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

North American rattlesnakes possess venom with primarily cytotoxic and hemotoxic properties. When persons are envenomated by these snakes, thrombocytopenia and coagulopathy commonly occur, yet patients rarely develop severe bleeding. This report describes a 44-year-old Native American man bitten on the index finger by an unknown species of rattlesnake. The man developed massive gastrointestinal hemorrhage that was ultimately treated with recombinant factor VIIa. He presented to an emergency department with a depressed level of consciousness, a blood pressure of 60/20 mm Hg, and heart rate of 148 beats per minute. He was diaphoretic and vomiting bright red blood. Initial laboratory results revealed thrombocytopenia and coagulopathy. Despite aggressive fluid resuscitation and administration of blood and antivenom in the emergency department, the patient continued to have profuse upper gastrointestinal bleeding, with hemoglobin as low as 1.8 g/dL. He received fluids, antivenom, and multiple blood products, with cessation of bleeding after administration of recombinant factor VIIa. Esophagogastroduodenoscopy revealed a single Mallory-Weiss tear as the source of hemorrhage. The patient stabilized after 6 hours of aggressive resuscitation but over the next several days developed several complications, including acute renal failure and gram-negative sepsis. The patient died on hospital day 5. In cases of life-threatening hemorrhage after rattlesnake envenomation in which traditional therapy with antivenom and aggressive supportive measures fail, recombinant factor VIIa should be considered as an additional therapeutic option to achieve hemostasis.
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PMID:Recombinant factor VIIa for treatment of gastrointestinal hemorrhage following rattlesnake envenomation. 1959 9

Background. A 61-year-old woman who had undergone an ileostomy closure 10 days previously presented to a tertiary medical center with abdominal pain, vomiting, diarrhea, dehydration, and oliguria. The patient had undergone a staged total proctocolectomy with ileal-pouch-anal anastomosis and a loop ileostomy 8 months previously to treat her steroid-refractory ulcerative colitis.Investigations. Physical examination, abdominal and pelvic CT scan, blood laboratory tests, pouch endoscopy, and fecal testing for Clostridium difficle toxins A and B.Diagnosis. Fulminant C. difficile-associated pouchitis and enteritis, which led to Psuedomonas aeruginosa septicemia, intravascular coagulopathy, acute renal failure, hemorrhagic ascites and respiratory failure and eventual death.Management. Intravenous hydration, aggressive therapy with oral and intravenous antibiotics, supportive care, hemodialysis, and intubation.
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PMID:Fulminant Clostridium difficile-associated pouchitis with a fatal outcome. 1965 2

A 24-year-old female at 34-week gestation, presented with malaise, nausea, vomiting, jaundice, and absent foetal movements. A clinical diagnosis of acute fatty liver of pregnancy was made. Although early caesarean section was performed, postoperative course was complicated by acute respiratory distress syndrome (ARDS) sepsis, and continuing coagulopathy. Supportive management in an intensive care unit resulted in successful outcome.
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PMID:Acute fatty liver of pregnancy: a case report of an uncommon disease. 1988 Nov 79

There is a lack of awareness of acutely presenting inborn errors of metabolism in adults, of which the X-linked urea cycle defect ornithine transcarbamylase (OTC) deficiency is an example, many comparatively mild mutations having been identified. In male hemizygotes clinical manifestations and age at presentation vary and depend on the mutation. In female heterozygotes the clinical spectrum depends on the extent to which the abnormal gene is expressed. Milder versions of the defect may not cause clear clinical symptoms and may remain unrecognized until the person is subjected to an unusually high nitrogen load when they develop severe hyperammonaemia. During acute episodes liver enzymes may be normal or only slightly elevated and occasionally accompanied by coagulopathy, but the key finding is hyperammonaemia. Boys with these milder forms may exhibit abnormal behaviour and be diagnosed with attention deficit hyperactivity disorder. This case illustrates how late presentation of OTC deficiency in a non-specialist centre can be difficult to differentiate from drug abuse, psychiatric illness or encephalopathy. Failure to measure blood ammonia in adults with unexplained key symptoms - particularly prolonged vomiting without diarrhoea and altered mental state/hallucinations, or to recognize the significance of elevated blood ammonia without evidence of liver decompensation can lead to delayed or missed diagnosis.
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PMID:Fatal ammonia toxicity in an adult due to an undiagnosed urea cycle defect: under-recognition of ornithine transcarbamylase deficiency. 2040 75

