complex week 11

Emergent Treatment of Hyperkalemia from Crush Syndrome

Normal saline IV fluid bolus IV NaHCO3 50 to 100 meq Aerosolized albuterol (2.5 mg in 3 cc) Less effective or practical : -IV dextrose (25 grams) & insulin (5 units IV) -PO or PR kayexalate Note that IV calcium is controversial (as it may just worsen intramuscular hypercalcemia) Emergent hemodialysis may be needed Albuterol- bronchodilator, beta-adrenergic. put K+ back into cells

Signs and Symptoms of rhabdo

Only 50% of adult patients present with triad In most patients the signs and symptoms are subtle, its history indicates the cause 1. muscle weakness 2. myalgia 3. dark urine

Gastrointestinal Surgery whipple

Whipple Procedure - Pancreaticoduodenectomy -the pancreatic head, the duodenum, part of the jejunum, the common bile duct, the gallbladder, and part of the stomach are removed -The continuity of the GI tract is restored by anastomosing the remaining portion of the pancreas, the bile duct, and the stomach to the jejunum -usually for people with pancreatic cancer Standard and pylorus-preserving Whipple procedures. A, The standard Whipple procedure involves resection of the gastric antrum, head of pancreas, distal bile duct, and entire duodenum with reconstruction as shown. B, The pylorus-preserving Whipple procedure does not include resection of the distal stomach, pylorus, or proximal duodenum.] Head of pancreas is gone- portions of dueodenum is still there Infection- high risk Post op leakage/abscesses

Differential diagnosis ileus v. mechanical obstruction

general s/s: abdominal discomfort, distention, vomiting ileus- steady pain, gas throughout bowel (x-ray) mechanical obstruction- colicky pain, gas cutoff (x-ray or CT)

SBO diagonsis

history**, s/s*8, x-ray- less radiation, but not as effective unless something sticking out, CT/MRI, WBC- b/c of inflammation, possible leakage?, BMP- lose a lot of mg and k cardiac!

Post-op Ilues

look @ pic

Use of IV Bicarbonate for Crush Syndrome

Goal is to have alkaline urine (check with pH paper) Can bolus supplement the normal saline with 50 meq (1 amp) doses -Up to 300 meq per 24 hours may be needed Or add 3 amps (150 meq) to one liter D5W and infuse as first or second IV bolus

Comparison of Gastric, Duodenal and Stress (Physiologic Ulcers) Type of Pain Associated Symptoms Role of H. Pylori Mortality Complication

"Burning", "gaseous" | "Burning",, "cramp-like" | N/A Occasional nausea, vomiting and weight loss | Occasional nausea and vomiting | N/A 50-70% of cases | 90-95% of cases | N/A Higher than D.U. | Lower than G.U. | N/A Hemorrhage, less perforation, outlet obstruction and intractability | Hemorrhage, more perforation, outlet obstruction | N/A

Portosystemic Shunt Procedures-what is TIPS? post procedural care? for what kind of patients? Portal hypertension is confirmed by ____

-Patient with a history of chronic gastritis or peptic ulcer disease is at high-risk -Patient who has had one major bleeding episode is more likely to have another -Patient with cirrhosis or previous UGI bleed is also at high-risk TIPS is an angiographic interventional procedure for decreasing portal hypertension. TIPS is advocated for (1) patients with portal hypertension who are also experiencing active bleeding or have poor liver reserve (2) transplant recipients or as a bridge to liver transplantation if the candidate becomes hemodynamically unstable. (3) patients with other operative risks. (4) bleeding varices orrefractory bleeding varices The TIPS procedure is usually performed by a gastroenterologist, vascular surgeon, or interventional radiologist. Portal hypertension is confirmed by direct measurement of the pressure in the portal vein. Cannulation is achieved through the internal jugular vein, and an angiographic catheter is advanced into the middle or right hepatic vein. The midhepatic vein is then catheterized, and a new route is created connecting the portal and hepatic veins using a needle and guidewire with a dilating balloon. A polytetrafluoroethylene (PTFE)-coated stent is then placed in the liver parenchyma to maintain that connection. The increased resistance in the liver is bypassed. Postprocedural care includes: - observation for overt (cannulation site) or covert (intrahepatic site) bleeding -hepatic or portal vein laceration - inadvertent puncture of surrounding organs. -hepatic encephalopathy -liver failure -bacteremia -stent stenosis.

Liver Function Test (LFT) Aspartate Aminotransferase (AST) conventional units Increased Level decreased level

0-45U/L Female 0-55 Male Very high levels of ALT (more than 10 X normal) are usually due to acute hepatitis. In acute hepatitis, levels usually stay high for about 1-2 months but can take as long as 3-6 months to return to normal. Levels of ALT may also be markedly elevated (sometimes over 100 X normal) because of exposure to drugs or other substances that are toxic to the liver or in liver ischemia. Moderate increases in ALT include obstruction of bile ducts, cirrhosis, heart damage, alcohol abuse, and with tumors in the liver. Low levels are generally not concerning and are not monitored.

Liver Function Test (LFT) Alanine aminotransferase (ALT) conventional units Increased Level decreased level

0-50 U/L Female 0-70 Male Very high levels of ALT (more than 10 X normal) are usually due to acute hepatitis. In acute hepatitis, levels usually stay high for about 1-2 months but can take as long as 3-6 months to return to normal. Levels of ALT may also be markedly elevated (sometimes over 100 X normal) because of exposure to drugs or other substances that are toxic to the liver or in liver ischemia. Moderate increases in ALT include obstruction of bile ducts, cirrhosis, heart damage, alcohol abuse, and with tumors in the liver. Low levels are generally not concerning and are not monitored.

