Blood Gases (Midterm 2)

**Blood Gases** -Priority: what does patient look like? Treat the patient not the numbers. -normal pO2 levels 80-100mmhg (partial pressure of oxygen in the blood) -Sats-the amount of HGB saturated with O2 -20:1 base to acid ratio: Low PH= acidic, high pH=basic (alkaline) -carbonic acid is what...

**Blood Gases** -Priority: what does patient look like? Treat the patient not the numbers. -normal pO2 levels 80-100mmhg (partial pressure of oxygen in the blood) -Sats-the amount of HGB saturated with O2 -20:1 base to acid ratio: Low PH= acidic, high pH=basic (alkaline) -carbonic acid is what causes acid/base balance. (H2CO3) **-what controls our acid/base balance?** -**Lungs**- react fast, getting rid of or retaining CO2 to balance but can only work for a little while. -lungs maintain normal pH by excreting CO2. CO2 combines with H2O to make carbonic acid (H2CO3). Carbonic acid breaks into hydrogen and bicarb. -**Kidneys**- reabsorb bicarb from urine, excrete hydrogen ions from blood. Slow, may take a few days for kidneys to kick in but will work for a long time. **Bicarb binds with hydrogen to neutralize.** -**buffers**- hydrogen ions are buffers, if blood is acidic then hydrogen will go into cell and potassium will leave (meaning serum potassium is high). If blood is basic, hydrogen leaves the cell causing potassium to leave the blood and go into the cell causing hypokalemia. **High C02= acidosis=hyperkalemia** **High Bicarb (HCO3)=alkalosis=hypokalemia** -**What is compensation?** CO2 increases, body absorbs bicarb (HCO3) to neutralize acidosis. Alkalosis: lungs blow off CO2 **Normal Values ABG's** **Component** **Range** --------------- ----------------------------- **pH** Acidic **7.35-7.45** Basic pO2 80-100mmhg **pCO2** Basic **35-45mmhg** Acidic O2 sats over 95% **HCO3** Acidic **21-28mEq/L** Basic A patient can have respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis. Will only have partial compensation until pH is normal. If pH is normal but other numbers are not normal will still have full compensation. **Respiratory acidosis:** Causes: airway obstruction (can't do gas exchange), CNS depression, sleep disorders (sleep apnea), neuromuscular impairment (Guillaume barre), increased CO2 production (increased metabolism (ex: seizures), malignant hypothermia (reaction to anesthesia)). -hypoventilation= increased CO2 in blood resulting in increased H+ in blood. =acidic -only way to correct blood gasses is to correct the cause. -Acidosis= will see hypoventilation, rapid shallow respirations, hyperkalemia, dysrhythmia. A diagram of a person\'s respiratory system Description automatically generated **Respiratory Alkalosis:** causes: CNS stimulation, hypoxia, stimulation of chest receptors (PE, pulmonary edema, pleural effusion), drugs/hormones. -hyperventilation= decreased CO2=decreased carbonic acid= decreased hydrogen ions=alkalosis  **Metabolic Acidosis:** causes: HCO3 loss, increased H ion production or ingestion (methanol intoxication), uremia, Lactic acidosis, bicarb loss from diarrhea, DKA ((ketones are acidic) (usually get DKA when sick, cortisol causes increase in sugar, so even though not eating still want to take long acting insulin to prevent DKA)), Accumulation of acid in the body or loss of bicarb=compensatory mechanism=increased CO2 excretion (Kussmaul respirations (abnormal, deep, and labored breathing pattern). A diagram of a human body Description automatically generated **Metabolic Alkalosis:** causes: GI loss of H+, vomiting/diarrhea, renal loss of H+, burns (usually treat with RL which has ++ bicarb. -acid is lost or bicarb increases. Compensation is decreased resp rate to increase CO2, symptoms are all general and nonspecific.  The Functions of the Liver and Signs You Need to Detox \... Splanchnic circulation: blood supply to GI tract, pancreas, liver, spleen.  -Gallbladder receives bile from common hepatic duct and holds it till it gets a signal that it is needed by the small intestine to digest fats and proteins. Bile goes from gallbladder through cystic duct to intestine. Pancreatic duct joins common bile duct at the same spot into the intestine. -Intrahepatic ducts: Tiny branching bile ducts inside the liver that collect bile as the liver makes it. These join outside the liver to form the common hepatic duct. -Common hepatic duct connects to gallbladder through the cystic duct forming the common bile duct. Half of the bile from the liver flows here which is the main trunk of the biliary tree. The other half goes to the gallbladder where its stored. -if ducts are blocked can have jaundice and elevated liver enzymes, can also have issues with pancreas and gallbladder. **Diagnostic Tests:** history/physical exam -lab tests: cbc, liver function tests (AST, ALT, GGT (**With acute liver failure look at AST, ALT, GGT** (when liver cells are damaged they excrete these enzymes), with chronic liver failure AST, ALT, GGT won't be elevated as the cells are no longer working enough to secrete these enzymes), bilirubin (if liver is unable to conjugate bilirubin will have high levels, seen more with chronic)), PT/INR (will see increased INR with chronic because liver cannot produce vitamin K/other clotting factors), Albumin (low because liver cant synthesize the proteins), stool for occult blood (watching for bleeding), analysis of ascites fluid (looking to see the components of the fluid), **(with chronic look at bilirubin, INR, and albumin),** liver biopsy (after biopsy have strict orders: vitals Q15 min x2, Q30 x2, Q1 x 2, then Q4 x2. Bed rest for 4-6 hours. Position the person on right side to put pressure on liver to prevent bleeding for first 2 hours). **Viral Hepatitis:** inflammation of the liver that's caused by a virus causing it not to function, 5 main strains (A,B,C,D,E), differ in modes of transmission, severity of illness, geographical areas and methods of prevention. Some preventable by vaccine (A+B). -types B and C lead to chronic disease **Acute liver failure:** Rapid deterioration of liver function with no known history of liver disease. Lasts 8-26 weeks. Most common cause is drugs, generally acetaminophen combined with alcohol. Can also occur after hepatitis A infection or mushroom ingestion (wild mushrooms). Usually presents with lab abnormalities, coagulation abnormalities and encephalopathy (confusion, jaundice). -treatment is to treat the underlying cause. Ex treat Tylenol with charcoal, mucomyst (acetylcysteine) (antidote for Tylenol as it neutralizes the toxic metabolite that comes from the breakdown of acetaminophen) - give between 4-8 hours after OD, can give it PO or IV. -sometimes acute liver failure can result in need for transplant. **Cirrhosis:** A chronic progressive disease of the liver. Characterized by fibrosis (scar tissue) and conversion of normal liver structure to abnormal nodules. -liver doesn't function how it should. -Scar tissue and inadequate blood flow are formed from irregular and disorganized regeneration resulting in poor cellular nutrition and hypoxia ending in decreased liver function. -13^th^ leading cause of death in Canada, twice as common in men (becoming more equal). -**Causes of cirrhosis**: -chronic ETOH use (produce a wide spectrum of hepatic lesions called steatosis) **-Steatosis**: deposits of fat into liver cells. Steatosis can progress to steatohepatitis. This can lead