph node biopsy - bone marrow biopsy - PET/CT scan - to know if metastasized The diagnosis and staging of HL is based on the patient history, physical examination, laboratory studies, and thoracic and abdominal CT scans. The most significant diagnostic feature of Hodgkin lymphoma is the presence of Reed–Sternberg cells. Treatment - depends on the nature and extent of the disease - combination chemotherapy - aggressive treatment - standard therapy is ABVD - A: adriamycin (doxorubicin), bleomycin, vinblas dacarbazine - Early stage: 2 to 4 cycles - Intermediate stage: 4 to 6 cycles - Advanced stage: 6 to 8 cycles - cycles = # of doses in a period of time - Radiation therapy depends on the extent of the disease - may be used as a supplement to chemotherapy - Consequences of treatment (SPECIFIC to ABVD) - later development of secondary cancers Non-Hodgkin Lymphoma Patho - a broad group of cancers containing primarily B,T, and natural killer cells - the most common hematological cancer - there are more than 75 types - most common are large B cell lymphoma (and aggressive) and follicular lymphoma - large B cell most commonly found in lymph nodes of neck and/or abdomen - can affect people of all ages - cause is unknown - more common in people who have inherited immunodeficiency syndromes, use immunosuppressive agents, or have received chemo/radiation Clinical Manifestations and Classification Clinical Manifestaions - spread unpredictable - most have WIDESPREAD disease on diagnosis - painless lymph node enlargement - hepatomegaly (liver involvement) - neurologic symptoms (CNS) - lymphadenopathy (high grade lymphomas) - B symptoms - fever - night sweats - weight loss Classification - differentiation - cell of origin - immunophenotype - genetic - clinical features Diagnotic Studies - generally starts in cervical area; ABOVE diaphragm - same as with HL - additional (due to extranodal sites) - MRI (Liver) - Lumbar puncture (CNS) - Bone marrow biopsy (bone marrow) - colonoscopy (GI) - prognosis based in histopathy Treatment Options - chemotherapy - biotherpay - radiation - immunotherapy - more aggressive, easier to treat - indolent lymphomas have a long course and more difficult to treat - usually go into remission - STEM cell transplants Multiple Myeloma Patho - cancerous plasma cells proliferate in the bone marrow and destroy the bone - over proliferation of plasma cells and over production of immunoglobulin and proteins cause end organ effects (liver, bone marrow, kidney) - excessive production of plasma cells - monoclonal antibodies - creates bence jones proteins - can be found in urine - more common in males and african american race - occurs between ages 65 to 74 - cause is unknown Clinical Manifestations - develops slowly - no symptoms until advanced disease - skeletal pain (outside of trauma) - pelvis, spine, ribs - osteoporosis (which is not common in men) - causes vertebral collapse - hypercalcemia due to bone destruction - high protein levels can cause renal failure Diagnostic Testing - H&P - CBC - CMP - calcium - urinalysis - increase protein - specifically “M” protein - skeletal survey - checking for fractures and osteoporosis - MRI/PET Treatment Options - corticosteroids - chemo - immunotherapy - targeted therapy - HSCT - stem cell transplant - Zoledronic acid and denosumab - inhibit bone breakdown - Goals - relieve symptoms - produce remission  - prolong life Shock Shock - Definition: syndrome characterized by a decreased tissue perfusion and impaired cellular metabolism - imbalance between the supply and demand of O2 and nutrients - Hypoperfusion of cells -> increased demand for O2 and nutrients -> ischemia -> cell injury and death - REMEMBER all shock starts with hypoperfusion - Classfifications: - cardiogenic (must have a cardiac injury) - hypovolemic (fluid/volume) - distributive - anaphylaxis (allergic rxn) - septic (infection/sepsis) - neurogenic (spinal cord injury) - obstructive - essentially nothing can flow through - common causes: PE, cardiac tamponade, and tension PTX Cardiogenic shock - there is a dysfunction in either the systolic or diastolic function of the heart -> reduced cardiac output (CO) -> stroke volume (SV), and BP - this leads to myocardial compromise, decreased myocardial function, and decreased CO and perfusion - the leading cause is MI Causes - cardiac tamponade, ventricular hypertrophy, cardiomyopathy - dysrhythmias (bradydysrhythmias and tachydysrhythmias) - ex: 3rd degree block is bradydysrhythmia - structural factors - valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax - MI - cardiac tamponade can be cardiogenic