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Grand Rounds

Grand Rounds. IVY DIMAYUGA-DE DIOS, M.D. Department of Medicine Makati Medical Center 2 August 2007. Objectives. To present a case in the ICU illustrating the development of ileus/intestinal pseudo-obstruction in the critically ill

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Grand Rounds

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  1. Grand Rounds • IVY DIMAYUGA-DE DIOS, M.D. • Department of Medicine • Makati Medical Center • 2 August 2007

  2. Objectives • To present a case in the ICU illustrating the development of ileus/intestinal pseudo-obstruction in the critically ill • To enumerate the risk factors and pathophysiology in the development of ileus/intestinal pseudo-obstruction in critically ill patients • To discuss the management options for ileus/intestinal pseudo-obstruction in the critically ill

  3. The Case

  4. H. T., 62/M, (+) HPN • admitted for unresponsiveness • 2-week history of dizziness, left-sided weakness, vomiting, LOC • diagnosed with Pontine infarct 2° complete basilar artery occlusion • comatose, intubated, s/p tracheostomy • treated with Enoxaparine and Co-amoxiclav

  5. Pertinent PE • BP: 110/70 HR: 88 bpm RR: 20, assisted T: 39.2 °C • pink conjunctivae, anicteric sclerae, (-) NVE, (-) CLAD, (-) TPC, (-) carotid bruits • equal chest expansion, fine crackles left basal lung field • adynamic precordium, good S1 and S2, apex beat displaced 2 cm lateral to 5th ICS LMCL , (-) murmur • abdomen soft, NABS, (-) masses • full and equal pulses, edematous upper and lower extremities • (+) multiple dry, irregularly-shaped erosions with erythematous base and surrounding hyperpigmentation over the L gluteal and L mid-back areas • DRE: (-) masses, lax sphincter tone, full rectal vault, yellowish stool

  6. Pertinent NE • comatose, non-responsive to painful stimuli • pupils 2mm ESRTL • (-) Doll’s eye and corneal reflexes • flaccid extremities • (+)1 DTRs on all extremities • (-) Babinski reflexes • supple neck

  7. Admitting Impression • Pontine infarct 2° to complete basilar artery occlusion • Acute respiratory failure 2° to CVA • Fever, probably 2° to infected decubitus ulcers vs. hospital-acquired pneumonia • Hypertensive cardiovascular disease

  8. Course in the Wards • Neurologic • Acute pontine infarct 2° to complete basilar occlusion • Tx: Somazine, Warfarin, Enoxaparine, Cilosatazol • Respiratory • Acute respiratory failure 2° to pontine infarct • Mechanical ventilator: tolerated SIMV weaning off pressure support, maximum PEEP at 10 cm H2O • Infection • Sepsis 2° to hospital-acquired pneumonia; Decubitus ulcers, grade 2 • Initial tracheal and blood cultures grew gram negative rods • Tx: broad-spectrum antibiotics; Calmoseptine and Bactroban ointment with duoderm dressing

  9. Course in the Wards • Renal • Dx: Acute renal failure, pre-renal, 2° to sepsis, t/c chronic Kidney Disease 2° to HPN nephrosclerosis; Hypoalbuminemia 2° to poor intake; Third space losses 2° to Hypoalbuminemia • Tx: Hydration, IV human albumin, Nutricomp added to feeding, IV Epoietin

  10. Course in the Wards: Gastrointestinal • Pt admitted with a soft abdomen, NABS, no palpated masses, normal DRE, NGT fed. • OF started at 2000 kcal/day, 222 cc + 50 cc H2O flushing q4°, drip < 1 hour. • Lansoprazole 30 mg OD • 2nd HD: increased NGT residuals = 200 cc • Next feeding withheld; OF given via drip x 1 1/2 hours and decreased to 1600 kcal/day, 178 cc + 50 cc H2O flushing q

