NURS 3608 Adult health Adult Exam 5 Blueprint | Download To Score A | {LATEST UPDATE

5th Adult Exam Blueprint Advice: o Read your portion of the assigned concept & highlight important keys, pay close attention to the nursing process assigned for those concepts. o I.e. Marianela is in charged of aging & would be in charge of posting information about aging from Tegrity AND the Medical Surgical Book. She would specifically focus on Assessment (AS). o Add important points as based per your judgment. o It is encouraged that you FIRST type out your portion in Word & then copy it onto here, ensuring that you are on the correct slide & order… Thank you! :) Rules: o Use Times Romans, 11 font, single space o PLEASE MAKE SURE THAT WHEN YOU ARE ASSIGNED A CONCEPT (I.E. AGING) ENSURE THAT YOU ARE COVERING THE RESOURCES (i.e. Tegrity AND Adult Book or Tegrity AND Critical Care Book)ASKED! o Add the source you are using & the corresponding page numbers! :D Bold & underline them i.e. Tegrity: o This is due Saturday, November 23, 2013 at 9 P.M.! Key: Liver 18 PH * Tegrity AND Medical Surgical Book must be incorporated 1. Marianela aging 1 (AS) This is all I found related to aging Textbook pg 697 Hepatitis A Virus. Typically, persons infected with hepatitis A virus spontaneously recover; however, adults over 50 years of age or with chronic liver disease may progress to fulminant liver failure. 2. Leo transplant 1 (I) Tegrity This is all that was shown for transplants in the tegrity… nothing was said about it. Med-Serg Book Page 708-710 Liver Transplant ● Liver transplant has become the treatment of choice for patients with End Stage Liver Disease and acute liver failure. ● Orthotopic Liver Transplantation: Total surgical removal of diseased liver and replacement with healthy one in same anatomical space. ● Survival Outcomes: over 85% at 1 year and 75% at 5 years. Indications and Contraindications: ● Indications o Advanced chronic liver disease o Fulminant hepatic failure o Metabolic liver disease, o HCC o Hepatocellular liver disease (viral, alcohol induced, Wilson’s) o Cholestatic disease. ● Contraindications o Uncontrolled infection o Extrahepatic malignancy or advanced hepatobiliary metastatic disease o Irreversible brain damage o Anatomic difficulties o Multiorgan failure Selection & Evaluation for Liver Transplant ● Requires assessment: complete medical, surgical, and psychosocial testing. ● Then put on wait list of meets criteria in the United Network for Organ Sharing (UNOS) ● Priority of who gets liver is determined by the Model of End Stage Liver Disease (MELD) score. ● The Highest Priority on the wait-list is given to those with acute or fulminant liver failure. Surgical Procedure ● This briefly describe the surgical procedure… I don’t think this will be on the exam, but feel free to read up about it. Surgical Complications ● Primary Graft Nonfunction: most severe complication, occurs in 5-10%. Signs of ongoing encephalopathy, coagulopathy, jaundice, metabolic acidosis, and hemodynamic instability. Requires immediate replantation and they get priority on the wait-list. ● Bleeding: Very common, can be from coagulopathy, portal hypertension, and fibrinolysis. Administer platelets, fresh frozen plasma, and other blood products. ● Rejection: Primary concern. Use of immunosuppressive agents. Nursing Management ● The nurse must be attuned to the emotional and psychological status of the client and family –referral may be needed. Preoperative Nursing Interventions ● Provide client and family with full explanation of procedure, chances of success, risks, and side effects of long-term immunosuppression. ● Nurse serves as advocate. Postoperative Nursing Interventions ● Maintain client in environment free of bacteria, viruses, and fungi, d/t use of immunosuppressives. ● In immediate postop monitor: cardiovascular, pulmonary, renal, and neurologic, metabolic. ● Hemodynamic status & Intravascular fluid volume are monitored with: Cardiac output (CO), central venous pressure (CVP), pulmonary artery pressures (PAPs), pulmonary capillary wedge pressure (PCWP), arterial and mixed venous blood gases, oxygen saturation, oxygen demand and delivery, urine output, heart rate, and blood pressure. ● Monitor: liver function tests, electrolyte levels, coagulation profiles, chest X-ray, electrocardiogram and fluid output. ● Monitor for excess bleeding (hypotension, tachycardia, tachypenea, decreased CO, CVP, PAPs, PCWP, melena, increasing abdominal girth, etc.. ● High Risk for Atelectasis and altered ventilation-perfusion ratio: caused by insult to diaphragm during surgery, prolonged anesthesia, immobility, and pain. ● Client will have endotracheal tube and ventilator post op (suction and humidify). ● After removal of ET, encourage client to use an IS to decrease risk for Atelectasis. Promoting Home Care ● Tell client to have lots of meds on hand and never skip a dose. ● During first months, client will require blood tests 2-3 times per week. ● Good oral hygiene with admin of prophylactic antibiotics because of immunosuppression. 3. Janie/ Estela Hepatitis A 2 (AS) Tegrity: o Hepatitis A started decreasing simply by ‘washing hands’ when there were no vaccines for it o Asymptomatic: The only abnormal thing is that the labs come out abnormal (high liver enzymes: high ALT, high AST); usually incidental findings. o Once they become symptomatic: Hepatitis’s mimics the flu; flu-like symptoms include: loss/no appetite (anorexia), weight loss, very fatigued (malaise), body aches, symptoms, nausea, vomiting, and right upper quadrant pain followed by jaundice and fever, splenomegaly, and ascites. o In the past, dismissed a lot because they thought it was just a stomach virus because it does mimic a stomach virus. o Preicteric Phase: which is right before your jaundice phase. This is your flu like symptoms & muscle aches in body, polyarthritis. o Icteric Phase: This is where jaundice sets in. Includes the characteristic clay colored stool r/t bilirubin not going through the liver, thus it is not turning stools a normal color. Sometimes it gets excreted through urine. It will turn your urine really dark like brownish color urine. o Postticteric/Convalescent Phase: Bilirubin level & enzymes start normalizing; GI symptoms subside & your jaundice goes away. o Transmission: Fecal- Oral; doesn’t lead to Chronic hepatitis o Hepatitis Epidemics usually caused by: Contaminated water, milk, food, raw shellfish from contaminated water o Incubation period: 15 to 30 days (2 to 6 wks) o More common near the border, Africa & middle East; usually along the west coast because there’s more immigration from other countries, Asian countries o With the new school entry laws for vaccinations, hepatitis A incidence went down. o Children are highest at risk for Hepatitis A. Why? They put everything in their mouth. o Not everybody gets jaundice. o If they’re less than 6yrs old, chances are they’re not going to get jaundice. They’re going to get all the GI symptoms, polyarthritis, malaise, fever, but chances are that less than 10% of them actually get jaundice. o 6-14yrs old, chances are you will see the jaundice (40-50%) o 14 years old = 70-80% likely to contract/ get o *So the older you are the more of the chance that you could be getting jaundice. o It has a low mortality rate because it is a virus & the body will slowly start to develop antibodies. Pathophysiology: Hepatitis A o Labs: Elevation of ALT/AST levels o Serum will positive for anti-HAV antibodies o IgM will be elevated at the onset of illness all the way up to 6 months o * IgM elevated along with Hepatitis antibodies means you are either acutely ill or have been exposed in the last 6 months; IgM is the one we test for o IgG peaks at one month and last for years &pretty much goes away o Jaundice may or may not be detected. Don’t count on jaundice as the final say. Clinical Manifestations o Early stage (prodromal): 1-2 weeks – Malaise – Anorexia – Nausea/vomiting – Low grade fever – Alteration in taste and smell – RUQ or epigastric o At end of prodromal – Jaundice – Pruritus o Energy level decreases with Hep. A HAV Prophylaxis • We give an Immune globulin (Gammar): Post-exposure Prophylaxis: o Any one exposed to HAV o Anyone traveling to high risk areas o Given IM, provides protection for up to 3 months To prevent Hep A: vaccinate! Recommended for any endemic area travelers, chronic liver disease patients, clotting factors disorders, animal handlers, bi & homosexual men, sewage workers, illicit drug users, food handlers, & day care center workers… these are all because of the fecal contamination. HAV Vaccination: o Routine vaccination for all school age children in state of Texas -12 months to 18 yrs. o For adults: -1ml of Havrix or Vaqta IM -2nd dose given 6 months later -Twinrix (A & B) - 4-dose (3 doses in 21 days) - Prior to planned exposure with short notice - 4th dose at 12 months (Pellico, pg 697) · Infection by HAV can present either asymptomatically or with acute symptoms such as fever, malaise, anorexia, nausea, diarrhea, vomiting, abdominal pain, and jaundice. Jaundice presents in over 70% of patients, primarily in adults. · Serologic testing is required for accurate diagnosis of hepatitis A infection. A positive anti- HAV (IgM) signifies serum IgM antibodies that are reactive to the hepatitis A virus and confirms an acute infect. 4. Jessica DL/Kelli Hepatitis B 2 (I) TEGRITY: The source of hepatitis B is: Blood - blood derived - body fluids. (percutaneous and mucosal routes) It can cause a chronic infection. How do you prevent it? Immunization!!! It leads to chronic hepatitis. If you have Hep B you’re more than likely going to get Hep D. Hepatitis B is the only one of all the Hepatitis that is a DNA virus. Transmitted by sexual or other intimate contact or by contact with infected blood. The incubation period is anywhere from 1-6 months or 6-24 weeks. Most cases are asymptomatic. High risk groups are your healthcare workers, that’s why as healthcare workers you are required to have your hepatitis B vaccination Hemodialysis patients, blood transfusion, homosexuality or homosexual active males and drug abusers need to have their hepatitis B vaccination. Vaccination from 1987- present: There is a Recombivax and Engerix- B: three injections. One now, in 1 month, then in 6 months. Given in the deltoid muscle For Postexposure: a combination of your immunoglobulin and vaccine is what's given. Again severe cases of acute Hep B can be treated with antiretroviral drugs, otherwise known as drugs that were previously used to treat HIV can also be used for chronic Hep B viruses and some of those (medications) are your: Heptovir, Hepsera, Baraclude, Entecavir which probably your strongest or most potent of your antiretroviral drugs. Then you have your combination vaccines which can have several things in it, so you have to be careful who you give them to: - Comvax: Hepatitis B with Haemophilus Influenzae type B - Cannot be administered before 6 weeks of age or after 71 - Pediarix: has Hepatitis B, Tetanus, Pertussis, and Polio - Twinrix: has Hepatitis A and Hepatitis B vaccines Hepatitis B vaccine safety: Side effects are very rare. There are some cases of anaphylaxis, in 1/600,000 doses. There is no link linking vaccines to autism, multiple sclerosis, or any autoimmune disorders. Med Surg: pgs 698-699 basically says the same thing as above Can be found in blood, saliva, and semen. Can be transmitted through mucous membranes and breaks in the skin. Close person to person contact via contact with open cuts and sores or by shared razors or toothbrushes, HBV contaminated surfaces. Perinatal, and sexual exposure. S/S: may be insidious and variable. Anorexia, fever, dyspepsia, abdominal pain, generalized aching and malaise, and weakness. Jaundice may or may not be evident. Chronic hep B may remain asymptomatic until development of cirrhosis and signs of hepatic decompensation. Risks: box 25-5 and not listed already above IV/injections users, close contact with carrier of HBV, recent history of sexual transmitted disease, travel to an area with uncertain sanitary conditions. Get labs such as CBC with platelets, hepatic function panel, prothrombin time and INR. Lab test to detect Hep B and other viral co- infections like HAV, HCV, HIV. Prevention: Get active immunization through Hepatitis B vaccine and to use passive immunization for unprotected people. Use barrier protection during sexual intercourse, avoid sharing toothbrushes and razors, cover open sores or lesions. Don’t donate blood, organs, or semen. The hepatitis vaccine is administered in three doses intramuscularly at 0, 1, and 6 month intervals for adults. Twinrix is a combined hepatitis A and B vaccine, given to those 18 and older with indications for both hepatitis A and B vaccination. FDA approved. Medical management: the goal is to prevent replication of active Hep B virus and reduce chronic liver inflammation. Ultimate goal is to prevent cirrhosis, liver failure and hepatocellular carcinoma. Get ultrasound screenings every 6 months. Antiviral therapy for hep B is pegylated interferon alfa, adefovir, entecavir, telbivudine, and tenofovir are the preferred medications. Nursing management: manage the symptoms by maintaining nutrition, fluid intake and adequate rest during recovery. 5. Jacob/Daniel Cirrhosis 2 (AS) Tegrity Cirrhosis is just an advanced stage of liver disease caused by a variety of inflammations or other injuries to hepatic parenchyma in which extensive fibrosis develops, with nodule formation and interruption of normal hepatic blood flow. It is pretty much destroyed. Types of Cirrhosis ● You have your Laennec’s cirrhosis which is your alcoholic cirrhosis. (most common) ● Micronodular : is postnecrotic which is your macronodular and toxic and then you have ● Biliary ● cardiac which is very uncommon. Extensive destruction of hepatocytes is usually what occurs in cirrhosis. - It alters flow in the vascular and lymphatic systems and bile duct channels. it becomes very congested and alters the flow - Increase in portal venous pressure Alcohol is the principal cause of cirrhosis in the us Chronic viral hepatitis B and C are also causes worldwide. - Alcoholism is the number 1 cause of cirrhosis in the US. But in worldwide, B and C are the number 1 causes. Clinical Manifestations Diagnosis is made after presenting with ● ascites, ● bleeding from esophageal varicies, ● bouts of hepatic encephalopathy, ● spontaneous bacterial peritonitis, ● Hepatorenal syndrome. Focused Assessment Findings Compensated Cirrhosis ● intermittent mild fever ● vascular siders ● palmar erythema ● unexplained epistaxis ● ankle edema ● vague indigestion ● flatulent ● dyspepsia ● abdominal pain ● firm enlarged liver ● splenomegaly Decompensated Cirrhosis ● ascites ● jaundice ● weakness ● muscle wasting ● weight loss ● continuous mild fever ● clubbing of fingers ● purpura ● spontaneous bruising ● epistaxis ● hypotension ● sparse body hair ● white nails ● gonadal atrophy On occasion, an abnormal physical finding can occur. Let’s say they come in and you’re doing an abdominal assessment, and you feel the liver being very enlarged. The spleen, you can feel the spleen. A lot of times, it can be an incidental finding. You’re like “your liver is a little enlarged. I wonder why?” Let’s do some liver testing on you, and sometimes it can come up. And a lot of the time it can come out abnormal. Or you can just take a look at some lab values and you can say, “oh this person came in for something else but look at these liver enzymes.” · Signs of hyperspenism or neutropenia · Spider angiomas · Palmar erythema (erythema on palm of hands) · Jaundice, ascites · Edema · Gynecomastia Those are some of the, on occasion, incidental findings that can be indicative of cirrhosis or liver dysfunction: Cirrhosis Complications Portal hypertension occurs when blood flow is completely altered. It builds up in the blood system, the blood can't