5/20/2021
Eleanor Fitzpatrick, DNP, RN AGCNS, ACNP, CCRN
Gastrointestinal Inflammation & Infection Cholecystitis Calculous & acalculous Colitis Clostridium difficile -related with toxic megacolon Cholangitis Diverticulitis Acute Pancreatitis Appendicitis Bowel perforation due to toxic megacolon Many other GI conditions seen in ICU patients which can result in high morbidity & mortality 50-80% of critically ill patients will experience a GI complication during hospitalization
1 5/20/2021
GI Infections & Inflammation Critically ill patients are often sedated and receiving narcotic analgesia Patients may also be receiving steroids or anti- inflammatory drugs Difficulty in identifying infectious/inflammatory conditions affecting the GI tract & few symptoms Elderly patients may not mount the pain response These GI issues & emergencies are relatively common & frequently life-threatening
Acute Ascending Cholangitis Obstruction & inflammation of the biliary ductal system results in bacterial infection Commonly in the setting of biliary stasis & obstruction Result is acute elevations in the biliary pressures leading to rapid bacteremia and sepsis
2 5/20/2021
Causes of Biliary Obstruction in Ascending Cholangitis Gallstones Neoplasms-usually after instrumentation Pancreatic Cholangiocarcinoma Fibrotic stricture Stones, trauma, postsurgical
Acute Ascending Cholangitis The 3 typical features of cholangitis were described in 1877 by Charcot Fever, often with rigors Jaundice Right upper quadrant pain- patients may not be able to communicate this 50-70% of patients develop all 3 features Severe disease results in Reynold’s pentad Hypotension Change in mental status
3 5/20/2021
Presentation of AAC Fever, often with rigors, is the most common sign Other signs of sepsis Lab findings Elevated white blood cell count and a left shift Elevated total bilirubin due to biliary obstruction Elevations in alkaline phosphatase and transaminases Elevated lactate level
Infection
If biliary system colonized by bacteria this does not lead to cholangitis When obstructed, infection results but pathophysiology is unknown Increased pressure in the biliary system may be causative Increased intestinal permeability & disrupted intestinal integrity may cause bacteria to enter the blood or lymphatics
4 5/20/2021
Diagnosis of AAC
Thorough history & physical exam Laboratory tests LFT’s Coagulation tests CBC with differential Lactate Metabolic panel Blood cultures
Diagnosis of AAC
Imaging tests Ultrasound CT scan MRCP EUS
5 5/20/2021
Management of Acute Ascending Cholangitis Immediate treatment with antibiotics & fluid resuscitation Semi-elective biliary drainage in stable patients Performed within 72 hours For those who do not respond or who deteriorate with severe signs & symptoms over 12 to 24 hours Urgent biliary decompression is needed Restore bile drainage Delay can have fatal results- sepsis, organ dysfunction
ERCP Cholangitis should be treated with endoscopic retrograde cholangiography and sphincterotomy Well tolerated Procedure of choice Common bile duct is accessed Sphincterotomy Nasobiliary tube drainage Stent drainage- tumors, strictures Stone removal Combination of interventions
6 5/20/2021
With permission from Wolters/Kluwer
The following video is used with permission from SAGES (Society of American Gastrointestinal and Endoscopic Surgeons) & author, Dr Vitale
7 5/20/2021
With permission from Wolters/Kluwer
Other Methods of Biliary Decompression Percutaneous transhepatic cholangiocatheter (PTC) If the ampulla of Vater cannot be cannulated with ERCP Open surgical drainage EUS guided catheter placement- on the rise Can be internalized No external drain- a good option for some
8 5/20/2021
Percutaneous Transhepatic Cholangiography & Catheter Insertion Invasive Small gauge needle to gain access to intrahepatic biliary system under flouroscopy-percutaneous A wire is passed followed by a drainage catheter Successful but a higher morbidity & mortality than ERCP
Surgical Drainage for AAC Because of surgical risk- emergency surgical decompression is rarely performed Reserved for anatomical issues or failed ERCP or PTC Open or laparoscopic common bile duct exploration In critically ill simplest procedure should be performed to shorten procedure time T-tube insertion
9 5/20/2021
Management of AAC Monitoring and supportive care for all interventions Fluids and antibiotics continue Monitor for response to treatment Assess and treat pain Preventing complications Correct any coagulopathy or metabolic derangements
Acute Acalculous Cholecystitis Acute inflammation of the gallbladder without evidence of calculi (stones) Due to bile stasis & gallbladder dysfunction Significant morbidity & 50% mortality with poorer outcomes than calculous
With permission from Wolters/Kluwer
10 5/20/2021
Conditions Associated with AAC Burns Severe trauma Total parenteral nutrition (TPN) Pancreatitis Sepsis Critical illness following cardiac or abdominal vascular surgery. Major cardiovascular disorders Complicated diabetes mellitus Autoimmune disease AIDS Vasculitis
Etiology of AAC
Bile stasis Dehydration during prolonged fasting Use of TPN Narcotics for pain with contraction of sphincter of Oddi Hypoalbuminemia Local inflammation with edema Multiple blood transfusions Gallbladder ischemia from hypoperfusion/shock
11 5/20/2021
Signs & Symptoms of AAC
Symptoms are similar to those of acute cholecystitis with gallstones May be difficult to identify because patients tend to be severely ill (eg, ICU setting) & unable to communicate Abdominal distention or unexplained fever may be the only clues Can rapidly progress to gallbladder gangrene and perforation, leading to sepsis, shock, and peritonitis Mortality approaches 65%
Acute Acalculous Cholecystitis
Underlying sepsis or state of shock is often associated with acalculous cholecystitis Early treatment with antibiotics and an intervention are warranted.