Liver Function Test (LFT) Total Bilirubin conventional units Increased Level decreased level Indirect (unconjugated) - 0.1-1.0 mg/dL Direct (conjugated) 0.1-0.3 mg/dL

0.2-1.3 mg/dL Increased total bilirubin that is mainly unconjugated (indirect) bilirubin may be a result of: • Hemolytic or pernicious anemia • Transfusion reaction • Cirrhosis If conjugated (direct) bilirubin is elevated more than unconjugated (indirect) bilirubin, there typically is a problem associated with decreased elimination of bilirubin by the liver cells. Some conditions that may cause this include: • Viral hepatitis • Drug reactions Alcoholic liver disease Low levels of bilirubin are generally not concerning and are not monitored.

Recommended IV Fluid Infusion Rates for Crush Syndrome

1 to 1.5 liters per hour for young adults 20 cc per kg per hour for children 10 cc per kg per hour for elderly Insert foley catheter as early as possible -Target urine output should be > 50 cc per hour for adults, and > 2 cc per kg per hour for children -Some references advocate 150 to 200 cc per hour target in early phase

Ligament of Treitz view pic of peptic ulcers

12 inches long Jejunum- iron is absorbed here. When you get bariatric surgery you may become anemic

Liver Function Test (LFT) albumin conventional units Increased Level decreased level

3.4-5.4 g/dL Dehydration Liver disease, chronic inflammation, shock Malnutrition, nephritic syndrome or nephrotic syndrome, Crohn's disease, celiac disease, burns, cancer, and hypothyroidism

Liver Function Test (LFT) Alkaline Phosphatase conventional units Increased Level decreased level

44-147 U/L Bone diseases, liver damage, hyperparathyroidism, biliary obstruction, rickets, Paget's disease, bone metastasis, Hodgkin's lymphoma, congestive heart failure, ulcerative colitis, and certain bacterial infections. Low levels of ALP may be seen temporarily after blood transfusions or heart bypass surgery.

Liver Function Test (LFT) Total Protein conventional units Increased Level decreased level

6.3-7.9 g/dL May be seen with chronic inflammation or infections such as viral hepatitis or HIV. It also may be associated with bone marrow disorders such as multiple myeloma. Liver disease, chronic inflammation, shock Malnutrition, nephritic syndrome or nephrotic syndrome, Crohn's disease, celiac disease, burns, cancer, and hypothyroidism Agammaglobulinemia

A patient is GI bleed is at risk for ____. Therefore assessment and interventions are geared towards ____ In pancreatitis the pancreatic enzymes get activated within the pancreas and cause the serious pathophysiologic changes explained in lecture. To differentiate between ileus and bowel obstruction the clinician would ask patient about the ____ Getting the patient out of bed is a nursing sensitive intervention in ____ ____ are needed to prevent recurrence of pancreatitis. Significant electrolyte imbalances are key features of pancreatitis, the nurse need to monitor the basic metabolic profile (BMP) ____ Peptic ulcer prophylaxis is most likely the reason why your patient is prescribed anti-ulcer/GERD meds if they don't have a GERD or PUD. Always correlate the meds with the history, if it is not on the list of co-morbidities - find out!

A patient is GI bleed is at risk for shock. Therefore assessment and interventions are geared towards shock. In pancreatitis the pancreatic enzymes get activated within the pancreas and cause the serious pathophysiologic changes explained in lecture. To differentiate between ileus and bowel obstruction the clinician would ask patient about the nature of the abdominal pain as there are distinct patterns. -obstruction, colicky pain and no gas Getting the patient out of bed is a nursing sensitive intervention in restoring bowel function after surgeries, not just bowel surgeries, but any surgery, especially those that involve general anesthesia. Lifestyle modifications are needed to prevent recurrence of pancreatitis. Significant electrolyte imbalances are key features of pancreatitis, the nurse need to monitor the basic metabolic profile (BMP) such as hyperNa, hypoK, and Ca (hypocalcemia is likely due to fatty acids combined with calcium to form insoluble salts in a process is known as saponification. Peptic ulcer prophylaxis is most likely the reason why your patient is prescribed anti-ulcer/GERD meds if they don't have a GERD or PUD. Always correlate the meds with the history, if it is not on the list of co-morbidities - find out!

Nursing Management - GI Bleed

Abdominal exam - Presence or absence of bowel sounds, tense, rigid abdomen may indicate perforation and peritonitis Laboratory - how often should we do CBC? Administering volume replacement Controlling the bleeding Gastric lavage Maintaining surveillance for complications Assess for shock Educating the patient and family - Religious preferences regarding blood or blood products If pt has cirrhosis lactated ringers is not good- could wind up with lactic acidosis

Collaborative Care of GI bleed drug therapy acid reducers and PPIs

Acidic environment can alter platelet function and clot stabilization Histamine2-receptor (H2R) blockers -Inhibits action of histamine at H2 receptors and decreases HCl acid secretion -Cimetidine (Tagamet), Ranitidine (Zantac) Proton pump inhibitors (PPIs) -Suppresses gastric secretion by inhibiting H+, K+, ATPase enzyme system -Inhibits gastric acid pump -Pantoprazole (Protonix), Esomeprazole (Nexium) Overuse of PPI- can have higher risk for pneumonia, cdiff, or hip fractures

