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

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Presentation on theme: "Grand Rounds IVY DIMAYUGA-DE DIOS, M.D. Department of Medicine Makati Medical Center 2 August 2007 IVY DIMAYUGA-DE DIOS, M.D. Department of Medicine Makati."— Presentation transcript:

1 Grand Rounds IVY DIMAYUGA-DE DIOS, M.D. Department of Medicine Makati Medical Center 2 August 2007 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 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 H. T., 62/M, (+) HPN

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

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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: Johnston JD et al, Crit Care Med, 1996, 24: Overhaus M et al, AJPGL, 2004, 287: G

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): 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): Vanek VW et al., Dis Colon Rectum, 1986, 29:203

27 Motor input from the CNS Parasympathetic cholinergic excitatory Sympathetic adrenergic inhibitory VagusSacral Distal colon Rectum Upper GIT Small bowel Right colon    Colon Celiac and mesenteric ganglia 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 Goyal RK et al., NEJM, 1996, 335: 215 Saunders MD. BPRCG, 2007, 21(4):

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

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): Mutlu GM et al, Chest 2001,119:

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

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

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): 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):

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): Sloyer AF et al. Dig Dis Sci, 1988, 33: Loftus CG et al. Am J Gastroenterol 2002, 97:

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): 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:

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): Ponec RJ et al. N Engl J Med 1999, 341: van der Spoel JI et al. Intensive Care Med 2001; 27: Mehta R et al. J Gastroenterol Hepatol 2006; 21:

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41 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): Sgouros SN et al. Gut 2006; 55:

42 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): 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:

43 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 cm (>10 cm) significant duration (>3-4 days) evidence of clinical deterioration or no improvement after 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:

44 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): Geller A et al. Gastrointest Endosc, 1996, 44:

45 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

46 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): Vanek VW and Al-Salti M. Dis Colon Rectum 1986; 29:

47 Saunders MD. BPRCG, 2007, 21(4): Eisen GM et al, Gastrointest Endosc, 2002, 56:789 Surgery/Percutaneo us cecostomy

48 end


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