get through the liver so it just creates altered access around the liver and it can’t really get through there. · There’s an increase in blood pressure in the portal venous system · Portal veins receive blood from the intestines and the spleen. · This results in increased pressure resistance You got a lot of blood flow in this area right here, okay, which is called portal hypertension. Enlargement of esophageal, umbilical, and superior rectus veins so your veins getting very engorged pretty much and when they do you get the dilated abdominal veins, which is called caput medusae. You can see the abdomen you can see the ascites. And then you have these little veins like varicose vein like us women on our legs. They actually start to get these veins in their abdomen, which is called caput medusae which is indicative of portal hypertension. Esophageal varices is one of the complications of cirrhosis and a very very serious complication. Is a common complication of portal hypertension because you have all this blood going everywhere and you got all these veins getting engorged · Some of the esophageal veins that are inside becoming engorged too so they can pop. They can burst and they’ll bleed. There’s: - increased portal venous blood pressure. - Increased intrathoracic pressure. (So any time these patients cough or strain or anything it just builds up that pressure.) - So can you imagine having these varicose veins also going into the esophagus and then you eat chips or you eat popcorn; something that’s going to irritate that. It’s just going to open up or cause bursting. - Any kind of juices, any kind of gastric juices; say you have GERD and you’re having that reflux, that can also irritate those varices and open them up and cause you to bleed. · Stomach and esophagus veins are the most at risk to rupture leading to medical emergency because these people will just bleed and bleed until they die. They will bleed to death. When they have the other not only vomiting blood but they are also expelling blood the other way as well so risk for hemorrhage is very high and should be avoided so if you start to see these varicose veins in the abdomen can you imagine what it looks from the inside as well Treatments to control hemorrhage are · Sclerotherapy: inject of morrhuate sodium directly to varices via endoscope · TIPS: percutaneous placement of expandable metal stent to the hepatic veins to create a channel, reduces portal hypertension only They put in little stents to open them up to create little channels so that the blood flow can continue on. It is very temporary. It does reduce portal hypertension but because the liver is still damaged the blood flow is still going to get altered. It’s like putting on a Band-Aid. It just controls the portal hypertension but doesn’t fix the problem; it can buy you time but it doesn’t fix the issue. · Vasopressin which gets infused directly to the superior mesenteric artery. It very effective but is also very dangerous. It can cause acute renal failure, MI, hypothermia, GI ischemia. If the pt starts to have chest pain while this is being infused it needs to be STOPPED (D/C). · Balloon tamponade, you apply pressure. It is just like apply pressure to a cut. You want to apply pressure to some of the varices that are in your esophagus. There is something called the Minnesota tube- or the Blakemore Tube. It is inserted into the stomach through the nose, and then they inflate it. It is an esophagus-stomach balloon. o They don’t leave it inflated for more than 24 hours. o It removes secretions & saliva to avoid aspiration. At the same time, it is applying pressure. Not enough pressure to completely obstruct, but it is applying pressure to stop the bleeding. o The Blakemore does not have a port for suction . o The Minnesota does have a suction. There may be other now out there. ● You need to keep a pair of scissors near the bedside, it’s very important, because in case a person becomes very anxious or you start to see signs of some kind of ischemia, then it needs to be cut very quickly to remove the tube very quickly ● Also the main thing is to avoid tissue necrosis so you don’t want to completely constrict that area too much. Hepatic encephalopathy with is also another cirrhosis complication. ○ It’s an extremely dangerous complication of portal hypertension ■ So when you have a lot of blood that’s being altered, you have portal hypertension ● What happens is that you get a lot of GI bleeds going on ○ So what happens when you have a lot of GI bleed? You have: ■ A lot of RBC’s ■ A lot of blood in the gut ● There’s a lot of blood in the gut and remember blood is a protein ● So blood in the gut is going to increase the ammonia levels because it’s going to break it down, it’s going to break down the blood, it’s going to break down the protein ● Ammonia levels are not good, increased ammonia levels in your blood will cause altered mental status, it disturbs the brain function it is not good for the brain it can lead to hepatic encephalopathy. ● Laxatives (lactulose) so that they can consistently be having bowel movements we don’t want those ammonia levels to rise because it will lead to hepatic encephalopathy and they can actually go into a coma. Medical management geared towards decreasing ammonia levels Stop the bleeding first Remove protein from gut or remove the blood from the gut. Acites is just an accumulation of fluid in peritoneal caused by: • Portal hypertension • Lowered plasma colloidal osmotic pressure, which is the leakage of plasma from the liver to the peritoneal cavity. So when you’ve got all this swelling going on you’re going to have leakage. • And then you have sodium retention as well that makes it even worse. Ascites Medical Management · Correct fluid and electrolyte imbalance because it’s not just taking out the fluid because once you take out all that fluid you will cause a big electrolyte imbalance in this patient. - Avoid aspirin, ibuprofen, indomethacin which impair renal sodium excretion. · Paracentesis – enough to relieve shortness of breath (SOB) · Albumin · Low sodium diet · Promote effective breathing pattern - Oxygen therapy - Semi-Fowlers to High-Fowlers - Measure abdominal girth – we’re not going to know if we’re getting anywhere if we’re not measuring abdominal girth · Maintain skin integrity – can you imagine someone like that when their skin integrity is pretty bad and mostly because of everything going on with the blood flow, portal HTN, pruritus. Nursing Diagnoses for Ascites: ● Excess/Deficient Fluid Volume ○ We need to restrict fluid ○ Monitor I&O's very well, because this is when it matters the most ○ Administer albumin, diuretics ○ Avoid any hepatotoxins ■ NSAIDs, Tylenol; anything that's metabolized by the liver ● Ineffective Breathing Pattern ● Impaired Skin Integrity ● Ineffective Health Maintenance ○ Patient teaching becomes a must with these patients Also in the effects of liver cell failure, there’s coma, the spider nive, jaundice, ascites, and the ankle edema. Then you also have something called the liver flap, which is a reflex that occurs; if you tell them to hyperextend their wrist, they’re going to feel the little slapping of the hand -- they are not going to be able to hyperextend their wrists back, when they do, their hand is going to flap. Cirrhosis Management, a low protein diet is going to be important, mostly because protein is metabolized by the liver. So you want to kind of eliminate anything that goes through the liver as much as possible: alcohol, toxic drugs. Rest is also crucial. Prevent any kind of infection because that’s just going to make it worse. Prevent hemorrhage. Prevent complications, and promote self-care. They're going to have to learn to really, really take care of themselves. A bilirubin not excreted. What is it? “Bilirubin not excreted, (5 )Jaundice” B vitamin K deficiency? (3) “Bleeding” C Backflow of blood to liver and Spleen? (1) Portal HTN D Impaired ammonia metabolism (6) Encephalopathy E Plasma leaking into the peritoneal cavity? (2) Ascites F kidneys unable to excrete solutes? (7) Hepatorenal Syndrome G Thin-walled distended veins (4) Esophageal varices 6. Araceli/Priss ascites 2 (AN, I) Focus on Adult Health: Medical-Surgical Nursing, PAGE 687 ANALYSIS Nursing Diagnoses: Ascites ● Excess/Deficient Fluid Volume ○ Restrict fluid ○ Monitor I&O ○ Administer albumin and diuretics ○ Avoid hepatotoxins ■ NSAIDs ● Ineffective Breathing Pattern ● Impaired Skin Integrity ● Ineffective Health Maintenance ○ Patient teaching MEDICAL AND NURSING MANAGEMENT Dietary Modifications ● Restriction of salt intake to 2,000 mg or less to achieve a negative sodium balance to reduce fluid retention ● Nutritional education and guidance on foods that contain high sodium content ○ All processed foods ○ Frozen and canned foods not indicated as low sodium ● Avoid the use of added salt in meals and food preparation Diuretics ● Combination drug therapy is the most effective regimen to control ascites and pedal edema and includes: ○ Spironolactone (Aldactone), a potassium-sparing agent ○ Furosemide (Lasix), a loop diuretic ● Monitor for daily weight changes ○ Not to exceed 0.5 kg/day (1.1 lbs) gain OR loss in patients WITHOUT peripheral edema ○ Not to exceed 1 kg/day (2.2 lbs) in patients WITH peripheral edema ● Complications of diuretic therapy ○ Dehydration ○ Volume depletion ○ Electrolyte abnormalities, such as hypokalemia, hyperkalemia, hyponatremia, renal impairment, and hepatic encephalopathy ○ Gynecomastia (man boobies) is a common side effect caused by spironolactone ○ If patients with ascites develop dilutional hyponatremia (serum sodium 134 mmol/L), diuretics should be discontinued and fluid restriction initiated Paracentesis ● Removal of fluid from the peritoneal cavity through a puncture or a small surgical incision through the abdominal wall under sterile conditions ● Ascites rapidly recurs, necessitating repeated fluid removal Transjugular Intrahepatic Portosystemic Shunt ● Cannula threaded into the portal vein by the transjugular route ● An expandable stent is inserted as an intrahepatic shunt between the portal circulation and the hepatic vein to reduce portal hypertension; this diverts blood flow from a high- pressure vascular bed to a lower-pressure vascular bed, allowing for the return of blood to the heart and decompressing portal hypertension ● It is extremely effective in decreasing sodium retention, improving the renal response to diuretic therapy, and preventing recurrence of fluid accumulation ● Does not increase survival benefit and increases hepatic encephalopathy 7. Veronica E. jaundice 1 (AS) Pg. 584 When the bilirubin concentration in the blood is abnormally elevated, all the body tissues, including the sclerae and the skin, become tinged yellow or greenish-yellow, a condition called jaundice. Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5 mg/dL. The elevated bilirubi9n stains tissues and fluid, but jaundice is most intense in the face, trunk, and sclera. Increased serum bilirubin levels and jaundice may result from impairment of hepatic uptake, conjugation of bilirubin, or excretion of bilirubin into the biliary system. Pg. 1336 Jaundice, a yellowing of the skin, is directly related to elevations in serum bilirubin and is often first observed in the sclerae and mucous membranes. The term icterus is used to describe yellowing of the sclerae (white of the eyes). Pg. 1337 Etiology: Increased serum bilirubin concentration (2.5 to 3 mg/dL) due to liver dysfunction or hemolysis, as after severe burns or some infections. Light skin: Yellow first in sclerae, hard palate, and mucous membranes; then over skin. Dark skin: Check sclerae for yellow near limbus; do not mistake normal yellowish fatty deposits in the periphery under eyelids for jaundice. (Jaundice is best noted at junction of hard and soft palate, on palms.) Tegrity Jaundice again is just the yellowing of the skin, sclera, and other tissues due to excessive circulating of bilirubin. Mild jaundice is best seen when you examine the sclera; it’s pretty much the best way, if you really are thinking that it is some kind of liver infection or hepatic infection look at the sclera, that’ll be your first indication that it is jaundice. Natural light; a lot of the times being in natural light will let you tell if you are jaundice. 8. Clau pruritus 1 (I) Tegrity· When bile pigment is deposited in the skin it’s very pruritic. So it’s going to cause a lot of itching and dryness. (hyperbilirubinemia) · The medical management of pruritus, I didn't see it in your book but I kind of kept it in here because I wanted to let you know that some of the treatments for pruritus are o Oral cholestyramine resin (Questran) o Binds to the bile salts in the intestines to assist with excretion of bilirubin, that's pretty much what it does to help with the pruritus. o You can also use antihistamines like Phenobarbital o It actually helps enhance the bile flow, and keeps relieving the itching. Nursing Diagnosis for Pruritus is skin integrity. If you having someone that is scratching so much they run the risk of running a secondary infection o They need to administer their Antihistamines on time o Cholestryramine resin (Questran). You need to make sure they use Tepid water. Don’t use too hot or too cold because that aggravates the itchiness. In Emolient baths avoid soaps especially antibacterial soaps are worse. Make sure you avoid some of these soaps. o Wear loose clothing. The tighter the close can cause itching and constriction of the area. o Soft bed linens. (Blanket from home that is a little softer). 9. Erika/Clavell hepatic encephalopathy 3 (AS, I) ● Then you also have hepatic encephalopathy with is also another cirrhosis complication. ○ It’s an extremely dangerous complication of portal hypertension ■ So when you have a lot of blood that’s being altered, you have portal hypertension ● What happens is that you get a lot of GI bleeds going on ○ So what happens when you have a lot of GI bleed? You have: ■ A lot of RBC’s ■ A lot of blood in the gut ● There’s a lot of blood in the gut and remember blood is a protein ● So blood in the gut is going to increase the ammonia levels because it’s going to break it down, it’s going to break down the blood, it’s going to break down the protein ○ So the breakdown of that causes the ammonia levels to go up Blood in the gut: · is going to increase the ammonia levels it will breakdown the blood, breakdown the protein, the breakdown of that causes the ammonia levels to go up. · ammonia levels are not good, increased ammonia levels in your blood will cause altered mental status, it disturbs the brain function it is not good for the brain it can lead to hepatic encephalopathy…How many of you have had patients where you have to give them laxatives pretty much around the clock so they can expel a lot of that bleeding? I used to hate those patients because I am going to be cleaning them all day long. Because we want to get rid of that blood in the gut, we want to get rid of it as fast as we can get rid of it, so these patients we give them · Laxatives (lactulose) so that they can consistently be having bowel movements we don’t want those ammonia levels to rise because it will lead to hepatic encephalopathy and they can actually go into a coma. · Hepatic encephalopathy is just another term for the liver’s inability to metabolize ammonia. That’s really what it is. There’s blood in the gut and it’s turning it into ammonia, and you know we can’t have that. · •Ammonia is a CNS depressant · •Ammonia produced in the GI tract when protein is broken down, like I said earlier. · •An increase in protein will cause ammonia levels to increase · •Medical management geared towards decreasing ammonia levels °Stop the bleeding first °Remove protein from gut or remove the blood from the gut. Adult book 693 - hepatic encephalopathy is a life threatening complication of liver disease. Due to