GI MOTILITY

BY GERESU G.(MSC, ACA LECTURER)

MARCH, 2020
 • Outlines
• GI motility
• Impaired GI transit
• Vomiting
• Regurgitation
• Aspiration

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 • Objectives:
• To describe GI motility
• Describe common motility disorders
• Identify patients with GI dysmotilities
• Explain management protocol for aspiration

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 INTRODUCTION

• Gastrointestinal (GI) motility is an essential function of

digestive and absorptive processes of the gut.
• The term given to an involuntary stretching and
contractions of the muscles in the GI tract.
• Required for propelling intestinal contents, mixing them
with digestive juices, and preparing unabsorbed
particles for excretion.
• Two types of movements in the GIT for this purpose
• Mixing movement
• Propulsive movement

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 CONT,….

• Each part of the GI tract has a unique function to

perform in digestion, and each has a distinct type of
motility and sensation.
• Better to have knowledge on GIT neurophysiology
and motor regulation in order to understand the
pathophysiology of various GI diseases arising from
aberrations in motility and neurophysiology.

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 REGULATION OF GI MOTILITY

• Myogenic control
• Hormonal
• Neurogenic

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 MYOGENIC CONTROL
• Like striated muscles, contraction and relaxation in the gut
smooth muscles preceded by changes in resting membrane
potential.
• Electrical potential can be elicited in any region in the smooth
muscle b/c GI pace maker cells can fire spontaneously
• Most gut smooth muscles except esophagus and proximal
stomach have spontaneous rhythmical fluctuation in resting
membrane potential or slow waves, generally between -40 and
-65 mV.
• Slow wave activity (BER) originate from interstitial cells of cajal
• The increase or decrease in RMP determines contraction or
relaxation to occur.

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 NEURONAL CONTROL

• Controlled by both intrinsic and extrinsic nerves

• Myenteric plexus control of bowel motility by

integrating neural information from the ANS and
other plexuses within the enteric nervous system to
provide control of contractile activity in the gut.

• Extrinsic control in mainly via autonomic nervous

system

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 NEUROHUMORAL CONTROL

• Regulated by balances of the effects from excitatory

and inhibitory regulatory agents (chemicals).
• Inhibitory agents generally work by stimulating
increases in cAMP or cGMP, secondary messengers
that appear to counteract the effects of increased
cytosolic Ca2+.
• Most excitatory agents of intestinal motility work by
stimulating increases in cytosolic Ca2+

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 • Dysfunction in any of the above control mechanisms
can end up with certain motility dysfunction.
• GI motility disorders pose a heavy burden of illness,
decreased quality of life, and decreased work
productivity.

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 VOMITING VS. REGURGITATION

• Vomiting is forceful expulsion of the contents of the

upper GI tract out of the mouth.
• It is an active process in w/c abdominal muscles
contracted as opposed to re-gurgitation, which is a
passive reflux of stomach contents into the
oesophagus.
• Regurgitation is a passive process that may occur at
any time & often silent.
• Regurgitation occurs when LOS function ceased or
impaired.
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 CONT,….

• Factors affecting the extent of regurgitation

• Decreased or absent LOST
• Gastric volume
• Gastric emptying
• vomiting serves as a protective mechanism in which
ingested toxins are detected and expelled from the
body.

• Pathophysiology and managements of N/V- assignment 1.

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 FULL STOMACH AND ASPIRATION

• What is full stomach?

• Which patients are at risk of aspiration?

• Five minutes

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 • Full stomach
• A patient with suspected increase in GI volume
• Who has had a recent oral intake
• With impaired GI motility
• With a certain pathologies I,e. trauma, DM, hiatal hernia,
GOO, bowel obstruction,….

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 ASPIRATION

• First recognized as a cause of an anesthetic-related

death in 1848
• Inhalation of material into the airway below the level
of the true vocal cords
• Rare but potentially devastating complication of
general anesthesia (1: 6000).
• Asymptomatic in some instances and resulting in
severe pneumonitis and ARDS.

