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Data from post-mortem and field studies were obtained that discussed poisoning in ostriches following ingestion of toxic plants. From the notes, all plants studied caused death in ostriches and there was systemic organ damage. Poisoning from Sarcostemma viminale (Melktou) resulted in beak patting, muscular tremors and head flopping, followed by collapse and violent kicking before death. Ingestion of Combretum oatesii (Red wings) seeds from plants in free grazing pastures resulted in vomiting, restlessness, eyelid flicking, collapse and kicking movements. Dichapetalum cymosum (Gifblaar) killed an ostrich after episodes of shaking legs, rapid respiration and bradycardia and hyperaemia of the lungs, liver and kidneys. Poisoning from Senecio sceleratus (Ragwort) caused skin haemorrhages and bleeding in tracheal mucous membranes, the pericardium, diaphragm and interperitoneal membrane. Consumption of drupes from Melia azedarach (Syringa berry) caused muscle tremors, kicking movements and respiratory distress. Lantana camara (Cherry pie) poisoning resulted in extremely inflamed eyes with copious yellow exudates extending down their beaks and onto their necks. Bentonite was administered by gavage at a dose of 5 g/kg. Poisoning in these cases is usually associated with the farmer allowing his/her birds to roam free-range in paddocks in which toxic plants are growing. Toxic plants should be removed from grass cut for hay.
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PMID:Poisoning in ostriches following ingestion of toxic plants--field observations. 1796 75

The clinical and ultrasonographic features of postoperative intestinal entrapment were assessed in five dogs. Four had vomiting and lethargy, and one had peracute collapse and hematochezia. Ultrasonographic findings in four of five dogs were similar, being characterized by focally hyperechoic mesentery and abdominal effusion, surrounding a single loop of amotile and dilated intestine. In some dogs, the affected intestinal loop had a thickened or corrugated wall, or alteration of wall layering. In one dog, the site of entrapment could be directly visualized. In the most severely affected dog, a large volume of echogenic peritoneal effusion was present, as well as fluid dilation of multiple intestinal loops. The ultrasonographic appearance of intestinal entrapment is similar to that of intestinal perforation or infarction by other causes.
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PMID:Ultrasonographic features of intestinal entrapment in dogs. 1940 Apr 70

Closed duodenal loops may be made in dogs by ligatures placed just below the pancreatic duct and just beyond the duodenojejunal junction, together with a posterior gastro-enterostomy. These closed duodenal loop dogs die with symptoms like those of patients suffering from volvulus or high intestinal obstruction. This duodenal loop may simulate closely a volvulus in which there has been no vascular disturbance. Dogs with closed duodenal loops which have been washed out carefully survive a little longer on the average than animals with unwashed loops. The duration of life in the first instance is one to three days, with an average of about forty-eight hours. The dogs usually lose considerable fluid by vomiting and diarrhea. A weak pulse, low blood pressure and temperature are usually conspicuous in the last stages. Autopsy shows more or less splanchnic congestion which may be most marked in the mucosa of the upper small intestine. The peritoneum is usually clear and the closed loop may be distended with thin fluid, or collapsed, and contain only a small amount of pasty brown material. The mucosa of the loop may show ulceration and even perforation, but in the majority of cases it is intact and exhibits only a moderate congestion. Simple intestinal obstruction added to a closed duodenal loop does not modify the result in any manner, but it may hasten the fatal outcome. The liver plays no essential role as a protective agent against this poison, for a dog with an Eck fistula may live three days with a closed loop. A normal dog reacts to intraportal injection and to intravenous injection of the toxic substance in an identical manner. Drainage of this loop under certain conditions may not interfere with the general health over a period of weeks or months. Excision of the part of the duodenum included in this loop causes no disturbance. The material from the closed duodenal loops contains no bile, pancreatic juice, gastric juice, or split products from the food. It can be formed in no other way than by the activity of the intestinal mucosa and the growth of the intestinal bacteria. This material after dilution, autolysis, sterilization, and filtration produces a characteristic effect when introduced intravenously. When in toxic doses it causes a profound drop in blood pressure, general collapse, drop in temperature, salivation, vomiting, and profuse diarrhea, which is often blood-stained. Splanchnic congestion is the conspicuous feature at autopsy and shows especially in the villi of the duodenal and jejunal mucosae. Adrenalin, during this period of low blood pressure and splanchnic congestion, will cause the usual reaction when given intravenously, but applied locally or given intravenously it causes no bleaching of the engorged intestinal mucosa. Secretin is not found in the duodenal loop fluid, and the loop material does not influence the pancreatic secretion. Intraportal injection of the toxic material gives a reaction similar to intravenous injection. Intraperitoneal and subcutaneous injections produce a relatively slow reaction which closely resembles the picture seen in the closed duodenal loop dog. In both cases there is a relatively slow absorption, but the splanchnic congestion and other findings, though less intense, are present in both groups. There seems, therefore, to be no escape from the conclusion that a poisonous substance is formed in this closed duodenal loop which is absorbed from it and causes intoxication and death. Injection of this toxic substance into a normal dog gives intoxication and a reaction more intense but similar to that developing in a closed-loop dog.
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PMID:INTESTINAL OBSTRUCTION : I. A STUDY OF A TOXIC SUBSTANCE PRODUCED IN CLOSED DUODENAL LOOPS. 1986 44