Laboratory Findings rhabdo renal failure

Acute Renal Failure Develops in 40% of patients. Measure BUN and creatinine levels Normal BUN is 10-20mg/dL Normal Creatinine is 0.5-1.1mg/dL In one study based on 97 adults with rhabdomyolysis, no patient with initial creatinine <1.7 developed acute renal failure. AST/ALT/LDH: marker for more severe muscle damage in exertional rhabdo; and for liver injury when exertional and heat related Chem 7, Phos, Calcium, ABG Uric acid: sensitive but not specific; normal is somewhat reassuring CBC PT/PTT/INR (r/o DIC) FDP (r/o DIC) Serum myoglobin

Acute Pancreatitis- description, etiology

Acute inflammatory process of the pancreas, varies from mild edema to severe necrosis African American rate three times higher than for whites Description -Ranson criteria Etiology -Gallstone migration and alcoholism (80% of cases) -Less common causes - surgical trauma, hypercalcemia, various toxins, ischemia, infections, and the use of certain medications. Doesn't have to be involved w/ alcohol Could be med side affects- EX: propofol

Emergency Assessment and Management Blood replacement

Blood replacement (cont'd) -Hb and Hct provide baseline for further treatment -Initial Hct may be normal and not reflect loss until 4 to 6 hours after fluid replacement ---Initially loss of plasma and RBC is equal Use of supplemental oxygen may help increase blood oxygen saturation Indwelling urinary catheter -Accurate urine volume assessment Central venous pressure line to monitor patient's fluid volume status Replace what is not there- if missing RBC give RBC, if platelets give platelets

Causes of Mass Casualties with Crush Syndrome

Building collapse Earthquakes Landslides Bombings Construction accidents Heavy snow on roof Mine or trench collapse

Renal Toxicity of Myoglobin

Bywaters' studies showed acid urine is required for myoglobin to cause renal injury At pH < 5.6, myoglobin dissociates into its 2 components : -Globin (shown nontoxic if infused) -Ferrihemate (probably the toxic component) Worse when you have acidosis or dehydration Ultimate - could lose kidney Must correct acidosis and dehydration to prevent this Put on a lot of fluids Correct pH

Cardiac Action Potential

Cardiac Action Potential has 5 phases These phases define transient depolarization followed by repolarization: i.e., Cardiac Contractions Caused by electrolyte transfer through cardiac muscle cell membrane

Acute Gastrointestinal Hemorrhage description---upper to lower etiology

Description Upper - pharynx to ligament of Treitz Lower - ligament of Treitz to rectum Etiology Peptic ulcer disease Stress-related mucosal disease (SRMD) Esophagogastric varices Esophagus, stomach, small intestine- anywhere with pepsin Ligament of treitz- where upper and lower GI meet. Holds duodenum in a curve. Possible causes: SRMD- ulcer from having illness or sepsis (no perfusion to stomach, ulcers).

Associated Conditions

Direct Muscle Injury Excessive Physical Exertion Muscle Ischemia (compartment syndrome, arterial/venous occlusions) Temperature Extremes Drugs, Toxins, Venoms Electrolyte & Serum Osmolality Abnormalities Chronic hypokalemia significant total body loss of K+ disrupts Na+ K+ pump cell membrane failure, leak of toxic intracellular contents from muscle cells Overuse of diuretics or cathartic drugs, hyperemesis gravidarum, some drugs (amphotericin B), hyperglycemic hyperosmolar nonketotic coma Infections -Pneumococcal & Staphylococcus aureus sepsis, salmonella & listeria infections, gas gangrene Statins can cause this Metformin can cause this, glucophage Temp extremes

Collaborative Care of GI bleed drug therapy Injection therapy during endoscopy hemostasis

During acute phase used to -↓ Bleeding -↓ HCl acid secretion -Neutralize HCl acid that is present Injection therapy during endoscopy hemostasis 1. Epinephrine -Produces tissue edema → pressure on bleeding source -Usually combined with other therapies IV vasopressin (Pitressin) -For variceal bleeding - watch out for angina, HTN -Causes vasoconstriction, ↑ smooth muscle activity of GI tract -Used in patients who do not respond to other therapies and poor surgical risk IV infusion of IV protonix can reduce acid secretions with antacids (unless theyre NPO) Vasopressin- ADH, give to cause vasoconstriction of splancnic area (mesenteric, gastic, pancreatic area) to stop bleeding. But causes it everywhere which can cause HTN and variceal bleeding Shock- norepinephrine, epinephrine, vasopressin

Pathophysiology of Edematous pancreatitis leads to _____

Edematous pancreatitis - Mild and self-limiting, autodigestion of pancreas Acute necrotizing pancreatitis Local tissue injury When there is injury there is inflammation Pancreas causes a lot of inflammation inside GI tract ---Leads to Capillary leak, fluid shunting, hypovolemia/shock

Collaborative Care of GI bleed Endoscopic hemostasis therapy (4 techniques)

Endoscopic hemostasis therapy Goal: To coagulate or thrombose bleeding artery -Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and polyps Several techniques are used including 1. Thermal (heat) probe--Coagulates tissue by directly applying heat to site 2. Electrocoagulation probe (multi- and bipolar) 3. Argon plasma coagulation (APC) --Noncontact coagulation delivers a monopolar current to tissue 4. Neodymium yttrium-aluminum-garnet (Nd-YAG) laser Pt who is bleeding- stop bleeding Typically done in mallory-weiss tear- near cardiac sphincter, first two inches above stomach near esophagus

Therapeutic Management of GI bleed (2)

Endoscopic injection therapy Endoscopic variceal ligation ^^^mallory-weiss, where a lot of varices happen in portal hypertension Esophageal varices- outpouching of wall of vein, took on more blood than normal b/c theres a problem with backup from liver. Liver is fibrotic so blood volume is shunted away into esophagus, belly, rectum (hemorrhoids)