  11. 5th HD: episodes of hiccups • PPI and Domperidone continued; Baclofen given • 8th HD: (+) distended abdomen, (+) hypoactive bowel sounds, (+) tympany, soft, adequate BM, no significant residuals • still with intermittent fever; SIMV not tolerated • PFA: Mild gaseous dilatation of some small bowel segments due to ileus. • Domperidone + Omeprazole + Baclofen

  12. 11th HD: no BM x 24 hours, (+) hiccups, distended abdomen, hypoactive bowel sounds, (+) tympany, (+) NGT residuals = 150 cc, abdominal girth = 44 cm. • feeding discontinued temporarily → Vamin glucose started • NGT reinserted and hooked to bedside bottle • Laxatives given→ (+) BM • 12th HD: (+) BM, ↓abdominal distention and tympany, abdominal girth=40 cm • OF resumed with decreased amount (133 cc q4°) and decreased drip rate (drip for 2 hours, drainage for 1 hour prior to feeding • Iberet discontinued

  13. 13th HD: recurrence of fever with severe abdominal distention, hypotension, tachycardia, desaturation, anuria; vasopressors started • Abdomen globular and firm but not tense, absent bowel sounds; serum K normal • OF discontinued • Referred to GI service; Assessment: Generalized ileus probably 2° to mesenteric hypoperfusion due to multiple underlying medical illnesses, to r/o mechanical obstruction • PFA: progression of gaseous distention of the small and large bowels • whole abdominal USG: normal liver, spleen, kidneys; the rest could not be evaluated due to overlying loops of bowel

  14. 13th HD... • Tx: conservative GI decompression with NGT and rectal tube insertion • slow fleet enema → (+) BM • Metoclopromide RTC; plan to give Tegaserod but not available • serum K monitoring: no hypokalemia • other plans: imaging (ie, CT scan); endoscopic/surgical decompression

  15. 14th HD: abdomen clinically soft, absent bowel sounds, (+) tympany (Pt at this time was still anuric and acidotic; better BP control with vasopressors); (+) coffee-ground and bilious drainage per NGT • PFA: further progression of the gaseously distended small and large bowels; consider a distal colonic obstruction • concern: enlarged cecal diameter 10 cm • PPI dose increased; gastric lavage done • GIT decompression continued; Metoclopromide continued • repeat slow fleet enema → (+) BM • arrested during dialysis

  16. Final Diagnosis • Multiple organ failure 2° • Septic shock 2° hospital-acquired pneumonia • Pontine infarct 2° to complete basilar artery occlusion • Acute colonic pseudo-obstruction 2° to general medical condition • Hypertensive cardiovascular disease • t/c Chronic Kidney Disease 2° to HPN nephrosclerosis • Hypoalbuminemia 2° to poor intake • Decubitus ulcers, grade 2

  17. Discussion: Ileus and Intestinal Pseudo-obstruction

  18. Enteric Nervous System • a collection of neurons in the GIT that constitutes the “brain of the gut” • can function independently of the CNS • controls the motility, exocrine and endocrine secretions, microcirculation, immune and inflammatory processes • peristalsis - result of a series of local reflexes, each consisting of a contraction of intestinal muscle above an intraluminal stimulus and a relaxation of muscle below the stimulus • interstitial cells of Cajal - nonneural cells that serve as pacemakers responsible for the spontaneous, rhythmic, electrical excitatory activity of GI smooth muscle (slow waves) Goyal RK et al., NEJM, 1996, 335: 215

  19. Goyal RK et al., NEJM, 1996, 335: 215

  20. Adynamic Ileus • obstipation and intolerance of oral intake resulting from a non-mechanical insult that disrupts the normal coordinated propulsive motor activity of the GIT • abdominal distention, lack of bowel sounds, accumulation of gas and fluids in the bowel and decreased GI passage with delayed or absent defecation Goyal RK et al., NEJM, 1996, 335: 215 Madl C and Druml W. BPRCG, 2003, 17 (3): 445

