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Retching
Retching
Retching
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Retching
SpecialtyGastroenterology

Retching (also known as dry heaving) is the reverse movement (retroperistalsis) of the stomach and esophagus without vomiting.[1] It can be caused by bad smells or choking, or by withdrawal from certain medications, or after vomiting has completed. Retching can also occur as a result of an emotional response or from stress, which produces the same physical reaction. The function is thought to be mixing gastric contents with intestinal refluxate in order to buffer the former and give it momentum in preparation of vomiting.[2] Treatments include medication and correction of the fluid and electrolyte balance.

Physiology

[edit]

The retching phase is characterized by a series of violent spasmodic abdomino-thoracic contractions with the glottis closed. During this time, the inspiratory (inhalatory) movements of the chest wall and diaphragm are opposed by the expiratory contractions of the abdominal musculature. At the same time, movements of the stomach and its contents take place. Whereas a patient will complain of disagreeable sensations during nausea, speech is not possible during retching. The characteristic movements furnish a ready diagnostic sign of the retching phase. Schindler (1937)[3] studied retching on two occasions during gastroscopy and noted that longitudinal folds appeared in the previously smooth antrum, thickened quickly, came together and completely closed the antrum.[4] Retching involves a deep inspiration against a closed glottis. This, along with contraction of the abdomen, leads to a pressure difference between the abdominal and thoracic cavities. As a result, the stomach and gastric contents are displaced upwards toward the thoracic cavity.[5]

Retching comprises a rhythmically alternating (about once per second) elevation and descension of the entire pharyngolaryngo-esophago-gastric apparatus in synchrony with the movement of the diaphragm. The function of retching may be to mix gastric contents with intestinal refluxate to buffer gastric contents before gastroesophageal reflux and to impart a momentum to the gastric contents before vomiting. Airway protection during retching is accomplished by glottal closure during retches and constriction of the upper esophageal sphincter between retches.[2]

Versus vomiting

[edit]

Vomiting (the expulsion of gastric contents) is usually preceded by retching, but retching and vomiting can occur separately[6] and involve different sets of muscles.[7] During a retch, thoracic pressure is decreased and abdominal pressure is increased, which may serve to position gastric contents and overcome esophageal resistance.[6] Conversely, a vomit occurs with increased thoracic and abdominal pressure. Retches and vomits are commonly lumped together in behavioral analyses and consequently the neural controls for these processes are not well delineated.[8]

Treatments

[edit]

The treatments for significant retching include correction of fluid and electrolyte balance, nutritional support and medications like phenothiazines (such as Compazine and Phenergan), 5-HT3 antagonist (such as Zofran), dopamine receptor antagonists (such as Reglan), antihistamines (Antivert, Dramamine, Benadryl) and anticholinergics (scopolamine). Alternative approaches are also available. The best-studied alternative therapy is perhaps the use of acupressure for pregnancy-related nausea and vomiting.[citation needed] Wristbands with acupressure buttons are commercially available. An implanted device with attached electrodes into the gastric wall can be an option for patients with refractory nausea and vomiting.[9]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Retching

View on Grokipedia
from Grokipedia
Retching is the involuntary, rhythmic contraction of the abdominal and respiratory muscles that attempts to expel the contents of the but does not result in . Also known as dry heaving or gagging, it represents a preliminary phase of the emetic response, often accompanied by and characterized by the absence of gastric content ejection. It is typically preceded by —an unpleasant, subjective awareness of impending —and may involve associated features such as , , , diaphoresis, or . The hallmark symptom is forceful, spasmodic abdominal and thoracic contractions producing a heaving sensation, often without emesis but occasionally with expulsion of or . Recent research has advanced understanding of the neural circuits regulating retching as part of the emesis cascade, with emerging treatments like gastric electrical stimulation showing promise for chronic cases.

Overview

Definition

Retching is defined as the involuntary, spasmodic contraction of the diaphragm and abdominal muscles that attempts to expel gastric contents from the , but results in no actual expulsion due to closure of the upper esophageal sphincter and during the process. This distinguishes retching from productive , as it involves coordinated respiratory and abdominal efforts without the propulsion of material beyond the . Retching often precedes as an initial phase in the emetic response. The term "retching" originates from the "hrǣcan," meaning to clear the or cough up , which evolved over time to describe futile efforts at without expulsion. Physiologically, retching serves to prepare the by mixing gastric contents with duodenal refluxate, thereby buffering acidity and imparting momentum to the material in anticipation of potential emesis. This mixing occurs even when retching happens independently of full .

