Acute Gastrointestinal and Genitourinary Disorders Christiana E. Hall, MD MS Division of Neurocritical Care University of Texas Southwestern Medical Center Dallas, Texas Upper & Lower GI bleeding UGIB CAUSES • • • • Peptic ulcer disease most common Variceal hemorrhage most feared Aortoenteric fistula deadly Other causes: esophagitis, mallory-weiss tear, Dieulafoy’s lesion, angiodysplasia, tumors Upper & Lower GI bleeding LGIB CAUSES • • • • • Diverticular Dz most common Angiodysplasia second most common Ischemic colitis most feared Postpolypectomy bleeds most annoying Other causes: (LGIB) Colitis, Dieulafoy’s lesion, tumors, anorectal fissures/varices/ hemorrhoids. • **Meckel’s diverticulum – rare, small bowel, ALWAYS rule out in young people Upper & Lower GI bleeding Initial approach & management • • • • • UGIB more likely hemodynamically unstable than LGIB Adequate IV access ie 2 large bore IVs Stat type & cross, CBC, coags, chemistry, LFT Up to 2 liters crystalloid; consider O(-) Transfuse as appropriate correct coagulopathy and consider holding additional PRBC units • NGT for room temp saline lavage unless clearly LGIB • Consult GI endoscopist • If massive, initiate massive bleeding transfusion protocol to include FFP & Plts etc; rapid infuser/warmer to BSD Upper & Lower GI bleeding UGIB Non-variceal UGIB Variceal • Begin resuscitation Hgb > 7 • Arrange endoscopy for dx and tx (w/in 24 hrs) • Consider pre-endoscopy PPI; definite PPI post treatment • No promotility agents, no somatostatin, no H2 antagonists • Surgery or intravascular tx when endoscopy fails • F/U testing for H pylori • Home on PPI • antiplt or NSAID tx safer with PPI • Prompt attn. Hgb ~ 8 • Urgent endoscopy for dx & tx (w/in 12 hrs) • Consider protective intubation • Balloon Tamponade – temporize (Sengstaken-Blakemore Tube) • somatostatin immediately3-5 d • *TIPS if endoscopy + pharmacotherapy unsuccessful • Cirrhotics: I week SBP prophylaxis w/ quinolone or Ceftriaxone *TIPS – transjugular intrahepatic portosystemic Shunt Ann Intern Med. 2010;152(2):101-13. Ann Intern Med. 2003 Nov 18;139(10):843-57 Am J Gastroenterol. 2007 Sep;102(9):2086-102. Upper & Lower GI bleeding LGIB PEARLS Acute & Fulminant Hepatic Failure • Acute Liver Failure = onset of hepatic encephalopathy and coagulopathy (INR > 1.5) within 26 weeks of initial jaundice in a patient without preexisting liver dz: – Fulminant = within 8 wks – Subfulminant = > 8 < 26 wks • Causes – – – – – – – Acetaminophen Drugs & toxins Viral hepatitis Malignancy/ Budd-Chiari Wilson’s disease Autoimmune Pregnancy related • HELLP syndrome • Acute Fatty Liver of pregnancy Acute & Fulminant Hepatic Failure Am J Dig Dis 1978;23:398- 406 Acute & Fulminant Hepatic Failure Gastroenterology 1989;97:439–55 Gastroenterology 2003;124:91–6 Acute & Fulminant Hepatic Failure Acute & Fulminant Hepatic Failure Treatments • Acetaminophen  N-acetylcysteine – Oral NAC 140 mg/kg load  then 70 mg/kg q 4 hrs – Oral NAC 150 mg/kg over 15-60 mins, then 12.5 mg/kg/hr x 4 hrs, then 6.25 mg/kg/hr – Until clinical improvement*** • Amanita phalloides  penicillin – PCN G 1 gm/kg daily IV plus NAC protocol as per APAP tx • Herpes Simplex  acyclovir 30 mg/kg/day • Autoimmune  methylprednisolone 60 mg/kg/day • HBV  Lamivudine 100-150 mg/daily PO Crit Care Med. 2007 Nov;35(11):2498-508 Acute & Fulminant Hepatic Failure Approach to ALF pt in ICU • • Determine if pt is TPL candidate If not can pt be salvaged without TPL Goals of care 1. 2. 