to the development of fibrosis where there are excessive deposits of extracellular matrix proteins which cause bumps. This causes liver scarring and vascular alterations, meaning decreased blood flow=liver failure. -**NAFLD** **(Nonalcoholic fatty liver disease),** usually caused by obesity, a spectrum of diseases characterized by hepatic steatosis and can progress to cirrhosis. This is likely an important cause of cryptogenic cirrhosis (can't figure out what is going on with the cirrhosis). Management of NAFLD is reducing risk factors like controlling diabetes, loosing weight, heart healthy diet. -2 stages of NAFLD= NAFL= see the fatty deposits with no symptoms, and NASH (nonalcoholic steatohepatitis)-more severe- lobular inflammation and cell death that can lead to fibrosis and cirrhosis. -nutrition related causes: malnutrition, inadequate intake of essential nutrients (chronic malnutrition can impair the livers' ability to regenerate and repair itself contributing to cirrhosis), -environmental causes (exposure to chemicals, pollutants), -genetic predisposition: hemochromatosis (increased absorption of iron) or Wilsons disease (disorder of copper metabolism causing copper to accumulate in the liver), -biliary causes (buildup of bile in the liver): primary sclerosing cholangitis (autoimmune disease associated with Crohn's or colitis, inflammation, fibrosis, and strictures in the medium and large bile ducts, making them hard and narrow resulting in liver damage), primary biliary cholangitis (inflammation and destruction of small bile ducts in the liver leading to fibrosis and cirrhosis). -cardiac cirrhosis: cirrhosis related to right sided heart failure. Blood is backing up causing increased portal hypertension resulting in cirrhosis. **Two clinical stages of cirrhosis:** **Compensated:** Generally asymptomatic or have vague symptoms which can include abdominal pain, fatigue, slight weight loss, enlargement of liver or spleen. The lack of symptoms is because the liver is still functioning. If caught early enough may be able to prevent advancing but usually doesn't get diagnosed. =survival time greater than 12 years. **Decompensated:** Early symptoms are abrupt and include anorexia, dyspepsia, nausea and vomiting, weakness, muscle loss, and diarrhea or constipation. These symptoms are due to the livers altered metabolism of carbohydrates, fats, and proteins. (advanced). At least one complication including ascites, jaundice, variceal hemorrhage, or hepatic encephalopathy. Late symptoms are a result of portal hypertension and liver failure. Survival time of 2 years. **Advanced Cirrhosis:** jaundice, usually seen in sclera, palms of hands/soles of feet, this is as the liver is unable to excrete conjugated bilirubin, urine is dark brown and foamy when shaken, stool is grey or tan. -peripheral edema (low albumin), -ascites (excess fluid related to low albumin and increased pressure in portal vein (portal hypertension) =excess fluid, lymphatic system can't deal)), -hematological disorders: Thrombocytopenia, leukopenia, anemia, and clotting problems. This is due to back up of blood from portal vein to spleen causing splenomegaly. Overactive spleen causes an increased removal of RBC especially platelets from circulation. Anemia is due to inadequate RBC production and survival. Coagulation issues are due to the livers inability to produce prothrombin. -peripheral neuropathies are due to dietary deficiency of thiamine, folic acid, and B12. -can see palmar erythema, petechiae, spider hemangiomas (to nose and cheeks). This is due to an increase in circulating estrogen because of the liver being unable to metabolize steroid hormones. -endocrine disorders due to decreased metabolization of hormones (gynecomastia, loss of axillary and pubic hair in men due to circulating estrogen, testicular atrophy, impotence, loss of libido), (in women: amenorrhea in younger women and vaginal bleeding in older women). **Management of Cirrhosis:** (can't fix damage but can decrease progression), Goal is to slow the progression of cirrhosis: rest, avoidance of ETOH, aspirin, acetaminophen, NSAIDs, Management of ascites, prevention and management of esophageal variceal bleeding, management of encephalopathy. **Complications:** Two main complications: less functioning liver and high blood pressure in the liver (portal hypertension) **-Portal hypertension**: structural changes (fibrosis) result in portal and hepatic veins being compressed and damaged resulting in obstruction of blood flow through the portal system causing portal HTN. -increased resistance to blood flow through the liver (also have blood backed up behind the liver), -collateral circulation develops in attempt to reduce high portal pressure and reduce the increased plasma volume and lymph flow. (try to get blood back to the heart) -can lead to esophageal and gastric varices (vessels get larger at top of stomach and esophagus due to increased pressure. Esophagus can't handle the pressure, so vessels blow causing esophageal varices), -umbilical vein decanalization (umbilicus pushes out) **-Esophageal and gastric varices:** vessels very fragile and used to low pressure (can easily burst), gastric varices located in upper portion of the stomach, bleeding esophageal varices most life-threatening complication of cirrhosis. -portal HTN and blood backing up is a direct cause of varices. Must be careful when providing care to prevent bursting. Ulceration and irritation can occur due to alcohol ingestion, swallowing poorly chewed food or coarse food like toast, acid reflux, increased intraabdominal pressure caused by nausea and vomiting, straining with BM, cough, sneeze. Need to treat respiratory infections early. No lifting heavy objects. **Management of esophageal varices:** Goal is to avoid bleeding/hemorrhage: -avoid ETOH, aspirin, acetaminophen, -treat respiratory infections promptly (avoid coughing), -if bleeding occurs stabilize, manage airway, and provide IV therapy. -Drug therapy may include Octreotide (acute bleed, reduce blood flow in GI tract, decrease gastric acid secretion, inhibits hormones that stimulate digestive enzymes), -vasopressin (acute bleed cause direct vasoconstriction of splenic arterioles and precapillary sphincters. Decrease blood flow to area, decrease risk of rupture), -beta blockers (nonselective, manage and prevent varices, noncardiac specific beta blockers (carvedilol, nadolol, propranolol), watch for hypotension. Decreased pulse, decreased blood to liver through adrenergic effects cause vasoconstriction in splanchnic circulation, decreased blood flow to liver). -Endoscopic sclerotherapy, -endoscopic ligation, -TIPS (trans jugular intrahepatic portosystemic shunt)- divert blood flow around the liver and back to the heart preventing blood backing up decreasing varices. **Measures for acute bleed:** crystalloids (NS or ringers bolus), blood products (PRBC), vitamin K (help with clotting), PPI (decreased acid in gastric tract), broad spectrum antibiotics (decreased risk of peritonitis that's associated with varices), give O2, (decreased BP, decreased consciousness). Balloon tamponade: sengstaken-blakemore (tube down esophagus with balloon to stop bleeding). Ensure intubated to prevent aspiration. **-Peripheral edema and ascites:** decreased colloidal osmotic pressure (related to impaired synthesis of albumin by the liver) (albumin doesn't pull fluid back into vessels), portal hypertension pushes fluids out of vessels, Na+ retention, ankles, and sacral region edematous. Large abdomen, stretch marks, decreased ability to take deep breath. -with portal HTN protein shifts from blood vessels into lymph space and lymph system is unable to carry all the excess proteins and fluid. This leaks through liver capsule and into peritoneal space. **Management of Ascites: -**Na+ restriction (sodium retains fluid so limit of 2g per day) Only restrict fluid with severe ascites. Measure ins/outs and abdominal girth. -diuretics (spironolactone (used more than furosemide, usually 100mg) (spironolactone blocks aldosterone release which results in less sodium reabsorption), furosemide 40mg (doesn't get absorbed as well because bile salts block absorption)) Have to be careful with diuretics and cirrhosis as they usually have lower blood pressure due to the fluid leaving the vessels) -paracentesis- watch out for rapid fluid shift as will bottom out BP. Give albumin to draw fluid into the vessel and increase BP.  **-Hepatic encephalopathy:** terminal complication of liver disease, disorder of protein metabolism (liver unable to convert ammonia to urea or blood shunted away from the liver (collateral circulation so not filtered by liver), ammonia crosses the blood brain barrier), changes in neurological and mental responsiveness. **Management of hepatic encephalopathy** (buildup of ammonia)**:** Goal is to decrease ammonia formation: lactulose (binds ammonia to excrete in stool, want 2-3 bm per day), antibiotics such as rifaximin (reduces ammonia producing enteric bacteria), treatment for precipitating factors. **Asterixis:** flapping tremors involving arms and hands. (unable to sign name due to tremor, stretch arms out and they flap) **Fetor Hepaticus:** musty, sweet-smelling odor on breath, accumulation of digestive products that liver is unable to breakdown. (urine dark due to inability to break down bilirubin). **Hepatorenal syndrome:** (portal HTN causes decreased blood flow). No structural abnormality of the kidney, splanchnic and systemic vasodilation and decreased arterial blood volume (decreased blood flow to liver), renal vasoconstriction, renal failure which leads to azotemia (increased nitrogenous waste in blood), oliguria, intractable ascites (renal dysfunction with liver failure so increased creatinine, decreased EGFR, and decreased urine output. This is related to the altered blood flow and increased pressure to liver altering blood flow to kidneys). -this is diagnosed with clinical criteria of cirrhosis, ascites, and impaired renal function (increased creatinine, decreased urine). Treatment is challenging and goal is to address underlying liver issue. Liver transplant can potentially reverse kidney and liver dysfunction. May need vasoconstrictive drugs and albumin transfusion to temporarily improve renal function. **Nutritional support:** diet for patient without complications (want to slow progression): high in calories (3000kcal/day), increase carbohydrate (can't access glucose stores, want high carb low protein), moderate to low fat, protein restriction may be justified in flare of symptoms, protein supplements if protein-calorie malnutrition, low-sodium diet for client with ascites and edema. **Shock --** characterized by decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and the demand for oxygen and nutrients. Mortality for non-traumatic shock is 20-30%, for septic shock is 50%. **Types of shock:** **1)Hypovolemic** **shock:** decreased circulating blood volume (blood loss: GI bleed, trauma, injury). develops from internal shifts (vascular to interstitial spaces, ex ascites) or external fluid losses (large amount vomiting, diarrhea, or both). Fluid losses accompanied by inadequate rehydration can lead to hypovolemic shock. (very important to do input/output). If we don't keep track of losses and replace then the shock may get more advanced before we notice it. -hypovolemic shock occurs when intravascular fluid volume is lost, and the remaining volume is inadequate to fill the vascular space. Absolute is when fluid is lost through bleeding or diarrhea etc., relative is through third spacing. -with children they have very low blood volume so must be very dehydrated before we see a drop in BP. (drop in bp is a late sign in kids but will see other signs like with adults like no tears, and altered behavior, altered LOC). -hypovolemic shock results in a decrease in intravascular volume resulting in decreased venous return, decreased preload, decreased stroke volume, and decreased CO. -SNS mediated response to compensate results in increased HR, increased CO, and increased resp rate and depth. **Categories of Hypovolemic Shock:** shock is progressive, want to ensure we catch it early. **-Mild:** under 20% of blood volume lost. Vasoconstriction begins (may see increase in BP). Body activates RAAS which tries to replace some of the lost fluid. -**Moderate:** 20-40% of fluid loss. Decreased perfusion to organs such as kidneys, spleen, and pancreas (may result in injury to spleen or pancreas (pancreatitis)). Body shunting fluid away from nonessential organs in attempt to get blood to lungs, brain, liver, heart. Can end up with prerenal acute kidney injury (tubular necrosis due to kidneys not getting enough O2, meaning kidneys can't activate RAAS). -**Severe:** over 40% fluid loss. Decreased perfusion to heart and brain. Loss of 40% results in irreversible tissue destruction. -**Early:** Altered LOC (agitation or restlessness) (this is important to watch for with kids), mild tachycardia and vasoconstriction (RAAS trying to increase blood volume, will have orthostatic HTN), orthostatic hypotension (body can maintain homeostasis when lying but dizzy when standing). -**Late:** marked tachycardia (140-150), hypotension (80/?), decreased level of consciousness (coma) **-**positioning: position patient with feet elevated and head maximum 30 degrees. On strict bedrest. -**Treatment of hypovolemic shock:** -oxygenation- can't trust sat monitor because testes amount of O2 on Hgb not amount of blood. Provide supplemental oxygen. -circulation- Aggressive with fluids IV NS or RL (isotonic fluid). Blood products (PRBC-rapid infuser) -Medication- no specific medications: may give vasopressors. -supportive therapies- warmed IV fluids (don't want body to have to work too hard to warm up fluids. Correct underlying cause- (bleeding, vomiting). -ensure with comorbidities that they can tolerate the amount of fluid at the rate you are giving. Keep a close eye on vitals, strict ins/outs, foley. Don't want to give meds that will make them drowsy because you won't know if drowsy from meds or shock. **2) Cardiogenic shock:** impaired tissue perfusion due to pump failure (for some reason heart can't pump effectively). Occurs when functioning myocardial muscle mass decreased by more than 40%. Lower cardiac output leads to impaired perfusion of the coronary arteries. Symptoms include hypotension, dyspnea, weakness, fatigue, respiratory crackles, and cyanosis. -cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in compromised cardiac output. **-Causes of cardiogenic shock:** MI, cardiac arrest, dysrhythmias, electrolyte imbalance. (Heart not getting oxygen rick blood to the tissues). -symptoms are like heart failure: tachycardia, hypotension, narrowed pulse pressure, pulmonary congestion, peripheral hypoperfusion, anxiety, confusion, agitation. -**Treatment of cardiogenic shock:** -Oxygenation: Supplemental O2, intubation and mechanical ventilation. -Circulation: Careful with fluids, blood flow restored with thrombolytics (break up clot), angioplasty (open vessels). -medications: Nitrates (vasodilation, reduce preload and afterload), inotropes (dobutamine (helps heart contract more effectively), diuretics (don't want heart to pump more fluid than it needs to), betablockers (help with rhythm and help with contractions of the heart). -supportive therapies: correction of dysrhythmias (fixing the cause of the cardiac problem). obstructive, distributive \*Causes of decreased cardiac output is different in cardiogenic vs obstructive. **3) Obstructive shock:** happens when there is a physical obstruction of blood flow resulting in a decrease in cardiac output. -cardiac tamponade (heart can't fully pump out blood to body, same with tension pneumothorax) -tension pneumothorax -pulmonary embolism -treatment is much the same as cardiogenic, need to treat underlying condition to help increase cardiac output. **4) Distributive shock:** caused by maldistribution of blood flow. **-**three types: anaphylactic, septic, neurogenic. **Sepsis**- (dysregulated immune response and inflammatory response). What happens in sepsis and septic shock: infection leads to normal immune response (warm and pink, BP can initially increase then drop). -2/3 of sepsis and septic shock are caused by gram negative bacteria but can also be cause by gram positive fungal or viral bacteria. -septic shock develops when hypotension from sepsis cannot be reversed with fluid resuscitation and tissue perfusion abnormalities are present. -dysregulated immune response: vasodilation and increased permeability, hypotension, microvascular dysfunction, coagulation abnormalities -when body detects infection the immune system initiates and inflammatory response. The immune cells release cytokines and other signaling molecules to combat the invading pathogens. This is normal. Then we get a dysregulated immune response (overactive) leading to an overwhelming release of inflammatory mediators including pro inflammatory cytokines like tumor necrosis factor and interleukin. This uncontrolled inflammation can damage tissue and organs. Then because of these mediators we get vasodilation and increased permeability. The excessive release of the inflammatory mediators causes blood vessels to dilate and become more permeable, so fluid is going to leak out of our blood vessels. This leads to loss of fluid from the blood stream into the surrounding tissues reducing the effective blood volume causing hypotension. vasodilation and loss of blood volume cause significant reduction of BP leading to inadequate blood flow to vital organs causing organ dysfunction. This can cause microcirculation dysfunction where the smallest blood vessels get impaired tissue oxygenation contributing to organ failure. Can also get coagulation abnormalities and can lead to DIC (disseminated intravascular coagulation). -Sepsis can be caused by lungs, skin, urinary tract, abdominal cavity. People we worry about are people getting chemo because of nadir (10-21 days after a round of chemo). **1^st^ phase (warm)** **2nd phase (cold)** ----------------------------------------------------------------------------------------------------------------------- ----------------------------------------------------------- Warm or hemodynamic phase (massive vasodilation, reduced peripheral vascular resistance, skin is warm, pink, and dry) Hypodynamic phase Massive vasodilation reduces peripheral vascular resistance Shock progresses, hypovolemia Skin is warm, pink, and dry Decrease cardiac output-vasoconstriction to compensate Skin is cool and clammy (decreased cardiac output and BP) -**Treatment of septic shock** **-**Oxygenation: supplemental oxygenation, intubation, and ventilation. -Circulation: aggressive fluid resuscitation (Isotonic IV solution). -Medications: Antibiotics (broad spectrum), vasopressors (dopamine), inotropes (dobutamine), anticoagulants (risk of clotting so use low molecular weight heparin, ensure you check platelets) -Supportive therapies: cultures (ensure blood cultures before abx), temperature monitoring, stress ulcer prevention (low blood volume going to GI tract makes them more at risk for ulcers. -HIIT: Platelets get halved, but platelets that are left can become 'super' resulting in clotting risk. -DIC: damage to microcirculation from inflammation so body sends out fibrin to clot off damage. This can block off blood flow to limbs. This uses up all fibrin resulting in bleeding. **Anaphylaxis:** (anaphylaxis reaction affecting at least 2 body systems) -reaction causes massive vasodilation, release of vasoactive mediators, and increased capillary permeability. -**Signs and symptoms:** -pruritis, urticaria, rash, periorbital edema, angioedema (swelling under tissues, look puffy) -Respiratory: hoarseness, coughing, dyspnea, wheezing, stridor, decreased O2 sats. -Feelings of doom, headache, dizziness, anxiety, disorientation, LOC -**What happens in anaphylactic shock**: (Allergen binds to Ige antibodies on mast cells and basophils which are a type of white blood cell. Binding triggers the release of chemical mediators such as histamine, leukotrienes, and prostaglandins from mast cells and basophils this causes vasodilation. 1)vasodilation (histamine and other mediators cause blood vessels to dilate leading to sudden drop in BP) 2)increased capillary permeability (increased capillary permeability-blood vessel walls become more permeable, allowing fluid to leak out of the blood vessels into the surrounding tissues causing swelling and hives). 3)smooth muscle constriction (smooth muscle contraction causing narrowing of the airways (bronchoconstriction) which can lead to difficulty in breathing). 4)increased mucous production (airways produce more mucus contributing to airway obstruction) 5)systemic effects (can affect multiple organ systems leading to GI distress (nausea, vomiting, and diarrhea), cardiovascular collapse and neurological symptoms like dizziness and confusion. -this combination of events leads to inadequate blood flow to vital organs which is life threatening if not promptly treated. **Treatment of anaphylactic shock:** -oxygenation: patent airway, supplemental oxygen, intubation/ventilation. -circulation: aggressive with NS or RL (fluid resuscitation) -Medications: epinephrine (first line, outer thigh, rapid absorption into bloodstream so can reach systemic circulation quickly. Also, outer thigh has fewer major arteries and nerves compared to other areas), antihistamine (given more for cutaneous symptoms, does nothing for airway), bronchodilators (for bronchoconstriction), corticosteroids (if hypotension persists) (helps with airway swelling). -epi dose 0.1mg/kg max dose of 0.5ml so if 50kg will be getting full dose. Epi needs to be given IM not SC as if given SC can cause tissue damage. Might need to be put on an epi drip if not responding to 4-5 doses IM. -supportive therapies: prevent by avoidance, premedicate if allergen is required (antihistamine or steroids). -biphasic reaction: recurrence of anaphylaxis after appropriate treatment. **Neurogenic shock** (potentially