Associated Symptoms

Retching episodes are characterized by intense , often described by patients as a profound and distressing urge to expel gastric contents. This is frequently accompanied by profuse salivation due to heightened parasympathetic activity, of the skin, diaphoresis or sweating, and a subjective sensation of tightening resulting from glottal closure during the spasmodic movements. Autonomic manifestations include tachycardia, elevated blood pressure, and anxiety-like sensations akin to dread or unease, though typically without progression to full-blown panic. These episodes typically consist of 1 to 22 retches (averaging 10), occurring at a rhythmic frequency of approximately 0.9 cycles per second, with clusters often lasting 10-30 seconds. Retching overlaps with early vomiting symptoms, particularly in the shared experience of and autonomic arousal.

Physiology

Muscular and Mechanical Mechanisms

Retching involves the coordinated of respiratory and abdominal musculature, beginning with the synchronous contraction of the diaphragm, , and muscles. This initial phase generates a forceful increase in intra-abdominal pressure while simultaneously engaging inspiratory efforts, positioning gastric contents for potential expulsion without actual release. Concurrently, the lower esophageal sphincter (LES) relaxes, facilitating retrograde movement of contents into the while the may partially open to allow duodenal . These muscular actions are initiated by neural signals from medullary centers, ensuring precise timing. The biomechanical hallmark of retching is the development of opposing gradients across the thoraco-abdominal compartments. Intra-abdominal surges dramatically, often reaching 50-100 mmHg due to the compressive force of the contracting diaphragm and abdominal muscles against the relaxed LES. In contrast, intrathoracic decreases to negative values, created by the inspiratory muscle contractions against a closed , which prevents aspiration of gastric material into the airways. This differential differs from the subsequent phase of , where thoracic becomes positive to drive expulsion; in retching, the closed and sustained negative thoracic maintain containment. The pharyngo-esophageal apparatus exhibits a characteristic rhythmic during retching, elevating orad during relaxation of the diaphragm and , followed by caudal descent as the diaphragm's dome and hiatal fibers contract. This alternating movement, driven by suprahyoid muscle contractions and upper esophageal sphincter (UES) closure between cycles, mixes gastric contents without propulsion beyond the . The hiatal fibers of the diaphragm contract around the LES during these cycles to limit , while the UES remains tonically closed, further safeguarding the airway. This rhythmic pattern repeats in bursts, typically lasting seconds per cycle, until transition to or cessation.

Neural Control

The neural control of retching is governed by a central pattern generator (CPG) situated in the Bötzinger complex within the medullary reticular formation of the brainstem, which orchestrates the synchronous, rhythmic contractions of the diaphragm and abdominal muscles during this pre-expulsive phase of emesis. This CPG integrates signals to produce the characteristic pattern of inspiratory efforts against a closed glottis, distinguishing retching from full vomiting. Coordination occurs primarily through interactions with the nucleus tractus solitarius (NTS) and the area postrema (AP), the latter serving as the chemoreceptor trigger zone due to its location on the floor of the fourth ventricle and lack of a blood-brain barrier, allowing detection of circulating emetogens. The NTS acts as a primary relay station, processing and relaying these signals to the CPG to initiate and modulate the retching sequence. Afferent pathways convey emetogenic stimuli to the NTS via the (cranial nerve X), which transmits signals from gastrointestinal mechanoreceptors and chemoreceptors detecting irritants in the gut, and the (cranial nerve IX), which relays from the and upper airways. Vestibular , critical for motion-induced retching, project to the NTS through secondary vestibular neurons, integrating balance-related signals that can trigger emetic responses during . These peripheral afferents onto second-order neurons in the NTS, where excitatory neurotransmitters like glutamate facilitate transmission to the CPG and AP. Efferent outputs from the CPG and dorsal motor nucleus of the vagus project motor commands to V (trigeminal, for jaw and pharyngeal muscle activation), VII (facial, for orofacial coordination), and X (vagus, for esophageal and gastric relaxation), as well as to spinal nerves innervating the intercostal, , and diaphragmatic muscles via phrenic and somatic motor pathways. This descending control ensures the precise timing of muscle groups, with reverse contractions of the diaphragm and generating intra-abdominal pressure without expulsion. Modulation of these pathways involves key receptors in the AP and NTS, including dopamine D2 receptors, which respond to stimuli and contribute to centrally mediated retching; serotonin 5-HT3 receptors, activated by serotonin release from enterochromaffin cells and vagal afferents; and acting on NK1 receptors, which amplify emetic signaling in the . These receptors enable fine-tuned responses to diverse triggers, with antagonists targeting them to suppress retching in clinical contexts.