12 5/20/2021
Identifying AAC AAC on ultrasound (gold standard) No gallstones but ultrasonographic thickened gallbladder wall and pericholecystic fluid. CT identifies extrabiliary abnormalities Cholescintigraphy
Management of AAC In patients with acute cholecystitis/associated physiological compromise, surgery is unattractive A percutaneous cholecystostomy offers an alternative treatment before definitive repair & is recommended. Bedside drainage procedure removes septic source with minimal physiological stress- ultrasound guided Focus on restoring stability, definitive surgical removal of gallbladder deferred until the patient is more stable Antibiotics, fluids, NG suction .
13 5/20/2021
Life-Threatening Complications of AAC
Gangrenous gallbladder Gallbladder perforation Empyema Sepsis
Prevention & Management of AAC in Critical Care Prompt initiation of enteral nutrition prevents bacterial translocation and further gallbladder dysfunction vs non-feeding Aggressive volume resuscitation of hypovolemic shock prevents hypoperfusion Close monitoring & high index of suspicion for those with risk factors Mortality rate as high as 40% due to infection in critical illness & associated co-morbid conditions
14 5/20/2021
Acute Pancreatitis Acute inflammatory condition of the pancreas caused by activation of digestive enzymes Ranges in severity from mild glandular edema to severe hemorrhagic disease or infected pancreatic necrosis
Etiology of Pancreatitis Gallstones and ETOH are the most common causes Gallstones- most common cause in women Alcohol common cause in men Other disorders Lipid abnormalities Medications Surgery/Trauma ERCP Idiopathic
15 5/20/2021
Pathophysiology of Acute Pancreatitis Obstruction of ampulla of Vater by gallstone, etc Bile reflux in pancreatic duct Activation of trypsin in acinar cells Result is pancreatic autodigestion Inflammation beyond gland into peripancreatic tissue
With permission from Mayo Clinic
Pathophysiology of Acute Pancreatitis Local injury and inflammation activates systemic inflammatory factors Complement Interleukins Phospholipase A Result is the systemic inflammatory effects
16 5/20/2021
Two Types of Acute Pancreatitis Interstitial Edematous Pancreatitis The majority of patients (80-90%) have this more mild form Lack of pancreatic necrosis Diffuse inflammatory edema Clinical picture usually resolves quickly
Two Types of Acute Pancreatitis Necrotizing Pancreatitis Presence of tissue necrosis in pancreatic parenchyma or peripancreatic tissue Infected or sterile ETOH is risk factor *
*Jeyarajah, DR, 2014.Current Problems in Surgery, 51, 374-408.
