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Prolonged nausea and vomiting after high dose chemotherapy and autologous peripheral stem cell transplantation in the treatment of high risk breast carcinoma.

BACKGROUND: Nausea and vomiting immediately after chemotherapy is a well recognized complication of cancer drug treatment; it is usually short-lived and controllable by modem antiemetics. The authors report a high incidence of prolonged nausea and vomiting after high dose chemotherapy with autologous peripheral stem cell transplantation (PSCT) in the treatment of high risk breast carcinoma patients. METHODS: Patients with high risk breast carcinoma were conditioned with high dose carmustine, cisplatin, and cyclophosphamide followed by autologous PSCT. In Part I of the study, patients who received PSCT at UCLA Medical Center were identified if they were either readmitted with dehydration secondary to nausea and vomiting or referred to a gastroenterology specialist for the treatment of intractable nausea and vomiting. In Part II of the study, the authors examined a series of 38 women treated at UCLA Medical Center in 1993 for high risk breast carcinoma to determine the incidence of prolonged postchemotherapy nausea and vomiting (PPNV) after PSCT. These women were followed at 2-week intervals with a quality of life evaluation that included questions about nausea and vomiting. RESULTS: In Part I of the study, the authors identified 9 women with more than 1 month of significant nausea and vomiting after PSCT without evidence of obstruction or mucositis. Hospitalization was frequently required for hydration. Gastroparesis was found in all four patients who underwent gastric emptying studies. The nausea and vomiting responded to the promotility drug cisapride and high dose corticosteroids. In Part II of the study, the authors found that PPNV was frequent; 24% of patients had significant nausea and 18% had significant vomiting 6 weeks after PSCT, despite treatment with standard antiemetics. CONCLUSIONS: PPNV is a frequent complication of high dose chemotherapy with the aforementioned regimen. It may be due to gastroparesis and represents a form of gastrointestinal toxicity to chemotherapy not previously reported.

Adult↗

Acupuncture-point stimulation for chemotherapy-induced nausea or vomiting.

BACKGROUND: There have been recent advances in chemotherapy-induced nausea and vomiting using 5-HT(3) inhibitors and dexamethasone. However, many still experience these symptoms, and expert panels encourage additional methods to reduce these symptoms. OBJECTIVES: The objective was to assess the effectiveness of acupuncture-point stimulation on acute and delayed chemotherapy-induced nausea and vomiting in cancer patients. SEARCH STRATEGY: We searched MEDLINE, EMBASE, PsycLIT, MANTIS, Science Citation Index, CCTR (Cochrane Controlled Trials Registry), Cochrane Complementary Medicine Field Trials Register, Cochrane Pain, Palliative Care and Supportive Care Specialized Register, Cochrane Cancer Specialized Register, and conference abstracts. SELECTION CRITERIA: Randomized trials of acupuncture-point stimulation by any method (needles, electrical stimulation, magnets, or acupressure) and assessing chemotherapy-induced nausea or vomiting, or both. DATA COLLECTION AND ANALYSIS: Data were provided by investigators of the original trials and pooled using a fixed effect model. Relative risks were calculated on dichotomous data. Standardized mean differences were calculated for nausea severity. Weighted mean differences were calculated for number of emetic episodes. MAIN RESULTS: Eleven trials (N = 1247) were pooled. Overall, acupuncture-point stimulation of all methods combined reduced the incidence of acute vomiting (RR = 0.82; 95% confidence interval 0.69 to 0.99; P = 0.04), but not acute or delayed nausea severity compared to control. By modality, stimulation with needles reduced proportion of acute vomiting (RR = 0.74; 95% confidence interval 0.58 to 0.94; P = 0.01), but not acute nausea severity. Electroacupuncture reduced the proportion of acute vomiting (RR = 0.76; 95% confidence interval 0.60 to 0.97; P = 0.02), but manual acupuncture did not; delayed symptoms for acupuncture were not reported. Acupressure reduced mean acute nausea severity (SMD = -0.19; 95% confidence interval -0.37 to -0.01; P = 0.04) but not acute vomiting or delayed symptoms. Noninvasive electrostimulation showed no benefit for any outcome. All trials used concomitant pharmacologic antiemetics, and all, except electroacupuncture trials, used state-of-the-art antiemetics. AUTHORS' CONCLUSIONS: This review complements data on post-operative nausea and vomiting suggesting a biologic effect of acupuncture-point stimulation. Electroacupuncture has demonstrated benefit for chemotherapy-induced acute vomiting, but studies combining electroacupuncture with state-of-the-art antiemetics and in patients with refractory symptoms are needed to determine clinical relevance. Self-administered acupressure appears to have a protective effect for acute nausea and can readily be taught to patients though studies did not involve placebo control. Noninvasive electrostimulation appears unlikely to have a clinically relevant impact when patients are given state-of-the-art pharmacologic antiemetic therapy.