shock or obstructive shock - if the cardiac tamponade is caused by pericarditis then it is cardiogenic shock - if the cardiac tamponade is caused by trauma then it is obstructive shock - tension pneumothorax can be either cardiogenic or obstructive -> depends what surrounds it - remember although MI is #1 cause ANY cardiac injury can lead to this - THERE MUST BE CARDIAC INJURY FOR CARDIOGENIC SHOCK TO OCCUR Patient Presentation - tachycardia - hypotension - narrow pulse pressure - decreased capillary refill (>3 sec) Assessment: Remember cardiac problems lead to fluid problems - tachypnea, crackles on auscultation - peripheral hypoperfusion - cyanosis, pallor, weak peripheral pulses, cool and clammy skin, delayed capillary refill - decreased renal perfusion: decreased urine output - anxiety, confusion, and agitation due to impaired cerebral perfusion Treatment - goal is to restore heart function in the balance between O2 supply and demand - restoration of blood flow: - angioplasty wiht stenting - emergency revascularization - valve replacement - devices - intra-aortic balloon pump - ventricular assist device (VAD) - drug is chosen based on clinical goal *** - nitrites (nitroglycerine): decrease the workload by dilating coronary arteries - vasodilators: reducing preload/afterload, decrease BP - sodium nitroprusside (nipride) - beta-adrenergic agnoists - epinephrine (low dose) - cardiac stimulation, bronchodilation, peripheral vasodilation - norepinephrine (levophed) - POST MI - cardiac stimulation - revascularization is priority, then drugs, then devices (which are a last ditch effort) Hypovolemic Shock - inadequate fluid volume in the intravascular space to support perfusion - Absolute (THINK FLUID OUT): fluid is lost through hemorrhage, GI loss (vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis (too much diuretics) - Relative (THINK third spacing (seen a lot in burns)): fluid volume moves out of the vascular space in the extravascular space Causes - external loss of whole blood - examples: - GI loss  - trauma - postpartum hemorrhage - miscarrage can cause this too - loss of other body fluid - relative hypovolemia - fluid shifts - internal bleeding - massive vasodilation (DIC) - pooling of blood or fluids - bowel obstruction Patient Presentation - extent of injury, age and general state of health contribute to the patient’s response - the body can compensate for up to 750 mL blood loss (15% of total volume) - blood loss over 750 mL a patient starts to become symptomatic - tachycardia (bradycardia is a late sign) - cool, clammy, pallor skin - decreased capillary refill - absent bowel sounds may be present - anxiety, confusion, agitation - decrese in urine output Lab Studies - Hemoglobin - Hematocrit - Electrolytes (BUN, creatinine) - Lactate (increased) - Blood gases - Urine output - Depending on the cause of the shock determines which lab is priority Treatment - Fix cause first THEN - The goal of fluid resuscitation is to restore tissue perfusion - 1 to 2 large bore IV (18 g) catheters, an intraosseous access device, or a central venous catheter can be used - NS is most often used but choice of fluid is controversial - NS - LR - PRBCs may be given to treat hypovolemic shock related to bleeding Distributive Shock - Relative hypovolemia due to intravascular volume redistribution r/t loss of vascular tone or disordered permeability - Types:  - Neurogenic - Hemodynamic consequence of spinal cord injury - Spinal anesthesia - Anaphylactic - Hypersensitivity - Septic - At-risk patients - Infection Neurogenic - Transient condition after acute spinal cord injury - absence of all voluntary and reflex neurologic activity below the level of the injury - Can occur within 30 minutes of spinal cord injury lasting up to 6 weeks - Usually associated with cervical or high thoracic injuries - Spinal anesthesia -> blocks transmission of SNS impulses - Ex: epidural Clinical Manifestions: - Hypotension - Bradycardia - Difficulty with temperature regulation (high or low temp) - bowel/bladder dysfunction - Dysfunction related to evel of injury - Decreased skin perfusion - Can be cool or warm, DRY SKIN Treatment - Treatment is bsed on the cause - Spinal cord injury - FIRST promote spinal stability (spinal precautions, c-collar for cervical stabilization) - Once stabilied then treat hypotension and bradycardia to prevent further damage - Vasopressors to maintain BP and organ perfusion - phenylephrine - Atropine - bradycardia - Infuse fluids CAUTIOUSLY because hypotension is NOT related to fluid loss - Monitor for hypothermia and hypotonic dysfunction - Remember! Pt