Upper GI Bleeding Common Causes of UGI Bleeding 150,000 to 200,000 hospital admissions each year for UGI bleeding Mortality rate 6% to 10% for past 40 years Increased incidence of UGI bleeding in older adults, especially women, and use of NSAIDs Occult bleeding - stools Undetectable by appearance Detectable by guaiac test 80% to 85% of patients who have massive hemorrhage spontaneously stop bleeding

Esophageal origin - Chronic esophagitis, Mallory-Weiss tear, Esophageal varices Stomach and duodenal origin - Gastric cancer, Hemorrhagic gastritis, Peptic ulcer disease (PUD), Polyps, Stress-related mucosal disease (SRMD) Drug-induced origin - ASA, NSAIDS, steroids Systemic disease origin - Blood dyscrasias, Leukemia, Aplastic anemia, Renal failure, cirrhosis

Medical Management of pancreatitis

Fluid management if in shock- not LR! Nutritional support - High-carbohydrate, low-fat, high-protein diet, bland diet, fat-soluble vitamins. Systemic complications - Pleural effusion, Atelectasis, Pneumonia, Cardiovascular, Hypotension, Tetany (caused by hypocalcemia) Local complications - Pseudocyst, Abscess - Pancreatic abscess - A large fluid-containing cavity within pancreas. Results from extensive necrosis in the pancreas. Upper abdominal pain. Abdominal mass Initial management of the patient with severe acute pancreatitis includes ensuring adequate fluid and electrolyte replacement, providing nutritional support, and correcting metabolic alterations. Careful monitoring for systemic and local complications is critical. Because pancreatitis is often associated with massive fluid shifts, intravenous crystalloids and colloids are administered immediately to prevent hypovolemic shock and maintain hemodynamic stability. Electrolytes are monitored closely, and abnormalities are corrected. If hyperglycemia develops, exogenous insulin may be required. Randomized clinical trials have demonstrated that enteral feeding (gastric or jejunal) is safe and cost effective and that it is associated with fewer septic and metabolic complications than other methods. Early initiation of enteral feeding is preferred over total parenteral nutrition (TPN), although TPN is still used in select situations. The most serious complications are hypovolemic shock, acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and GI hemorrhage. Other possible pulmonary complications include pleural effusions, atelectasis, and pneumonia. [Review Box 30-8, Signs and Symptoms of Pancreatic Infection, with students.] Local complications include the development of infected pancreatic necrosis and pancreatic pseudocyst. The necrotic areas of the pancreas can lead to development of a widespread pancreatic infection (infected pancreatic necrosis), which significantly increases the risk of death. Pseudocyst Cavity surrounding outside of pancreas filled with necrotic products and liquid secretions Abdominal pain Palpable epigastric mass Nausea, vomiting, and anorexia Elevated serum amylase May resolve spontaneously within a few weeks or may perforate, causing peritonitis Treatment: Internal drainage procedure Pancreatic abscess (cont'd) High fever Leukocytosis Requires surgical drainage Nutrition- give a lot of carbs to build up energy. Liver stores glycogen. Low fat b/c triggers pancreatic enzymes. vitamin K lack leads to bleeding .vitamin A- eyes. Must give fat soluble vitamins to person who is NPO (DONT STIMULATE PANCREAS) give through enteral nutrition or TPN When pancreatitis is severe enough- could send to ARDS Pleural effusion from direct infiltration from inflammaed pancreas-could hypoventilate b/c it's painful to breathe

Comparison of Gastric, Duodenal and Stress (Physiologic Ulcers) Gender Peak Age Pain Pain location

Greater in women | Greater in men (increasing in post menopausal women | N/A 50-60 | 35-45 | N/A When stomach is empty, or with food ingestion. About 1-2 hours after meals | 2-5 hours after meals, mid-morning, mid-afternoon, middle of the night, periodic and episodic | N/A Left (high) epigastrium, back and upper-abdomen | Mid-epigastric region beneath xiphoid, back pain for ulcers on the posterior duodenum | N/A

Assessment and Diagnosis GI bleed Diagnostic procedures. hematemesis? hematochezia? melena? lab studies? H&H is low? kidney?

Hematemesis - bright red or brown, "coffee grounds"--- upper GI Hematochezia - bright red stools-- lower GI Melena - black, tarry, or dark red stools-- upper GI Laboratory studies - (CBC, LFTs, Coags, ABG, Type and Screen, UA) - It may take 24 to 72 hours for the redistribution of plasma from the extravascular space to the intravascular space to occur and cause the patient's H/H to decrease. Think of the kidney! Diagnostic procedures - EGD, fiberoptic endoscopy, colonoscopy, hemostasis Tx, endoscopic retrograde cholagiopacreatography (ERCP) Hemoglobin is low? Want to know where H&H is. Look @ liver to see if there is liver damage or connection to GI bleed. EX: if you are really jaundiced something is wrong with liver. EX: tylenol overdose would damage liver but you wouldn't know until you look at high PT Do serial CBCs to keep track of blood loss. H&H could be artificially high or low due to dehydration etc. trend is more important Loosing blood- prerenal failure? If blood goes down GI tract you digest blood, blood is made of protein, why your BUN is so high Burdening glomerulus from too much nitrogen/protein and prerenal failure- you may lose kidney ERCP- examine pancreatic ducts and bile ducts. Scope the ducts, can squirt dye, take pictures, take out gallstones (can also be a treatment for pancreatitis), place stent