Causes

Physiological Triggers

Retching, as a precursor to , can be elicited by various benign physiological stimuli that activate the emetic circuitry in the . Sensory inputs play a prominent role, where strong odors, visual cues such as the sight of , and gustatory irritants stimulate the and , integrating emotional and cognitive processing to signal the nucleus tractus solitarius (NTS) via pathways. Gustatory irritants, in particular, engage vagal afferents in the , prompting the release of serotonin (5-HT) and , which further amplify signals to the NTS and (CTZ) in the . The CTZ, lacking a robust blood-brain barrier, sensitively detects these irritants when they influence circulating emetogens, initiating retching through 5-HT3 and neurokinin-1 (NK1) receptor activation. Vestibular influences represent another key physiological trigger, primarily through arising from conflicting sensory inputs between the vestibular apparatus, , and . These discrepancies activate neurons in the vestibular nucleus and , which project to the NTS, coordinating the emetic and often culminating in retching before full emesis. This pathway is mediated by H1 and muscarinic M1 receptors, with the NTS serving as a central that relays signals to the dorsal motor nucleus of the vagus for coordinated abdominal and diaphragmatic contractions. Neural pathways for these triggers converge at the NTS, facilitating rapid processing without requiring pathological disruption. Hormonal factors, particularly elevated levels of cholecystokinin (CCK) following a meal, contribute to retching in scenarios of gastric overdistension by modulating gastrointestinal feedback. CCK, secreted from enteroendocrine cells in response to nutrient ingestion, stimulates vagal afferents to enhance signals while influencing gastric , potentially leading to discomfort and retching when the is excessively distended. Overdistension itself activates visceral mechanoreceptors in the gastric wall, transmitting signals via vagal and splanchnic afferents to the NTS, where integration with CCK-mediated inputs heightens the emetic response to prevent further intake. This mechanism underscores CCK's role in normal postprandial regulation, promoting adaptive retching to alleviate mechanical stress on the upper . Pregnancy can also trigger retching through hormonal changes, such as elevated human chorionic gonadotropin and levels, contributing to .

Pathological and Iatrogenic Causes

Pathological causes of retching often stem from disruptions in the that irritate vagal afferents, leading to exaggerated emetic reflexes. , typically viral in origin, commonly induces retching as part of acute and episodes due to mucosal inflammation and toxin release. , characterized by delayed gastric emptying from impaired motility, frequently results in persistent retching secondary to gastric distension and retained . Intestinal obstruction, such as gastric , causes unproductive retching by mechanical blockage that builds abdominal pressure without expulsion. Neurological conditions can trigger retching through involvement of central emetic pathways, including the nucleus tractus solitarius (NTS) and . Migraine attacks often feature retching alongside severe headache and nausea, attributed to activation of trigeminovascular pathways that converge with emetic centers. Vestibular neuritis, an inflammation of the usually from viral infection, provokes intense retching and vomiting during acute vertigo episodes due to mismatched sensory inputs to the . Central lesions affecting the NTS or , such as in certain tumors or strokes, can cause recurrent vomiting and retching by disrupting emetic control. involves recurrent episodes of intense retching and vomiting without clear structural cause, often triggered by stress or infections. Iatrogenic factors, particularly those from cancer therapies, elicit retching via serotonin (5-HT) release and direct toxicity to the gastrointestinal mucosa and . with highly emetogenic agents like can induce retching as part of acute and in up to 90% of patients through 5-HT release from enterochromaffin cells, stimulating 5-HT3 receptors on vagal afferents. can precipitate retching as part of its symptoms, including , , and autonomic hyperactivity. to the abdomen or can cause retching by damaging mucosal linings and releasing inflammatory mediators, with risks varying by site and comparable to moderate emetogenic for upper abdominal fields. Psychological contributors amplify retching through conditioned responses or stress-mediated autonomic activation, often without primary organic pathology. Anxiety disorders, including generalized anxiety and panic attacks, can manifest as psychogenic retching or gagging via heightened sympathetic arousal and cortical modulation of the emetic center. In eating disorders like , retching may occur during unsuccessful purging episodes, driven by behavioral reinforcement and electrolyte imbalances that sensitize emetic pathways. Organ dysfunction, such as (), (), or , can lead to retching through accumulation of toxins activating the CTZ. Intense pain, shock, and food allergies also commonly trigger retching via visceral afferents or allergic mediator release.

