GASTROPARESIS 

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GASTROPARESIS 


Delayed gastric emptying in the absence of mechanical gastric outlet obstruction.


Epidemiology

  • 40–70% mechanically ventilated patients
  • Up to 60% septic shock patients
  • Common after major surgery
  • More common in:
    • Head injury
    • Stroke
    • Burns
    • Trauma
    • Pancreatitis
    • Multiple organ dysfunction

Delayed gastric emptying contributes significantly to

  • Underfeeding
  • Aspiration pneumonia
  • Ventilator-associated pneumonia (VAP)
  • Increased ICU stay

Pathophysiology

Cause

Mechanism / Effect on Gastric Emptying

Autonomic dysfunction

Critical illness causes ↓ vagal tone and ↑ sympathetic activity, leading to fundic dysfunction, weak antral contractions, and pyloric spasm, resulting in delayed gastric emptying.

Inflammatory cytokines

Sepsis-related TNF-α, IL-1, IL-6, and nitric oxide (NO) suppress gastric smooth muscle activity and impair enteric neurons, reducing gastric motility.

Nitric oxide excess

Excess NO causes gastric atony, abnormal pyloric relaxation, and loss of coordinated gastric contractions.

Enteric nervous system dysfunction

Inflammation damages the myenteric plexus and interstitial cells of Cajal, impairing gastric pacemaker activity and coordinated peristalsis.

Hormonal disturbances

Increased cholecystokinin (CCK), peptide YY (PYY), and GLP-1 inhibit gastric motility and slow gastric emptying.

Hyperglycemia

Blood glucose >180–200 mg/dL causes antral hypomotility, increased pyloric contraction, and reduced vagal function. This is one of the most important reversible causes; glycemic control often improves gastric emptying.

Electrolyte abnormalities

Hypokalemia: ↓ smooth muscle contraction.

Hypomagnesemia: ↓ neuromuscular transmission.

Hypophosphatemia: ↓ ATP production, impairing muscular function.

Drugs

Most common ICU-related cause.

• Opioids (most important): μ-receptor stimulation → ↓ acetylcholine release → ↓ antral contraction + ↑ pyloric tone (e.g., morphine, fentanyl, remifentanil, hydromorphone).

• Sedatives: Midazolam > Propofol (mild); Dexmedetomidine has relatively less effect.

• Vasopressors (high-dose noradrenaline, vasopressin): ↓ splanchnic perfusion → ↓ motility.

• Anticholinergics: Glycopyrrolate, atropine reduce gastric motility.

• Calcium channel blockers: May worsen gastric emptying.

• GLP-1 receptor agonists: Semaglutide, liraglutide, tirzepatide markedly delay gastric emptying, especially in awake patients.

• Dopamine agonists: May impair gastrointestinal motility.

Mechanical ventilation

High PEEP reduces venous return and splanchnic perfusion; associated sedation further contributes to delayed gastric emptying.

Increased intracranial pressure (ICP)

Seen in traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and stroke. Autonomic dysfunction results in gastric paralysis (neurogenic gastroparesis).

Clinical Features

Gastrointestinal

  • High GRV
  • Vomiting
  • Regurgitation
  • Nausea
  • Fullness
  • Bloating
  • Abdominal distension
  • Epigastric discomfort

Nutritional

  • Failure to reach calorie targets
  • Protein deficit
  • Weight loss
  • Muscle wasting

Pulmonary

  • Aspiration
  • Desaturation
  • VAP
  • Increased oxygen requirement

Consequences

  • Underfeeding
  • Protein-energy malnutrition

Diagnosis

1. Clinical Assessment

Evaluate

  • Vomiting
  • Distension
  • High GRVs
  • Feeding intolerance
  • Bowel sounds (poor predictor)
  • Bowel movements

2. Exclude Mechanical Obstruction

Consider

  • Gastric outlet obstruction
  • Small bowel obstruction
  • Volvulus
  • Ileus
  • Anastomotic complications

Investigations

  • CT abdomen
  • Contrast study
  • Upper GI endoscopy (if indicated)

3. Gastric Residual Volume (GRV)

Historically used but now de-emphasized in modern ICU nutrition guidelines.

Current guideline recommendations

  • Routine GRV monitoring is not recommended for all ICU patients because it does not reliably predict aspiration and may unnecessarily interrupt enteral nutrition.
  • If GRVs are measured, isolated elevated values should be interpreted in the context of vomiting, regurgitation, abdominal distension, and overall clinical status.