Acupuncture Points↗

Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents.

BACKGROUND: Vomiting caused by acute gastroenteritis is very common in children and adolescents. Treatment of vomiting in children can be problematic and the use of antiemetics remains a controversial issue. There have been concerns expressed about apparently unacceptable levels of side effects such as sedation and extrapyramidal reactions, which are associated with some of the earlier generation of antiemetics. OBJECTIVES: To assess the effectiveness of antiemetics on gastroenteritis induced vomiting in children and adolescents. SEARCH STRATEGY: We searched the Cochrane Central register of Controlled Trials (CENTRAL), which includes the Cochrane Upper Gastrointestinal and Pancreatic Diseases Group Trials Register (searched 28 July 2005), MEDLINE (1966 to July 2005) and EMBASE (1980 to July 2005). Published abstracts from conference proceedings from the United European Gastroenterology Week and Digestive Disease Week were handsearched. Members of the Cochrane UGPD Group were contacted for details of any ongoing or relevant unpublished clinical trials. The search was re-run on 12th July 2006 and one new trial was found. SELECTION CRITERIA: Randomised controlled trials comparing antiemetics and/or placebo in children and adolescents, under the age of 18, with vomiting due to gastroenteritis. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Study authors were contacted for additional information. Adverse effects data was collected from the studies. MAIN RESULTS: Three trials involving 396 participants were included. Although no data were available for the precise time to cessation of vomiting (the primary outcome specified in the protocol for this review), one trial reported that the proportion of patients without vomiting over a 24 hour period was higher in the ondansetron and metoclopramide groups than placebo. In the second trial, ondansetron ensured complete anti-emesis for 8/12 (67%) patients within the first 4 hours and in 7/12 (58%) patients in the first 24 hr period. A few secondary outcomes were reported in the included trials. The third trial reported that 14% of patients who received ondansetron vomited during oral rehydration (which was given over one hour period after randomization) compared to 35% of the placebo group. AUTHORS' CONCLUSIONS: The small number of included trials provided some, albeit weak and unreliable, evidence which appeared to favor the use of ondansetron and metoclopramide over placebo to reduce the number of episodes of vomiting due to gastroenteritis in children. The increased incidence of diarrhea noted with both ondansetron and metoclopramide was considered to be as a result of retention of fluids and toxins that would otherwise have been eliminated through the process of vomiting.

Acute Disease↗

Effect of cannabinoids on lithium-induced vomiting in the Suncus murinus (house musk shrew).