Relation to Vomiting

Key Differences

Retching and , though often conflated, exhibit distinct physiological profiles in their execution and outcomes. Retching represents a preparatory phase characterized by rhythmic contractions without the expulsion of gastric contents, whereas culminates in the forceful ejection of those contents through the oral cavity. A primary distinction lies in the absence of expulsion during retching, which is maintained by the sustained contraction of the upper esophageal (UES). In retching, the UES remains closed or constricts between retch cycles, preventing gastric contents from entering the despite retrograde esophageal movements that oscillate the material below the sphincter. In contrast, involves complete relaxation and maximal opening of the UES, driven by hyoid and pharyngeal muscle , allowing the propelled bolus to exit the body. This sphincter behavior ensures retching serves as a non-ejective priming action, while achieves material clearance. Pressure dynamics further differentiate the two processes. During retching, abdominal muscles contract to generate positive intra-abdominal , while the costal diaphragm's downward pull creates negative intrathoracic , resulting in opposing forces that mix and position gastric contents without net propulsion into the . , however, synchronizes these pressures: the crural diaphragm relaxes, enabling abdominal compression to transmit positive into the , facilitating coordinated expulsion alongside retrograde giant contractions in the . In terms of duration and outcome, retching manifests as cyclic, repetitive episodes that provide no relief, often prolonging discomfort as a buildup mechanism. follows as a singular, decisive event yielding post-expulsion resolution through content evacuation. Both processes originate from shared neural circuitry in the medullary emetic center, but diverge in motor output execution.

Role in the Emesis Cascade

Retching constitutes the second phase of the emesis cascade, following the initial phase of and preceding the expulsion phase of . This phase involves coordinated spasmodic contractions of the diaphragm and abdominal muscles against a closed , which generates intrathoracic and intra-abdominal pressure changes without expelling gastric contents from the mouth. In retching, the gastric contents are repeatedly propelled into the through retrograde , facilitating the mixing and homogenization of material with protective fluids such as and duodenal secretions to neutralize acidity and prepare a cohesive bolus. This preparatory function enhances the efficiency of potential expulsion while minimizing esophageal damage from corrosive . The transition from retching to full occurs when sustained activation of the nucleus tractus solitarius (NTS) in the surpasses a physiological threshold, integrating from vagal afferents and the . This escalation triggers coordinated responses, including pyloric sphincter closure to prevent duodenogastric reflux, relaxation of the lower esophageal sphincter, and further esophageal dilation to accommodate the bolus for expulsion. Unlike the mechanics of , which involve opening and forceful oral ejection, retching maintains a closed airway to build pressure without release. Retching can occur independently of , terminating without progression to expulsion in a substantial proportion of episodes, thereby acting as a protective mechanism to clear minor gastrointestinal irritants without full emetic commitment. This incomplete cascade allows for resolution of mild stimuli while conserving energy and avoiding unnecessary or loss associated with complete .