accumulation of ammonia. Damage liver cells fail to detoxify and convert the ammonia to urea and the elevated ammonia enters the bloodstream. Serum ammonia is decreased by elimination of protein from the diet and by the administration of antibiotic agents. Factors that can cause hepatic encephalopathy is susceptible patients include excessive diuresis, dehydration, infections, constipation, surgery, fever, and some medications (sedatives, tranquilizers, analgesics and diuretics that cause potassium loss). The increased ammonia concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy. Some of the clinical symptoms that is important to assess:LOC, mental changes, and motor disturbances. The patient appears slightly confused unkempt and has alterations in mood and sleep patterns. The patient tends to sleep during the day and have restlessness and insomnia at night. As hepatic encephalopathy progresses, the patient may become difficult to awaken, eventually resulting in coma. 10. Irish portal hypertension 1 (AS) Pellico p. 687 - Portal hypertension: - It is caused by increased resistance to blood flow through the liver and increased blood flow due to vasodilation in the splanchnic circulation. - The two major complications of portal hypertension are ascites and gastroesophageal varices. 1) Ascites: - Clinical manifestations/assessment: - Increased abdominal girth, weight gain, and swelling of the lower extremities. Dyspnea may be present. Abdominal hernias may be visible. Patient may experience satiety, anorexia, and general weakness. With the pt supine, the free fluid in the abdomen will accumulate in the flanks. Percussion of the abdomen will reveal tympany over the anterior abdomen and dullness over the flanks. There will be shifting dullness on percussion. 2) Gastroesophageal varices: - Clinical manifestations/assessment: - Hematemesis, melena, general deterioration in mental or physical status. Signs and symptoms of shock may be present. Hepatic Disorders Tegrity/PPT - Portal hypertension - Increase in blood pressure in the portal venous system - Occurs when blood flow is completely altered. It builds up in the blood system, the blood can’t get through the liver so it just creates altered access around the liver. - Portal vein receives blood from the intestines and spleen - Resulting in increase in pressure resistance - Enlargement of esophageal, umbilical, and superior rectus veins - Caput Medusae: dilated abdominal veins (indicative of portal hypertension) 11. Armando/David esophageal varices 2 (AS, I) MED SURG BOOK PG 706 Clients with cirrhosis are at increased risk for bleeding because of a decreased production of prothrombin and decreased ability for the liver to produce substances for blood coagulation. The nurse should: • Observe for melena and assess the stools for blood. • Monitor vital signs regularly °Avoiding increases in portal pressure minimizes rupture of varices • Keep readily available: °Equipment (e.g., balloon tamponade tube) °IV fluids °Medications needed to treat hemorrhage If bleeding occurs the nurse will: • Aid the physician in stopping the bleeding • Administer fluid, blood component therapy and/or medications • If the client has massive hemorrhage they are transferred to the ICU and will require surgery or other treatment TEGRITY Esophageal varices are a complication of cirrhosis. It is a complication of portal hypertension. Dilation can lead to rupture by: • Increased portal venous blood pressure • Increase in intrathoracic pressure °coughing, straining • Irritation from food or alcohol • Erosion by gastric juices Esophageal varices can lead to a medical emergency because these clients will keep bleeding. Risk for hemorrhage is high and should be avoided. Treatments to control hemorrhage: • Sclerotherapy °injecting morrhuate sodium directly to varices via endoscope • TIPS °Percutaneous placement of expandable metal stent to hepatic veins to create a channel, this improves blood flow °Only reduces portal hypertension °Blood flow is still going to be altered, so this is temporary. It only buys you time but does not fix the problem. • Vasopressin °It is infused directly to superior mesenteric artery °Very effective, but at the same time very dangerous. °It can cause acute renal failure, MI, hypothermia °Can cause GI ischemia, if the client is having chest pain it needs to be stopped. • Balloon tamponade °Applies pressure to ruptured varices via balloon tamponade, like applying pressure to a cut. °Sengstaken Blakemore/Minnesota tube -Inserted into the stomach through the nose. -Inflates an esophageal and stomach balloon -Do not leave inflated for 24 hrs (can cause tissue necrosis) -Remove secretions and saliva to avoid aspiration -Sengstaken does not have a port for suction -Minnesota pas a port for suction -Keep a pair of scissors at bedside for emergency removal of tube -Avoid tissue necrosis by periodical release Shock 17 (1)PH AN *Tegrity AND Med. Surg. Book MUST be used. 12. Karla vasoactive medication 1(I) Vasoactive Medications pg.1398 (I used some information from the book and Tegrity because Ms.Voss mentioned names and in the book it didn’t have any just categories) · Vasoactive medication can be used in all forms of shock to improve the patient’s hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Different medication work on different aspects of CO, and specific medications are selected depending on the underlying cause. · Although the most of the medications have several effects, these medications are used to: (1)Increase the strength of myocardial contractility Positive Inotropes: Epinephrine and Dopamine (2) Regulate the heart rate Antidysrhythmic’s: Amiodarone, beta blockers and calcium channel blockers will be used. (3) Reduce myocardial resistance: Vasodilators (decrease afterload decrease venous return, decrease systemic vascular resistance) Nitroprusside and Nitroglycerine (4) Initiate vasoconstriction: Vasocontrictors (increase after load by increasing systemic vascular resistance by improving BP and tissue perfusion): Epinephrine, Dopamine, Vasopressin, Norepinephrine · When vasoactive medications are administered, the nurse must monitor vital signs frequently (at least every 15 minutes until stable, or more often if indiacted). · Vasoactive medication should be administered through a central venous line, because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing. · IV pump must be used to ensure that the medications are delivered safely and accurately. · Invasive monitoring using an arterial line is used to titrate medications accurately. 13. Crystal/Joseph hypovolemic 2(I, AS) Tegrity (Tegrity had WAY more info than the book, plus Voss said specifically what she was going to ask on the test plus the book didn’t really have much assessment info on hypovolemic shock so I didn’t add anything from the book. If you want to read up on it, the info is on pg 1399 of the Pellico book)-Joseph Assessment: 4 initial stages of assessment of shock: Initial, compensatory, progressive, and refractory Initial stage: 15% loss of volume (750mL) Patient is symptom free Compensatory stage: 15-30% loss of volume (700-1500mL) Patient has an increase heart rate, increase sympathetic nervous system response, narrowing of pulse pressure, increase respirations, decreased urinary output, skin vasoconstriction, pale and cool skin, and decreased LOC. Progressive stage: 30-40% loss of volume (mL) Dysrhythmias start to occur because they start having respiratory distress, oliguria-the kidneys start to fail, the skin will be ashen, cool and clammy, patient is lethargic and unresponsive. Refractory stage: 40% loss of volume (2000mL) Severe tachycardia, severe hypotension, absent pulses, cyanotic, mottled skin, and unresponsiveness Assessment is going to show decreased cardiac output, decreased preload, vasoconstriction, and an increased afterload. In Hypovolemic shock your pressures will be low, particularly your wedge pressures will be low *she said this