RATIONALE: Marijuana has been reported to interfere with nausea and vomiting in chemotherapy patients. The principal cannabinoids found in marijuana include the psychoactive compound Delta-9-tetrahydrocannabinol (THC) and the non-psychoactive compound cannabidiol (CBD). The experiments reported here evaluated the potential of THC and CBD to interfere with vomiting in the Suncus murinus (house musk shrew) produced by lithium chloride (LiCl), which is the most commonly employed unconditioned stimulus for taste avoidance. OBJECTIVES: To evaluate the potential of the principal components of marijuana, THC and CBD, to suppress Li-induced vomiting in the house musk shrew. METHODS: Shrews were injected with vehicle or one of two cannabinoids [Delta-9-THC (1-20 mg/kg), or CBD (2.5-40 mg/kg)] 10 min prior to an injection of LiCl (390 mg/kg of 0.15 M) and were then observed for 45 min. The frequency of vomiting episodes and the latency to the first episode were measured. The role of the CB1 receptor in these effects was also evaluated by pretreatment with SR-141716. RESULTS: Delta-9-THC produced a dose-dependent suppression of Li-induced vomiting, with higher doses producing greater suppression than lower doses. CBD produced a biphasic effect with lower doses producing suppression and higher doses producing enhancement of Li-induced vomiting. The suppression of Li-induced vomiting by THC, but not by CBD, was reversed by SR-141716. CONCLUSIONS: These results indicate that two major cannabinoid compounds found in marijuana, THC and CBD, are effective treatments for Li-induced vomiting; however, only THC acts by the CB1 receptor. The effects of THC and CBD on vomiting were dose dependent; with THC the effect was linear, but with CBD the effect was biphasic.

Animals↗

Vomiting after mild head injury is related to migraine.

OBJECTIVE: To determine whether vomiting after mild head injury in children is related to migraine and to identify predictors of vomiting after head injury. METHODS: A series of consecutive children admitted to the observation unit of an emergency department after mild head injury was identified by chart review. A telephone interview with the parents or child or both was then conducted by using a structured questionnaire. RESULTS: Of 47 eligible children with acute head injury, 44 (94%) were contacted. The mean age at head injury was 7.4 years. Twenty-nine children (66%) vomited after the head injury. The likelihood of vomiting was increased if the child had a history of recurrent headache (p = 0.05). If the headaches were migrainous, the likelihood of vomiting increased further (p <0.002). All 15 children with a history of motion sickness vomited after the head injury. Family history of migraine, particularly maternal (n = 21), also predicted recurrent vomiting (p <0.001). If more than one of these predictive variables was present, the likelihood of vomiting was 100%. CONCLUSIONS: History of motion sickness, migraine headaches, and family history of migraine are highly predictive of vomiting after a mild head injury.

Acute Disease↗

Post-operative nausea and vomiting following orbital hydroxyapatite implant surgery.

Fifty-five consecutive patients undergoing a short-stay ophthalmic operation (orbital hydroxyapatite implantation) were recruited over 1 year to assess the frequency and duration of post-operative nausea and vomiting over 7 days. The incidence of nausea and vomiting in hospital was recorded. Patients scored their nausea and vomiting four times daily at home. By the end of the first day after surgery, 31 (75%) patients had experienced mild to severe nausea. Eighteen (38%) patients became nauseated on five or more occasions. Nineteen (35%) patients had vomited by the end of the first day after surgery and, over 7 days, 24 (43%) patients had vomited on one or more occasion. Three patients reported that they had vomited during the journey home. Vomiting was not correlated with pain or a past history of post-operative nausea and vomiting. However, there was a statistically significant correlation between nausea and pain. The high incidence of nausea and vomiting observed in this study appears to provide additional evidence of an oculo-emetic reflex. The timing of discharge and appropriate patient education are discussed.

Adult↗

Droperidol and dimenhydrinate alone or in combination for the prevention of post-operative nausea and vomiting after nasal surgery in male patients.