Treatments and Management

Pharmacological Interventions

Pharmacological interventions for retching focus on antiemetic agents that interrupt the emetic reflex at central and peripheral sites, particularly effective against triggers like chemotherapy, postoperative recovery, and gastrointestinal disorders. These medications, including serotonin receptor antagonists and dopamine blockers, target neurotransmitter pathways to suppress the involuntary contractions and neural signaling associated with retching without necessarily addressing underlying causes such as gastroparesis. Evidence from randomized controlled trials (RCTs) supports their use in reducing retching frequency and severity, often as part of multimodal prophylaxis. Serotonin 5-HT3 receptor antagonists, such as , are first-line agents for retching in (CINV), where they block s in the nucleus tractus solitarius (NTS) to inhibit emetic signal transmission from the gut. demonstrates high efficacy, with meta-analyses of RCTs showing complete response rates (no retching or , no rescue medication) of 60-75% in patients receiving moderately emetogenic when administered prophylactically. In postoperative settings, intravenous at 8 mg significantly reduces retching incidence compared to , with dose-response studies indicating a 20-30% improvement in preventing emesis over lower doses. Dopamine D2 receptor antagonists, exemplified by metoclopramide, serve as prokinetics and antiemetics for retching linked to delayed gastric emptying in conditions like , by antagonizing D2 receptors in the (CTZ) and enhancing gastrointestinal motility. Systematic reviews of clinical evidence indicate metoclopramide improves retching and symptoms in 50-70% of diabetic patients, with FDA approval for short-term use in gastroesophageal reflux-related emesis based on RCTs demonstrating symptom relief. Typical dosing involves 10 mg orally or intravenously before meals, though long-term use requires monitoring for extrapyramidal side effects. Neurokinin-1 (NK1) receptor antagonists, such as , target delayed-phase retching in CINV by competitively binding NK1 receptors in the NTS and blocking substance P-mediated emetic signaling. Phase III RCTs establish 's superiority over standard therapy alone, increasing the proportion of patients free from retching or by 18% during the 25-120 hour post-chemotherapy period, particularly when combined with 5-HT3 antagonists. Oral is dosed at 125 mg on day 1 followed by 80 mg on days 2-3 for prophylaxis. Antihistamines like address retching from vestibular triggers, such as or vertigo, through H1 receptor antagonism that dampens central vestibular input to the vomiting center. Clinical guidelines and RCTs support 's efficacy in preventing and associated retching, with response rates exceeding 70% in prophylaxis when taken 25-50 mg orally one hour prior to exposure. It is particularly useful for acute episodic retching without systemic emetic involvement.

Non-Pharmacological Strategies

Non-pharmacological strategies for managing retching focus on supportive measures to alleviate symptoms, particularly in preventive or refractory cases associated with . Lifestyle and dietary modifications play a foundational role, including the consumption of small, frequent meals to minimize gastric distension and reduce the intensity of retching episodes. Avoiding environmental triggers such as strong odors or spicy foods can further prevent symptom onset by limiting sensory stimulation of the emetic reflex. Additionally, maintaining adequate hydration through small sips of clear fluids or ice chips helps counteract from excessive salivation during retching, promoting overall comfort without exacerbating discomfort. Behavioral techniques offer accessible interventions for symptom control, especially in psychogenic or anticipatory retching. at the P6 (Neiguan) point on the , often applied via bands, has demonstrated efficacy in reducing and associated retching, with meta-analyses indicating significant symptom relief in contexts like and postoperative recovery, comparable to some effects. For psychogenic retching linked to anxiety or phobia of vomiting (), (CBT) targets underlying thought patterns and avoidance behaviors, leading to sustained reductions in episode frequency through techniques such as exposure and relaxation training. These approaches empower individuals to manage triggers proactively, often yielding improvements in 60-80% of cases when tailored to psychological components. Procedural options provide targeted relief for persistent retching, particularly in chronic scenarios. Ginger supplementation at 1 g per day acts as a natural by modulating serotonin pathways, with meta-analyses confirming its ability to decrease the severity and incidence of nausea-induced retching, especially in or pregnancy-related cases when administered for at least three days. For refractory chronic retching unresponsive to conservative measures, implantable gastric electrical stimulators deliver low-frequency pulses to the wall, reducing frequency by up to 80% in patients with or , as evidenced by long-term clinical studies. These strategies can complement pharmacological interventions in multidisciplinary management plans.

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