would be a test question* Hypovolemic Shock Tegrity Interventions Everything in BOLD is what I think may be asked as a test question. - Crystal Management: ● To correct hypovolemia- vigorous fluid administration ○ ER nurse will put a large IV and hang normal saline to open it up and restore tissue perfusion. ○ They will get both crystalloids and colloids, really depending on what type of fluid loss and if they have chest trauma or massive hemorrhage. But especially in chest trauma a lot of the chest drainage compartment can be used for auto transfusion. Nursing care: ● Identifying the patient at risk ● Constantly assessing fluid balance (How do you constantly assess fluid balance?) Output and weight. ○ Foley catheter measures output ○ Daily weight checked just once a day *Test Question* When you replace fluid volume with crystalloids, it’s going to be 3:1. ● You’re going to have to give 3 liters of crystalloids for every 1 liter lost. Normal saline: ● Generally used in shock ● It may result in hyperchloremia (high chloride) because they are going to have a loss of base so the chloride is going to be retained. Ringer’s Lactate: ● Usually not used in shock ○ Because of the Lactate. Remember there’s lactate in ringer’s solution. The Lactate is converted by the liver to bicarbonate. It neutralizes, but if you were in a hypo perfusion state, your liver is hypo perfused, shocked liver. It’s going to maintain the lactate acidosis. ● Will be the fluid of choice in burn shock. Disadvantages with colloids: (mostly we’re talking about packed red blood cells for blood loss) ● They are expensive ● They cause allergic reactions Other colloids that can be used: ● Hetastarch ● Dextran- is high in sugar, but it is going to maintain volume Packed RBC’s: ● Typed and crossed matched ● Universal rule is that if the Hemoglobin is below 7 they need a transfusion Most common type of shock: ● Hypovolemic shock ● In a trauma patient they are going to have blood available and it’s going to be from the universal donor. Who is that? O positive ○ O positive can be donated to all other blood groups Vasoconstrictors: ● Increase afterload by increasing systemic vascular resistance ● They are going to improve: ○ Blood pressure ○ Tissue perfusion ● Vasoconstrictors that will be used: ○ Epinephrine ○ Dopamine ○ Vasopressin ○ Levophed And at times we will need to decrease afterload Vasodilators: ● Decrease afterload ● Decrease venous return ● Decrease systemic vascular resistance ○ That’s Nitroprusside & Nitroglycerin To increase cardiac contractility we use positive inotropes: ● Those are Epinephrine and Dopamine ● Also used to control heart rate, influence heart rate ○ Antidysrhythmics such as Amiodarone ● For very Tachy arrhythmias especially with cardiogenic shock: ○ Use Beta blockers and Calcium Channel Blockers Shock Position: · Position the patient in a modified trendelenburg To maximize respiratory function: · Have the head of the bed elevated 30 degrees If put in just trendelenburg (not modified) what’s the problem? · Increased ICP 14. Sanzabeedee anaphylactic 1 (AN) ● Test Question Voss stated on Tegrity-If you got someone with laryngeal edema airway is really hard to maintain without someone right in there to trache them. So what is going to stop the mediators? Epinephrine (Epinephrine pen) that’s the test question. So epinephrine now is IM but it used to subcutaneous. If you are in the hospital it can be given IV, is 0.1 gm/kg. ● Diphenhydramine(Benadryl), given IM is used to reverse the effects of histamine, thereby reducing capillary permeability. Nebulized medication such as albuterol(proventil), may also be given to reverse histamine induced bronchospasm, and systemic glucocorticoids are used to prevent rebound. 15. Paula neurogenic 1 (AN) Focus on Adult Health- p. 1406 ● Neurogenic shock- vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation ● Sympathetic stimulation causes vascular smooth muscles to constrict, and parasympathetic stimulation causes vascular smooth muscles to dilate ● Patient experiences a predominant parasympathetic stimulation that causes vasodilation lasting for an extended period. ● Blood volume is adequate because the vasculature is dilated, the blood volume is displaced producing hypotensive. ● The overriding parasympathetic stimulation that occurs with neurogenic shock causes a severe decrease in the patient’s systemic vascular resistance and sometimes bradycardia. ● Inadequate BP results in the insufficient perfusion of tissue and cells. ● Caused by spinal cord injury (commonly above level T6), spinal anesthesia, or nervous system damage, depressant action of medications or lack of glucose. ● May have prolonged course or a short one (syncope or fainting). ● In Neurogenic shock, the sympathetic system is not able to respond to body stressors. Tegrity ● Neurogenic shock is a type of distributive shock that caused by loss of sympathetic tone. ● Occurs within minutes to several days, weeks or months after an injury. ● Usually occurs because of a spinal cord injury above T5 . Can also occur after spinal anesthesia ● Without the sympathetic nervous system you have a massive vasodilation with a decrease SVR, decrease preload, decrease cardiac output and tissue perfusion. ● The patient is going to be bradycardic and won't be able to maintain their temperature (They are the same temperature as the room *NCLEX) People with spinal cord injuries you warm the room because they are very cold because they have no sympathetic nervous system. 16. Yesenia cardiogenic 1 (AN) Tegrity: “so I ask questions on the exam with this- When someone has cardiogenic shock what do their pressures look like? We are kind of looking at the difference of parameters in someone with hypovolemic shock and cardiogenic shock parameters such as: CVP – this is the simplest; But then I could go to pulmonary artery pressures particularly the wedge- so it is an easy question; In hypovolemic shock pressures are going to be low; in cardiogenic shock- Blood is there but the heart cant pump- so all the pressures are going to be high” Critical Care book page 549 Assessment of the hemodynamic parameters of a patient in cardiogenic shock revels decreased cardiac output with a CI less than 2.2 L/minute/ m in the presence of an elevated PAOP of more than 15-18 mm Hg. A proportional pulse pressure less than 25 % is indicative of left ventricular failure. Increased filling pressures are necessary to rule out hypovolemia as the cause of circulatory failure The increase in PAOP reflects an increase in the left ventricular end-diastolic pressure and left ventricular end-diastolic volume resulting from decreased SV. With right ventricular failure, the RAP also increases. compensatory vasoconstriction results in an increase in the SVR. 17. Veronica D./Francoise/Angie septic 3 (AS, I, AN) 17. Veronica D Assessment (Tegrity) · Massive vasodilation Venous -decreased preload -low RAP & PAWP Arterial -Decreased afterload -low SVR -Drop in Blood pressure · Skin pink, warm, flushed, · Increased HR and CO · Widening pulse pressure and full bounding pulse · Decrease myocardial contractility · Lungs -increased RR, hypoxemia, crackles · ABG’s -Respiratory alkalosis, hypoxemia, metabolic acidosis -Respiratory & metabolic acidosis · Change in LOC, urine ouput declines, elevated Temperature · Elevated WBC and glucose · Impaired tissure perfusion -MODS Angie: Assessment (Pellico, Pg.1404) ● Septic shock has been described as having two phases: a hyperdynamic (warm) phase and a hypodynamic (cold) phase ● Hyperdynamic (warm) phase: ○ Massive vasodilation (aka hyperdynamic state) ■ Venous ● Decreased preload (decrease in venous return to the heart) ● Low RAP & PAWP ■ Arterial ● Decreased afterload ● Low SVR ● Drop in blood pressure (hypotensive), but responsive to fluids ○ Blood pressure may remain within normal limits ● Warm, flushed, pink skin ● Decrease in myocardial contractility ○ Increased HR, progressing to tachycardia ■ Response