life-threatening condition that results from a disruption of the autonomic nervous systems sympathetic outflow leading to a loss of sympathetic tone. Can be due to various things like spinal cord injuries, brain injuries or certain medical conditions). -neurogenic shock can occur within 30 min of a spinal cord injury at T5 or above and lasts up to 6 weeks. The injury results in a massive vasodilation without compensation that is caused by the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the vessels, tissue hypoperfusion and impairment of cellular metabolism. -spinal shock is a transient condition that is present after an acute spinal cord injury and symptoms are absence of all voluntary and reflex neurological activity below the level of the injury. -failure of the sympathetic nervous system: regional anesthetics, spinal cord injuries, sympathetic blocking agents, emotional distress/pain. **Low BP and Low pulse** -disruption of sympathetic nervous system activity. Autonomic nervous system is responsible for regulating involuntary body functions including heart rate, blood vessel constriction and organ function. The sympathetic nervous system plays a crucial role in maintaining blood pressure and heart rate. So with neurogenic shock there is a sudden and severe disruption of the sympathetic nervous system activity which leads to vasodilation so the primary effect of loss of sympathetic tone is widespread vasodilation of blood vessels. (causing blood vessels to relax and expand resulting in decreased systemic vascular resistance). -can also get bradycardia which is related to loss of sympathetic tone because there is often a compensatory increase in the parasympathetic activity resulting in bradycardia as parasympathetic opposes the sympathetic systems action of the heart. **Treatment of neurogenic shock** -oxygenation: airway patency, supplemental O2, intubation and ventilation (if sympathetic system not working) -circulation: fluid administration with caution- need to be careful as with the loss of the sympathetic tone the body can't handle massive amounts of fluid. -Medication: Vasopressors (phenylephrine, norepinephrine (works to try and get vasopressin on body vessels)), Atropine (for bradycardia). -Supportive therapies: minimize trauma with stabilization (stabilize spine), monitor temperature (autonomic nervous system is responsible for temperature regulation). **Stages of shock** -compensated shock symptoms: increased heart rate, increased resp rate, constriction of peripheral circulation, pale cool skin. -decompensated shock starts with low blood volume, lack of perfusion, symptoms are falling BP. **1)Initial: -**decrease in oxygenation (buildup of lactic acid) -acidosis (lactic acidosis- tissues not getting O2 they need-causing tissue death = metabolic acidosis (look at lactate with shock)), -no signs of hypoperfusion yet (not clinically obvious they are in shock, more at the cellular level. See aerobic metabolism become anaerobic leading to lactic acidosis). **2)Compensatory stage:** body activates compensatory mechanisms to overcome the consequences of anaerobic metabolism and maintain homeostasis. -sympathetic nervous system reacts to the low blood pressure and decreased cardiac output causing vasoconstriction and release of epinephrine and norepinephrine. So, in compensatory stage might see a rise in BP due to vasoconstriction. -increase heart rate (heart trying to pump as much oxygen around the body as it can), **Parameter** **Clinical changes** ------------------- --------------------------------------------------------- Blood pressure Adequate to perfuse vital organs-widened pulse pressure Heart rate Increased Skin Warm and flushed Peripheral pulses Rapid, weak, thready Urine output Decreased, under 30cc/hr LOC Follows commands, restless, confused but rousable respirations Increased Pupils Dilated, PERL Bowel sounds Hypoactive, mild abdominal distension **3)Progressive stage:** loss of circulating blood flow, loss of fluid. Leaking out of blood vessels into the interstitial space. Autoregulatory mechanisms are starting to fail. Body is no longer able to maintain homeostasis by its normal mechanisms. -compensatory mechanisms fail- aggressive interventions are needed to prevent MODS -loss of autoregulation (very dangerous for patients) -increased capillary permeability -decreased venous return -decreased cardiac output -cardiac ischemia which leads to MODS, Multi organ system failure. **Parameter** **Clinical changes** ------------------- ----------------------------------------------------------------------------------- Blood pressure Inadequate to perfuse vital organs, under 80-90 systolic, narrowed pulse pressure Heart rate Over 150bpm, irregular Skin Cyanotic, mottled, cold Peripheral pulses Very weak, thready, absent Urine output Decreased (under 20ml/hr) LOC Painful stimuli or unresponsive Respirations Increased, change in depth Pupils Dilated, sluggish, fixed Bowel sounds Absent (GI tract not getting blood flow it needs) **Changes in organs:** (from organs not getting enough O2) **Brain:** decrease cerebral blood flow, decrease LOC **Kidneys:** renal tubular necrosis, AKI **GI Tract:** ulcerations on gastric and intestinal surfaces, GI bleed, infection **Liver:** failure, buildup of wastes **Lungs:** decrease O2 and increase CO2. (body can't do the exchange it needs to), atelectasis, respiratory failure (ARDS) Adult respiratory distress syndrome. **4)Refractory stage** -decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism. Blood leaves vessels and pools, cerebral blood flow can not be maintained resulting in cerebral ischemia. \- people in refractory stage have profound hypotension and hypoxemia. Failure of the liver, lungs, and kidneys results in accumulation of waste products. Organs start to fail, and body's compensatory mechanisms are overwhelmed. Recovery is unlikely. -irreversible damage (refractory shock is variably defined as persistent hypotension with end organ dysfunction. Despite fluid resuscitation, high dose vasopressors, oxygenation and ventilation, no matter what is done leads to irreversible damage to the body. -Systemic inflammatory response syndrome (SIRS) to a variety of insults including infection, ischemia, infarction, and injury, characterized by 2 or more symptoms: fever, edema, hypotension, tachycardia, impaired oxygenation, and elevated WBC. SIRS progresses to MODS. -Multiple organ dysfunction syndrome (MODS)- medical condition characterized by the failure of two or more organ systems in the body. Typically occurs as a complication of severe illness or injuries and can be life threatening (ex-kidneys and liver failing-\> this can have a major impact on ability to survive). -Acute respiratory distress syndrome (ARDS): severe and life-threatening medical condition characterized by rapid onset of widespread inflammation in the lungs which leads to a significant decrease in the lungs ability to exchange oxygen and carbon dioxide. This results in severe respiratory failure and can be fatal if not treated promptly. It's marked by hypoxemia, bilateral infiltrates, and severe respiratory distress. Oxygen Sats drop very quickly, they are in a lot of distress and doesn't seem to matter how much oxygen you put on them the lungs are so full of fluid and inflamed that oxygen co2 transfer can't occur. So frequently require