Acute Pancreatitis Drug Therapy

IV morphine Nitroglycerin or papaverine Antispasmodics Carbonic anhydrase inhibitor Antacids Histamine (H2) receptor Nitro- vasodilator Have gastritis, peptic ulcer disease- give PPIs

Causes of Crush Syndrome

Immobility against firm surface for > one hour : Drug or alcohol intoxication Carbon monoxide poisoning Cerebrovascular accident Head trauma with coma Elderly with hip fracture Improper positioning of surgical patient Assault with beating Pneumatic Antishock Garment (PASG or MAST) Military- lots of this during training Places w/ lots of earthquakes/disasters Falls

Contribution of Inflammation in rhabdo

In addition, neutrophils enter the damaged muscle, producing an inflammatory reaction The swollen and inflamed muscle compresses structures in the fascia causing compartment syndrome The swelling compromises blood supply to the area Hydroxyl free radicals are produced causing nephrotoxicity by vasoconstriction through interaction with nitric oxide and endothelin receptors So swollen b/c sodium went into cell. There is tissue hypoxia No volume in intravascular space- BP drops and cause hypoxia Free radicals by tissue breakdown are nephrotoxic- causes intrarenal failure

When Should Fasciotomy be Done for Crush Injury?

In most reports of mass casualties from earthquakes, most of the fasciotomies were done more than 12 hours after the time of trauma -Reviews of these cases showed high infection rates with increased mortality and amputations, and poor long term function Israeli experience has shown better results with not routinely performing delayed fasciotomies So fasciotomy would be indicated if the victim can be extricated and receive definitive medical care within 6 hours of injury, but not later If initial compartment pressures are normal, and delayed compartment syndrome develops, fasciotomy may be needed

Small Bowel Obstruction (SBO) 2 types

Interruption to the flow of intraluminal contents Can be caused by extrinsic or intrinsic factors Two types of obstructions -Partial -Complete- nothing is getting through, so people vomit (things come up from up top). n/v

Pathophysiology of rhabdo---Na and K

Intracellular and extracellular balance is maintained by the cell membrane Damage to tissues which breaks cell membrane The sodium pump preserves essential intracellular and extracellular distribution of electrolytes. This pump is energy dependent, fueled by adenosine triphosphate (ATP). A steady supply of oxygen is needed to produce ATP. In falls tissue compression and vascular occlusion occur causing hypoxia to muscle cells. Without oxygen delivery and ATP production , pump dysfunction occurs. -Potassium (K+), Magnesium, and Phosphate are intracellular -Sodium (Na+), Calcium(Ca+), Chloride(Cl), Bicarbonate (HCO3) are chiefly extracellular -When a fall, crush injury or obstruction by confinement in a fixed position occur, the cell membrane breaks -Massive influx of sodium occurs -Followed by water -Causing increased swelling of muscle cells Massive influx of sodium- cell is swollen K+ exists and may cause cardiac problems- hyperkalemia Rearrange electrolytes from damage of cell membrane- sodium potassium pump damaged.

Pathophysiology of rhabdo-general

Large amounts of intravascular fluid leave circulation and are trapped in damaged muscle tissues This fluid shift produces intravascular hypovolemia The dramatic decrease in intravascular fluid volume leads to vasoconstriction and renal failure Compartment syndrome- swelling, ischemia Large fluid now in cell- cell is swollen and interrstitial leak. Causes shock Potassium leaks into the extracellular space causing cardiac toxic effects and dysrhythmias. Potassium leaks causing hyperkalemia Metabolic acidosis

Prognosis Related to Crush Syndrome Major risk factors for renal failure (3)

Major risk factors for renal failure : -2 or more limbs crushed -Insufficient early IV fluid -Delayed in presentation to hospital Children at lesser risk to need dialysis 50 % or more may have severe long term limb disability if fasciotomy done Need for long term physical therapy and counseling Need to have access to increased number of hemodialysis machines The Renal Disaster Relief Task Force of the International Society of Nephrology has been organized to bring multiple machines to a disaster region

Main Treatment for Crush Syndrome: IV Fluid Resuscitation

Normal saline (0.9 %) preferred -(lactated Ringers contains 4 meq / liter of potassium, & so may worsen hyperkalemia, & also has calcium) If started early, may prevent later development of renal failure Best if IV fluids can be started even prior to extrication Meausre urine pH--- want it to be 6.5-7. usually its 5 but you want it to be higher w/ dipstick READ RHABDO ARTICLE

Use of Mannitol for Crush Syndrome Other Advantages of Mannitol for Treating Crush Syndrome

May help eliminate myoglobin from the kidney & prevent renal failure May be useful to initiate diuresis in a patient who has adequate normal saline on board but whose urine output is still < 2 cc per kg per hour, or if adequate urine output is still not achieved 4 hours after treatment started Other Advantages of Mannitol for Treating Crush Syndrome: May scavenge free radicals in muscle thus limiting necrosis Positive inotropic effect on the heart *Most important *: may help decompress compartment syndrome by mobilizing fluid from damaged muscle (thereby preventing need for fasciotomy)

Pathophysiology of GI hemorrhage. severity?