Droperidol and dimenhydrinate are inexpensive antiemetic drugs. Droperidol, especially, has been studied extensively, but there are no studies on the combination of both drugs for prevention of post-operative nausea and vomiting. One hundred and forty male hospitalized patients undergoing nasal surgery were randomized to receive one of four anti-emetic regimes: placebo, dimenhydrinate (1 mg kg-1), droperidol (15 micrograms kg-1), or the combination of both drugs (droperidol 15 micrograms kg-1 + dimenhydrinate 1 mg kg-1) administered after induction of anaesthesia. Patients in the dimenhydrinate-group and the combination-group received a second dose of dimenhydrinate 6 h after the first administration to mitigate the short half-life of the drug. For general anaesthesia a standardized technique, including benzodiazepine premedication, propofol, desflurane in N2O/O2, vecuronium, and a continuous infusion of remifentanil, was used. Post-operative analgesia and anti-emetic rescue medication were standardized. Episodes of vomiting, retching, nausea, and the need for additional anti-emetics were recorded for 24 h. The main endpoint of this study was the number of patients who were completely free of post-operative nausea and vomiting (Fisher's Exact Test). Furthermore, the severity of post-operative nausea and vomiting was analysed using a standardized scoring algorithm. The incidence of patients completely free of post-operative nausea and vomiting was 62.9% in the placebo-group, 77.1% in the dimenhydrinate-group (P = 0.21), and 82.9% in the droperidol-group (P = 0.07). This increased to 94.3% in the combination-group (P = 0.0015). In all three treatment groups the severity of post-operative nausea and vomiting was reduced significantly compared with placebo treatment (P = 0.0003). The incidence of side effects was similar in the four groups. Dimenhydrinate was ineffective in reducing the incidence of post-operative nausea and vomiting and droperidol only reduced the severity of post-operative nausea and vomiting. However, the combination of both drugs significantly reduces the incidence of post-operative nausea and vomiting when compared with placebo treatment.

Adult↗

Prevention of vomiting after strabismus surgery in children: dexamethasone alone versus dexamethasone plus low-dose ondansetron.

BACKGROUND: Postoperative vomiting is a common complication after strabismus surgery. The combination of dexamethasone and ondansetron decreases vomiting after strabismus surgery, while dexamethasone alone decreases vomiting after tonsillectomy in children. We compared the effect of dexamethasone alone to ondansetron plus dexamethasone on postoperative vomiting among children undergoing strabismus surgery. METHODS: Healthy children, aged 2-14 years, who were undergoing strabismus surgery were entered into this randomized, blocked and stratified study. Patients were administered 0.5 mg.kg(-1) midazolam p.o., 20-30 min preoperatively when indicated. The patients had an intravenous induction with 2.5-3.5 mg.kg(-1) propofol or an inhalation induction of anaesthesia with halothane and N2O. All patients were given 20 microg.kg(-1) atropine i.v. Study drugs were administered in a double-blind fashion. Both groups received 150 microg.kg(-1) dexamethasone i.v. Group D patients received placebo and group OD received 50 microg.kg(-1) of ondansetron i.v. Anaesthesia was maintained with halothane and N2O. Postoperative fluid, vomiting and pain management were standardized. Patients were followed for 24 h. We studied 193 patients with 111 patients in the OD group. Demographic data were similar. RESULTS: The overall incidence of vomiting was 23%; in group D and 5%; in group OD (P < 0.001). Each episode of vomiting increased the in-hospital length of stay by 29 min (P < 0.001). CONCLUSIONS: There was a remarkably low incidence of postoperative vomiting of 5%; with the combination of dexamethasone plus a low-dose of ondansetron which more effectively decreased vomiting after strabismus surgery in children when compared with dexamethasone alone.

Adolescent↗

Bilious vomiting in the newborn: How often is it pathologic?