  21. Ileus vs. Pseudo-obstruction • Intestinal ileus - lack of motor activity in the intestine • activity can be inhibited by the selective suppression of excitatory motor reflexes through sympathetic nerves or by sustained intrinsic inhibitory neural overactivity • activation of non-neuronal inducible NOS ⇒↑ nitric oxide • cannot be produced by the generalized suppression of neural activity in the gut • All neural transmission inhibited→ (-) tonic, neurogenic inhibition →unmasks spontaneous, myogenic excitation → increased contractile activity →uncoordinated, non-propulsive activity ⇒ functional bowel obstruction (chronic) Goyal RK et al., NEJM, 1996, 335: 215

  22. Etiology • post-op ileus - inhibitory neural reflexes and inflammatory processes • opioids • catecholamines • intraperitoneal/retroperitoneal infection • edema/ascites 2° to massive fluid resuscitation • abdominal arterial or venous injury • diffuse inflammation of the intestinal wall (IBD, acute intestinal infections, pseudomembranous colitis) • mesenteric ischemia • intraabdominal/retroperitoneal hematomas • metabolic disturbances (ie, ↓K) • renal function - strong predictor of impairment of intestinal motility

  23. Etiology • Sepsis on GI motility in ICU patients • Exogenous LPS from gram-negative bacteria • nitric oxide and prostaglandins • cytokines (IL-6, TNF-α, IL-1β): alter the enteric neuromuscular transmission • increased intestinal permeability (increase in the large pores in the intestine despite an overall decreased functional absorptive area) Cullen JJ et al., Dig Dis Sci, 1997, 42: 731-7 Johnston JD et al, Crit Care Med, 1996, 24: 1144-9 Overhaus M et al, AJPGL, 2004, 287: G685-694

  24. Pathophysiology • Intestinal dilatation/inflammation ⇒ neutrophils release proteolytic enzymes and cytokines ⇒ release of NITRIC OXIDE ⇒ smooth muscle paralysis aggravating intestinal dilatation • NOS amount and activity correlates significantly with intestinal dilatation • animal studies: NOS inhibitors ⇒ improvement of intestinal dilatation, intestinal contractility and gut luminal pressure Madl C and Druml W. BPRCG, 2003, 17 (3): 445

  25. Acute colonic pseudo-obstruction: Ogilvie’s syndrome • intestinal ileus with massive colon dilatation (usually the cecum and right hemicolon) without mechanical obstruction that develops in hospitalized patients with serious underlying medical or surgical conditions • M > F; >60 y/o • >95% of patients: associated with a predisposing factor or clinical condition • 3 most common associations: trauma, infection, cardiac disease • 32%: (+) metabolic, cancer, respiratory failure, renal failure • >50%: (+) metabolic imbalance (esp. hypoK, hypoCa, hypoMg) and opiate administration • sole association in <5% of cases Saunders MD. BPRCG, 2007, 21(4): 671-87 Vanek VW et al., Dis Colon Rectum, 1986, 29:203 Jetmore AB et al. Dis Colon Rectum, 1992, 35: 1135

  26. Acute colonic pseudo-obstruction: Ogilvie’s syndrome • Clinical manifestations • abdominal distention → labored breathing • abdominal pain, nausea, vomiting • (+) tympany; (+) bowel sounds in >90% • (+) peritoneal signs: impending perforation • leukocytosis: underlying disease; impending perforation • PFA: dilated colon, often from the cecum to the splenic flexure (occasionally to the rectum) • normal haustral markings • CT scan or gentle water soluble enema: for confirming Dx and excluding mechanical obstruction and toxic megacolon Saunders MD. BPRCG, 2007, 21(4): 671-87 Vanek VW et al., Dis Colon Rectum, 1986, 29:203