to increased SNS, metabolic, and adrenal gland stimulation ■ If volume and preload are adequate, it results in normal-to-high CO and CI despite impaired contractility ○ Higher demand of heart à high CO ■ Patient with a pulmonary artery catheter will get a CO as high as 10 ○ Widening pulse pressure ○ Full bounding pulse ○ Lungs (mismatch of the V/Q ratio) ■ Pulmonary vasoconstriction ■ Formation of pulmonary emboli à increased RR, hypoxemia ■ Noncardiogenic pulmonary edema (w/ increased pulmonary capillary membrane permeability) à crackles ○ ABG’s ■ Initially, elevated respiratory rate à Respiratory alkalosis, hypoxemia & metabolic acidosis, hypocarbia ● Low PaO2, low PaCO2, and low HCO3 ■ They’re going to breathe so fast. Eventually, they will retire à Respiratory ■ Lack of oxygen to the cells and development of lactic acidemeia à metabolic acidosis ○ Change in LOC (mental status) due to decreased cerebral perfusion, immune mediator activation, hyperthermia, and lactic acidosis à confusion, combative, disoriented, agitation, lethargy ○ Urine output may remain at normal levels or decline b/c of decreased renal perfusion ○ GI status may be compromised, as evidenced by nausea, vomiting, diarrhea, or decreased bowel sounds ○ Elevated temperature (fever) b/c of the pyrogens that is stimulating the CNS, which further increases the metabolic activity ○ Elevated WBC in response to invading microorganisms ■ Elevated procalcitonin level is a valuable indicator of significant infection. ○ Signs of hypermetabolism include increased serum glucose and insulin resistance ○ Impaired tissue perfusion ■ Multiorgran dysfunction syndrome (MODS) à all systems affected ■ This is a hyperdynamic state. This is warm shock. Eventually it leads to MODS. When it leads to cardiac failure and MODS, it is going to be a low output failure aka “cold shock” (vasoconstriction, low cardiac output). The same shock Voss has talked about before. This is a high hyperdynamic shock. ● Hypodynamic (cold) phase: …occurs with progression of sepsis ○ Tissues become more underperfused and acidotic, compensation beings to fail, and the patient becomes more hypodynamic ○ The cardiovascular system begins to fail, the BP does not respond to vasoactive agents and fluid resuscitation, and signs of end-organ damage are visible (ex. renal failure, pulmonary failure, hepatic failure) ○ As sepsis progresses to septic shock, the BP drops, and the skin becomes cool and pale ○ Temperature may be normal or below normal ○ Heart and respiratory rates remain rapid ○ Urine output decreases, and multiple organ dysfunction develops ● URDEN P. 558 BOX 26-12 CLINICAL MANIFESTATIONS OF SEPTIC SHOCK ○ Increased HR ○ Decrease BP ○ Wide pulse pressure ○ Full, bounding pulse ○ Pink, warm flushed skin ○ Increased RR (early) or decreased RR (late) ○ Crackles ○ Change in sensorium ○ Decreased urine output ○ Increased temperature ○ Increased CO and CI ○ Decreased SVR ○ Decreased right atrial pressure ○ Decreased PAOP ○ Decreased left ventricular stroke work index ○ Decreased PaO2 ○ Decreased PaCO2 (early) or increased PaCO2 (late) ○ Decreased HCO3 ○ Increased SVO2 and SCVO2 17 Francoise Castillon Pathophysiology of septic shock Book pg(1404) · Microorganisms invade the body tissues and body produces an immune response · Immune response activates biochemical cytokines and mediators associated with an inflammatory response. · It produces a complex cascade of physiologic events that leads to poor tissue perfusion. · Increased capillary permeability, which leads to fluid seeping from the capillaries, and vasodilation are two such side effects that interrupt the ability of the body to provide adequate perfusion, oxygen, and nutrients to the tissues and cells. · Proinflammatory and anti-inflammatory cytokines released during the inflammatory response activate the coagulation system. · Activation of coagulation system leads to clot formation in areas where a clot may or may not be needed. Tegrity Pathophisiology · It is initiated by a microorganism that stimulates the inflammatory immune response. · This response phagocytes the organisms and they shed protein and this protein, the endotoxin and the exotoxin, activates plasma enzyme cascades such as: o the compliment, o the kinin, o and the coagulation/fibrinolytic cascades. · It also mounts the inflammatory response with: o the neutrophils, o the macrophages, o and the platelets. · Once activated, these symptoms release a variety of mediators that initiate a complex interaction that causes massive vasodilation. · With massive vasodilation, and I should have moved this out, sluggish circulation and microemboli form. · There is selective vasoconstriction that occurs and because of the inflammatory immune response there is increased capillary permeability · The inflammatory immune response is overwhelmed feedback mechanism fail and the process that is designed to protect the body actually harms it. · Hyper-metabolic state occurs because of the activation of the central nervous system and the endocrine system, increased the oxygen demand of the cells and lactic acidosis occurs. o The glucocorticosteroids, ACTH, the epinephrine the glucagon cause a catabolic state. It causes glucose intolerance and hyperglycemia, insulin resistance. o Protein is used for injury, energy and catabolism occurs. § These patients in ICU, very quickly lose all their muscle mass and their visceral organs along with their skeletal muscles are catabolized. Quickly go from a healthy looking individual down to no muscle mass. When you see the deterioration in their skeletal muscle at the same time, because in their shock state are on ventilators, all kind of support and not able to maintain respiration on their own until you are able to rebuild that muscle. Those visceral organs so again feeding them. They have to be fed. Angie: Treatment ● FIRST GUIDELINE: Finding and eradication infection ○ Culture everything: blood, urine, wound, sputum using aseptic technique ■ At least two cultures should be obtained before antibiotic therapy is initiated. ■ Sometimes tips of central lines are cultured, although recently that practice has been called into question ■ Any potential routes of infection must be eliminated. ● IV lines are removed and reinserted at other body sites ● If possible, urinary catheters are removed or replaced ■ Additional cultures may be obtained from the CSF (in case of suspected meningitis) or pleural space (if empyema is suspected) ○ Antibiotics as quick as possible (w/in 1 hour of recognition) ■ Depends on the site of the expected infection ■ If the infecting organism is unknown, empiric broad-spectrum antibiotics are started ■ When culture and sensitivity reports become available, the antibiotic agents can be changed to those that are more specific to the infecting organism and less toxic to the patient ■ Combination therapy is recommended for known of suspected Pseudomonas infection and for neutropenic patients but should be limited to less than 3-5 days. ○ (Pellico, Pg. 1405) Glucocorticoids ■ IV corticosteroids reduce mortality in catecholamine-dependent septic shock patients with relative adrenal insufficiency. ● IV hydrocortisone is recommended only for the pt. in septic shock who is poorly responsive to fluid resuscitation and vasopressor therapy. ■ The general concept is that, since septic shock represents a significant physiologic stress, dysfunction of the hypothalamic-pituitary-adrenal axis may be one factor that leads to increased mortality. ■ Drawbacks of steroid administration include increased infection rate, worsening glycemic control, and impaired wound healing ■ A recent literature review suggests that administration of hydrocortisone to patients with severe sepsis, whose systolic BP remains inadequate even after vasopressor support, might be beneficial. ○ Surgical debridement must be done if they have any infected necrotic tissue; abscesses are drained ● SECOND GUIDLINE: Cardio-pulmonary support: Enhance