BACKGROUND/PURPOSE: Intestinal obstruction is one of the most common reasons for admission to a neonatal surgical unit and frequently is manifest by bilious vomiting. Not all cases of neonatal bilious vomiting are caused by intestinal obstruction. This study aimed to investigate the outcome of neonates with bilious vomiting. METHODS: A prospective audit was undertaken of all neonates with a history of bilious vomiting referred to a regional pediatric surgical unit during a 2-year period (1998 to 2000). Infants with bilious nasogastric aspirates but no vomiting were not included. Demographic details, symptomatology, investigations, and final diagnoses were recorded. Subsequent clinical progress was ascertained by out-patient review or telephone interview. RESULTS: Sixty-three consecutive neonates (35 boys, 28 girls) were identified with a median gestational age of 40 (range 31 to 42) weeks and median birth weight of 3.5 kg (range 1.67 to 4.64). Median age at presentation was 26 hours (range, 9 hr to 28 days). A surgical cause of bilious vomiting was identified in 24 (38%): Hirschsprung's disease (n = 9), small bowel atresia (n = 5), intestinal malrotation (n = 4), meconium ileus (n = 3), meconium plug (n = 1), colonic atresia (n = 1), and milk inspissation (n = 1). Nineteen of these had both abdominal signs and an abnormal plain abdominal radiograph, and 4 had an abnormal abdominal radiograph only. In one infant with intestinal malrotation, clinical examination and plain radiography were unremarkable. After definitive surgery, all 24 infants were well at a median age of 14 (7 to 28) months. No surgical cause for bilious vomiting was found in 39 (62%) neonates whose symptoms resolved with conservative management. CONCLUSIONS: These data emphasize the maxim that bilious vomiting in the newborn should be attributed to intestinal obstruction until proved otherwise. However, in this prospective audit, bilious vomiting was not caused by intestinal obstruction in 62% of cases, and most of these infants suffered no further sequelae.

Bile↗

Nausea and vomiting after gynaecological surgery: a meta-analysis of factors affecting their incidence.

A total of 1442 patients who had major gynaecological surgery were recruited into three multicentre studies using a standard general anaesthetic technique in order to assess the efficacy of various doses of orally administered ondansetron in the prevention of postoperative nausea and vomiting. A total of 1257 patients were included in this analysis: 420 received oral formulations of placebo and 212, 296 and 329 received ondansetron 1, 8 and 16 mg, respectively. The following factors were measured in these studies and were considered to have a possible influence on the proportion of patients experiencing postoperative nausea and vomiting: age of patient; volatile anaesthetic; intraoperative dose of fentanyl; postoperative dose of morphine; country; anaesthesia duration; neuromuscular blocker; neuromuscular block antagonist; premedicant; recovery time; type of surgery; antiemetic treatment; body weight. Using a process of elimination based on logistic regression techniques, the factors found to be the most important influences on the frequencies of nausea and vomiting were antiemetic treatment, type of surgery, neuromuscular blocker, country, volatile anaesthetic and age. A statistically significant interaction between type of surgery and age was observed. Adjusted probabilities of nausea and vomiting were obtained from the model, including all the above factors, together with the type of surgery by age interaction. Ondansetron 8 mg showed the smallest adjusted probability of nausea (0.54) and vomiting (0.34) and placebo the greatest (nausea 0.75, vomiting 0.61). A similar pattern of adjusted probabilities over neuromuscular blocking agents was seen for nausea and vomiting, with the greatest occurring in patients receiving pancuronium (nausea 0.74, vomiting 0.57) and the least in patients receiving alcuronium (nausea 0.59, vomiting 0.38).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Investigations using logistic regression models on the effect of the LMA on morphine induced vomiting after tonsillectomy.