Most serious loss of blood from UGI (sudden onset Insidious occult bleeding Severity depends of bleeding origin -Venous -Capillary -Arterial Pathophysiology -Hypovolemic Shock -Shock Response -Multiple Organ Dysfunction Syndrome Swelling, sequesters blood in third space- why BP drops. SIRS- decreases blood flow, coagulopathy, capillary leak in lungs can lead to ARDS -GI bleed can lead to ARDS Bleeding from arterial source is profuse, and the blood is bright red The bright red color indicates that the blood has not been in contact with the stomach's acid secretions "Coffee ground" vomitus reveals that the blood has been in the stomach for some time and has been changed by gastric secretions Melena: Slow bleeding from an upper GI source

Pathophysiology of rhabdo myoglobin

Myoglobin, the dark red protein that gives muscle cells their red-brown color, leaks out of the muscle cells and flows into the urine causing a noticeable reddish-brown urine Myoglobin can precipitate (particularly with hypovolemia and acidosis) and directly obstruct renal tubular flow Myoglobin is also directly toxic to the renal tubular cells

SBO s/s

N/V (feculent) distention, pain, obstipation, fever, tachycardia from fluid loss, hypotension from fluid loss, dehydration -Feculent- stool vomit. Abdominal distention- inflammation where there is obstruction

GI Intubation - GI Tubes

Nasogastric or orogastric suction tubes - Salem Sump tube (LIS or LCS) Long intestinal tubes Gastric Lavage Feeding tubes - small bore tubes - how do you know it's in the right place? Complications of NGT Nursing Considerations

Paralytic Ileus causes s/s treatment

Non-mechanical insult that disrupts peristalsis. Absence of lesions causing obs. Causes: sepsis, surgery (POI), intra-abdominal abscess, peritonitis, meds (opiates, anticholinergics), hypo K, hypo Ca/Mg, spinal sx, hypothyroid, general anesthesia Symptoms: N/V (feculent) distention, pain, obstipation, fever, tachycardia from fluid loss, hypotension from fluid loss, dehydration Treatment: early ambulation, non-opioid pain meds, pro-kenetic agents (Cisapride), stimulant laxative, early feeding, avoid surgery No consensus exists to differentiate ESBO from postoperative ileus Non-operative management improve both diseases. Reoperation in the presence of ileus prolongs hospitalization/complication Hurts if you have section of bowel that doesn't move. Move everything to a stop -hurts Treament for ileus- move to pick up peristalsis, treat cause (EX: if anesthesia let it wear off, if meds then take back opiates)

Compartment Syndrome in Crush Injury and when fasciotomy is indicated normal compartment pressure? Irreversible muscle damage occurs after ___ hours, & irreversible nerve damage may occur after ___ hours of ischemia

Normal muscle compartment pressure is < 15 mm Hg Pressure > 30 mm Hg produces muscle ischemia, so fasciotomy indicated if pressure is persistent above this Irreversible muscle damage occurs after 6 hours, & irreversible nerve damage may occur after 4 hours of ischemia Patients with higher diastolic pressure can tolerate higher tissue pressure without ischemia, so fasciotomy recommended when compartment pressure approaches 20 mm Hg below diastolic pressure However, if patient is hypotensive, they can have significant ischemia at lower compartment pressures

Nursing Management of pancreatitis

Pain Relief - IV morphine with antispasmodic agent Aggressive hydration Maintaining surveillance for complications Management of metabolic complications - Fingerstick Minimizing stimulation - Suppression of pancreatic enzymes, NPO, NG suction Monitor for signs of hypocalcemia - Tetany (jerking, irritability, twitching), Numbness around lips/fingers, Chvostek or Trousseau sign*** Observe for paralytic ileus, renal failure- BUN/Cr Lifestyle changes, Pancreatic enzyme replacement Monitor for hypoglycemia- stress of illness Nursing management of the patient with pancreatitis incorporates a variety of nursing diagnoses. Administration of around-the-clock analgesics to achieve pain relief is essential. Morphine, fentanyl, or hydromorphine are the commonly used narcotics for pain control. Relaxation techniques and the knee-chest position can also assist in pain control. The patient must be routinely monitored for signs of local or systemic complications. Organ failure is a major indicator of the severity of the disease. The patient must be monitored for signs and symptoms of pancreatic infection, which include increased abdominal pain and tenderness, fever, and increased white blood cell count. Early in the patient's hospital stay, the patient and family should be taught about acute pancreatitis and its causes and treatment. As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the recurrence of the precipitating disorder. Pancreatic enzymes- don't chew

Cardiac Action Potential phase 0-4

Phase 0 Rapid depolarization; influx Na+ Phase 1 Initial repolarization; end Na+ influx Phase 2 Plateau; influx Ca++; prolongs contraction Phase 3 Rapid repolarization; efflux K+ Phase 4 Resting membrane potential between heartbeats

Assessment and Diagnosis of pancreatitis physical lab diagnositcs

Physical examination - Abdominal pain is predominant symptom. Pain in the left upper quadrant, may be in the midepigastrium, radiates to the back, Sudden, Severe, deep, piercing, steady, Aggravated by eating, Not relieved by vomiting. Low-grade fever, Leukocytosis, Hypotension, Tachycardia, Jaundice , Abdominal tenderness. Steatorrhea Frothy urine/stool Laboratory studies - ↑ Serum amylase and ↑ lipase, BMP, hypocalcium, triglyceride, WBC, ↑ Serum bilirubin, ↑ Alkaline phosphatase Diagnostic procedures - Flat plate of abdomen, ultrasound, Endoscopic retrograde cholangiopancreatography (ERCP), Chest x-ray, CT of pancreas, Magnetic resonance cholangiopancreatography (MRCP) Strip + flip Severe LUQ pain Swelling infiltrates bile duct- jaundice occurs secondary-> Steatorrhea -> more diarrhea /bmp- look for prerenal failure/shock, hypocalcemia b/c pancreatic enzymes absorb calcium, no enzymes

Gastrointestinal Surgery Complications and medical management

Pulmonary complications Anastomotic leak Deep vein thrombosis (DVT) and pulmonary embolism (PE) Bleeding Postoperative nursing management Pulmonary management Pain management Psychososial