can have autonomic dysreflexia if injury above T6 Anaphylactic - Acute, life-threatening hypersensitivity reaction to a sensitizing substance - drug, chemical, food, insect venom (ex: bee and wasp), or vaccine - PATHO: massive vasodilation -> release of vasoactive mediators -> increase in capillary permeability -> fluid leaks from the vascular space into the interstitial space  - Can result from inhalation, ingestion, or injection with an antigen that the individual is sensitized to - IM administration of the antigen is the route most likely to cause anaphylaxis - Oral, topical, and inhalation route (especially peanut dust) can also cause anaphylactic reaction - Quick action is needed to prevent progression to anaphylactic shock - REMEBER airway!!! - This is a MEDICAL EMERGENCY Clinical Manifestions - Laryngeal edma or severe bronchospasm -> respiratory distress - Dizziness, chest pain, incontinence, swelling of lips and tongue, wheezing, stridor - Skin changes- flushing, pruitis, urticaria (a skin condition that causes itchy, red, raised bumps or blotches to appear on the skin), angioedema (swelling of mouth + tongue + face) - Anxious confused and severe impending doom Treatment - assess airway first then give the 3 meds - history is key to avoiding risk for anaphylaxis - Medications: - Epinephrine - peripheral vasocontrition, bronchodilation, opposes effects of histamine - NEVER give epi IV push !!! only subq or IM (heart could not handle it) - 1,000 to 1 for a code - 10,000 to 1 for anaphylaxis - Diphenhydramine and histamine receptor blockers - adjunctive therapy to block ongoing release of histamine - IV - Corticosteriods: decrease inflammation - IV - Airway (#1): - Maintain a patent airway - Laryngeal edema or bronchoconstriction can quickly develop - Nebulizer, bronchodilators, aerolized epinephrine, and ET intubation - Depends on the pts O2 stat; 85-86% we would intubate - Least invasive to most - Bare minimum we give a nonrebreather - Hypotension due to increase vascular permeability and vasodilation - Aggressive fluid resuscitation with crystalloids is needed Septic - Dysregulated patient response along with new organ dysfunction related to the infection - Infection that keeps getting worse - Septic shock is a subset of sepsis - increased mortality risk due to profound circulatory, cellular and metabolic abnormalities - Causes: - Gram-negative and gram-positive bacteria - Parasites, fungi and viruses can also cause septic shock - 2 common causes - Pneumonia - UTI Clinical Manifestations - persistent hypotension (we’re treating and its not getting better) - tachycardia - Dysregulated temperature - Decrease ejection fraction - GI bleed - Paralytic ileus - Altered LOC - Decreased urine output Labs - Elevated BGL - Elevated lactate - Decreased platelets - Positive blood cultures (gram + or -) - High or low WBC - Elevated procalcitonin - Increased urine SG Fluids - The goal is to restore the intravascular volume and organ perfusion - Initial volume resuscitation is given by 30 mL/kg of isotonic crystalloid solution - Fluid challenge techniques may be done and repeated until hemodynamic improvement is seen - increased MAP - Potential problem is FLUID OVERLOAD Drugs - If the patient is hypotensive after fluid resuscitation, vasopressors are added - Norepinephrine - alpha adrenergic agonist - drug of choice when BP reminds low - If norepi isnt working, a beta-adrenergic agonist will be added  - Epinephrine - Dobutamine - increases O2 delivery - Broad - spectrum antibiotics started within the first hour of sepsis or septic shock - Obtain cultures BEFORE starting antibiotics - Glucose level should be reduction in CO - Cardiac tamponade, tension pneumothroax, super vena cava syndrome -> restricted diastolic filling of the right ventricle - Abdominal compartment syndrome - increased abdominal pressure - Compresses the inferior vena cava decreasing venous return to the heart - Pulmonary embolism - Patients have - Decreased CO - Increased after load - Rapid assessment and treatment are important to prevent further compromosing cardiac arrest Clinical Manifestations - Tachycardia - Hypotension - Decreased bowel sounds - Anxiety, confusion, agitation - Decreased urine output - Pulsus paradoxus - Tachypnea (bradypnea is a late sign) Treatment - Early recognition and treatment is needed to relieve and manage obstruction - Essentially no meds just reat the cause !!! - Mechanical decompression - pericardial, tamponade tension, pneumothorax, or hemopneumothroax may be done by needle or tube insertion - Pulmonary embolism - immediate anticoagulation