3. Support and bridge TPL candidates to operation Support survival candidates through non-op course Provide comfort care to non-TPL candidates with unsurvivable ALF Crit Care Med. 2007 Nov;35(11):2498-508 Acute & Fulminant Hepatic Failure • Ammonia – – – – gut nitrogen escapes liver metabolism & crosses BBB detoxified by astrocytes  osmotically active moieties Injures astrocytes  cytotoxic edema If used, lactulose with precautions avoid neomycin • Surveillance Cultures & empiric ABX tx (90% infex rate) – Stage III/IV HE -- Overt SIRS – Refractory HypoTN -- TPL waiting list – Suggested  3rd gen cephalosporin; vanc for all catheter-related infex; antifungal if no improvement • Seizures – Common subtle SZ in III/IV – Prophylaxis not recommended, low threshold for EEG tx if sz Crit Care Med. 2007 Nov;35(11):2498-508 Acute & Fulminant Hepatic Failure • Coagulopathy – – – – – – Vit K Targets for intervention/ active bleeding  plt 50K & INR 1.5 Avoid prophylactic FFP / do use GI prophylaxis  H2 or PPI Hypfibrinogenemia  cryoprecipitate oozing  aminocaproic acid If rVIIa then low dose 40 mcg/kg & FFP for other fx • Nutrition – Adequate protein -- Avoid hypoglycemia • Circulatory – SBP > 90 -- MAP > 65 – judicious hydration -- Norepinephrine preferred – Hydrocortisone if adrenal insufficiency Crit Care Med. 2007 Nov;35(11):2498-508 Acute & Fulminant Hepatic Failure • Cerebral Edema ICP – – – – – ICP montoring HE III/IV only (SA Bolt or IP fiberoptic) ICP < 25 -- CPP 50 - 80 Mannitol 1st line -- Hypertonic saline 2nd line Hypothermia controversial -- Barbiturate Coma Indomethacin rescue 25 mg IV push  mech vasoconstriction • Renal failure – CRRT -- Avoid prerenal azotemia  fluid challenges • Pulmonary – ARDS-NET approach Crit Care Med. 2007 Nov;35(11):2498-508 Ileus & Toxic Megacolon Ileus • Common, multiple medical & surgical precipitants • N&V, distension, absent stool & flatus • Conservative management – Bowel rest – Suck and drip -- Remove offending drugs -- Ambulation where feasible Ogilvie’s • Massive colonic dilation without obstruction • precipitants  trauma, infections, cardiac dz, pelvic region surgery (hip and c-section) • abdominal distension, pain, N&V. Flatus & stool passed. • Illness severity, old age, ischemia or perforation cecal diameter (> 12cm) duration (>6 days) Ileus & Toxic Megacolon Ogilvie’s Gastrointest Endosc 2002; 56:789–792. Best Practice & Research Clinical Gastroenterology 2007; 21:671–687. Toxic Megacolon • deadly form of colitis • vicious cycle of inflammation in the colonic wall with atony and dilation • grave systemic illness – – – – Diarrhea Constipation abdominal pain distension -- bloody diarrhea, -- obstipation, -- tenderness, -- decr bowel sounds. – CT: dilated colon, bowel wall thickening, submucosal edema, pericolic stranding, ascites, perforations, abscesses, ascending pyelophlebitis Toxic Megacolon • Toxic Megacolon classically associated with inflammatory colidites: – ulcerative colitis – Crohn’s disease • frequently reported in association with infectious diarrheas – C. difficile • Jalan’s Diagnostic Criteria: – Fever > 101.5°F (38.6°C) + Heart rate > 120 bpm + WBC >10.5 OR – Anemia + one of the following criteria: dehydration, mental changes, electrolyte disturbances, or hypotension Toxic Megacolon • • • • • General Measures Intravenous fluid support Correct electrolyte abnormalities Complete bowel rest Discontinue anticholinergics and narcotics Rule out infectious etiology Am J Gastroenterol 2003;98:2363–2371 Gastroenterology 1969;57:68–82 Decompressive therapies • Rectal tube • Nasogastric or long nasointestinal tube • Repositioning maneuvers (prone, knee elbow) • Endoscopic treatment is NOT a usual intervention Radiology • Frequent assessment with plain films • Abdominal CT scanning may aid in management Toxic Megacolon Medical Care (7 day trial in non-worsening patients may be “colon sparing”) • Specific treatment for infections – (i.e. metronidazole if C diff) • Intravenous corticosteroids for inflammatory bowel disease – (e.g. hydrocortisone 100 mg q 8 hr or methylprednisolone 15 mg q 6 h) • Broad spectrum antibiotics – consider empirically if only to reduce mortality in case of perforation) Surgical intervention (total or subtotal colectomy) • Failed medical care • Progressive toxicity or dilation • Signs of perforation Am J Gastroenterol 2003;98:2363–2371 Acute GI Tract Perforations • Esophagus  rectum • Many causes • GI Spillage into sterile spaces – inflammation, sirs, infection and sepsis. • longer interval between perforation to diagnosis to definitive treatment  the higher is the M&M • • • • Contamination: Colon >>>>stomach Free Air: Stomach & colon >>>> small bowel Rapid dx and operative cleansing & repair are key Pts have acute abdomen, do not breathe with abdominal muscles and lie motionless on stretcher Acute GI Tract Perforations • Esophagus – – – – CT surgery territory Free air in mediastinum, neck st, prevertebral on plain film Gastrographin swallow to localize tear Risk life threatening mediastinitis • Stomach – – – – Anterior wall and duodenal ulcers by far most common Large free air “3 way of abdomen” plain films Spillage has low bacterial content but causes severe SIRS (acid) X-lap unless posterior and contained • Small bowel – Lesser gas, CT may be needed to see free air – X-lap, run bowel, antibiotics Acute GI Tract Perforations • Colon – Divertucular rupture – by far most common – Walled off diverticular ruptures may respond to abx + percutaneous drainage – Free air and perfs due to other causes require operation • Patients and risks – – – – – – – – Often older & sicker bringing in many medical comorbities Third spacing and intravascular contraction Bacteremia Peritonitis, pancreatitis ARDs  MOF Multiple Ors for washout, abd compartment syndrome Exacerbations of CAD etc. X-lap unless posterior and contained Late comps: dehiscences, abscess formation, PE, DVT Acute GI Tract Perforations • Preop – – – – – – – – Fluid resuscitation Correct electrolyte derangements CVP monitoring for the critically ill ABX: Ampicillin + Metronidazole + fluoroquinolone (alt. aminoglycoside) combination chosen represents the best empiric estimate to cover the likely organisms depending on location. goal of antibiotics is to minimize risks of postoperative infectious complications. Suck & drip To OR urgently Acute GI Tract Perforations • Post-op – Fluid management to maintain intravascular volume, CVP & UOP – Bowel rest  suck & drip until GI output minimal & flatus returns – ABX continued as preop unless cultures dictate change – All ABX by IV route – maintain electrolytes – Vigilance for compartment syndrome – Adequate pain management • Failure of clinical improvement (@ 2-3 days) – – – – inadequacy of initial operative procedure secondary complications superinfection at a remote site antibiotic dosing is inadequate or spectrum of coverage is insufficient Acute Intestinal Vascular Disorders & mesenteric infarction • final common pathway for infarcted bowel is necrosis and perforation • By the time perforation occurs with its obvious symptoms, irreversible tissue death has long since completed • Infarction of long segments of small bowel such as is the territory of the superior mesenteric artery (SMA) is incompatible with life • Goal: recognize gut ischemia early and rescue tissue at risk before infarction occurs • This is no easy task Acute Intestinal Vascular Disorders & mesenteric infarction • Causes: – trauma, obstruction with severe dilation or torsion, Atherosclerotic vascular disease, low flow states as in shock, in vasospasm, with prolonged procedures with clamping or on cardiac bypass or due to thromboembolization. Iatragenic from IA Procedures! • Classic neuroscience patient at risk is the vasculopath on the stroke service • patients may give an episodic history of intestinal angina typically postprandial (increased blood flow demand) • “Pain out of proportion to exam.” is the classical presentation – sudden in onset of severe abdominal pain but the exam remains rather benign, not an acute abdomen Acute Intestinal Vascular Disorders & mesenteric infarction • diagnosis: – – – – – – Classic exam, history, setting Labs may include leukocytosis, lactic acidosis, elevated amylase KUB may be mistaken for partial SBO leading to delays Angiography is gold std Some surgeons bypass angio and go straight to OR (time is gut) Goals of operation are revascularization and resection of infarcted bowel – Second looks allow for gut sparing – Compassionate care involves peak and shriek when extensive completed infarction incompatible with life id found and return to ICU for comfort care • Angiographic tx – Definate role for IA