GRV

Interpretation

<250 mL

Usually acceptable

250–500 mL

Monitor closely; optimize feeding and consider prokinetics if persistent

>500 mL

Suggests significant gastric intolerance; evaluate causes and initiate management

Important: Do not stop feeds based solely on a single elevated GRV in an otherwise asymptomatic patient.


Management 

Step 1. Identify Reversible Causes

Correct:

  • Hyperglycemia (target generally 140–180 mg/dL in most ICU patients)
  • Hypokalemia
  • Hypomagnesemia
  • Hypophosphatemia
  • Dehydration
  • Acid-base disturbances
  • Sepsis
  • Hypoxia
  • Hypoperfusion

Review medications:

  • Reduce opioids if feasible (multimodal analgesia)
  • Minimize deep sedation
  • Stop anticholinergics if unnecessary

Step 2. Feeding Optimization

  • Elevate head of bed 30–45°
  • Continuous feeding rather than bolus feeding
  • Slow advancement of feed rate
  • Avoid overfeeding
  • Consider lower-fat formulas if appropriate
  • Flush feeding tubes regularly
  • Ensure correct tube position

3. Pharmacological Therapy

Metoclopramide + erythromycin is more effective than either agent alone in patients with persistent intolerance but should generally be limited to short courses because of tachyphylaxis and adverse effects.

Parameter

Metoclopramide

Domperidone

Erythromycin

Levosulpiride

Mechanism
  • Dopamine (D₂) receptor antagonist
  • 5-HT₄ agonist (weak)
  • Tachyphylaxis-3 days
  • 2nd line

Peripheral D₂ antagonist
  • Motilin receptor agonist
  • Tachyphylaxis-3 days
  • Ist line 
  • Peripheral D₂ receptor blockade
  • Enhances cholinergic activity(Improves gastric smooth muscle contraction.
  • Antiemetic

Dose

10 mg IV every 6–8 hours (reduce dose in renal impairment)


200–250 mg IV every 6–8 hours

25 mg three times daily

CNS Side Effects

Yes (crosses BBB) 

• Dystonia 

•Parkinsonism 

  • Tardive dyskinesia
  • Hyperprolactinemia

Minimal (does not cross BBB significantly)

None specific

Low but possible EPS

Serious Warning

⚠ Black box warning: Tardive dyskinesia 

➡ Use ≤12 weeks

QT prolongation, arrhythmia risk,Hyperprolactinemia

QT prolongation, drug interactions (CYP3A4)

Hyperprolactinemia, QT prolongation

Other Agents

Drug

Role

Prucalopride

5-HT₄ agonist; limited ICU evidence

Neostigmine

Reserved for acute colonic pseudo-obstruction, not isolated gastroparesis

Ghrelin agonists (e.g., relamorelin)

Investigational

Cisapride

Withdrawn in many countries because of arrhythmias

Bethanechol

Rarely used

Step 4. Post-Pyloric Feeding

Indications include:

  • Persistent intolerance despite prokinetics
  • Recurrent aspiration
  • Recurrent vomiting
  • GRV persistently >500 mL with inability to meet nutritional goals
  • Severe pancreatitis
  • High aspiration risk

Options:

  • Nasojejunal tube
  • Naso-duodenal tube
  • PEG-J (long-term)

Benefits:

  • Improves delivery of enteral nutrition
  • Reduces vomiting and regurgitation
  • May reduce aspiration in selected patients

Step 5. Parenteral Nutrition

Consider supplemental or total PN when:

  • Enteral nutrition remains insufficient despite optimization
  • Post-pyloric feeding is not feasible or unsuccessful
  • There are contraindications to enteral nutrition

Step 6. Gastric Decompression

Useful in patients with:

  • Marked gastric distension
  • Persistent vomiting
  • High aspiration risk
  • Gastric outlet obstruction while awaiting definitive therapy

Step 7. Surgery or Endoscopic Intervention

Rarely required in ICU unless there is:

  • Mechanical obstruction
  • Gastric volvulus
  • Ischemia
  • Perforation
  • Refractory chronic gastroparesis requiring specialized interventions (e.g., G-POEM or gastric electrical stimulation) after recovery from critical illness

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