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 PATHOGENESIS

• LOS acts as a valve preventing the reflux of gastric

contents.
• Barrier pressure, a major mechanism preventing
reflux of gastric contents into esophagus.
• is the difference between LOS pressure (normally 20-
30mmhg) and intra-gastric pressure (normally 5-
10mmhg)
• Negative barrier pressure and raised gastric pressure
overcomes lower esophageal sphincter pressure and
aspiration likely to occur.
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 FACTORS AFFECTING LEST

• High volume
• Pregnancy
• Hiatal hernia
• Obesity
• DM
• Anesthetics
• Cricoid pressure
• Succinyl choline

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 DRUGS AFFECTING LOST

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 • Mechanisms of injury
• Aspiration pneumonia
• Aspiration pneumonitis

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 ASPIRATION PNEUMONIA

• Due to Inhalation of infected GI material into airways

or Secondary to bacterial infection following
chemical pneumonitis.
• Pulmonary inflammatory response to bacterial
products
• Tachypnea, tachycardia, cough, and fever are major
features.
• Confirmed by CXR.
• Lobar consolidation, cavitation and abscess

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 ASPIRATION PNEUMONITIS

• Also known as Mendelsohn's syndrome or acid

aspiration syndrome.
• Aspiration of acidic and usually sterile gastric
contents into the lungs.
• Due to the irritation of bronchioles by gastric acid,
producing bronchiolar spasm, a peribronchiolar
exudates, and congestion.
• Solid aspiration plugs in the airways and causes
obstruction w/c is fatal.

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 PREVENTIONS

• Pre-operative fasting guidelines

• Premedication with drugs which decrease risk of
aspiration
• Specialized induction techniques
• Gastric decompression by a wide bore orogastric
tube

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 1. PREOPERATIVE FASTING

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 2. ASPIRATION PROPHYLAXIS

• Goals
• To decrease acidity
• To decrease gastric volume
• Decrease gastric acidity
• prophylaxis to raise gastric PH>2.5
• Sodium citrate, H-2 antagonists and proton pump inhibitors
(PPIs)

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 • Sodium citrate
• a clear, soluble, non-particulate alkali to neutralize gastric
contents.
• Effective at raising gastric pH, but may cause an increase in
gastric volume.
• 30 ml, 0.3 M sodium citrate 10 minutes before surgery
• inadequate mixing with stomach contents may lead to
inadequate failure to neutralise
• s/e: short duration of action, N/V

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 • An oral H2 antagonist (ranitidine 150-300mg PO) must be
given night before and 1-2 hours before anesthesia

• Ranitidine superior to PPIs in both reducing gastric fluid

volume and acidity.

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 • Proton pump inhibitors
• Proton pump inhibitors can alter the volume and pH of
gastric contents.
• Suppress gastric acid secretion via inhibiting H-K-ATPase
• Omeprazole, fantoprazole
• omeprazole 40mg before the night and 2hr preoperatively

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 • Prokinetics
• stimulates gastric motility
• Metoclopramide has D2 receptor antagonist
• Antagonizes inhibitory effect of dopamine
• treats N/V
• Usual pre-medication for caesarean section under general
anesthetic.
• 10mg/PO 15min before surgery

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 RSI

• Administration of a sedative and a paralytic to

facilitate the rapid placement of an endotracheal
tube with cricoid pressure
• RSI can help to diminish risk of aspiration
• High risk of aspiration? Do a RSI, unless difficult
airway to warrant an awake fibreoptic intubation.
• Adequate depth of anesthesia is important to avoid
coughing, laryngospasm and vomiting.

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 CONT,….

• Techniques
• Preoxygenate
• Prepare the equipments
• Premedicate
• Put the patient down (sedate)
• Pressure (cricoid)
• Paralyse
• Place the tube

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 ASPIRATION MANAGEMENT

• Early recognition is crucial for timely intervention and

decrease mortality
• Recognition of aspiration visible gastric contents in
the oropharynx, or
• More subtle indications such as hypoxia, increased
inspiratory pressure, cyanosis, tachycardia or
abnormal auscultation

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MANY THANKS