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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Water-electrolyte abnormalities while pregnancy or for infant are very serious. We present a case of a woman at 26 weeks who had gestation pernicious vomiting that led to major extracellular dehydration, water intoxication and acute renal insufficiency. The etiology was a volvulus on common mesentery. Hyperemesis disappeared thanks to surgical treatment. The mother and her fetus would later present serious complications due to the water-electrolyte imbalance correction. The fetus suffered from cerebral hemorrhage and subdural hematoma subordinate to brain edema resorption. The mother presented centropontine myelinolysis. The treatment of electrolyte abnormalities during pregnancy could lead to serious complications for the mother and fatal for the foetus.
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PMID:[Water-electrolyte abnormalities during pregnancy: maternal and fetal complications (about a case)]. 1882 18

Pancytopenia is a rare but serious adverse effect of low-dose methotrexate (MTX) sodium therapy, and this case report describes a very early-onset of pancytopenia and cutaneous lesions after three days of ingestion. A 64-year-old man was presented to Emergency Department with weakness, fever, poor appetite, nausea, and vomiting after he had had accidentally ingested MTX tablets (2.5 mg) twice a day for the last three days. On initial examination, several painful lesions in his oral mucosa and a cutaneous ulceration on his right foot were also observed. He had severe pancytopenia, poor kidney functions, and abnormal coagulation parameters. The blood level of MTX was found to be within therapeutic range. He was treated with leucovorine, intravenous antibiotics, and appropriate blood transfusions; he was discharged from hospital without any sequela. Pancytopenia associated with low-dose (cumulative dose of 15 mg in 3 days) MTX therapy had not been reported previously. The Naranjo probability scale showed pancytopenia and skin ulcer associated with low-dose MTX therapy as probable adverse reactions. Risk factors for pancytopenia such as renal insufficiency, hypoalbuminemia, low folate levels, concomitant infections, concomitant use of drugs, and folate supplementation were not identified in our patient. Although pancytopenia associated with low-dose MTX therapy is not expected as early as 3 days after initiation of the therapy, physicians should also be aware of this life threatening adverse effect during the very first days of MTX therapy for rheumatoid arthritis patients.
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PMID:Early-onset pancytopenia and skin ulcer following low-dose methotrexate therapy. 1882 35

Defined by the association of hemolysis, hepatic dysfunction and thrombocytopenia, the Hemolysis, Elevated Liver enzyme, Low Platelets (HELLP) syndrome can complicate preeclampsia and worsen maternal and fetal prognosis. It can be diagnosed in the immediate postpartum (30%) or in the absence of preeclampsia (10-20%). Clinical diagnosis can be difficult because there is no specific symptom. Abdominal pain or vomiting during the third trimester must lead to think about this diagnosis. Biological criteria are well defined: hemolysis by the presence of schistocytes, increased serum total bilirubin >12 mg/L or LDH >600 IU/L, hepatic dysfunction by increased transaminases and thrombocytopenia by a platelet count <100,000/microL. The evolution of those parameters is a major prognostic factor. With the HELLP syndrome, maternal morbidity is dramatically increased compared to isolated preeclampsia with complications such as eclampsia, placental abruptio, disseminated intravascular coagulation, pulmonary edema, acute renal insufficiency, subcapsular liver hematoma. The management of a HELLP syndrome requests level 3 hospital with intensive care units for neonate and mother. The treatment of this syndrome requires termination of the pregnancy as soon a possible, either by cesarean section or by vaginal delivery if cervical conditions are optimal (without any maternal or fetal complications). Before 32 weeks, a more expectative attitude could be acceptable with the prematurity permitting corticotherapy for fetal pulmonary maturation. This corticotherapy can improve temporary biological parameters but there are no proven benefits to consider improvement for long term maternal or fetal prognosis. During the postpartum, evolution is usually spontaneously favorable. Recurrences are not frequent.
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PMID:[Management of the HELLP syndrome]. 1900 44

