Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN

 inflammatory response and potential necrosis of pancreatic endocrine and exocrine cells as the result of premature activation of pancreatic enzymes

Presenting Signs & Symptoms  pain (upper abdomen) – 95% – edema and distension – chemical burn – release of kinin – obstruction of biliary tree

Presenting Signs & Symptoms  protracted vomiting  abdominal tenderness  guarding  distension  tympany Acute Abdomen

Presenting Signs & Symptoms  Severe disease – hypovolemic shock – Grey Turner’s sign – Cullen’s sign

Diagnostics  Serum amylase – elevated during 1st 24 hours after onset of signs – may remain elevated for only 2 days – > 300 mcg/dL

Diagnostics  Serum lipase – elevates within 24 to 48 hours of disease – remains elevated for days – can indicate pseudocyst

 Hypocalcemia – free fatty acid-albumin complexes bind calcium – decreased PTH function

Diagnostics  Elevated WBC count – inflammatory response

Diagnostics  Hyperglycemia – beta cell damage – increased glucagon production

Radiographic Studies  Computed tomography (CT) – gold standard for diagnosis

Complications  Pancreatic Abscess high fever, palpable mass, abdominal tenderness, N & V, leukocytosis & hyperglycemia surgery required

Complications  Pancreatic Pseudocyst abdominal pain, fever, N & V > 1 week WBC or amylase remains elevated

Complications  Pancreatic Pseudocyst usually subsides on its own within a few weeks CT guided needle aspiration

Medical Goals  prevent & control shock  relieve pain  suppress pancreatic stimulation

Medical Goals  support the patient  minimize the occurrence of complications

64 year old woman develops upper abdominal pain late last night. Band-like with radiation to back. Initially not severe, but awoke and had several episodes of non-bloody emesis. The first 8 hours in ED/Hospital the patient required 36 mg MSO 4 to control pain.

PMHx: HTN, Hyperlipidemia MEDS: Estrace, Plendil SOCIAL: no tobacco or ETOH use BP: 94/45  160/90, HR: 76, T: 97.9, GEN: awake alert HEENT: no icterus, mouth is dry CARDIO: ST ABD: no rebound tenderness, no bruising

ABD CT: marked peri-pancreatic fluid, streaking around pancreas, normal enhancement, no clear gallstones, CBD not dilated LABS: AST/ALT both slightly elevated. T.bilirubin normal Amylase 2620 Lipase 26,625 Hct normal WBC 14.8

Ranson’s Criteria Admission Age > 55 WBC > 16,000 Glucose > 200 LDH > 350 AST > 250 During first 48 hours Hematocrit drop > 10% Serum calcium < 8 Base deficit > 4.0 Increase in BUN > 5 Fluid sequestration > 6L Arterial PO 2 < 60 5% mortality risk with <2 signs 15-20% mortality risk with 3-4 signs 40% mortality risk with 5-6 signs 99% mortality risk with >7 signs

At 36 hrs the patient has increased work of breathing, crackles at bases of lungs. She is 4 liters ahead on fluids. What do you want to do?

“Vigorous intravenous hydration alone is the best available option in the prevention of pancreatic necrosis.” Pitchhumoni et al. “Mortality in Acute Pancreatitis,” Journal of Clinical Gastroenterology

AGGRESSIVE FLUID RESUSCITATION May require cc/hr for first 48 hrs –6 L of fluid is sequestered in abdomen alone –Third spacing can consume up to 1/3 of total plasma volume 1/3 of people die in the first phase  50% of these are associated to ARDS PULMONARY EDEMA ≠ CHF

How do you know you have resuscitated the patient? Blood pressure Heart rate Urine output SaO 2 /ABG’s show good oxygenation and no acidemia

AGGRESSIVE FLUID RESSUCITATION may create electrolyte imbalances that need to be corrected may need CVP monitoring (central line) CXRs help (CHF vs ARDS) ABGs help (still hypoxic  need more fluids?) 23% of SAP pts get ARF  80% mortality 0.5 cc/kg/hr urine output is goal (need a Foley)

NECROSIS Starts to occur within 4 days of disease CT with oral & IV contrast is gold standard necrotic areas do not enhance will NOT see it on CT before 48hrs

NECROSIS once diagnosis of necrosis is made - mortality jumps 40-60% get secondary infection mortality then approaches 80%

secondary infection symptoms: N/V, epigastric pain, distension, fever, elevated WBC diagnosis of sterile vs infected necrosis CT-guided needle aspiration the most devastating complication and marks the second peak in mortality 2 weeks)

SECONDARY INFECTIONS n What bugs? n Gram (-) bacteria cross from gut E. coli (35%) Klebsiella (24%) Enterococcus (24%) Staph (14%) Pseudomonas, proteus, strep, enterobacter, bacteroides, anaerobes

ANTIOBIOTICS Controversial DO decrease incidence of infection in necrosis, but do NOT decrease mortality Gotta cover multiple bugs Gotta get into pancreas If you see necrosis  start antibiotics