therapy, thromobolytic therapy, or embolectomy - Decompression laparotomy - abdominal compartment syndrome due to high intra-abdominal pressure and hemodynamic stability Stages of Shock - Initial stage  - Shock occurs at a cellular level and is not usually clinically apparent - Don’t see much - Compensatory stage - Body trys to compensate but we’re seeing symptoms - Body’s initial response to inadequate blood flow, where physiological mechanisms attempt to maintain perfusion and stabilize vital functions despite decreased circulation - Body activates compensatory mechanisms - If shock is not corrected and the body is unable to compensate, the body will then enter the progressive stage of shock - Progressive stage - ALL OUT shock; vitals showing it; organs failing; no compensation at all - This phase will begin if compensatory mechanism start to fail and results in results in a further decrease of circulating blood volume - Refractory stage - Decreased perfusion and decrease CO -> worsening of anaerobic metabolism - Cerebral ischemia develops - Failure of one organ system will affect several other organ systems - Goes to SIRS and MODs - mottling/black fingers shows more than one organ failing - Irreversible cellular and organ damage - These are a continuum of overlapping stages and a patient can move back and forth between the stage Nursing Management of Shock Assessment - ABC’s - airway, breathing, circulation - Tissue perfusion - VS, LOC, peripheral pulses, capillary refill skin temp, color, moisture and urine output - Tissue perfusion will only go to vital organs - Urine output should be >30mL/hr - As shock progresses - Neuro status - Urine output decreases - Skin becomes cooler and mottled - Peripheral pulses decrease - Obtain a history - including events leading to shock state, onset and duration of symptoms, and health history - This can tell us what kind of shock Planning  - Goals for a patient in shock: - Monitor all patients for infection - Stop the progression from infection to sepsis and shock - Immunocompromise patients are at a higher risk for opportunistic infections - Reduce risk for healthcare associated infections - Decreasing the number of invasive catheters - Using aseptic technique during invasive procedures - Paying attention to handwashing - Change equipment per policy and santitize and discard equipment between patient use Acute Care - Your role in shock: 1. Monitor the patients ongoing status (BP, labs) 2. Identifying trends to detect changes in patient’s condition (multiple VS and watching the trends) 3. Planning and implementing nursing interventions in therapy (turning pt, hand washing) 4. Evaluating the patients response to therapy (ex: after giving vasopressors is the BP improving) 5. Emotional support to the patient and caregiver 6. Collaborating with other healthcare team members to coordinate care - Neurological status: orientation and LOC Q1-Q2; best indicator of cerebral blood flow - Cardiovascular status: assess CO, SVR, SV, and SPV (HR, BP and MAP) - Respiratory status: RR, pulse ox, and ABGs - Renal status: urine output, BUN, and creatinine - Body temperature: fever - G.I. status: auscultate bowel sounds, NG tube, and occult blood - Skin integrity: hyigene, positinal changes, and oral care - Emotional support: fear, anxiety, pain, spiritual needs, and caregiver - Would you like to talk to a chaplin SIRS and MODS - SIRS comes first and leads to MODS - SIRS + MODS + shock -> identify and treat the cause Systemic Inflammatory Response Syndrome (SIRS) - It’s a clinical condition characterized by an exaggerated inflammatory response to a variety of stimuli  - Infection - Trauma - Pancreatitis - SIRS can lead to severe complications and is often associated with sepsis when caused by infection - It requires prompt medical attention to identify and treat the underlying cause SIRS Triggers - Have to have one of these to happen in order for SIRS - Mechanical tissue trauma - burns, crush injuries, and surgery - Abscess formation - intraabdominal or extremities - Ischemic or necrotic tissue - pancreatitis, vascular disease, MI - Microbial invasion - bacteria, viruses, fungi, parasites - Infection plus a low BP or decreased tissue perfusion - Endotoxin release - gram-negative and gram-positive bacteria - Global perfusion deficits - postcardiac resuscitation, shock - When you resuscitate someone it is because they have decreased perfusion to entire body - Regional perfusion deficits - distal perfusion deficits SIRS Criteria - 2 or more of the following criteria are REQUIRED: - Temp ⪰ 101 F or ⪯ to 96.8F - Pulse ⪰ 90 BPM - RR ⪰ 20/min