mechanical ventilation to get their O2 up. If that doesn't work, they might need ECMO, which is extracorporeal membrane oxygenation, to help get the blood oxygenated. Mechanical ventilation: positive pressure pushes fluid out of alveoli to allow space for air exchange to happen. **-**Disseminated intravascular coagulation (DIC)- characterized by abnormal blood clotting and bleeding throughout the body. Not a disease but a complex response to an underlying medical condition. In DIC the bodies normal blood clotting mechanism becomes overactive leading to the formation of tiny blood clots and blood vessels while simultaneously causing a decrease in the body's ability to form larger more stable blood clots. Instead, the body creates all these little clots and then runs out of the clotting fibers it needs like fibrin. Body's clotting factors are used up faster then can be replaced leading to both bleeding and clotting. Small clots block blood vessels and cause tissue damage, while depletion of clotting factors can result in uncontrolled bleeding. Need to watch for excessive bleeding (nose, gums, heavy menstrual bleeding, bruising, petechiae), Can also cause organ damage like kidney or liver dysfunction. Excessive bleeding and clotting will cause low BP. \- AKI -MI (heart not getting O2 it needs) -cerebral ischemia/infarction **Bloodwork expected in shock: elevated:** BUN, creatinine, CK, D-dimer, INR (high or normal), lactate, ALT, AST, GGT, sodium (early) potassium (late), glucose (early), Urine specific gravity. **Low:** pH, HCO3, potassium (early), platelet count (normal or low), glucose (late). **Trauma and Burns** **Trauma team activation:** Prehospital: EMS report: patient age and sex, mechanism and time of injury, vital signs, apparent injuries, activation criteria. **In hospital: Primary survey** (done in the order of what will kill the patient the fastest). Systemic evaluation reduces the risk of undiscovered injuries. Can assess ABCD in 10 seconds by asking name and what happened. Appropriate response by pt shows there is no major airway compromise. If can speak clearly then breathing is not severely compromised, able to generate enough air movement to permit speech and the LOC is not markedly decreased if they are alert enough to tell you what happened. **A-Airway with cervical spine stabilization:** **-**assume C-spine injury in all blunt trauma patients until proven otherwise. -assess for airway obstruction, facial trauma (edema). Do jaw thrust to open airway. -suction secretions, remove foreign objects (teeth, blood, vomit) -insert artificial airway if needed (ET tube). **B-Breathing:** airway patency alone does not ensure adequate ventilation and oxygenation so need to assess work of breathing, look for tracheal deviation or accessory muscle use. -assess work of breathing- assess resp rate and depth. -inspect chest wall- assess for injury of asymmetric expansion which can indicate a pneumothorax. -auscultate breath sounds- stridor, snoring resps, or absent breath sounds. -palpate the chest: deformity or crepitus (pneumothorax) -chest tube insertion (if pneumothorax) -pulse oximetry and supplemental O2 **C-Circulation:** once airway and breathing are stabilized preform an initial evaluation of circulatory status. -palpate central pulses- carotid and femoral pulses bilaterally. Rapid and thready pulse is a sign of hypovolemia. -assess skin characteristics- color and temp (cool and clammy?) -focused assessment with sonography for trauma (FAST) exam- ultrasound areas susceptible to hemorrhage including the pericardium, spaces within the peritoneal cavity, and pelvis. Use pelvic binder to stabilize the pelvis. -establish IV access x2, (Peripheral, CVAD, IO) **D-Disability:** rapid neurological evaluation -Glasgow coma scale (under 8 intubate as not alert enough to protect airway) -pupillary size and reaction -decrease in loc can be an indication of decreased cerebral perfusion or direct injury. -hypoglycemia, alcohol, narcotics, or drugs can alter LOC. **E- Exposure and environmental control** -undress to assess for injuries- need to cut off garments -prevent and treat hypothermia- can develop quickly if given rapid infusion of room temperature fluids. Want to ensure fluids are warmed. Cover with blankets. A close-up of a medical information Description automatically generated **Traumatic injuries can occur due to multiple factors. 4 categories:** -blunt trauma: fall, motor vehicle accident (MVA) (direction of impact (front? side?), did the car roll? seatbelt? injected from vehicle? motorcycle-helmet? -Penetrating trauma: stab wounds, gunshot wound (GSW) (the anatomical location of the injury is most important) -Burns: fire, inhalation (smoke inhalation injury is from breathing noxious chemicals or hot air which can cause damage to resp tract tissues), smoke, electrical, chemical -other: sport (traumatic head injuries), near drowning **Secondary survey:** doesn't start until primary survey is completed, resuscitation efforts are underway and improvement in patient status has been demonstrated. -if have additional members secondary survey can start while primary is being completed. **F-Full set of vitals** **G-Get resuscitation adjuncts:** labs, monitor ECG, nasogastric tube, oxygenation assessment, pain assessment, give pain medications. **H-History/head to toe assessment** **A**llergies, **M**edications (scripts etc), **P**ast medical history, **L**ast meal or PO intake, **E**vents related to injury (mechanism of injury), **T**etanus immunization (especially with burns or open wounds), **I-Inspect posterior surface:** ensure back and spine assessment is done. **Burns:** burn injuries are highly complex and result in substantial morbidity and mortality, so need a good grasp on how to treat. Inflammatory response during initial 24-48 hours, myocardial depression and increased capillary permeability result in rapid and extensive fluid shifts and the depletion of intravascular volume. **Structures and functions of the skin.** **Epidermis:** Thin, avascular, protects from external environment, made up of: Keratinocytes (fibrous protein that waterproofs the skin), melanocytes (give pigment to the skin and protect from UV), Langerhans cells (or dendritic cells). **Dermis:** highly vascular connective tissue made up of primary collagen which is responsible for the mechanical strength of the skin. Also contains elastin which is a stretchy protein that give the skin its flexibility. Contains: collagen, elastin, appendages (nerve endings, sebaceous and sweat glands, hair follicles, lymphatic and blood vessels. Dermis contains nerve endings which provide sensory info on the environment and sebaceous glands. Also lubricates the skins surface. Helps regulate body temperature though vasoconstriction or vasodilation of blood vessels and secretion of sweat glands. **Hypodermis:** makes up subcutaneous layer, acts as a shock absorber, heat insulator, and energy source. Also provides a point of attachment for the skin to deeper muscles. Contains subcutaneous tissue. **Burn mechanism:** Burns occur when there is injury to the tissues of the body cause heat, chemicals, electrical current, or radiation. **Thermal** (heat, flames, hot liquids, steam, hot objects, oil, grease). -most common -can occur at temp over 44 degrees -severity depends on contact temp and duration **Chemical -**treatment is continuous water irrigation. -Higher the pH of the agent, the greater the damage -Acidic agents-coagulation necrosis (eschar forms and limits further damage) -alkaline agents-liquefactive necrosis (causes more damage then acidic) (cause the tissue to turn to liquid that continues to cause damage until the alkali is neutralized or diluted -poison control should always be consulted in chemical burns. -acids, alkalis, petroleum-based agents. The duration of contact and nature of agent is important. **Electrical:** electrical burns cause direct damage to nerves and vessels causing tissue anoxia and death. -passive electricity through the body destroying tissues so volts and type of current, current pathways, tissue resistance (tissue density affects the amount of resistance, fat and bone have most resistance, nerves, and blood vessels the least), and duration of contact are all influencing extent of injury. Will usually have entrance and exit wounds so hard to assess full extent of injury as mostly internal and invisible. -determine voltage and type of current -most damage isn't visible (iceberg effect) -cardiac dysrhythmias- electrical injuries may interfere with the cardiac cycle and cause lethal dysrhythmias like asystole or ventricular fibrillation. Can also cause immediate asystole or ventricular fibrillation. Cardiac issues can occur without warning during first 24 hours. -fractures (C-spine), the technic contractions of muscles cause by electrical current can also be significant enough to produce bony fractures including the c-spine. -neurovascular tissue has less resistance than bone. Cardiac tissue can hold electricity so need to be on continuous cardiac monitor. Need to watch for compartment syndrome with deep muscle injury. -want urine output of 75-100ml/hr to prevent AKI in electrical burns. **Radiation** -most commonly sunburns or related to therapeutic radiation. - radiation burns will result from excessive exposure to radiation. Will usually see burns that are relatively superficial. **Depth and extent: zones of burn injury** -it may take up to 48-72 hours to determine the depth and extent of a burn injury. -can't fully see full depth of a burn immediately after the burn because there is a dynamic nature to the local tissue response of a burn. The localized response is characterized by 3 zones of injury. These zones evolve and change over the course of 48-72 hours following the injury. Therefore, classification of burn can change.  Jackson\'s Burn Wound Model -The zone of coagulation is the center of a burn injury, and it represents the site of direct injury and cellular death. There is no perfusion to the tissue in this zone and tissue loss is irreversible. No blood flow=tissue death. -the zone of stasis is the middle zone and tissue damage results from decreased perfusion so the tissue is potentially salvageable in this zone if perfusion can be restored with adequate resuscitation if perfusion is not quickly restored tissue loss in the zone will lead to the burn getting deeper and wider over time. So much of the treatments are targeted at salvaging the zone of stasis. Can salvage and becomes zone of hyperemia, or if not salvaged becomes zone of coagulation. Need to debride and graft. After 72 hours you can see what you salvaged and what you didn't. -zone of hyperemia is the outer zone where tissue perfusion and edema is actually increased as a result of inflammatory vasodilation and damage to this zone is usually reversible. **Depth of burn** 5 designations of burn depth  **-**depth of burn largely determines the healing potential and the need for surgical intervention -superficial: most sunburns, only the epidermal layer -superficial partial thickness: red weepy wounds, can be difficult to distinguish from superficial burns. The blistering shows the difference between the two, -partial thickness burns involve the entire epidermis and a portion of the dermis. -Deep partial thickness: extend to lower dermis, damage hair follicles, glandular tissue, and some nerve endings so often less painful. May need surgical intervention depending on size of injury. Often leave thick raised, hypertrophic scars if no surgical intervention. -full thickness: extend through all layers often into hypodermis. Leathery look due to elastin damage and may vary in color. Skin does not blanch with pressure and blisters don't develop. Usually, painless due to destruction of nerve endings and take a long time to heal with severe scarring and contractures which usually need surgery. -Deep tissue injury: deep tissue is potentially life or limb threatening, extend through the skin and underlying soft tissue to involve the muscle, fascia, and bone. Usually painless, the margins of all burns often have a lot of damaged nerve endings and can be painful. These injuries will not heal without surgical intervention and may require amputation. **Depth of burn:** -depth of tissue damage is dependent on 4 factors: -temperature of the offending agent, duration of contact with the offending agent, thickness of the epidermis and dermis, blood supply to the area. -burn injuries are often a combination of varying depths. (makes it difficult to assess) -need to be reassessed in the first 24-72 hours. (due to zones of injury) Diagram of a diagram showing the structure of the skin Description automatically generated **Location:** Location of the burn can predispose a patient to initial complications or complications in healing. **Face, neck, chest, thorax:** associated with respiratory distress (due to edema to airway), inhalation injury. **Hands, feet, joints, eyes:** altered range of motion, mobility (bones over joints will affect range of motion, especially if they develop hypertrophic scars or contractures during healing), body function (significantly alter mobility and ADL's) **Perineum:** high risk for infection (from urine or feces) **Circumferential burns:** circulatory compromise, compartment syndrome. (to thorax can impair chest wall expansion), circular burns around circumference of a body part and cause circulatory compromise and compartment syndrome due to the combination of decreased skin elasticity and increased edema. An intervention for this is escharotomy which is an incision into the necrotic tissue like a fasciotomy. This will release pressure as burn acts like a tourniquet. **Size:** -the extent of burns is estimated expressed as the % of total body surface area (TBSA), superficial (first degree) burns are not included in % TBSA. -3 methods widely accepted and used: rule of nines, lund-Browder chart, palmar method. -to estimate size of a body surface burned there are 3 methods. Rule of 9's: body divided into anatomical surface areas of 9% or multiples of 9%. This is not very accurate in pediatric. In pediatric preferred method is the lund browder chart. This is more accurate assessment of burn size calculations because it divides the body surfaces into smaller regions and provides a greater consideration for the age of the patient. -palmar method uses the palmar surface of the patient's palm and fingers to represent 1% of the total body surface area. This method is helpful when you are calculating patchy and noncontinuous burn areas. Like the depth of the burn injuries the extent or size of the burn is often revised after edema subsides or if wounds are debrided. Assessing the extent of burns is important because we know that burns involving 20% or more total body surface area in adults leads to systemic complications.  **Systemic complications** **Emergent phase:** (resuscitative): Care most about airway management, fluid therapy, and wound care. Want to resolve the immediate life-threatening problems resulting from the burn injury (lasts 72h) concerns are the onset of hypovolemic shock and formation of edema. Phase ends when fluid mobilization and diuresis begin. Occur in burns over 20% TBSA in adults. -**Fluid and electrolytes:** third spacing, insensible H2O loss, intravascular volume deficit, hypovolemic and distributive shock, hyponatremia, and hyperkalemia. -Fluid and electrolyte shifts occur due to increased capillary permeability and sensible losses. Intravascular deficits are most severe in the 1^st^ 24 hours post injury. -with hypovolemic shock capillary walls become more permeable and fluid goes into interstitial space. -the combined hypovolemic and distributive burn shock require adequate fluid replacement to avoid organ hyper perfusion and cell death. Hyponatremia and hyperkalemia also develop in the first 24 hours then when fluid is remobilized the opposite occurs. These fluid shifts can also lead to pulmonary edema and ARDS. -**Respiratory:** pulmonary edema, ARDS -**Cardiovascular:** decreased cardiac output, peripheral vasoconstriction. -Burn injuries also depress cardiac function within the first few hours of injury and lasts 24-48 hours. This is due to oxidative stress in the release of inflammatory mediators and cellular alterations. So, a marked decrease in cardiac output accompanied by increased peripheral vascular resistance will further decrease blood flow to tissue and organs and further contribute to the development of shock. Some of these system specific complications of burn shock within the GI system are a paralytic ileus. Within the first 24 to 48 hours, you can also see stress ulcers develop so starting enteric feeds ASAP helps keep the bowel tract patent. -**GI:** paralytic ileus, stress ulcer -**Urinary:** AKI, hypovolemia, muscle and RBC breakdown, urine output 30-50ml/hr -in the urinary system, acute kidney injury is common due to not only hypovolemia but also with full thickness burns or compartment syndrome. Myoglobin from injured muscle and Hgb from damaged RBC are released into circulation, this can lead to rhabdo and subsequent acute tubular necrosis. AKI can also occur because you have hemolysis of RBC due to direct injury or by circulating factors which releases potassium and Hgb which can build up in the kidneys. Monitor output with a foley and want 30-50mls per hour. -**Hypothermia:** other complication is hypothermia as the skin integrity is compromised and no longer able to fulfil its function of thermal regulation. Also getting large amounts of IV fluid which can also contribute to hypothermia. So increase room temperature and give warm fluids. Major burns: Part 1. Epidemiology, pathophysiology and initial management - BJA Education **Fluid Resuscitation:** **Parkland formula:** 4ml of ringer's lactate per kilogram of body weight per percentage or TBSA burned= total fluid requirement for first 24 hours after burn. 50% of total in first 8 hours, 25% of total in second 8 hours, 25% of total in third 8 hours.  -most complications are due to fluid shifts so fluid resuscitation is a pillar of burn management. -because of increased capillary permeability only 25% of the RL infused will stay in IM space. -parkland formula 4mls of RL/Kg per % of total burn surface area= total fluid requirement for first 24 hours post burn. ½ of the fluid is give in first 8 hours. -first 24 hours is when fluid resuscitation is most important. -fluid resuscitation-look at how patient is responding. If tolerating can increase, if not then decrease. Know if giving enough fluid if have urine output of 30-50mls per hour. If myoglobin in urine want higher urine output. -in emergent phase harder to take fluid away then add more. -too much fluid=confusion (cerebral edema), crackles, puffy, electrolyte imbalance. -ensure to look every hour at urine output. -use fluid equation if over 20% burn as will have systemic effects. -insensible losses-skin holds fluid in so no skin=no holding fluid in. Fluid also goes in tissue (third spacing), can cause pulmonary edema, compartment syndrome, ++ edema. **Acute phase:** begins with mobilization of extracellular fluid and subsequent diuresis. This phase ends when burned area is completely covered by grafts or wounds are healed. This may take weeks or months. **Complications: Acute Phase** **-Local infection-\> sepsis:** private room, protective isolation, sterile linins, wound cleansing (warm NS, remove debris, necrotic tissue, slough), wound debridement (sharp debridement- remove necrotic tissue or eschar), topical antimicrobials (prevent bacteria from growing on skin) (flamazine, aquacel ag (prevent infection or if signs and symptoms of local infection), acticoat, polisporin (keeps wound bed moist which is essential for healing)), sterile dressing changes (do one dressing at a time to prevent heat loss and avoid cross contamination). **Primary goal is to prevent infection.** -**Contractures:** Contractures develop because of the shortening of scar tissue in the flexor tussues of a joint. Tendons and ligaments tend to shorten in the healing process. Positioning and elevating limbs, splinting, ROM exercises (can result from improper positioning). -**Pain:** opioids, IV route (PO may not work especially if GI tract not working. IM and SC are not absorbed in burns or edematous areas so use IV route (IM and SC are not absorbed adequately and meds pool in the tissue). Will need frequent doses. -medications are sequently metabolized because patients with significant burns have an increased metabolic rate. Up to 40-100x the norm due to increased catecholamines and automatic nervous system response meaning they have significantly increased caloric requirements so consult dietician. Also increase protein intake to help promote wound healing. Increased cortisol levels from burns cause insulin resistance and hyperglycemia. This hyper metabolic state can persist for years following a burn injury. **-**systemic abx are not used because decreased blood supply=decreased abx getting to the wound. -**Nutrition:** hypermetabolic, increased calories and protein. Start feeding tube early to prevent ileus and want to give increased protein to promote healing. Enteral feeds preserve gastro-intestinal function, increases intestinal blood flow, promotes optimal conditions for wound healing. Paralytic ileus can occur within a few hours after burn because of body's response to major trauma. -**psychological:** ++emotional needs. **Skin grafts:** if have active infection grafts are not going to stick. -deep partial-thickness and full thickness burns usually require grafting (unless burn area is small like less than 4cm). **-Autograft:** tissue from a donor site on the patient's body. Only permanent graft (other types of grafts will eventually get rejected). -**Donor site:** very painful. Covered with bulky dressing and topical agent. Don't remove for 24 hours. -grafting site can be fixed in place with staples or sutures or laid in place and covered with a dressing. -face cherry red= Co2 poisoning: apply high flow O2.