Treatment rhabdo

Rapid fluid infusion will restore intravascular volume and flush kidneys 1. IV Normal Saline rate of 500-1000ml/hr to maintain hourly urine output of 150-300ml/hr- to flush our myoglobin and prevent acidosis, correct dehydration and save kidney Telemetry/EKG/ABG 2. Alkalize the urine to a pH of 6.5-7.0 to prevent increased nephrotoxic effects by adding sodium bicarb to IV NS Place Foley catheter to monitor fluid output. 3. DIAMOX Acetazolamide (250 mg PO tid) may help excrete bicarbonate in the urine When kidneys do not respond, emergency hemodialysis is necessary to manage oliguria, metabolic acidosis and fluid overload Oxygen supplementation (even if patient isn't hypoxemic) Pain medications Tetanus immunization Furosemide may initiate diuresis but not favored since it makes the urine acidic Do you diurese or not? Furosemide may make pH of tubules acidic and cause kideny failure in context. Mannitol may be better

Definition of Rhabdomyolysis. results in ____

Rhabdomyolysis is the rapid breakdown of skeletal muscle due to injury to muscle tissue. Damaged skeletal muscles release products such as myoglobin into the blood stream leading to acute kidney failure. Clinical syndrome in which contents of injured muscles cells leak into circulation and results in electrolyte abnormalities, acidosis, clotting disorders, hypovolemia, ARF Previously known as 'crush injury syndrome' but now known also for other precipitating factors Pts feel muscle pain, urine is really dark black/grey Kidney failure from hemepharetine Traumatic and nontraumatic conditions lead to rhabdomyolysis. Intervention consists of early detection, volume replacement, and aggressive diuresis or hemodialysis.... Nurses are instrumental in both early detection and management of this life-threatening syndrome."

Collaborative Care of GI bleed drug therapy Somatostatin analog octreotide (Sandostatin) antacids Gastric Mucosal Agent

Somatostatin analog octreotide (Sandostatin) -Used with upper GI bleeding -Reduces splanchnic blood flow and acid secretion -Given in IV boluses up to 5 to 6 days after initiation of bleeding Gastric Mucosal Agent - Sucralfate (cytoprotective) - binds with HCL, creates paste-like substance, adheres to the surface of ulcer = shield it from pepsin, acid and bile Antacids -Neutralize HCl acid, maintain gastric pH above 5.5 -Elevated pH inhibits activation of pepsinogen ---Sodium bicarbonate (Alka-Seltzer), calcium carbonate (Tums) ---Magnesium hydroxide (Mag-Ox) -Calcium carbonate and Na bicarb can lead to systemic alkalosis Sandostatin- form of growth hormon. Used to reduce splanchnic perfusion

Medical/Surgical Management of GI bleed

Stabilization - Crystalloids, blood products, vasopressors Controlling the bleeding -Peptic ulcer disease - injection therapy/thermal or hemostatic clips -SRMD - vasopressin and intra-arterial embolization -Esophagogastric varices Transjugular Intrahepatic Portosystemic shunt (TIPS) Disadvantage- blood is not cleaned up by liver. Liver is sanitation department, ammonia is still there. When someone is on TIPS you worry about ammonia elevation- put them on lactulose

Comparison of Gastric, Duodenal and Stress (Physiologic Ulcers) Lesion Incidence/Risk Factors Location of Lesion Gastric Secretion

Superficial; smooth margins, round oval or cone shaped | Penetrating(deformity of duodenal bulb from healed recurrent ulcer) | Multiple superficial erosion Less common than duodenal ulcer, increased with smoking, drug and alcohol use | More common than gastric ulcer, increased with smoking, drug and alcohol use | Common in patients with respiratory failure, trauma, surgery, shock, extensive burns Any part, predominantly antrum, also in body and fundus | First 1-2 cm of the duodenum, mid-epigastric below xiphoid, back | fundus Normal/Decreased | Increased | N/A

Ranson Criteria for Severity of Acute Pancreatitis At Admission At 48 Hours

The Ranson score was developed for alcoholic AP and comprises five clinical criteria measured at admission and six clinical criteria measured at 48 hours. The criteria measured at admission reflect the local inflammatory effects of pancreatic enzymes; those measured at 48 hours represent the later systemic effects. Three or more Ranson criteria predict a severe course and increased mortality. If the patient has 0 to 2 factors present, the predicted mortality rate is 2%; with 3 to 4 factors, the rate is 15%; with 5 to 6 factors, the rate is 40%; and with 7 to 8 factors, the predicted mortality rate is 100%. At Admission: Age >55 yr WBC >16,000/mL LDH >350 IU/L AST >250 IU/L Glucose >200 mg/dL At 48 Hours: Hematocrit decrease >10% BUN increase >5 mg/dL Calcium <8 mg/dL Pao2 <60 mm Hg Base deficit >4 mg/dL Fluid sequestration >6 L

Laboratory Findings rhabdo-CK

The actual diagnosis of rhabdomyolysis is confirmed by lab tests. Total Creatine Kinase (CK) is the most reliable test for rhabdomyolysis. ---Normal CK levels are 45-260 U/L. ---CK high alone is wont hurt your kidney- myoglobin does the real damage Greater than 5 times normal is considered + ...maybe! With rhabdomyolysis CK levels are massively elevated 10,000 to 200,000 U/L (Craig, 2009)