  27. ACPO: alteration in the autonomic regulation of colonic motor function transient parasympathetic impairment at the sacral plexus hyperactivity of inhibitory neurons to the large bowel colo-colonic reflex: Distention→Mechanoreceptors→reflex via efferent sympathetic nerves targeting the myenteric plexus or smooth muscle layers ➜ inhibition of colonic motility Motor input from the CNS Parasympathetic cholinergic excitatory Sympathetic adrenergic inhibitory ⇓ ⇓ Celiac and mesenteric ganglia Vagus Sacral ⇓ ⇓ Upper GIT Small bowel Right colon Distal colon Rectum Colon Goyal RK et al., NEJM, 1996, 335: 215 Saunders MD. BPRCG, 2007, 21(4): 671-87

  28. Differential Diagnosis of Acute Colonic Dilation • Mechanical obstruction • Clostridium difficile infection (Toxic megacolon) • Acute colonic pseudo-obstruction Saunders MD. BPRCG, 2007, 21(4): 671-87

  29. ACPO vs. mechanical obstruction • (+) crampy abdominal pain • “cut-off sign” (lack of gas in the distal colon or rectum) • small bowel air-fluid levels

  30. ACPO vs. Toxic Megacolon • very ill: (+) fever, tachycardia, abdominal tenderness • (+) history of bloody diarrhea • PFA: (+) “thumbprinting” due to the presence of submucosal edema, or thickening of the colonic wall • flexible sigmoidoscopy: (+) active colitis

  31. Martin B, AACN Adv Crit Care, 2007, 18(2):158-66 Mutlu GM et al, Chest 2001,119: 1222-41

  32. Pathophysiology of systemic consequences of ileus Madl C and Druml W. BPRCG, 2003, 17(3): 445-56

  33. Systemic Consequences Madl C and Druml W. BPRCG, 2003, 17(3): 445-56

  34. Factors influencing outcome in ACPO • Severity of underlying illness • Increasing age • Cecal diameter (>12 cm) • Duration of colonic distention (>6 days) • Presence of ischemia or perforation Saunders MD. BPRCG, 2007, 21(4): 671-87 Eisen GM et al, Gastrointest Endosc, 2002, 56:789

  35. Treatment Options • Supportive measures • Pharmacologic therapy • Colonoscopic decompression • Surgery

  36. Supportive therapy for ACPO • NPO, maintain on IV fluids • Correct fluid and electrolyte imbalances; treat underlying reversible causes; discontinue unnecessary medications • Nasogastric suction • Rectal tube decompression - (+) sigmoid colon and rectal involvement • Limit offending medications • Frequent position changes (ambulate if possible) • Serial PE and abdominal radiographs Saunders MD. BPRCG, 2007, 21(4): 671-87

  37. Supportive therapy for ACPO • successful as the primary treatment in the majority of patients • Sloyer et al on 25 cancer patients with ACPO: 96% improved by clinical and radiologic criteria • retrospective series of 151 patients with ACPO: 77% had spontaneous resolution • initial management of ACPO should be directed towards eliminating or reducing contributory factors Saunders MD. BPRCG, 2007, 21(4): 671-87 Sloyer AF et al. Dig Dis Sci, 1988, 33:1391-96 Loftus CG et al. Am J Gastroenterol 2002, 97:3118-22

  38. Pharmacologic agents for ACPO • Gentle enemas • Neostigmine - reversible acetylcholinesterase inhibitor • PEG electrolyte solution • Erythromycin - motilin receptor agonist • Metoclopramide - reverses the inhibitory effects of dopamine on GI motility (more for gastric emptying) • Cisapride, Tegaserod - 5-HT4 receptor agonist • Alvimopan - peripherally-restricted µ-opioid antagonist Saunders MD. BPRCG, 2007, 21(4): 671-87 Loftus CG et al. AJG, 2002, 97: 3118 Bonacini M et al. J Clin Gastroenterol, 1991, 13:475 Sgouros SN et al, Gut, 2006, 55: 638-42

