Transcript 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
To enumerate the risk factors and pathophysiology in
the development of ileus/intestinal pseudoobstruction in critically ill patients
To discuss the management options for
ileus/intestinal pseudo-obstruction in the critically ill
The Case
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
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
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
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
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
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
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
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
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
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
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
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
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
Discussion: Ileus and
Intestinal Pseudoobstruction
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
Goyal RK et al., NEJM, 1996, 335: 215
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
Intestinal ileus - lack of motor activity in the
intestine
Ileus
vs.
activity
canPseudo-obstruction
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
Goyal RK et al., NEJM,
1996, 335: 215
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
Sepsis on GI motility in ICU patients
Etiology
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 largeCullen
pores
in the
JJ et al., Dig Dis Sci, 1997, 42: 731-7
Johnston JD et al, Crit Care Med, 1996, 24: 1144-9
intestine despite an overall
Overhaus M et al,decreased
AJPGL, 2004, 287: G685-694
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
Madl C and
Drumlluminal
W. BPRCG, 2003, 17 (3): 445
pressure
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
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
Motor input from the CNS
Parasympathetic
Sympathetic
cholinergic
excitatory
adrenergic
inhibitory
Vagus
Sacral


Upper GIT
Small bowel
Right colon
Distal colon
Rectum
Celiac and mesenteric
ganglia
Colon
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): 671-87
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
ACPO vs. mechanical obstruction
(+) crampy abdominal pain
“cut-off sign” (lack of gas in the distal colon or rectum)
small bowel air-fluid levels
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
Martin B, AACN Adv Crit Care, 2007, 18(2):158-66
Mutlu GM et al, Chest 2001,119: 1222-41
Pathophysiology of systemic
consequences of ileus
Madl C and Druml W. BPRCG, 2003, 17(3): 445-56
Systemic Consequences
Madl C and Druml W. BPRCG, 2003, 17(3): 445-56
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
Treatment Options
Supportive measures
Pharmacologic therapy
Colonoscopic decompression
Surgery
NPO, maintain
on IV fluids
Supportive
therapy
for ACPO
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)
Saunders MD. BPRCG, 2007, 21(4): 671-87
successful astherapy
the primaryfor
treatment
in
Supportive
ACPO
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
Saunders MD. BPRCG,
2007, 21(4): 671-87
Sloyer AF et al. Dig Dis Sci, 1988, 33:1391-96
contributory factors Loftus CG et al. Am J Gastroenterol 2002, 97:3118-22
Gentle enemas
Pharmacologic agents for ACPO
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
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
Alvimopan - peripherally-restricted µ-opioid
antagonist
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 antimotility 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
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
Saunders MD. girth
BPRCG, 2007, 21(4): 671-87
Sgouros SN et al. Gut 2006; 55: 638-42
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
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
withdrawn due to cardiovascular side effects
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
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
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
Ramage JI Jr, et al. Gastrointest Endosc, 2003, 57:752
patients)
Invasive
strategies
for
ACPO:
associated with significant mortality and
Surgery
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
Saunders
MD. BPRCG 2007; 21(4):671-87
exteriorisation or primary
anastomosis
- if with
Vanek VW and Al-Salti M. Dis Colon Rectum 1986; 29: 203-10
Saunders MD. BPRCG, 2007, 21(4): 671-87
Eisen GM et al, Gastrointest Endosc, 2002, 56:789
Surgery/Percutaneo
us cecostomy
end