Related Causes of Rhabdomyolysis

Viruses directly attack muscle cell membrane. The most common are Influenza A and B, Salmonella, herpes. Legionella directly invades and degenerates muscle fibers. Any microbe that causes sepsis may cause muscle damage and necrosis Alcohol abuse causes metabolic abnormality and immobilization leading to muscle compression and muscle ischemia Narcotic overdose causes altered sensorium and immobilization for long periods. Pressure necrosis develops Cocaine damages muscle tissue by vasoconstriction. Antipsychotics may cause neuroleptic malignant syndrome and muscle rigidity leading to rhabdomyolysis Statins cause muscle cells to break down Statin medications impair the production of proteins involved in muscle metabolism The higher the dose of statins the higher the risk of rhabdomyolysis

The kidney damage caused by myoglobin is worsened when ____. This is why the goal is to ____ Significant ____ is a diagnostic criterion in rhabdo as well as history and signs and symptoms such as ____ ____ levels require immediate pharmacologic interventions and ECG monitoring. The management of rhabdo requires ____ because of fluid sequestration. When the hemodynamic parameters indicate that the patient is ____, ____! With specific IV, of course. To goal of treatment is to ____, ____and avoid ____ Rhabdo is a reversible adverse effect of ____

The kidney damage caused by myoglobin is worsened when the kidney pH is low. This is why the goal is to alkalinize the urine. Significant CPK increase is a diagnostic criterion in rhabdo as well as history and signs and symptoms such as hyperkalemia etc. Critically high levels of potassium require immediate pharmacologic interventions and ECG monitoring. The management of rhabdo requires hemodynamic monitoring because of fluid sequestration. When the hemodynamic parameters indicate that the patient is dry, water them! With specific IV, of course. To goal of treatment is to get rid of the myoglobin, increase urine output and avoid compartment syndrome. Rhabdo is a reversible adverse effect of statin.

Pathophysiogy of rhabdo DIC

Thromboplastin and tissue plasminogen are released from injured muscle cells making patients susceptible to disseminated intravascular coagulation (DIC)

Small Bowel Obstruction (SBO) treatment

Treatment: gastrografin challenge, surgery, IV fluids, antibiotics, NPO, NGT, TPN/PPN -Fluid replacement!!!! NPO!!- don't want them to vomit more. Put in NG tube to suction intermittently- Antibiotcs prophylactically Gastrografin- contrast dye. Liquid that they drink, can track through x ray or CT. hyperosmolar- pulls fluid into GI tract as it moves along. Helpful b/c then you can hydrate the patient and possible cure constipation/hard stools. You want to see the contrast for the entire tract and you cant if theres a huge hard stool activating the movement of water into the small bowel lumen by osmosis and decreasing edema of the small bowel wall. It probably also enhances smooth muscle contractile activity. The combination of these effects is thought to generate effective peristalsis, enabling the small bowel to overcome ASBO

Trypsinogen Elastase Phospholipase A

Trypsinogen Activated to trypsin by enterokinase Inhibitors usually inactivate trypsin Enzyme can digest the pancreas and can activate other proteolytic enzymes Elastase Activated by trypsin Plays a major role in autodigestion Causes hemorrhage by producing dissolution of the elastic fibers of blood vessels Phospholipase A Plays a major role in autodigestion. Activated by trypsin and bile acids Causes fat necrosis

Laboratory Findings rhabdo urine dipstick

Urine dipsticks are a quick way to screen for myoglobinuria Urine dipsticks are positive in <50% of patients with rhabdomyolysis If dipstick is positive for blood and UA microscopy is negative for RBCs, myoglobin is present. Confirm with elevation of Total CK and normal CKMB and normal troponin.

The Physical Assessment SBO

What are we going to do first in our physical assessment? AUSCULTATE! You found the patient lacks bowel sounds in all four quadrants. The abdomen is distended and tender in the right quadrants.

Small Bowel Obstruction (SBO) causes

adhesions (75%)- pulls on bowel and interrupts flow surgery (laparoscopic)-causes a lot of adhesions strangulations, volvulus- intestines twist around themselves. Strangulate themselves intussusception-intestines sldie back into themselves (telescoping back in). Narrowing of intestines inside lumen so stool cant pass strictures, dehiscence, gastric bypass, ovarian cancer, "objects", hernias, Crohn's, tumors -Other possible causes: blockages from opiate use Adhesion puts intestine into weird shape that blocks flow

Cullen Sign and Turner's Sign

cullen- blotches all over stomach/umbilicus -retroperitoneum to the umbilicus through the round ligament turner- sides -retroperitoneum to the subcutaneous tissues of the flanks These discolorations are a result of liberated pancreatic enzymes causing the diffusion of fat necrosis and inflammation with retroperitoneal or intraabdominal bleeding are associated with severe acute pancreatitis and high mortality.

Comparison of Gastric, Duodenal and Stress (Physiologic Ulcers) Other factors and Associated Diseases

gastric: Common in person with lower socio-economic status, stress ulcer, burns duodenal: Increased incidence in people with type O blood, Zollinger-Ellison syndrome, COPD, cirrhosis, pancreatitis, associated with alcohol and smoking stress: AKA - Stress-Related Mucosal Disease. Patients are given PUD prophylaxis such as a PPI or H2 blockers if at risk

pancreatitis etiologic factors and autodigestive effects of pancreatic enzymes patho

etiologic factors: alcoholism biliary tract disease trauma infection drugs postop GI surgery unknown -> activation of pancreatic enzmes or injury to pancreatic cells autodigestive effects of pancreatic enzymes trypsin: edema, neccrosis, hemorrhage elastase- hemorrhage phospholipase A- fat necrosis lipase- fat necrosis kallikrein: edema, vascular permeability, smooth muscle contraction, shock