or PCO2 < 32 mmHg - WBC - >12,000 cells/mm^3 - OR 10% immature (band) forms Clinical Manifestaions - Tachycardia - Tachypnea - hyper/hypothermia - Hypotension - Flushing or pallor or mottling - Skin is essentially anything BUT normal - Mottling is like bruising where is shouldn’t be Diagnostic Studies - CBC - Elevated or decreased WBC - BMP - Electrolyte imbalances  - Elevated creatinine - LFT - Blood cultures - ABGs - Elevated lactate levels - As circulation decreases lactate goes up - PT/INR, PTT - Xray - CT - Looks for intraabdominal disease process Treatment Options - Identify and treat underlying cause - Fluid resuscitation - Maintain BP and tissue perfusion - Hypotension comes first, it leads to decreased tissue perfusion - Decreased capillary refill and decreased urine output show decreased tissue perfusion - Vasopressors - Treat hypotension when fluid resuscitation does not work - O2 - Especially in cases of respiratory distress (ex: O2 is < 92%) - Corticosteroids - Especially in patients wiht septic shock - Timely intervention and a multidisciplinary approach are crucial for improving outcomes Nursing Implications - Monitor VS closely (for deterioration) - Assess for signs of infection, organ dysfunction and changes in mental status - We see organ dysfunction through labs and assessment - Monitor urinary output - Tells us how well the kidneys are function and tissue perfusion - Strict hand hygiene - Prevent secondary infections - CAUTI, hospital acquired pneumonia, central line infection, etc. - Patient education - About treatment plan Multiple Organ Dysfunction Syndrome (MODS) - Failure of two or more organ systems in an acutely ill patient resulting in an inability to maintain homeostasis without intervention - Mortality rates for MODs are poor - 40 to 60% - Increases as more organ systems fail - The most common cause of death is sepsis  - The most important goal is to prevent SIRS from progressing to MODS - We fix the cause of SIRs to hopefully increase the tissue perfusion Underlying Causes - Essentially comes from something BIG happening - Sepsis - Severe trauma - Triggered a systemic inflammatory response - Pancreatitis (cells dying) - Burns - Shock - ARDS - Severe Hemorrhage - Acute MI - Acute Liver failure - Neruogenic shock - Systemic inflammatory response - Autoimmune diseases - Toxic shock syndrome (ex: forgein substances left in for too long) Clinical Manifestaions - Based on what organ is affected - Tachypnea - Hypoxemia - Signs of ARDS - Crackles or decreased breath sounds - Hypotension - Tachycardia - Decreased cardiac output - Peripheral edema - Poor capillary refill - Decrease or absent urine output - Jaundice - Altered Mental status - Abd pain - N/V - GI bleeding Diagnostic Testing - directly related to whichever organ is failing - CBC - Anemia, leukocytosis (increased WBC) or leukopenia (decreased WBC) - BMP - Electrolytes, kidney function  - LFT - Elevated ALT, AST, bilirubin - PT/INR, PTT - ABG - Blood cultures - Elevated lactate - Chest xray - Pneumonia, ARDS - CT scan - Assess abdominal organs, pancreatitis - Neuro - ECG Treatment Options - Focus on addressing the underlying cause and providing supportive care to the affected organ systems - Also deal with the problems that come from the organ failing - Infection: antibiotics - Sepsis: antibiotics and fluid resus - Fluid and vasopressors (if fluid not working) - O2 or mechanical ventilation - Monitor and treat electrolyte imbalance - Treat AKI (if indicated) - Monitor Neuro for seizures or ICP (this is how you know the brain is involved) - Monitor for GI bleed and treat - Stress ulcer prophylaxis: protonix - Monitor for addition complications - Pressure ulcer - Contractures - UTI - Hospital acquired pneumonia - REMEBER we cannot just ignore these ^^^ Aortic Aneurysm Patho - Aortic aneurysms can involve the aortic arch and thoracic and/or abdominal aorta - Most AAA occur below the renal arteries - DEF: localized, outpouching or dilation of the vessel wall - The larger the aneurysm the greater the risk for rupture - There is a genetic link, if a family member has had one then you’re more likely to have one Classification  - Two types - True: wall of the artery forms aneurysm with at least 1 vessel layer still intact - Fusiform - circumferential and relatively uniform in shape - Saccular - pouchlike with a narrow neck connecting the bulge to 1 side of the arterial wall - False/pseudoaneurysm: disruption of all arterial wall layers with bleeding that is contained by surrounding anatomic structures - Can result from trauma, infection, peripheral artery bypass graft, or