A definite intoxication develops as a result of a closed intestinal loop and toxic material accumulates in the closed loops. Much evidence has been submitted to show that this loop poison causes the intoxication observed after producing a closed intestinal loop. Sufficient evidence has been presented to prove that the essential poison is present in these closed intestinal loops, and usually in concentrated form. Chemical study of the contents of closed intestinal loops shows that a single substance or group of substances possesses toxic properties. This resists autolysis and pancreatic and ereptic digestion. It is thrown out of solution by five volumes of alcohol or by half saturation with ammonium sulphate. It is readily soluble in water and is not injured by boiling. It is not removed by dialysis. The method of isolation excludes practically all substances except primary proteoses. The characteristic resistance to digestive enzymes suggests a heteroproteose. Proteose intoxication in dogs gives a picture identical with that described after poisoning with intestinal loop fluid: early salivation and vomiting, followed by diarrhea and prostration, fall in temperature and blood pressure, and finally death in collapse. Autopsy shows essentially a splanchnic paralysis and remarkable engorgement of liver and spleen, but especially of the mucosa of the duodenum and small intestine. The blood shows great concentration due to loss of fluid and may remain incoagulable because of an excess production of antithrombin. Proteoses escaping from the blood are excreted in the urine. This toxic proteose concerned in intestinal obstruction has not yet been isolated in the urine, but may be excreted by the kidneys. This probably explains the clinical improvement and lessened intoxication noted after transfusion. Experimental evidence points to a primary proteose as the essential poison concerned in the intoxication of closed intestinal loops and intestinal obstruction.
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PMID:INTESTINAL OBSTRUCTION : V. PROTEOSE INTOXICATION. 1986 66

A patient who was given metoclopramide for vomiting and diarrhoea developed circulatory collapse with his blood pressure dropping to 50/20 mm Hg. A gastrinoma was diagnosed histologically. The extent of the tumour was defined by octreotide scanning and magnetic resonance imaging. Metoclopramide was again given for colicky abdominal pain and the patient developed circulatory collapse a second time. A laparotomy involving extensive resection of the tumour was performed. The MEN1 mutation was not detected in blood or tumour tissue. Follow-up octreotide scanning did not show any residual tumour. Possible causes for the circulatory collapse are discussed. Our case is probably the first patient with gastrinoma to develop circulatory collapse after being given metoclopramide.
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PMID:Circulatory collapse in a patient with gastrinoma after metoclopramide administration. 2012 83