The effect of intraoperative airway management on postoperative vomiting after tonsillectomy is unknown. Logistic regression was used in a retrospective study to investigate the effect of the laryngeal mask airway (LMA) on a morphine dose-vomiting response curve. Charts were reviewed in 351 children in whom the airway was managed with either a LMA (n=177) or a tracheal tube (n=174). A mean perioperative morphine dose of 0.10 mg.kg(-1) (SD 0.09) was used in 248 children and a further 103 children were given no opioid. One hundred and eighteen of these 248 children vomited (47.6%) compared to 14 of 103 children given no morphine (13.6%). The probability of vomiting was related to morphine dose using logistic regression with both a linear and an E(max) model. Both the calibration (Hosmer-Lemishow goodness of fit chi-squared test lambda(2), P=0.81) and discrimination (area under the receiver operating characteristic plot, AUC ROC=0.67) of the E(max) model were better than the linear model (lambda(2), P=0.49; AUC ROC=0.64). Pharmacodynamic parameter estimates for the Emax model were P(0) (the baseline probability of vomiting) 0.139, P(max) (the maximal probability of vomiting due to morphine) 0.96, ED(50) (morphine dose that induces an effect equivalent to 50% of the logit P(max)) 0.09 mg.kg-1. The probability of vomiting was 50% after morphine 0.125 mg.kg-1. The use of the LMA had no effect on this dose-response curve. A covariate analysis investigating propofol for induction or isoflurane for the intraoperative maintenance of anaesthesia, however, showed that both drugs shifted the curve to the right. The probability of vomiting was 50% after morphine 0.17 mg.kg(-1) and 0.21 mg.kg(-1) for the isoflurane and propofol use curves, respectively. The concomitant use of propofol and isoflurane, but not the use of the LMA, decreases the probability of vomiting due to morphine.

Adolescent↗

Significance of vomiting after head injury.

OBJECTIVES: To determine whether the presence and severity of post-traumatic vomiting can predict the risk of a skull vault fracture in adults and children. METHODS: Data were analysed relating to a consecutive series of 5416 patients including children who presented to an emergency service in the United Kingdom during a 1 year study period with a principal diagnosis of head injury. Characteristics studied were age, sex, speed of impact, level of consciousness on arrival, incidence of skull fracture, and the presence and severity of post-traumatic vomiting. RESULTS: The overall incidence of post-traumatic vomiting was 7% in adults and 12% in children. In patients with a skull fracture the incidence of post-traumatic vomiting was 28% in adults and 33% in children. Post-traumatic vomiting was associated with a fourfold increase in the relative risk for a skull fracture. Nausea alone did not increase the risk of a skull fracture and multiple episodes of vomiting were no more significant than a single episode. In patients who were fully alert at presentation, post-traumatic vomiting was associated with a twofold increase in relative risk for a skull fracture. CONCLUSION: These results support the incorporation of enquiry about vomiting into the guidelines for skull radiography. One episode of vomiting seems to be as significant as multiple episodes.

Adult↗

Mechanisms of abdominal muscle activation during vomiting.

The possible contribution of spinal reflexes to abdominal muscle activation during vomiting was assessed in decerebrate cats. The activity of these muscles is partly controlled by bulbospinal expiratory neurons in the caudal ventral respiratory group (VRG). In a previous study it was found that the abdominal muscles are still active during vomiting after midsagittal lesion of the axons of these neurons between C1 and the obex (A.D. Miller, L.K. Tan, and I. Suzuki. J. Neurophysiol. 57: 1854-1866, 1987). The present experiments indicate that this postlesion activity was due to spinal stretch reflexes because 1) such midsagittal lesions eliminate abdominal muscle nerve activity during fictive vomiting in paralyzed cats in which there are no abdominal stretch reflexes, 2) the abdominal muscles are activated during vomiting by spinal reflexes after upper thoracic cord transections, and 3) the normal 100-ms delay between diaphragmatic and abdominal activation during vomiting is reduced to approximately 20-25 ms after both types of lesions, which is consistent with postlesion abdominal reflex activation. Our results also suggest that, during normal vomiting, abdominal stretch and tension reflexes have only a minor role if any and abdominal muscle activation is probably mediated primarily or exclusively by expiratory neurons in the caudal ventral respiratory group. However, our finding that phrenic activity is reduced both during vomiting after thoracic transections and during fictive vomiting after paralysis is consistent with a contribution of reflex activity from abdominal and/or intercostal muscles to phrenic discharge during normal vomiting.

Abdominal Muscles↗

Control of abdominal and expiratory intercostal muscle activity during vomiting: role of ventral respiratory group expiratory neurons.