NUTRITION normal pancreas secretes up to 2 liters/day of secretions pancreatic stimulation during AP releases proteolytic enzymes  autodigestion oral feeding increases release of secretin and cholecystokinin  stimulates pancreas “rest the pancreas”  “NPO”

ENTERAL vs TPN Feedings: If distal to Ligament of Treitz (nasojejunal tube or J-tube) pancreatic secretion = basal rate Both started after 48 hours –Easier to restart po feedings –Average length of nutritional support shorter 7 vs 11 days –Fewer septic complications –$23/day vs $222/day

NEW THOUGHTS Meta-analysis of 15 randomized studies: Compared early vs delayed ENTERAL feedings in 753 critically ill pts Early was 36 hrs! Improved: Wound healing Host immune function Preservation of intestinal mucosal integrity Decreased infections BUT, no decreased mortality

Case continues By 48 hours patient’s abdominal pain is worsening HR is 140, afebrile, BP normal Abdomen shows very subtle guarding WBC: 27.6 Ca ++ : 6.6

Case continues PO 2 : 61 Base deficit: 8 BUN rise: 9 LDH: 976 RANSON SCORE: 3

Case continues Patient transferred to ICU Central line & Arterial line Repeat Abdominal CT: new bilateral pleural effusions, pancreas enhanced in tail only. Patient died 5 weeks after admission

SUMMARY They may look good, but… Score severity early Use lots of IVF Go to ICU early Early enteral feedings work better

Hepatic Failure  cirrhosis: –alcoholic with malnutrition –biliary cirrhosis  hepatitis  hepatatoxins  hypoperfusion

Hepatic Failure  Signs & Symptoms –asterixis –jaundice –obtundation –distended abdomen & ascites –renal failure –GI bleed

Hepatic Failure  Treatment –encourage rest –limit protein, amino acids & fat –prevent exposure to stress

Hepatic Failure  Treatment: Monitor –hemodynamic status –serum drug levels –lab tests

Hepatic Failure  Treatment –monitor EEG –maintain glucose –monitor for  ICP

Hepatic Failure  Treatment –jaundice = vitamin K –thrombocytopenia = folic acid & FFP, platelets –DIC = fibrinogen & heparin

Hepatic Failure  Treatment for varicies –saline lavage –administer blood –IV vasopressin or somastatin –Sengstaken – Blakemore tube –portacaval shunt

On May 3 (approx hours) a 35 year old alcoholic male began to take 2-3 acetaminophen 500 mg tablets per hour because of a toothache. He continued this through the night until 0800 hours. What is the recommended therapeutic dose for acetaminophen?

Adults: 4 grams per day. Children: 75 mg/kg/day to a maximum of 4 grams per day.

On May 4,the patient presented to the ED because of his toothache and was discharged home with Tylenol #3. He went home and took 3-4 Tylenol #3 at 0900 hours. At approx hours he developed abdominal pain and N/V and returned to the ED.

His acetaminophen level was 212 umol/L and his AST was 990 IU/L. How do you interpret these numbers?

Because it is a chronic ingestion you can not plot it on the nomogram. In instances where it is a chronic ingestion or the time of ingestion is unknown, send an acetaminophen level and an AST(ALT) and if either are elevated start N-acetylcysteine

Rumack-Matthew Nomogram

IV NAC is initiated. How does ethanol affect acetaminophen toxicity?

Chronic alcoholics are at increased risk with an acetaminophen overdose. Chronic ethanol consumption induces the cytochrome P450 pathway resulting in increased metabolism through this pathway and therefore increased NAPQI formation. Malnourishment decreases glutathione stores.

On May 5 his acetaminophen level was non- detectable and his AST was 22,733 (2305 hours) and his INR was 19. Is his liver failure secondary to chronic alcohol abuse or acetaminophen toxicity? How long would you continue his NAC and why?

Aminotransferase elevation in chronic ethanol abuse rarely exceeds 1000 IU/L. It is not unusual for severe acetaminophen toxicity to have elevations in the 10,000’s IU/L. In alcoholics with acetaminophen overdoses and elevated aminotransferases, err on the side of caution and treat with IV NAC.

How long would you continue his NAC and why? Continue IV N-acetylcysteine until his INR is less than 2. N-acetylcysteine has antioxidant and free radical scavenging effects which have been shown to decrease mortality in fulminant hepatic failure.

When would you transfer this patient to a hospital that could do liver transplants? What are the indications for a liver transplant?

Transfer for transplant consideration! INR > 5 at anytime. Metabolic acidosis (pH <7.35 or CO 2 <18) Hypoglycemia. Renal Failure (creatinine >200 umol/L) Encephalopathy

Indications for Transplant! pH <7.3 after adequate fluid replacement. Grade III or IV encephalopathy plus either: PT >100 seconds Creatinine > 292 umol/L

The patient was continued on IV N- acetylcysteine and on May 14 his INR was Will this patient have any chronic liver damage from his acetaminophen overdose?

No, patients who recover from an acetaminophen overdose go on to have completely normal liver function with no chronic sequelae