Blood tests: CBC, glucose, potassium, creatinine, total protein, albumin, calcium, amylase, pregnancy
Radiological tests: plain abdominal series
Evaluate structural disease
Upper endoscopy and/or radiological tests (UGI series, small bowel follow-through)
Evaluate motility disorder
Solid-phase gastric emptying test (4 h) or pH/pressure capsule (SmartPill)
If gastroparesis diagnosed, obtain thyroid function, antinuclear antibody, HbA1C
Treatment
Prokinetic or antiemetic agent
Refractory symptoms
Electrogastrography
Antroduodenal manometry
CT enterography
CBC, complete blood count; CT, computed tomography; UGI, upper gastrointestinal.
Diabetic gastroparesis is due to a neuropathy and generally coincides with other complications of diabetes mellitus including retinopathy, nephropathy, and peripheral neuropathy. Orthostatic hypotension may be present as a manifestation of autonomic neuropathy. While generally a complication of type 1 diabetes, gastroparesis is also a complication of type 2 diabetes. Note that hyperglycemia itself decreases antral contractility, induces gastric dysrhythmias and delays gastric emptying; however, this is a reversible phenomenon and not necessarily indicative of neuropathy.
Idiopathic gastroparesis
Many patients (25–30%) with gastroparesis have no predisposing factor for their disease. In most series the majority of affected patients are young women. In a subset of these individuals, fever, myalgias, nausea, and diarrhea precede the onset of gastroparesis, which suggests an underlying viral cause.
Postoperative gastroparesis
A minority of patients (<5%) who have undergone surgery for peptic ulcer disease or malignancy experience nausea, vomiting, and early satiety secondary to postoperative stasis. Abnormalities in antral peristalsis and fundus tone have been demonstrated in this condition. Gastric stasis may also complicate gastroplasty or gastric bypass operations for morbid obesity, producing early satiety, anorexia, and weight reduction. Patients undergoing fundoplication for gastroesophageal reflux develop gastroparesis, possibly by intraoperative damage to the vagus nerve.
Table 20.2 Effects of medications on gastric emptying
| Delay gastric emptying Ethanol (high concentration) Aluminum hydroxide antacids Anticholinergics β-Adrenergic receptor agonists Calcitonin Calcium channel antagonists Dexfenfluramine Diphenhydramine Glucagon Interferon-α L-Dopa Octreotide Opiates Progesterone Proton pump inhibitors Sucralfate Tetrahydrocannabinol Tobacco/nicotine Tricyclic antidepressant Accelerate gastric emptying β-Adrenergic receptor antagonists Clonidine Domperidone Erythromycin/other macrolides Nizatidine Metoclopramide Naloxone Tegaserod |
Functional dyspepsia
Delayed gastric emptying is reported in 30–82% of cases of functional dyspepsia. Many affected patients also exhibit increased sensitivity to gastric balloon distension, suggesting that sensory nerve abnormalities may be involved in symptom induction.
Medication-induced delays in gastric emptying
Many prescription and over-the-counter medications delay gastric emptying (Table 20.2). Nonmedicinal compounds, including tobacco, marijuana, and intoxicating quantities of ethanol, also inhibit gastric motor function. Total parenteral nutrition has been associated with delayed gastric emptying, which may relate in part to the induction of hyperglycemia.
Disorders with diffuse gastrointestinal involvement
Rheumatological disorders
Scleroderma produces dysphagia, heartburn, nausea, vomiting, bloating, abdominal pain, and bowel disturbances as a result of diffuse dysmotility that involves the esophagus, stomach, small intestine, and colon. In most patients, gastroduodenal manometry demonstrates diffuse low-amplitude contractions that are consistent with myopathic involvement. However, a subset of patients with early disease exhibits high-amplitude, unco-ordinated contractile activity, which indicates neuropathic disease.
Chronic idiopathic intestinal pseudo-obstruction
Patients with this disorder may have associated gastric dysmotility with prominent nausea, vomiting, bloating, and early satiety. The presence of bladder dysfunction or orthostatic hypotension suggests diffuse neuromuscular disease. Pseudo-obstruction may be familial, it may occur after a viral prodrome, or it may be a paraneoplastic consequence of certain malignancies such as small cell lung carcinoma.
Nongastrointestinal disorders
Eating disorders
Delayed gastric emptying with reduced antral contractility is a common manifestation of anorexia nervosa. Causes of gastroparesis with anorexia nervosa include central nervous system inhibition and malnutrition, but no specific gastric pathology has been demonstrated. Some patients with bulimia nervosa exhibit delayed solid emptying. Rumination syndrome usually is not associated with delayed emptying, although small reductions in postprandial antral motor activity have been documented.
Cyclic vomiting syndrome
Cyclic vomiting syndrome is a disorder of unknown etiology that is characterized by intermittent symptomatic periods that begin abruptly and last for 3–5 days followed by prolonged asymptomatic intervals that last for months. Some patients with cyclic vomiting syndrome exhibit delayed gastric emptying, which suggests underlying gastric motor dysfunction although motility may also be normal. Metabolic derangements, mitochondrial disorders, atopy, and migraine headaches are associated with distinct subsets, suggesting a heterogeneous pathogenesis.
Neurological disorders
Altered gastric motility or emptying has been demonstrated after cerebrovascular accidents, with migraines, and after high cervical spinal injury. Gastric stasis may occur with disorders of autonomic function (e.g. Shy–Drager syndrome, Parkinson disease, Guillain–Barré syndrome, and multiple sclerosis).
Endocrinological and metabolic disorders
Nausea, vomiting, and anorexia are frequently reported by patients with end-stage renal disease, even after adequate dialysis, but only a minority of these patients exhibit abnormal gastric emptying. Hypothyroidism causes gastroparesis and hypothyroidism, hyperthyroidism and hypoparathyroidism are associated with intestinal pseudo-obstruction.
Diagnostic investigation
Laboratory studies
Laboratory studies may assist in determining the severity and chronicity of the patient’s disorder. Hypokalemia and contraction alkalosis result from severe vomiting, whereas anemia and hypoproteinemia are consistent with long-standing malnutrition. Specific serological tests may suggest rheumatological diseases such as systemic lupus erythematosus or scleroderma, whereas antineuronal antibody tests can screen for paraneoplastic dysmotility syndromes. Blood tests also can detect diabetes, uremia, or thyroid and parathyroid disease.
Radiographic and endoscopic studies
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