5/20/2021

Eleanor Fitzpatrick, DNP, RN AGCNS, ACNP, CCRN

Gastrointestinal &  Calculous & acalculous   Clostridium difficile -related with toxic  Cholangitis   Acute  Bowel perforation due to  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 during hospitalization

1 5/20/2021

GI & Inflammation  Critically ill patients are often sedated and receiving narcotic analgesia  Patients may also be receiving steroids or anti- inflammatory  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  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

2 5/20/2021

Causes of Biliary Obstruction in Ascending Cholangitis   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  , 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 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 & 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 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 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  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/

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  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   common cause in men  Other disorders  Lipid abnormalities  Medications  Surgery/Trauma  ERCP  Idiopathic

15 5/20/2021

Pathophysiology of  Obstruction of ampulla of Vater by , 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 , sometimes radiating to back  Associated & 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 , 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 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 - 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, 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  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

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 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 & 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 *  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 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 , 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 , 36(1), 89-104.

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