vasodilator therapy in vasospasm – Possible role for embolectomy in very early partial obstructions where infarction has not yet occurred (repersfion injury, endotoxin shock) Acute Intestinal Vascular Disorders & mesenteric infarction •Don’t let this patient be yours : • Eliminate drivers of shock • Resuscitate adequately, avoid excessive pressors Pancreatitis • • In pancreatic inflammation, pancreatic enzymes are stimulated resulting in autodigestion and necrosis This pancreatic parenchymal process may have far reaching systemic effects 3 phase model 1. trypsin is prematurely activated within the acinar cells and then in turn activates a cascade of injurious pancreatic enzymes designed for digestive processes in the gut lumen 2. intrapancreatic inflammation perpetuates through numerous pathways 3. Extrapancreatic inflammation develops taking the form of such entities as SIRS and ARDS Pancreatitis • leading causes of pancreatitis – • alcoholism and gall stones. Other etiologies: – – – trauma including the postoperative state Hypercalcemia drugs (classic examples are HCTZ and steroids.) Diagnose when 2 of the following 3 factors are present: 1. abdominal pain characteristic of acute pancreatitis a. b. 2. 3. classical pain is epigastric, continuous and often radiates to the back Pain is usually severe and often attended by nausea and vomiting amylase and/or lipase ≥3 times upper limit of normal CT findings compatible with pancreatitis Pancreatitis • Initial laboratory evaluation – CBC with diff, complete serum chemistry including calcium, liver functions, lactate dehydrogenase, amylase, lipase and triglycerides. Pancreatitis • distribution of severity in acute pancreatitis – – 85% Simple interstitial pancreatitis 15% of cases are necrotizing – 1/3 necrotizing cases develop infected necrosis • Interstitial Pancreatitis – • • • only 1 in 10 will develop any organ failure, it tends to be reversible necrotizing pancreatitis – median prevalence for organ failure is about 50% Overall mortality for pancreatitis is 5% – range of 3% for interstitial to 17% for necrotizing. In the absence of organ failure mortality is nil; 3% for single organ failure & nearly 50% for MOF. Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400. Pancreatitis • Predicting who will have necrotizing course – – – – Older age, obesity Increasing Apache II in first 48 hrs Increasing Hemoconcentration in first 48 hours Dynamic CT with contrast, best if delayed ~ 48 hrs • • Shows pancreatic necrosis where present Work-up – – – Urgent US of RUQ for stones If obstruction ERCP for relief urgently if cholangitis and if none, after 72 hrs if failure to improve Delayed cholecystectomy when stones present Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400. Pancreatitis • management – – – – – – • Fluid support up to 6 liters may be reguired in 3rd spacing Hypovolemia perturbs necrosis via hypoperfusion Pain control Feeding tubes distal duodenum or jejunum PPI to compensate for insufficient pancreatic bicarb Prophylactic ABX not recommended, but empiric tx of suspected sepsis or SIRS indistinguishable from sepsis during work up Suspicion of infected pancreatic necrosis – – CT guided percutaneous aspiration, may repeat q week GS = GNR  carbipenum + fluoroquinolone + metronidazole – – – GS = GPC  Vancomycin Surgical debridement of infected necrosis urgently or after period of organization Sterile necrosis may or may not require delayed debridement Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400. Pancreatitis • There are 3 complication situations in which a patient with sterile necrosis may require emergent operation. – – – development of abdominal compartment syndrome, suspected secondary bowel obstruction, perforation or ischemia, for bleeding of a pseudoaneurysm where hemostasis cannot be achieved endovascularly. Delayed pancreatic abscesses respond well to percutaneous drainage Am Coll of Gastroenterology. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006; 101:2379-2400. BEST WISHES FOR SMOOTH SAILING THROUGH YOUR BOARDS