arterial leakage from removal of catheter Clinical Manifestations: Thoracic Aortic Aneurysm (TAA) - Thoracic aortic aneurysms (TAA) are usually asymptomatic - Symptoms (associated w/its location, its higher up) - Deep, diffuse, chest pain that may extend to the interscapular area - Ascending aorta and aortic arch aneurysms can cause: - Angina from decreased blood flow to coronary arteries - TIAs from decreased blood flow to the carotid arteries - Coughing, SOB, and/or difficulty swallowing from pressure on the laryngeal nerve - If the aneurysm presses on the superior vena cava decreased venous return can result in JVD and edema on the face and arms AAA Clinical Manifestations: - Abdominal aortic aneurysms (AAA) are often asymptomatic - Found during routine physical assessment or evaluation for another problem - abdominal x-ray, CT - Pulsatile mass in the periumbilical area slightly to the left of the midline may be present - Bruits may be auscultated over aneurysms - Physical findings are hard to detect in the obese - Symptoms: - May mimic pain associated w/abdominal or back disorders - Compression of nearby anatomic structures and nerves cause - - EXCRUCIATING BACK PAIN - Epigastric discomfort - Altered bowel elimination - Intermittent claudication - Pain in the calf when moving but goes away with rest - “Blue toe syndrome” - patchy mottling of the feet and toes in the presence of palpable pedal pulses Complications of AAA  - Aneurysm rupture (broke open) - Can also have a slow leak - More likely to occur in those who smoke tobacco - Peritoneal space: bleeding may be controlled by surrounding anatomical structures preventing exsanguination and death - Grey turner sign - Thoracic or abdominal cavity: pts can die from massive hemorrhage presenting with hypovolemic shock: - Tachycardia - Hypotension - Pale clammy skin - Decreased urine output - Altered LOC - Abdominal tenderness - Simultaneous resuscitations and immediate surgical repair - Pts are generally flown to other hospitals if needed; helps avoid bumps in the road - Mortality rate is 53% - Increases if pt is on blood thinners, age, smoking, comorbidities Diagnostic Studies - Chest x-ray: abnormal widening of thoracic aorta - Abdominal x-ray: calcification within the aortic wall - ECG: to rule out MI - Echo: assess aortic valve function - Ultrasound: useful for aneurysm screening and to monitor size - CT/MRI: to diagnose and assess location and severity - CT is the go to!! - Angiography: used to map the aortic system using contrast Treatment - Goal of care: to prevent rupture - Prevent increasing pressure - Conservative therapy: - Small, asymptomatic AAA (65) - Graft patency - CV status - Infection - GI status - Neuro status - Peripheral perfusion status - Renal perfusion status Aortic Dissection - A tear in the inner layer of the aorta, leading to separation (dissection) of the layers of the aortic wall - slow , layer by layer Etiology (causes) - Chronic HTN - Connective tissue disorders: - Marfan syndrome and ehlers- danlos - Atherosclerosis - Trauma - Pre-existing aortic aneurysm - Genetic predisposition - Iatrogenic causes: - Complication from heart surgeries or catheterization - Smoking is NOT a common cause Patho  - Tear - Blood flow in between layers - False lumen - Disruption of blood supply - Complications - Aortic rupture - Cardiac tamponade - Organ failure Clinical Manifesations - Sudden, severe chest or upper back pain (often described as “tearing” or “ripping”) - Shortness of breath - Fainting or loss of consciousness - Weak pulse in one arm compared to the other - To verify you can also check BP in both arms, one will be significantly lower than the other Diagnotic Studies - CT scan, MRI, or TEE - Chest x-ray may show a widened aorta Treatment - EMERGENCY (immediate bleed out) - Surgical repair for severe cases - Endovascular Dissection Repair - A minimally invasive surgical procedure used to treat aortic dissection by placing a stent-graft within the aorta to reinforce the vessel wall and restore normal blood flow - Medications to lower BP and HR Nursing Management - Preoperative - H/P - Obtain necessary laboratory tests (e.g., CBC, coagulation profile) - Postoperative - Neurovascular checks: assess extremities for circulation, sensation, and movement - Graft patency - Pain management - Observe for signs of infection at the access site - Monitor for complications such as endoleak, graft migration, or bowel ischemia - Patient education - Activity restrictions - s/s to report - Bruising, back pain, epigastric pain - Discuss lifestyle modifications (e.g. BP control, smoking cessation)