17 5/20/2021
Diagnosis Clinical findings Central upper abdominal pain, sometimes radiating to back Associated nausea & vomiting Laboratory Serum amylase or lipase 3 times normal Radiographic-CT or MRI/MRCP Used acutely only when the diagnosis is unclear Helpful later in course of the disease for local complications Ultrasound Assess for gallstones as source if no other etiology is apparent
Management of Acute Pancreatitis
Fluid resuscitation SIRS response & fluid losses sequestered- retroperitoneum NSS or LR Management of the systemic and local complications Caused by enzyme activity & release of inflammatory mediators from damaged pancreatic cells
18 5/20/2021
Local Complications of Acute Pancreatitis: Source of a Hot Belly
Infected Pancreatic Necrosis Area of nonviable pancreatic parenchyma Abdominal pain Fever Leukocytosis Radiologic findings: Air in an area of pancreatic necrosis on CT scan Gram stain and culture on a fine needle aspirate of the necrosis identifies the organism
Step-Up Approach Management of Acute Pancreatitis Placement of percutaneous drainage catheters & antibiotics used first Outcomes better if surgery delayed til necrosis organized, usually 4 weeks after disease onset Minimal access necrosectomy by percutaneous (transgastric) or endoscopic routes Video- assisted retroperitoneal debridement
19 5/20/2021
Surgical Management of Acute Pancreatitis Moderate the inflammatory response Surgical interventions- debridement Reserved for infected pancreatic necrosis after catheter drainage fails Pancreatic necrosectomy with closed, continuous irrigation via indwelling catheters Necrosectomy and open packing Necrosectomy with closed drainage without lavage Removes toxins, minimizes systemic absorption
Infected Pancreatic Necrosis Systemic antibiotics should be reserved for the treatment (not prophylaxis) of infected pancreatic necrosis Fungal infections occurs in 25% of cases Require anti fungals
20 5/20/2021
Management of Acute Pancreatitis Remove or reduce inciting agents Those with alcoholic pancreatitis should be referred for counseling services Gallstone pancreatitis Prompt cholecystectomy and/or Endoscopic sphincterotomy, extraction of bile duct stones post severe inflammation
Case Study After a 5 ½ month hospital stay complicated by multiple septic episodes and pancreatic abscess, patient was transferred to acute rehab Patient & family education Collaborated with Social work on counseling & education re: ETOH Later discharged to home with family with extensive education on need for follow up & abstinence from ETOH Now working and abstaining from alcohol Has continued with alcohol counseling and is involved in A.A.
21 5/20/2021
GI Infections: Clostridium Difficile
Organism responsible for antibiotic associated colitis C. diff colonizes and over-grows GI tract after the normal flora has been altered by antibiotic therapy Two protein exotoxins released by the C. diff bacteria (toxin A and toxin B) Mucosal injury and inflammation
Clostridium Difficile- Associated Colitis & Toxic Megacolon Toxic megacolon-active, acute colitis with massive colonic distension caused by C Difficile, common hospital-acquired infection Frequent cause of morbidity & mortality in hospitalized patients
22 5/20/2021
Clinical Manifestations
Moderate to severe colitis Profuse diarrhea- 10 + liquid foul smelling stools/day Abdominal distension with pain Occult colonic bleeding Fecal leukocytes A minority of patients (3% to 12%) can progress to severe disease, toxicity & shock with ICU admission, colectomy or death
Pathophysiology
C. diff toxins cause shedding of cells of basement membrane into lumen of colon Shallow ulcer left on the mucosal surface-yellow raised plaques which slough Serum proteins, mucus and inflammatory cells flow out from the ulcer
23 5/20/2021
Risk Factors Risk Factors Antibiotic exposure Flouroquinolones most common Institutionalization Advanced age Severe illness Gastric acid suppression (especially with PPI)
Clinical Presentation Presentation Watery diarrhea Range of no symptoms to fulminant septic shock Could be an absence of diarrhea with: Unexplained leukocytosis Pancolitis on imaging to evaluate other symptoms such abdominal pain, nausea, vomiting, fever
24 5/20/2021
Diagnostic Testing Stool sample to detect C. difficile toxin in the stool Toxin DNA NAAT (Nucleic Acid Amplification Test) to detect the toxin gene 2-step testing algorithm. If the 1st test is positive, a 2nd test will be automatically performed to detect the toxin antigen Testing may be institution-specific Abdominal radiograph and helical CT-colonic thickening Colonoscopy- for clinical suspicion but negative lab tests or no stool due to ileus
Management Supportive care Replete volume and electrolyte losses Avoidance of antiperistaltic agents Strict adherence to infection control practices Withdrawal of antibiotic therapy Enteral feedings whenever possible Oral Vancomycin Recommended first line agent