By cooling fresh suprarenal gland tissue immediately on removal from the animal, and by defatting, and mincing the same at low temperatures, and drying at 37 degrees C. with the least loss of time, a preparation is obtained which in daily doses of 3 grm. per os, is effective in restoring a large measure of health to sufferers from Addison's disease.It is essential that a potent extract of suprarenal cortex be available for (a) restoring the patient sufficiently to enable whole gland treatment to be instituted and (b) to treat any return of abdominal symptoms or circulatory collapse induced by intercurrent illness or failure to retain the whole gland through vomiting.It is desirable to increase the intake of sodium chloride to 10 to 15 grm. daily.Neither saline alone, nor cortical extract alone produces the same effective result as whole suprarenal gland prepared as above administered per os.Commercial preparations of whole suprarenal can be entirely without effect.Subcutaneous injection of adrenalin in a phase of weakness may have disastrous results.Trials, using the whole gland preparation on normal subjects, further establish the observations of Rowntree, that the gastric musculature is stimulated by injection of whole suprarenal gland. In certain cases, considerable elevation of blood-pressure may also result.
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PMID:The Treatment of Addison's Disease by Whole Adrenal Gland: (Section of Therapeutics and Pharmacology). 1999 Mar 13

Venomous animals occur in numerous phyla and present a great diversity of taxa, toxins, targets, clinical effects and outcomes. Venomous snakes are the most medically significant group globally and may injure >1.25 million humans annually, with up to 100 000 deaths and many more cases with long-term disability. Scorpion sting is the next most important cause of envenoming, but significant morbidity and even deaths occur following envenoming with a wide range of other venomous animals, including spiders, ticks, jellyfish, marine snails, octopuses and fish. Clinical effects vary with species and venom type, including local effects (pain, swelling, sweating, blistering, bleeding, necrosis), general effects (headache, vomiting, abdominal pain, hypertension, hypotension, cardiac arrhythmias and arrest, convulsions, collapse, shock) and specific systemic effects (paralytic neurotoxicity, neuroexcitatory neurotoxicity, myotoxicity, interference with coagulation, haemorrhagic activity, renal toxicity, cardiac toxicity). First aid varies with organism and envenoming type, but few effective first aid methods are recommended, while many inappropriate or frankly dangerous methods are in widespread use. For snakebite, immobilisation of the bitten limb, then the whole patient is the universal method, although pressure immobilisation bandaging is recommended for bites by non-necrotic or haemorrhagic species. Hot water immersion is the most universal method for painful marine stings. Medical treatment includes both general and specific measures, with antivenom being the principal tool in the latter category. However, antivenom is available only for a limited range of species, not for all dangerous species, is in short supply in some areas of highest need, and in many cases, is supported by historical precedent rather than modern controlled trials.
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PMID:Venomous animals: clinical toxinology. 2035 86

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

For nearly five decades now, lithium has been used as a drug for treatment of bipolar affective disorder [1]. Adverse effects of lithium have been reported, but still lithium continues to be an effective prophylactic agent for bipolar disorder. Serious and fatal toxicity can occur with levels of lithium considered to be in the therapeutic range [2, 3, 4, 5, 6]. We are reporting a patient who was on lithium for bipolar disorder and was admitted with a history of sudden collapse following vomiting, and sinus bradycardia with ST-T changes. The patient expired with levels of lithium being within therapeutic range.
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PMID:Fatal lithium toxicity with therapeutic levels--a case report. 2154 37

The key points of acupoint selection and manipulations of Professor WU Bing-huang's experiences on emergency treatment with acupressure are introduced. It includes emergency treatment on coma (collapse, faint, faint at the sight of blood, faint during acupuncture, faint during moxibustion, shock, etc.), and pain, cough as well as asthma relieving with acupressure (include abdominal pain, vomiting, diarrhea, headache, toothache, dysmenorrhea, lumbago, neck stiffness after sleep, cough, asthma, etc.). At the same time, typical cases are given as examples.
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PMID:[Clinical experiences of professor WU Bing-Huang on emergency treatment with acupressure]. 2164 19


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