A 19-year-old female diagnosed with Graves' disease had treatment initiated with propylthiouracil (PTU). Pretreatment complete blood count and liver-associated enzymes (LAEs) were normal, but no further LAEs were obtained, reflecting U.S. guidelines written in 1995. Three months later, she presented with nausea, vomiting, abdominal pain, and jaundice. LAEs were markedly elevated with: total bilirubin, 6.5 mg/dl; aspartate aminotransferase (AST), 1747 IU/L; and alanine aminotransferase (ALT) 1589 UL/L. After 6 days at an outside hospital, she was transferred to our tertiary care center in acute liver failure with coagulopathy and stage II encephalopathy. Liver transplant evaluation was promptly initiated and she was listed as status 1. PTU was the only medication she had taken; and all serologic, autoimmune, and metabolic studies were negative. She demonstrated rapid clinical deterioration, and on hospital day 7 she underwent orthotopic liver transplant but succumbed to tonsillar herniation immediately after surgery. Pathology from her explanted liver revealed marked necrosis and collapse, consistent with her acute liver failure. PTU-associated hepatotoxicity and myelotoxicity have been well-recognized serious adverse effects for more than 50 years. However, as deaths related to hepatic injury from PTU are rare, American Thyroid Association guidelines do not call for routine monitoring of LAEs, although monitoring of white blood cell count levels is advised. Given the wide spectrum of PTU-related liver injury, ranging from asymptomatic elevations in ALT to fatal acute liver failure, we urge consideration of an LAE monitoring program to prevent irreversible liver damage and call for a reappraisal of monitoring guidelines in the United States.
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PMID:Gone (from the Physicians' desk reference) but not forgotten: propylthiouracil-associated hepatic failure: a call for liver test monitoring. 2057 20

Galactosemia is a treatable metabolic disorder caused by the deficiency of enzyme galactose-1-phosphate uridyl transferase (GALT) and inherited as an autosomal recessive trait. A case of neonate manifesting with recurrent Escherichia coli sepsis is presented here which turned out to be a classic galactosemia. No other common presenting features were observed in this infant except cataract on slit lamp examination. To the best of our knowledge, there is no case of galactosemia reported in literature which presented with recurrent neonatal sepsis without hepatomegaly, hyperbilirubinemia, bleeding disorder, vomiting, diarrhea, failure to thrive, hypoglycemia, coagulopathy, hemolysis or renal tubular acidosis.
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PMID:Galactosemia presenting as recurrent sepsis. 2132 Oct 7

A 7-week-old girl showed vomiting after feeding, facial pallor, loss of muscle tone and respiratory depression. An emergency doctor performed successful resuscitation and after arrival in hospital, cranial ultrasound showed left-sided subdural hemorrhage, cerebral edema with a shift of the midline, and a decrease in cerebral perfusion. Ophthalmologic examination showed retinal hemorrhage. In view of this, the doctors suspected shaken baby syndrome and approached the parents with their suspicions, but they denied any shaking or trauma. Despite surgery for the subdural hemorrhage the girl died a few hours later with a severe coagulopathy. Autopsy verified subdural hemorrhage, cerebral edema and retinal hemorrhage, but also revealed intact bridging veins and a lack of optic nerve sheath hemorrhage, therefore shaken baby syndrome could not be proven by autopsy. Histological examination showed severe neonatal giant cell hepatitis as the cause of the severe coagulopathy and the associated spontaneous subdural bleeding. Neonatal giant cell hepatitis may be responsible for unexpected deaths in infancy and, although rarely associated with subdural bleeding, must be considered as a potential differential diagnosis of shaken baby syndrome.
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PMID:Fatal spontaneous subdural bleeding due to neonatal giant cell hepatitis: a rare differential diagnosis of shaken baby syndrome. 2194 36

