Autonomic dysfunction - gastroparesis

Description

Delayed gastric emptying in the absence of mechanical obstruction, with compatible symptoms
Cardinal symptoms: early satiety, postprandial fullness, nausea, vomiting (often of undigested food hours after eating), bloating, upper abdominal pain
- Pain is present in up to 90% but is rarely the dominant complaint - if it is, reconsider the diagnosis

Causes

	Share	Note
Idiopathic	~35-40%	Often young women, post-viral onset
Diabetic	~25-30%	Long-standing T1DM > T2DM, with other microvascular complications
Post-surgical	~10-15%	Vagal injury - fundoplication, oesophagectomy, bariatric surgery
Drug-induced		Opioids, GLP-1 receptor agonists, anticholinergics, TCAs, clonidine, CCBs
Other		Parkinson disease, scleroderma, amyloidosis, paraneoplastic, hypothyroidism, MS, mesenteric ischaemia

Gastroparesis and functional dyspepsia overlap heavily and shift between each other over time - the distinction is less clean than it looks

Prevalence ~10-50/100,000; F:M ~4:1
~5% of type 1 diabetes and ~1% of type 2 diabetes develop symptomatic gastroparesis
Delayed emptying on scintigraphy is far commoner than symptomatic disease and correlates poorly with symptoms
GLP-1 receptor agonist use has become a major and rising iatrogenic cause - and a preoperative aspiration concern

Normal gastric emptying requires
- Fundic accommodation (vagally mediated, nitrergic)
- Antral contractions driven by the pacemaker interstitial cells of Cajal in the greater curve
- Pyloric relaxation coordinated with antral contraction
Diabetic gastroparesis
- Vagal autonomic neuropathy -> impaired antral contraction and fundic accommodation
- Loss of interstitial cells of Cajal - the key histological finding, and correlates with severity
- Loss of nNOS-expressing neurons -> failure of pyloric relaxation -> functional outlet obstruction
- Acute hyperglycaemia itself delays emptying (a BSL >15 mmol/L slows the stomach and confounds any emptying study)
Vicious cycle in diabetes: erratic emptying -> mismatched insulin absorption and food delivery -> unpredictable glycaemia -> worse emptying

Three requirements

1. Compatible symptoms

2. Mechanical obstruction excluded - endoscopy first (also excludes ulcer, malignancy, bezoar)

3. Objectively delayed gastric emptying

Gastric emptying scintigraphy - the gold standard

The gold-standard investigation for confirming diabetic gastroparesis once mechanical obstruction has been excluded endoscopically
Standardised low-fat egg-white meal, imaged at 0, 1, 2 and 4 hours
- Imaging must continue to 4 hours - a 2-hour study misses ~30% of cases
- Delayed = >60% retention at 2 h, or >10% retention at 4 h
Preconditions that invalidate the test
- Blood glucose must be <15 mmol/L (ideally <10)
- Cease prokinetics and opioids for 48-72 h
- Also cease anticholinergics, GLP-1 agonists and cannabis

Alternatives

Wireless motility capsule or 13C-octanoate breath test where scintigraphy is unavailable
Contrast studies and gastric ultrasound are not diagnostic

Look for the cause and the consequences

HbA1c, TSH, UEC, FBE, coeliac serology, ANA/scleroderma serology
Full drug review - opioids and GLP-1 agonists are the two most commonly missed causes
Nutritional assessment, weight trajectory
Consider cannabinoid hyperemesis and rumination syndrome as mimics - both are frequently misdiagnosed as gastroparesis

A. Correct the reversible

Cease or reduce opioids, anticholinergics, GLP-1 receptor agonists where possible
Optimise glycaemic control - improves emptying and symptoms; consider insulin pump or CGM
Correct hypokalaemia, hypomagnesaemia, hypothyroidism

B. Dietary - the foundation

Small, frequent, low-fat, low-insoluble-fibre meals (4-6 per day)
Liquid and semi-solid calories empty normally even when solids do not - the key practical manoeuvre
Chew thoroughly; sit upright for 1-2 h after eating; avoid alcohol and carbonated drinks
Dietitian referral; high-fibre "healthy eating" advice makes this worse and risks bezoar formation

C. Prokinetics

Drug	Note
Metoclopramide	D2 antagonist + 5-HT4 agonist. Limit to the shortest course - tardive dyskinesia risk rises with duration; avoid beyond 12 weeks[[c2]] and in the elderly and in Parkinson disease
Domperidone	Peripheral D2 antagonist, does not cross the blood-brain barrier - preferred in Parkinson disease. *QT prolongation: baseline ECG, avoid with other QT-prolonging drugs and in significant cardiac disease*
Erythromycin	Motilin agonist; effective IV in the acute setting; tachyphylaxis within weeks limits oral use
Prucalopride	5-HT4 agonist; emerging evidence

D. Antiemetics

Ondansetron, prochlorperazine, cyclizine
- Prochlorperazine and metoclopramide worsen parkinsonism - use ondansetron or domperidone in PD
Avoid opioids for pain - they worsen the underlying problem. Consider TCA (nortriptyline), mirtazapine, or gabapentinoid
- Mirtazapine helps nausea, appetite and weight together

E. Refractory disease

Gastric peroral endoscopic myotomy (G-POEM) - increasingly first-line intervention for refractory disease
Pyloric botulinum toxin - negative in randomised trials, not recommended routinely
Gastric electrical stimulation - reduces vomiting in refractory diabetic gastroparesis
Enteral feeding: nasojejunal trial, then surgical jejunostomy if sustained
- Gastrostomy alone is inadequate; venting gastrostomy may help bloating
Parenteral nutrition only as a last resort

F. Acute decompensation

IV fluid and electrolyte correction, IV antiemetic, IV erythromycin, NG decompression
Treat concurrent DKA; gastroparesis and DKA each precipitate the other

Type 1 diabetes with retinopathy, nephropathy and peripheral neuropathy - gastroparesis rarely occurs in isolation
Other autonomic dysfunction - orthostatic hypotension, erectile dysfunction, gustatory sweating
Systemic sclerosis, amyloidosis, Parkinson disease, paraneoplastic (anti-Hu, small cell lung cancer)
Post-fundoplication and bariatric surgery
Opioid use, GLP-1 receptor agonist therapy, cannabis use
Eating disorders - bidirectional and often difficult to disentangle
Malnutrition, bezoar, Mallory-Weiss tear, dental erosion

Chronic and fluctuating; symptom severity correlates poorly with the degree of emptying delay
Idiopathic post-viral gastroparesis often improves over 1-2 years; diabetic gastroparesis usually does not
Diabetic gastroparesis predicts poor glycaemic control, more hospital admissions and increased mortality, largely reflecting the burden of associated microvascular disease
Complications: weight loss and malnutrition, electrolyte disturbance, recurrent admission, bezoar, aspiration, opioid dependence

Monitor

Weight, nutritional markers, HbA1c
ECG if on domperidone; duration of metoclopramide exposure
Anaesthetic risk: full stomach despite fasting - flag before any procedure, particularly in patients on GLP-1 agonists

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