25 5/20/2021
Management Alternative first line drug is oral Fidaxomycin* Both drugs are effective Duration of therapy 10 to 14 days Fecal Microbiota transplant for refractive cases
*May be Institution dependent
Mechanism of C Diff Colitis & Toxic Megacolon Progression of the infection to the severe inflammation of the colon with Ileus Bowel dilatation Loss of GI wall integrity Systemic inflammatory response syndrome causing toxic megacolon with perforation, MODS
26 5/20/2021
Toxic Megacolon Severe inflammatory reaction Damage to smooth muscle layers and necrosis Disruption of gut barrier Absorption of bacteria into mesenteric & portal circulation Sepsis Perforation occurs in 25% of cases Immediate surgical decompression is required NPWT Second-look surgery Antibiotics if perforation or positive operative cultures
Clinical Evaluation of GI Perforation
Radiologic Evaluation As described Do not await diagnostic testing to intervene
27 5/20/2021
Management of Toxic Megacolon Aggressive treatment of volume depletion Early surgery-offers the best chance for cure when performed before severe MODS has developed Organ system support & nutrition support
Surgery for Toxic Megacolon Subtotal colectomy Perform end ileostomy & restore GI continuity when acute illness resolves If surgery performed rapidly necrosis & frank perforation is rare Continue Vancomycin PO/NG for 7 days to treat residual disease in the rectum* May add IV Metronidazole* *Institution-specific
28 5/20/2021
Management of Gastrointestinal Perforation Most important therapy of GI perforation is source control
Postoperative Management Management of pain & anxiety Wound management NPWT Monitor for abdominal compartment syndrome Fluid resuscitation continues Ostomy assessment and management Supportive care Prevention of additional complications Continued infection surveillance
29 5/20/2021
Getting a Handle on C. Difficile Prevention of initial and additional cases Careful use of antibiotics If needed-- treat for the shortest interval Hand hygiene, equipment sterilization Huddles on units when cases arise Recurrent, recalcitrant disease (institution preference) Fidaxomicin-bacteriocidal Tapered, intermittent Vancomycin plus other meds Fecal bacteriotherapy (fecal microbiata transplant)
Summary Severe acute inflammatory & infectious conditions of the gastrointestinal tract are life-threatening disorders and can lead to multi-organ involvement Multidisciplinary interventions have improved survival statistics Critical care nurses are at the forefront in rapidly identifying & assessing these conditions Aggressive & rapidly institute treatment
30 5/20/2021
References Alemi, F., Seiser, N., & Ayloo, S. (2019). Gallstone Disease: Cholecystitis, Mirizzi Syndrome, Bouveret Syndrome, Gallstone Ileus. Surgical Clinics, 99(2), 231-244. Barreto, S. G., Habtezion, A., Gukovskaya, A., Lugea, A., Jeon, C., Yadav, D., ... & Pandol, S. J. (2021). Critical thresholds: key to unlocking the door to the prevention and specific treatments for acute pancreatitis. Gut, 70(1), 194-203. Desai, J., Elnaggar, M., Hanfy, A. A., & Doshi, R. (2020). Toxic megacolon: background, pathophysiology, management challenges and solutions. Clinical and experimental gastroenterology, 13, 203. Iqbal, T., & DuPont, H. L. (2021). Approach to the patient with infectious colitis: clinical features, work-up and treatment. Current Opinion in Gastroenterology, 37(1), 66-75. Krishnamoorthi, R., & Ross, A. (2019). Endoscopic management of biliary disorders: diagnosis and therapy. Surgical Clinics, 99(2), 369-386. Mederos, M. A., Reber, H. A., & Girgis, M. D. (2021). Acute Pancreatitis: A Review. JAMA, 325(4), 382-390. Mishra, B. M., Sethy, S., & Rath, B. K. (2021). Management outcome of non-traumatic small intestinal perforation: A prospective study. International Journal of Surgery, 5(1), 26-30. Olson, E., Perelman, A., & Birk, J. W. (2019). Acute management of pancreatitis: the key to best outcomes. Postgraduate Medical Journal, 95(1124), 328-333. Pisano, M., Ceresoli, M., Cimbanassi, S., et al. (2019). 2017 WSES and SICG guidelines on acute calculous cholecystitis in elderly population. World Journal of Emergency Surgery, 14(1), 10. Rincon, J. E., Rasane, R. K., Aldana, J. A., Zhang, C. X., Fonseca, R. A., Zhang, Q., ... & Bochicchio, G. V. (2021). Acute acalculous cholecystitis-associated bacteremia has worse outcome. Surgical infections, 22(2), 182-186. Zhang, V. R. Y., Woo, A. S. J., Scaduto, C., Cruz, M. T. K., Tan, Y. Y., Du, H., ... & Siah, K. T. H. (2021). Systematic review on the definition and predictors of severe Clostridiodes difficile infection. Journal of Gastroenterology and Hepatology, 36(1), 89-104.
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