Clinical features can be used to identify which patients with minor brain injury need CT scanning. A systematic review and meta-analysis was undertaken to estimate the value of these characteristics for diagnosing intracranial injury (including the need for neurosurgery) in adults, children, and infants. Potentially relevant studies were identified through electronic searches of several key databases, including MEDLINE, from inception to March 2010. Cohort studies of patients with minor brain injury (Glasgow Coma Score [GCS], 13-15) were selected if they reported data on the diagnostic accuracy of individual clinical characteristics for intracranial or neurosurgical injury. Where applicable, meta-analysis was used to estimate pooled sensitivity, specificity and likelihood ratios. Data were extracted from 71 studies (with cohort sizes ranging from 39 to 31,694 patients). Depressed or basal skull fracture were the most useful clinical characteristics for the prediction of intracranial injury in both adults and children (positive likelihood ratio [PLR], >10). Other useful characteristics included focal neurological deficit, post-traumatic seizure (PLR >5), persistent vomiting, and coagulopathy (PLR 2 to 5). Characteristics that had limited diagnostic value included loss of consciousness and headache in adults and scalp hematoma and scalp laceration in children. Limited studies were undertaken in children and only a few studies reported data for neurosurgical injuries. In conclusion, this review identifies clinical characteristics that indicate increased risk of intracranial injury and the need for CT scanning. Other characteristics, such as headache in adults and scalp laceration of hematoma in children, do not reliably indicate increased risk.
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PMID:Diagnostic accuracy of clinical characteristics for identifying CT abnormality after minor brain injury: a systematic review and meta-analysis. 2180 74

Mycoplasma pneumoniae (Mp) is a unique pathogen that causes not only pulmonary but also extrapulmonary manifestations that must be rapidly diagnosed. A 12-year-old boy, with no relevant medical history, presented with fever, severe epigastric pain, and vomiting. Laboratory findings showed fulminant and cholestatic hepatitis, hemolytic anemia, thrombocytopenia, acute kidney injury, disseminated intravascular coagulopathy, acute myocardial infarction, and rhabdomyolysis. His clinical condition rapidly deteriorated during intubation and continuous renal replacement therapy. Despite intensive treatment, he did not recover. We report a case of fulminant and fatal multiple organ failure in a previously healthy boy with Mp infection, describing the possible pathomechanisms of multiple organ failure involved in the disease.
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PMID:Fulminant and Fatal Multiple Organ Failure in a 12-Year-Old Boy With Mycoplasma pneumoniae Infection. 2221 Nov 73

The development of intramural duodenal haematoma (IDH) after small bowel biopsy is an unusual lesion and has only been reported in 18 children. Coagulopathy, thrombocytopenia and some special features of duodenal anatomy, e.g. relatively fixed position in the retroperitoneum and numerous submucosal blood vessels, have been suggested as a cause for IDH. The typical clinical presentation of IDH is severe abdominal pain and vomiting due to duodenal obstruction. In addition, it is often associated with pancreatitis and cholestasis. Diagnosis is confirmed using imaging techniques such as ultrasound, magnetic resonance imaging or computed tomography and upper intestinal series. Once diagnosis is confirmed and intestinal perforation excluded, conservative treatment with nasogastric tube and parenteral nutrition is sufficient. We present a case of massive IDH following endoscopic grasp forceps biopsy in a 5-year-old girl without bleeding disorder or other risk for IDH, which caused duodenal obstruction and mild pancreatitis and resolved within 2 weeks of conservative management. Since duodenal biopsies have become the common way to evaluate children or adults for suspected enteropathy, the occurrence of this complication is likely to increase. In conclusion, the review of the literature points out the risk for IDH especially in children with a history of bone marrow transplantation or leukaemia.
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PMID:Intramural duodenal haematoma after endoscopic biopsy: case report and review of the literature. 2237 65


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