The role of ventral respiratory group (VRG) expiratory (E) neurons in the control of abdominal and internal intercostal (expiratory) muscle activity during vomiting was examined in decerebrate cats by recording from these neurons during fictive vomiting in paralyzed animals and comparing abdominal muscle activity during vomiting before and after sectioning the axons of these descending neurons. Fictive vomiting was defined by a series of bursts of coactivation of abdominal and phrenic nerves elicited by either subdiaphragmatic vagus nerve stimulation or emetic drugs. Such coordinated activity would be expected to produce vomiting if the animals were not paralyzed. Data were recorded from 27 VRG E neurons that were antidromically activated from the lower thoracic (T13) or lumbar spinal cord. During fictive vomiting, almost two-thirds of these neurons (17/27) were mainly active in between periods of abdominal and phrenic nerve coactivation, when the internal intercostal motoneurons are known to be active. This group of neurons was termed INT neurons. INT neurons were subdivided according to whether they were active between every burst of phrenic and abdominal nerve coactivation (INTa neurons, n = 10) or only between some bursts (INTb neurons, n = 7). Another one-third of the VRG E neurons had normal or increased levels of activity when the abdominal nerves were active during fictive vomiting (ABD neurons). The one remaining neuron was mainly silent throughout fictive vomiting. ABD neurons were indistinguishable from INT neurons on the basis of their location in the VRG, type of firing pattern (ramp versus step ramp), conduction velocity, or extent of projection in the lumbar cord. However, INTa neurons had a significantly higher discharge rate during respiration than either ABD or INTb neurons. Abdominal muscle EMG and nerve activity were recorded from six unparalyzed cats before and after cutting the axons of VRG E neurons as they cross the midline between C1 and the obex. The lesions abolished or almost eliminated expiratory modulation of abdominal muscle activity. In contrast, the abdominal muscles were always active during vomiting; however, the amplitude of postlesion abdominal activity varied from approximately 70-100% of prelesion values in three cats to 60-70% of normal in a fourth animal to only approximately 20% of prelesion values in two other cats.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdominal Muscles↗

Diaphragmatic and external intercostal muscle control during vomiting: behavior of inspiratory bulbospinal neurons.

1. The role of dorsal and ventral respiratory group (DRG and VRG) bulbospinal inspiratory (I) neurons in the control of diaphragmatic and external intercostal (inspiratory) muscle activity during vomiting was examined by recording from these neurons during fictive vomiting in decerebrate, paralyzed cats. Fictive vomiting was defined by a characteristic series of bursts of coactivation of phrenic and abdominal muscle nerves, elicited either by electrical stimulation of abdominal vagal afferents or by emetic drugs, which would be expected to produce vomiting if the animals were not paralyzed. 2. Data were recorded from 22 DRG and 29 VRG I neurons that were antidromically activated from the fourth cervical spinal segment (C4). Only 10% (5/51) of these neurons started to fire near the beginning of phrenic discharge during fictive vomiting and thus had the appropriate discharge pattern to contribute to the initial activation of the diaphragm and coactive external intercostal muscles during vomiting. The frequency of occurrence of these Active neurons was not significantly different in the DRG (3/22) and VRG (2/29) (chi 2 test). Most remaining neurons were either totally silent (n = 7) or had only sporadic, infrequent firing (n = 16) (Silent neurons, 23/51 = 45%), or else fired near the end of phrenic discharge during fictive vomiting (End neurons, 21/51 = 41%). Two neurons were categorized as having miscellaneous (Misc) behavior. 3. No differences were found among neurons having different response patterns during fictive vomiting in regard to the following: the manner in which fictive vomiting was elicited: cell location: conduction velocity; and neuronal firing onset, rate, and pattern during respiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Sumatriptan in the treatment of cyclic vomiting.