tissue perfusion ○ Increase cellular oxygen supply and decrease cellular oxygen demand ○ Fluid administration PAWP 15 mmHg ■ Aggressive fluid resuscitation to augment intravascular volume and increase preload until CVP of 8-12 mm Hg is achieved. ■ Correct hypovolemia that results from the incompetent vasculature and the inflammatory response ■ Crystalloids, colloids, and blood products may be administered to increase intravascular volume ○ Goal-directed therapy—involves using CVP, MAP, urinary output, and SvO2 ■ The patient’s response to tx is closely monitored and resuscitation is continued until: ● CVP 8 ● MAP 65mmHg ● Urine output is 0.5mL/kg/hr or more ● SvO2 70% ○ SvO2 is an abbreviation of venous oxygen saturation. It determined tissue hypoxia. Normal values = 60-80% ■ This approach is associated with a decreased mortality and should be considered standard of care in the management of septic shock ■ Voss says… PAWP 15mmHg, but on her PPT she meant to write “CVP” instead of “PAWP” b/c all the guidelines say to maintain CVP between 8- 12 mmHg ○ Vasoconstrictors & positive inotropic ■ Arterial line placement is recommended for vasopressor therapy. ● Vasopressors (norepinephrine and dopamine) to maintain a MAP of at least 65 mm Hg. ● Epinephrine is recommended as an alternative agent if response to norepinephrine or dopamine is poor. ■ If SCVO2 is 70% or the SVO2 is 65% after CVP goal is achieved à administer PRBCs to achieve HCT of at least 30% or inotropic stimulation with dobutamine to counteract myocardial depression and maintain adequate CO ○ Intubation and mechanical ventilation to maintain a PaO2 70 ■ Ventilation with lower than traditional tidal volumes in patients with ALI and ARDS decreases mortality. ■ Goal: 6 ml/kg of predicted body weight and plateau pressures of no more than 30 cm H2O for pts. with severe sepsis or septic shock ● Increased PaCO2 may result and is acceptable if tolerated ■ Ventilator settings should include PEEP and adjusted to provide PaO2 70 mm Hg ● Pts. w/ mechanical ventilation should be maintained in semirecumbent position w/ HOB raised 45 degrees to decrease risk of ventilator-associated pneumonia ● Prone position considered for septic patients with ARDS requiring high levels of oxygen. ○ Sedation protocols using intermittent bolus or continuous infusion ○ Avoid neuromuscular blocking agents to prevent prolonged blockage after discontinuation ● Continuous infusion of insulin and glucose ○ To maintain a blood glucose level of 150 mg/dL or less improves outcomes. ○ Glucose levels should be monitored every 1-2 hours until stable and then every 4 hours. ● PLTs should be administered when counts are 5000/mm3 and RBC transfusions are recommended when HGB 7.0 g/dL to obtain target value 7-9 g/dL ● Temperature ○ Give antipyretics & cooling blankets ○ High temperature is going to increase metabolic demands ● Nutrition support ○ Goal: improve the patient’s overall nutritional status, enhance immune function, and promote wound healing. ○ Aggressive ○ Daily caloric intake of 25-30 kcal/kg of usual body weight ■ Enteral route preferred ■ Ideal nutrition: high protein ● Due to metabolic derangements that develop in the hypermetabolic state ● Amount depends on patient’s nitrogen balance ○ In the guidelines, it says to keep the blood sugar greater than 150 and less than 170 ○ Glutamine is considered by some to be an essential amino acid in critically ill patients and has the most empirical support. ○ Arganine has produced negative outcomes and is NOT recommended. ● There has been a study that drugs alters the immune response, but none of them have been effective. None of them are recumbent protein C. Corticosteroids have been studied and have showed of no benefit. Nursing Care ● Prevention* ● Identify patients at risk ● Early identification & treatment ○ #1 intervention: HANDWASHING! ○ Mrs. Voss is suspicious of anyone breathing too fast. Immediately look for an infection. Look at urine. Listen to lungs. Take temperature (may be absent for those who are immunocompromised or elderly). ○ Early identification will decrease mortality ● Nursing priorities directed toward: ○ Early identification of sepsis syndrome ○ Administering prescribed fluids and medications ○ Providing comfort and emotional support ○ Maintaining surveillance for complications ○ Severe Sepsis and Septic Shock Management Guidelines (Urden Pg. 562-564) 18. Sarah H. MODS 1 (PS, I) Med Surg book pg. 1409 - Multiple Organ dysfunction syndrome (MODS) is altered organ function in acutely ill patients that requires medical intervention to support continued organ function. It is defined as severe organ dysfunction of at least two organ systems lasting at least 24-48 hours in the setting of sepsis, trauma, burns or severe inflammatory conditions. MOSD may result from any form of shock because of inadequate tissue perfusion. The most common types of organ dysfunction seen with MODS are acute renal failure and acute respiratory distress syndrome. Prevention remains top priority in managing MODS. IF preventative measures fail, treatment measures to revers MODS are aimed at 1. Controlling the initial event 2. Promoting adequate organ perfusion 3. Providing nutritional support Primary nursing interventions are aimed at supporting the patient and monitoring organ perfusion until primary organs insults are halted. Providing information and support to family members is a critical role of the nurse. It is important that the health care team address end of life decisions to ensure that supportive therapies are congruent with the patient’s wishes. 19. Cassie/Sonia ARDS (ALI) 4 (PH, AN, I) ARDs (acute respiratory distress syndrome) life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood. Severe form of acute lung injury (ALI). Manifestations: ● Occurs within 24-72hours (tegrity) 4-48hours (book) ● Rapid onset of severe dyspnea that occurs 12-48hrs after the initiating event. ● hypoxemia; does not respond to oxygen therapy. ● Absence of left atrial pressure ● “increase work of breathing”- intubation & mechanical ventilation required. ‘ ● intercostal retractions and crackles Diagnostic test: ● BNP level, echocardiography, and pulmonary artery catherization Mediacal management: ● Intubation & Mechanical ventilation if required. ● Oxygen ● PEEP ● Nutrition (enternal, parenteal if needed) Nursing: ● Oxygen ● Turn patient to improve perfusion & ventilation ● Rest ● Ventilator considerations: PEEP assess tubing, for blockage or kinks, sedative may be required 20. Yari/Bibi DIC 2 (AN, AS) Tegrity slide 7 (Sarah Hilton) Disseminated intravascular coagulation The CNS, again its a result of hypoperfusion, there will be failure of SNS that will result in vasodilation, pooling of blood in the capillaries, increased capillary permeability and at this time with vasodilation occurring and increased capillary permeability there will be microemboli that forms and this sluggish circulation further decreasing perfusion to that tissue setting off the coagulation syndrome using up all the body’s clotting factors and bleeding will occur, and that’s called DIC. Disseminated intravascular coagulation. Its both a process where microemboli form in the capillary circulation and bleeding occurs because with all of that emboli the clotting factors are used up the patient is clotting and bleeding at the same time. Adult Health Book (Pellico) pg. 558-560 · DIC not a disease but a sign of an underlying condition · DIC may be triggered by sepsis, trauma, cancer, shock, abruption plancentae, toxins, or allergic reactions Pathophysiology · Normal hemostatic mechanisms are altered in DIC, so that a massive amount of tiny clots forms int eh microcirculation. · Initially, the coagulation time is normal, however as the platelets and clotting factors are consumed to form the microthrombi, coagulation fails. · Paradoxical result of excessive clotting is BLEEDING Clinical Manifestations & Assessment · Patients with frank CIC may bleed from muco