Platinum-based chemotherapeutic doublets have produced significant survival benefits for patients with non-small cell lung cancer of all disease stages. The optimal combination of chemotherapy has been the subject of much investigation, and the ideal platinum agent the subject of ongoing and heated debate. For patients with resected disease, all evidence of survival advantage rests with cisplatin, and the only clinical trial to evaluate carboplatin-based therapy failed to show a survival benefit. In the setting of locally advanced lung cancer, no comparative data exist, and even randomized phase III trials are largely lacking. Cisplatin-based doublets provide the most consistent evidence of superior survival when coupled with definitive thoracic radiation. Meta-analyses of palliative chemotherapy indicate consistent survival advantages with cisplatin-based therapy over carboplatin; however, the relative advantage is small. Cisplatin carries a higher toxicity profile, including nausea, vomiting, neuropathy, renal insufficiency, and alopecia in comparison to carboplatin. When the goal of therapy is curative, the survival benefits with cisplatin are in most circumstances worth the increased toxicities. When the goal of therapy is palliation, the relative price of toxicity needs to be weighed on the basis of the individual patient in an effort to maximize quality of life.
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PMID:Cisplatin versus carboplatin in NSCLC: is there one "best" answer? 1922 91

Autosomal dominant polycystic kidney disease may present to the emergency department (ED) with vomiting, abdominal pain or hernias, renal insufficiency or failure, or bleeding from cerebral aneurysms. A 37-year-old man presented to the ED with signs and symptoms of incarcerated inguinal hernia. Laboratory studies showed renal failure with anion gap acidosis, and bedside ultrasound showed multicystic kidneys. Computed tomography confirmed the diagnosis. Emergency physicians should be aware of this common connective tissue defect and its serious associated conditions.
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PMID:Polycystic Kidney Disease with Renal failure Presenting as Incarcerated Inguinal Hernia in the ED. 1956 70

Amphotericin B (AmB) is a crucial agent in the management of serious systemic fungal infections. In spite of its proven track record, its well-known side effects and toxicity will sometimes require discontinuation of therapy despite a life-threatening systemic fungal infection. The mechanism of action of AmB is based on the binding of the AmB molecule to the fungal cell membrane ergosterol, producing an aggregate that creates a transmembrane channel, allowing the cytoplasmic contents to leak out, leading to cell death. Most of the efforts at improving AmB have been focused on the preparation of AmB with a lipid conjugate. AmB administration is limited by infusion-related toxicity, an effect postulated to result from proinflammatory cytokine production. The principal acute toxicity of AmB deoxycholate includes nausea, vomiting, rigors, fever, hypertension or hypotension, and hypoxia. Its principal chronic adverse effect is nephrotoxicity. AmB probably produces renal injury by a variety of mechanisms. Risk factors for AmB nephrotoxicity include male gender, higher average daily dose of AmB (> or = 35 mg/day), diuretic use, body weight > or = 90 kg, concomitant use of nephrotoxic drugs, and abnormal baseline renal function. Clinical manifestations of AmB nephrotoxicity include renal insufficiency, hypokalemia, hypomagnesemia, metabolic academia, and polyuria due to nephrogenic diabetes insipidus. Human studies show convincingly that sodium loading in excess of the usual dietary intake notably reduces the incidence and severity of AmB-induced nephrotoxicity.
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PMID:Amphotericin B: side effects and toxicity. 1983 85

1. Uranium and cantharidin, in the smallest doses capable of producing a distinct nephritis, tend to increase the elimination of nitrogen, probably by stimulating tissue katabolism. 2. Uranium, cantharidin, and potassium chromate, in larger doses, impair the power of the kidney to eliminate nitrogen; but this may not be evident unless the animal is on a high nitrogen diet, and the impairment, when due to potassium chromate, may not persist more than a day. 3. Small doses of uranium and of cantharidin cause a transient increase of chloride elimination which corresponds in a general way to the excess of diuresis. 4. Large doses of uranium and of chromate cause a fall, usually transient, in the chloride elimination. The chloride elimination may, however, be diminished forty per cent. for twenty-four hours without evidences of intoxication (vomiting). 5. The anatomic appearance of the kidney varies somewhat with the poison used and greatly with the period of survival after administration of the poison, but bears no definite relation to the nitrogen, chloride, or phenolsulphonephthalein elimination; marked anatomic alteration is compatible with normal elimination of all these substances and with freedom from symptoms of intoxication (vomiting). 6. The decrease in the elimination of phenolsulphonephthalein, which occurs in uranium, chromate, and cantharidin nephritides, and which, in a general way, is proportional to the dose of the poison, bears no constant relation to the changes in the nitrogen or chloride elimination. 7. A marked decrease in the elimination of the phenolsulphonephthalein occurs synchronously, as a rule, with the onset of the symptoms of intoxication (vomiting), and therefore the phenolsulphonephthalein test would seem to be a better indicator of the ability of the kidney to eliminate the toxic substance responsible for the symptoms of renal insufficiency than are either the anatomic changes or the elimination of total nitrogen or of chlorides.
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PMID:EXPERIMENTAL ACUTE NEPHRITIS: THE ELIMINATION OF NITROGEN AND CHLORIDES AS COMPARED WITH THAT OF PHENOLSULPHONEPHTHALEIN. 1986 82