  39. Pharmacologic agents for ACPO • Neostigmine - the only randomized, double-blind, placebo-controlled therapeutic trial for ACPO • Ponec et al.: (+) clinical response in 91% of patients • van der Spoel et al: 85% of critically ill ventilated patients passed stool • (+) several non-controlled, open label and retrospective series supporting the use of neostigmine for ACPO • Mehta et al.: response to neostigmine more likely in the post-op setting, and less likely in those with electrolyte imbalance or receiving anti-motility agents • Contraindications: mechanical obstruction, ischemia/perforation, severe bronchospasm, pregnancy, uncontrolled cardiac arrhythmias, renal failure Saunders MD. BPRCG, 2007, 21(4): 671-87 Ponec RJ et al. N Engl J Med 1999, 341: 137-41 van der Spoel JI et al. Intensive Care Med 2001; 27: 822-27 Mehta R et al. J Gastroenterol Hepatol 2006; 21: 459-61

  40. Pharmacologic agents for ACPO • PEG solution may decrease the recurrence rate of colonic dilation • Sgouros et al: RCT in 30 ACPO patients with cecal diameter > 10 cm • none in the PEG group had recurrence • significant increase in stool and flatus output, decrease in colonic distention or radiographic measurements, and improvement in abdominal girth Saunders MD. BPRCG, 2007, 21(4): 671-87 Sgouros SN et al. Gut 2006; 55: 638-42

  41. Pharmacologic agents for ACPO • Erythromycin - successful in a few case reports • Armstrong et al: decompression in 2 patients with ACPO treated for 10 days • Bonacini et al: 1 patient had resolution after 3 days of IV erythromycin therapy • Cisapride and Tegaserod: been employed with some success • withdrawn due to cardiovascular side effects Saunders MD. BPRCG, 2007, 21(4): 671-87 Armstrong DN et al. Lancet 1991; 337: 378 Bonacini M et al. J Clin Gastroenterol 1991; 13:475-6 MacColl C et al. Gasteroenterology 1990; 98:773-6 Camilleri M. Aliment Pharmacol Ther 2001; 15: 277-89

  42. Colonoscopic Decompression for ACPO • role remains controversial: success rates vary from 69-90% • rate of dilation is more important than the absolute diameter of the colon • Indications: initial invasive procedure of choice • failed supportive measures • colonic diameter progressed to 11-13 cm (>10 cm) • significant duration (>3-4 days) • evidence of clinical deterioration or no improvement after 24-48 hours • contraindications to or fail neostigmine • recurrence occurs in 40% Sloyer AF et al. Dig Dis Sci, 1988, 33: 1391 Rex DK. Gastroenterologist 1994, 2: 233 Geller A et al. Gastrointest Endosc, 1996, 44: 144-50

  43. Geller et al: clinical success is poor (25%) in procedures where a decompression tube was not placed - versus 88% perforation rate approximates 3% Sloyer AF et al. Dig Dis Sci, 1988, 33: 1391 Saunders MD. BPRCG 2007; 21(4):671-87 Geller A et al. Gastrointest Endosc, 1996, 44: 144-50

  44. Invasive strategies for ACPO • Indications • failed medical and endoscopic management • (+) peritonitis, perforation • Percutaneous endoscopic cecostomy • caution: local infection, bleeding • for high surgical risk patients • definitive treatment in a small case series (5 patients) Ramage JI Jr, et al. Gastrointest Endosc, 2003, 57:752

  45. Invasive strategies for ACPO: Surgery • associated with significant mortality and morbidity, likely related to the severity of patients’ underlying conditions • Vanek et al: large retrospective series • 179 patients: 6% morbidity rate, 30% mortality rate • Cecostomy: procedure of choice if without perforation or ischemia • Segmental or subtotal resection with either exteriorisation or primary anastomosis - if with perforation or ischemia Saunders MD. BPRCG 2007; 21(4):671-87 Vanek VW and Al-Salti M. Dis Colon Rectum 1986; 29: 203-10

  46. Saunders MD. BPRCG, 2007, 21(4): 671-87 Eisen GM et al, Gastrointest Endosc, 2002, 56:789 Surgery/Percutaneous cecostomy

  47. end

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