OBJECTIVE: To describe a patient with cyclic vomiting who was treated successfully with sumatriptan, a serotonin, agonist. CASE SUMMARY: A patient with a 4-year history of cyclic vomiting was treated for an episode of nausea, vomiting, and abdominal pain. This patient had been hospitalized numerous times for cyclic vomiting over the previous 4 years, each hospitalization lasting from 3 to 11 days. Following a single subcutaneous injection of sumatriptan 6 mg, the patient ceased vomiting and was discharged 40 hours from the time of admission. DISCUSSION: The efficacy of sumatriptan in migraine headache appears to be mediated through its agonist activity at the serotonin1D receptor, resulting in constriction of dural blood vessels. According to published reports, therapeutic attempts at controlling cyclic vomiting often have included antimigraine therapies. Consistent with these reports, sumatriptan also appears effective in the treatment of cyclic vomiting. CONCLUSION: The pathogenesis of cyclic vomiting appears to share similarities with classic migraine, both of which may respond to sumatriptan therapy according to this report and previous work. Further study of the use of sumatriptan in the treatment of cyclic vomiting appears warranted.

Abdominal Pain↗

Anticipatory nausea in cyclical vomiting.

BACKGROUND: Cyclical Vomiting Syndrome (CVS) is characterised by discrete, unexplained episodes of intense nausea and vomiting, and mainly affects children and adolescents. Comprehending Cyclical Vomiting Syndrome requires awareness of the severity of nausea experienced by patients. As a subjective symptom, nausea is easily overlooked, yet is the most distressing symptom for patients and causes many behavioural changes during attacks. CASE PRESENTATION: This first-hand account of one patient's experience of Cyclical Vomiting Syndrome shows how severe nausea contributed to the development of anticipatory nausea and vomiting (ANV), a conditioned response frequently observed in chemotherapy patients. This conditioning apparently worsened the course of the patient's disease. Anticipatory nausea and vomiting has not previously been recognised in Cyclical Vomiting Syndrome, however predictors of its occurrence in oncology patients indicate that it could complicate many cases. CONCLUSION: We suggest a model whereby untreated severe and prolonged nausea provokes anxiety about further cyclical vomiting attacks. This anxiety facilitates conditioning, thus increasing the range of triggers in a self-perpetuating manner. Effective management of the nausea-anxiety feedback loop can reduce the likelihood of anticipatory nausea and vomiting developing in other patients.

Adult↗

Incidence, course, and severity of delayed nausea and vomiting following the administration of high-dose cisplatin.

Although many trials have evaluated the severity and treatment of nausea and vomiting immediately after cisplatin administration, no studies have focused on vomiting occurring more than 24 hours after chemotherapy--delayed emesis. Two consecutive trials were undertaken to evaluate the incidence, course (trial 1), and severity (trial 2) of delayed nausea and emesis and to develop methods to study these conditions. Eighty-six patients receiving cisplatin (120 mg/m2) for the first time were entered. On the day of cisplatin treatment, all received intravenous (IV) metoclopramide (3 mg/kg X 2 doses) plus dexamethasone (20 mg IV X 1 dose) with either diphenhydramine (50 mg IV) or lorazepam (1.0 to 1.5 mg/m2). Sixty-two percent of patients experienced no vomiting during the 24 hours immediately after administration of cisplatin. Overall, 93% of studied patients experienced some degree of delayed nausea or vomiting from 24 to 120 hours after cisplatin. In trial 1, the incidence of delayed vomiting ranged from 21% to 61% and delayed nausea from 24% to 78% in 58 patients. The highest incidence of both delayed nausea and emesis occurred during the period from 48 to 72 hours after administration of cisplatin. Patients who had no emesis during the initial 24 hours after cisplatin were less likely to experience delayed emesis. The severity of delayed nausea and vomiting was evaluated in 28 patients in trial 2. The amount of delayed nausea and vomiting was assessed daily by patients using a visual analogue scale and by an observer rating. The highest nausea and vomiting scores were seen during the period from 48 to 72 hours after administration of cisplatin, with acceptable correlation between patient scores and observer ratings. Although the nausea and vomiting occurring 24 or more hours after cisplatin administration is not as severe as that seen during the initial 24 hours after administration of cisplatin in patients not receiving antiemetics, it is a common condition that merits both further study and specific treatment.

Adult↗