A close cooperation between medical teams is necessary when calculating the fluid intake of parenterally fed patients. Fluids supplied parenterally, orally and enterally, other infusions, and additional fluid losses (e.g. diarrhea) must be considered. Targeted diagnostic monitoring (volume status) is required in patients with disturbed water or electrolyte balance. Fluid requirements of adults with normal hydration status is approximately 30-40 ml/kg body weight/d, but fluid needs usually increase during fever. Serum electrolyte concentrations should be determined prior to PN, and patients with normal fluid and electrolyte balance should receive intakes follwing standard recommendations with PN. Additional requirements should usually be administered via separate infusion pumps. Concentrated potassium (1 mval/ml) or 20% NaCl solutions should be infused via a central venous catheter. Electrolyte intake should be adjusted according to the results of regular laboratory analyses. Individual determination of electrolyte intake is required when electrolyte balance is initially altered (e.g. due to chronic diarrhea, recurring vomiting, renal insufficiency etc.). Vitamins and trace elements should be generally substituted in PN, unless there are contraindications. The supplementation of vitamins and trace elements is obligatory after a PN of >1 week. A standard dosage of vitamins and trace elements based on current dietary reference intakes for oral feeding is generally recommended unless certain clinical situations require other intakes.
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PMID:Water, electrolytes, vitamins and trace elements - Guidelines on Parenteral Nutrition, Chapter 7. 2004 67

Risk assessment of the amnesic shellfish poison, domoic acid, a potent neurotoxin, is evaluated based on its current knowledge and its harmful effects, and is presented under four headings, viz., (1) hazard identification, (2) dose response assessment, (3) exposure assessment and (4) risk characterization. Domoic acid binds the glutamate receptor site of the central nervous system (CNS) of humans and causes depolarization of neurons and an increase in cellularcalcium. In nature, domoic acid is produced by the algae, Pseudonitzschia spp. and they enter into the body of shellfish through their consumption. This toxin is reported to cause gastroenteritis, renal insufficiency confusion and memory loss in humans, since it affects the hippocampus of the brain. In rats, intraperitonial and oral administration of domoic acid result in scratching, tremor and convulsions, and in monkeys, the toxic symptoms like mastication, salivation, projectile vomiting, weakness, teeth grinding and lethargy are apparent. The no-observed-adverse-effect-level (NOAEL) in animals reveals that pure toxin is more effective than those isolated from shellfish. Based on LD50 values, it is found that intraperitonial administration of this toxin in animals is 31 fold more effective than oral administration. Low levels of domoic acid (0.20-0.75 ppm) show no toxic symptoms in non-human primates, but clinical effects are apparent in them and in humans, at a concentration of 1.0 ppm. The tolerable daily intake (TDI) of domoic acid for humans is calculated as 0.075 ppm, whereas for razor clams and crabs, the TDI are 19.4 and 31.5 ppm respectively. The hazard quotient (HQ) is found to be 2. Being an irreversible neurotoxin, domoic acid has severe public health implications. Death occurs in those above 68 years old. In order to ensure adequate protection to public health, the concentration of domoic acid in shellfish and shellfish parts at point of sale shall not exceed the current permissible limit of 20 microg g(-1) tissue. While processing shellfish, it maybe advisable to pay attention to factors such as environmental conditions, inter-organ variability in concentrations of domoic acid and cross contaminations.
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PMID:Risk assessment of the amnesic shellfish poison, domoic acid, on animals and humans. 2012 Apr 52

A 2-year-old male presented to hospital with a 5-day history of vomiting and pyrexia. He was initially treated with non-steroidal medication as an anti-pyretic. Initial investigations demonstrated a raised urea and creatinine and he was treated with intravenous fluids. Within 24 h he became anuric with progressive renal insufficiency. Ultrasound scan demonstrated minimal bilateral hydronephrosis with debris in the lower pole calyces. The bladder was empty. Cystoscopy and retrograde contrast imaging revealed bilateral ureteric obstruction. Double J stents were inserted and his renal function returned to normal within 4 days. We believe the aetiology to be renal papillary necrosis and bilateral ureteric obstruction secondary to the administration of ibuprofen in association with dehydration.
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PMID:Bilateral ureteric obstruction secondary to renal papillary necrosis. 2042 17


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